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White, Peter D., and Trudie Chalder. "Chronic fatigue syndrome: treatment without a cause." Lancet 379, no. 9824 (April 2012): 1372–73. http://dx.doi.org/10.1016/s0140-6736(12)60197-4.
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Blitshteyn, Svetlana, and Pradeep Chopra. "Chronic Fatigue Syndrome: From Chronic Fatigue to More Specific Syndromes." European Neurology 80, no. 1-2 (2018): 73–77. http://dx.doi.org/10.1159/000493531.
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In the last decade, a group of chronic disorders associated with fatigue (CDAF) emerged as the leading cause of chronic fatigue, chronic pain, and functional impairment, all of which have been often labeled in clinical practice as chronic fatigue syndrome (CFS) or fibromyalgia. While these chronic disorders arise from various pathophysiologic mechanisms, a shared autoimmune or immune-mediated etiology could shift the focus from symptomatic treatment of fatigue and pain to targeted immunomodulatory and biological therapy. A clinical paradigm shift is necessary to reevaluate CFS and fibromyalgia diagnoses and its relationship to the CDAF entities, which would ultimately lead to a change in diagnostic and therapeutic algorithm for patients with chronic fatigue and chronic pain. Rather than uniformly apply the diagnoses of CFS or fibromyalgia to any patient presenting with unexplained chronic fatigue or chronic pain, it may be more beneficial and therapeutically effective to stratify these patients into more specific diagnoses in the CDAF group.
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Eichner, Edward R. "Chronic Fatigue Syndrome: Searching for the Cause and Treatment." Physician and Sportsmedicine 17, no. 6 (June 1989): 142–52. http://dx.doi.org/10.1080/00913847.1989.11709812.
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Murray, John B. "Psychological Aspects of Chronic Fatigue Syndrome." Perceptual and Motor Skills 74, no. 3_suppl (June 1992): 1123–36. http://dx.doi.org/10.2466/pms.1992.74.3c.1123.
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Geraghty, Keith J., and Charlotte Blease. "Cognitive behavioural therapy in the treatment of chronic fatigue syndrome: A narrative review on efficacy and informed consent." Journal of Health Psychology 23, no. 1 (September 15, 2016): 127–38. http://dx.doi.org/10.1177/1359105316667798.
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Cognitive behavioural therapy is increasingly promoted as a treatment for chronic fatigue syndrome. There is limited research on informed consent using cognitive behavioural therapy in chronic fatigue syndrome. We undertook a narrative review to explore efficacy and to identify the salient information that should be disclosed to patients. We found a complex theoretical model underlying the rationale for psychotherapy in chronic fatigue syndrome. Cognitive behavioural therapy may bring about changes in self-reported fatigue for some patients in the short term, however there is a lack of evidence for long-term benefit or for improving physical function and cognitive behavioural therapy may cause distress if inappropriately prescribed. Therapist effects and placebo effects are important outcome factors.
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Gerwin, Robert D. "A Review of Myofascial Pain and Fibromyalgia – Factors that Promote Their Persistence." Acupuncture in Medicine 23, no. 3 (September 2005): 121–34. http://dx.doi.org/10.1136/aim.23.3.121.
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Chronic muscle pain (myalgia) is a common problem throughout the world. Seemingly simple, it is actually a difficult problem for the clinician interested in determining the aetiology of the pain, as well as in managing the pain. The two common muscle pain conditions are fibromyalgia and myofascial pain syndrome. Fibromyalgia is a chronic, widespread muscle tenderness syndrome, associated with central sensitisation. It is often accompanied by chronic sleep disturbance and fatigue, visceral pain syndromes like irritable bowel syndrome and interstitial cystitis. Myofascial pain syndrome is an overuse or muscle stress syndrome characterised by the presence of trigger points in muscle. The problem these syndromes pose lies not in making the diagnosis of muscle pain. Rather, it is the need to identify the underlying cause(s) of persistent or chronic muscle pain in order to develop a specific treatment plan. Chronic myalgia may not improve until the underlying precipitating or perpetuating factor(s) are themselves managed. Precipitating or perpetuating causes of chronic myalgia include structural or mechanical causes like scoliosis, localised joint hypomobility, or generalised or local joint laxity; and metabolic factors like depleted tissue iron stores, hypothyroidism or Vitamin D deficiency. Sometimes, correction of an underlying cause of myalgia is all that is needed to resolve the condition.
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HARTZ, A. J., S. BENTLER, R. NOYES, J. HOEHNS, C. LOGEMANN, S. SINIFT, Y. BUTANI, et al. "Randomized controlled trial of Siberian ginseng for chronic fatigue." Psychological Medicine 34, no. 1 (January 2004): 51–61. http://dx.doi.org/10.1017/s0033291703008791.
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Background. Chronic fatigue greatly affects quality of life and is a common reason for consulting a physician. Since conventional therapy is often of limited help, fatigued patients may use herbal treatments. This randomized controlled trial evaluated the effectiveness of Siberian ginseng.Method. Subjects were recruited from advertisements in Iowa (82%) and members of chronic fatigue syndrome support groups (18%). Potential subjects were required to have substantial fatigue [ges ]6 months with no identifiable cause. The mean change in a fatigue measure was compared for placebo and Siberian ginseng at 1 and 2 months. Comparisons were for all subjects and for subjects with characteristics previously identified in the literature as important for categorizing chronic fatigue.Results. Ninety-six subjects were randomized to treatment groups, and 76 provided information at 2 months of follow-up. Fatigue among subjects assigned to either placebo or Siberian ginseng was substantially reduced during the study, but differences between treatment groups were not statistically significant in the full sample. Fatigue severity and duration had a statistically significant interaction with response to Siberian ginseng at the P<0·05 level. Treatment was effective at 2 months for 45 subjects with less severe fatigue (P=0·04 unadjusted for multiple comparisons) and for 41 subjects with fatigue for [ges ]5 years (P=0·09 unadjusted for multiple comparisons).Conclusion. Overall efficacy was not demonstrated. However, the findings of possible efficacy for patients with moderate fatigue suggests that further research may be of value.
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Pinikahana, Jaya, Geoff Holloway, and Neville Millen. "The Limits of Medicine and the Social Consequences for Sufferers of Chronic Fatigue Syndrome." Australian Journal of Primary Health 8, no. 2 (2002): 70. http://dx.doi.org/10.1071/py02030.
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Chronic Fatigue Syndrome (CFS) appears to be made up of several clusters of illness categories acting alone or in tandem to cause the decline of health through; fatigue/exhaustion, sensitivity/allergies, pain, general muscle and joint pains, cognitive impairment and gastro-intestinal problems. This study investigated how patients interpret, evaluate and respond to the complex and varied symptoms of Chronic Fatigue Syndrome. Data were collected from persons with CFS using a survey (n=90) and an interview (n=45). The researchers investigated how chronic fatigue syndrome is diagnosed by medical practitioners, how the label of CFS is determined and the social consequences for the patient. The results confirm the limited ability of the biomedical paradigm to diagnose adequately and treat effectively 'socially constructed' and medically ambiguous illnesses like CFS. In the absence of a legitimated regime of medical treatment for CFS, a range of often expensive treatments are employed by CFS sufferers, from formal use of pharmaceutical drugs through to 'alternative' therapies, including herbal, vitamin, homeopathic, esoteric meditative techniques, spiritual healing and general counselling are taken in no particular order.
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Sîrbu, Oana, Victoriţa Șorodoc, Alexandra Stoica, Alexandr Ceasovchih, Mihai Constantin, Laura Huiban, Gabriela Dumitrescu, Luminiţa Vâţă, and Laurenţiu Șorodoc. "A Rare Cause of Chronic Hepatitis: Celiac Disease." Internal Medicine 15, no. 4 (August 1, 2018): 55–60. http://dx.doi.org/10.2478/inmed-2018-0030.
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AbstractIntroduction. Celiac disease is a chronic bowel disease with a prevalence of 1% in the general population. This condition, immune-mediated, may exhibit multiple extra-intestinal changes, including the liver.Case presentation. We present the case of a 43-year-old patient presenting in our clinic for fatigue, associated with cytolytic and cholestatic hepatic syndrome with an onset of 10 years. During this time, the patient performed multiple investigations with the exclusion of viral, autoimmune etiology, primitive biliary cirrhosis and Wilson's disease. An abdominal ultrasound recorded an elongated, with an infundibular septum gallbladder. Abdominal computer tomography did not detect any changes. The final diagnosis is chronic alithiasic cholecystitis receiving hepatoprotective treatment with symptom relief and improved hepatic disorders. Over the past 2 years, the patient was diagnosed with osteoporosis (T score = -2.7 followed by treatment with Calcium and Vitamin D and improvement in T score to -2.1), and an iron deficiency anemia corrected with oral iron treatment. Upon resuming the anamnesis, we notice the presence of an intermittent bloating associated with diarrhea. Positive anti-transglutaminase antibodies required upper endoscopy with biopsy witch confirmed celiac disease.Conclusion. Despite the rather low prevalence of celiac disease in the etiology of hepatocytolysis, it is important to investigate its presence in the context of hepatic changes with uncertain etiology. This case motivates us to be rigorous in looking for secondary causes of hepatic impairment even in patients with apparently benign changes.
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Missailidis, Daniel, Sarah J. Annesley, and Paul R. Fisher. "Pathological Mechanisms Underlying Myalgic Encephalomyelitis/Chronic Fatigue Syndrome." Diagnostics 9, no. 3 (July 20, 2019): 80. http://dx.doi.org/10.3390/diagnostics9030080.
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The underlying molecular basis of myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) is not well understood. Characterized by chronic, unexplained fatigue, a disabling payback following exertion (“post-exertional malaise”), and variably presenting multi-system symptoms, ME/CFS is a complex disease, which demands a concerted biomedical investigation from disparate fields of expertise. ME/CFS research and patient treatment have been challenged by the lack of diagnostic biomarkers and finding these is a prominent direction of current work. Despite these challenges, modern research demonstrates a tangible biomedical basis for the disorder across many body systems. This evidence is mostly comprised of disturbances to immunological and inflammatory pathways, autonomic and neurological dysfunction, abnormalities in muscle and mitochondrial function, shifts in metabolism, and gut physiology or gut microbiota disturbances. It is possible that these threads are together entangled as parts of an underlying molecular pathology reflecting a far-reaching homeostatic shift. Due to the variability of non-overlapping symptom presentation or precipitating events, such as infection or other bodily stresses, the initiation of body-wide pathological cascades with similar outcomes stemming from different causes may be implicated in the condition. Patient stratification to account for this heterogeneity is therefore one important consideration during exploration of potential diagnostic developments.
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Collins, Shannon, Audrey Anna Bolyard, Tracy M. Marrero, Lan Phan, and David C. Dale. "Barth Syndrome and Severe Chronic Neutropenia." Blood 116, no. 21 (November 19, 2010): 3787. http://dx.doi.org/10.1182/blood.v116.21.3787.3787.
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Abstract Abstract 3787 Barth syndrome is an X-linked recessive genetic condition characterized by neutropenia, cardiomyopathy, growth delay, muscle weakness, and 3-methylglutaconic aciduria (an increase in organic acid caused by abnormal mitochondria). Its clinical manifestations are variable and can include fatigue, hypotonia, and dilated cardiomyopathy. Symptoms usually appear at birth or within the first few months of life. Mutations in the tafazzin (TAZ) gene cause Barth syndrome. The Severe Chronic Neutropenia International Registry (SCNIR) is building a base of information about the natural history and response to granulocyte colony stimulating factor (G-CSF) treatment for patients with Barth syndrome and other causes of chronic neutropenia. Through the SCNIR, we follow the clinical course and treatment of seven male subjects (median age 17 years, range: 6–28 years) with Barth syndrome observed for up to 11 years (median 9, range 3–11). Six of these seven subjects were neutropenic prior to G-CSF treatment, the median absolute neutrophil count (ANC) was 0.293 × 109/L (range 0 – 1.260). The seventh subject was not consistently neutropenic, median ANC 2.107 × 109/L (range 0.779 – 3.520). Sixteen bone marrow evaluations were performed on four of the seven subjects. Four of 16 bone marrows were prior to G-CSF exposure (3 subjects). Two of three subjects manifest eosinophilia in the marrow but not in the blood. Marrow exams for two of the three subjects' evaluations were read as normocellular marrow, and one of the three was read as hypocellular with a decrease in cells of the myeloid series. Twelve of the 16 bone marrow evaluations were performed in two subjects who were receiving G-CSF. One of the four subjects had bone marrow evaluations both before and after G-CSF exposure. His pre G-CSF evaluations displayed hypocellular bone marrow, and his post G-CSF evaluations showed normocellular bone marrow and eosinophilia. None of the marrow evaluations before or on G-CSF suggested myelodysplasia or showed evidence of acute myeloid leukemia. The six neutropenic subjects have all received G-CSF for a median of 96 months (range 28 – 137) at a median dose of 1.57 mcg/kg/day (range 0.43 to 2.18). The total G-CSF exposure for all six subjects is 507 months. The median ANC of the six subjects prior to G-CSF treatment was 0.293 × 109/L (range 0–1.260). The median ANC on G-CSF was 2.056 × 109/L (range 1.640–3.403). Prior to receiving G-CSF, three of the seven subjects reported mouth ulcers. Two of seven subjects reported skin infections, including one subject who reported infections around the G-tube used to maintain his nutritional status. One of seven subjects reported an episode of bacteremia. Of the six subjects who received G-CSF, three reported a reduced number of mouth ulcers and two of six reported reduced skin infections (G-tube, port-a-cath). None of the subjects experienced unusual side effects or clinically significant complications associated with G-CSF therapy. These data indicate that patients with Barth syndrome and neutropenia have ulcers and patterns of infections similar to other patients with chronic neutropenia. They are responsive to G-CSF treatment and it appears to be safe and effective to reduce their predisposition to bacterial infections. Disclosures: Dale: Amgen: Consultancy, Research Funding.
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Baddam, Sujatha, and Jorge Diaz Castro. "Does Venetoclax Cause Vitiligo?" Blood 134, Supplement_1 (November 13, 2019): 5139. http://dx.doi.org/10.1182/blood-2019-130854.
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Introduction: Venetoclax is a highly selective, orally bioavailable BCL2 inhibitor which binds to the BH3 domain of BCL2, displacing proapoptotic proteins such as BIM and BAX that once released facilitate induction of apoptosis. Venetoclax is indicated for the treatment of patients with newly-diagnosed acute myeloid leukemia (AML) who are 75 years or older or have other medical conditions that prevent the use of standard chemotherapy. There are many side effects associated with use of venetoclax. Vitiligo has not been reported as a side effect of Venetoclax. We are presenting a case of vitiligo induced by Venetoclax in a patient with AML. Case description: 71-year-old Caucasian female with ECOG performance status of 2, presented to Hematology/oncology clinic for evaluation for persistent thrombocytopenia. Past medical history is significant for hypothyroidism, essential tremor and chronic fatigue and weakness. Review of systems revealed fatigue, generalized weakness, easy bruising, tremors and weight loss of 10 pounds in 6 months. She denied any fevers, chills, gross bleeding. or any other systemic symptoms. Family history is significant for sarcoma (father). Denied any smoking, alcohol or illicit drug use. Vitals were stable. Physical examination revealed bruising on both arms and legs. Initial laboratory data showed hemoglobin of 10.7, White blood cell count of 3000 with 43% lymphocytes, and platelet count of 15000. Flow cytometry showed 17% blasts and Bone marrow biopsy revealed AML, non-APL type with 30 % blast cells. Karyotype 46, XX. FISH did not reveal any of the common abnormalities observed in MDS. Molecular analysis showed no abnormalities in FLT-3, IDH1/IDH2, NPM1 or CEBPA. Given her performance status, she was not considered a candidate for intense chemotherapy. She was started on low dose cytarabine 20 mg/m2 SQ QD from days 1 to 10 every 28 days with venetoclax 100 mg PO q daily titrated up to 600mg per day. Venetoclax was discontinued on day 10 of treatment due to neutropenia, diarrhea and fatigue. Bone marrow biopsy after one cycle of treatment showed a complete response. Cytarabine was discontinued due to poor tolerability and venetoclax was restarted at 200mg per day. 6 weeks after restarting venetoclax, she developed a mildly painful erythematous macular rash, initially noted in her hands but then extending to neck and chest. The rash then became hypochromic. She was evaluated by dermatology and diagnosed with venetoclax induced Vitiligo. Venetoclax was discontinued secondary to recurrent diarrhea and pancytopenia and then restarted at 100mg per day after recovery from pancytopenia. There was complete resolution of the vitiligo during discontinuation of venetoclax, with recurrence shortly after reinitiating the medicine. She was treated with topical corticosteroids and kept on venetoclax. Discussion: Venetoclax is a selective small-molecule inhibitor of BCL-2, an antiapoptotic protein. It is indicated for the treatment of patients with chronic lymphocytic leukemia (CLL) or small lymphocytic lymphoma (SLL) and newly diagnosed AML in patients who are not candidates for intense chemotherapy. Adverse events associated with venetoclax include pancytopenia, electrolyte abnormalities, fatigue, edema, tumor lysis syndrome, increases serum AST, diarrhea, upper respiratory infections, fever and rash. To our knowledge, this is the first reported case of vitiligo induced by venetoclax. Skin reactions, including vitiligo should be considered as potential side effects of this medication. Figure Disclosures No relevant conflicts of interest to declare.
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Powell, Pauline, Richard H. T. Edwards, and Richard P. Bentall. "THE TREATMENT OF WHEELCHAIR-BOUND CHRONIC FATIGUE SYNDROME PATIENTS: TWO CASE STUDIES OF A PRAGMATIC REHABILITATION APPROACH." Behavioural and Cognitive Psychotherapy 27, no. 3 (July 1999): 249–60. http://dx.doi.org/10.1017/s1352465899273067.
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Chronic fatigue syndrome is a disabling condition characterized by persistent mental and physical fatigue. Its aetiology is controversial, and it has been attributed to both physical and psychological causes. Previous controlled trials with ambulatory patients have shown that a proportion of CFS patients respond to cognitive-behaviour therapy. In this paper, we report two case studies of patients who are wheelchair-bound, who have been treated by a pragmatic intervention designed to increase activity and challenge dysfunctional illness beliefs. The patients received 60 and 55 contacts with the therapist, some of which were face-to-face and some of which were by telephone. At the end of treatment, the patients experienced clinically significant reductions in fatigue, were not using wheelchairs, showed an increase in occupational and social functioning and were leading relatively independent existences.
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Taylor, Anna K., Maria Loades, Amberly LC Brigden, Simon M. Collin, and Esther Crawley. "‘It’s personal to me’: A qualitative study of depression in young people with CFS/ME." Clinical Child Psychology and Psychiatry 22, no. 2 (October 14, 2016): 326–40. http://dx.doi.org/10.1177/1359104516672507.
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Background: Paediatric chronic fatigue syndrome/myalgic encephalomyelitis (CFS/ME) has a prevalence of 0.4–2.4% and is defined as ‘generalised disabling fatigue persisting after routine tests and investigations have failed to identify an obvious underlying cause’. One-third of young people with CFS/ME have probable depression. Little is known about why depression develops, the relationship between depression and CFS/ME, or what treatment might be helpful. Methods: We conducted nine semi-structured interviews with young people with CFS/ME (aged 13–17 years, 8/9 female) and probable depression, covering perceived causes of depression, the relationship between CFS/ME and depression, and treatment strategies. Results: Most thought CFS/ME caused depression. Many discussed a cyclical relationship: low mood made CFS/ME worse. A sense of loss was common. CFS/ME restricted activities participants valued and changed systemic structures, causing depression. There was no single helpful treatment approach. Individualised approaches using combinations of cognitive behavioural therapy (CBT), medication, activity management and other strategies were described. Conclusion: This study suggests that depression may be secondary to CFS/ME in young people because of the impact of CFS/ME on quality of life. Clinicians treating young people with CFS/ME need to consider strategies to prevent development of depression, and research is needed into approaches that are effective in treating CFS/ME with co-morbid depression.
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Kim, Joa, Yun-Sung Kim, and Sung-Hwan Park. "Metformin as a Treatment Strategy for Sjögren’s Syndrome." International Journal of Molecular Sciences 22, no. 13 (July 5, 2021): 7231. http://dx.doi.org/10.3390/ijms22137231.
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Sjögren’s syndrome (SS), a chronic inflammatory disease involving the salivary and lacrimal glands, presents symptoms of sicca as well as systemic manifestations such as fatigue and musculoskeletal pain. Only a few treatments have been successful in management of SS; thus treatment of the disease is challenging. Metformin is the first-line agent for type 2 diabetes and has anti-inflammatory potential. Its immunomodulatory capacity is exerted via activation of 5’ adenosine monophosphate-activated protein kinase (AMPK). Metformin inhibits mitochondrial respiratory chain complex I which leads to change in adenosine mono-phosphate (AMP) to adenosine tri-phosphate (ATP) ratio. This results in AMPK activation and causes inhibition of mammalian target of rapamycin (mTOR). mTOR plays an important role in T cell differentiation and mTOR deficient T cells differentiate into regulatory T cells. In this manner, metformin enhances immunoregulatory response in an individual. mTOR is responsible for B cell proliferation and germinal center (GC) differentiation. Thus, reduction of B cell differentiation into antibody-producing plasma cells occurs via downregulation of mTOR. Due to the lack of suggested treatment for SS, metformin has been considered as a treatment strategy and is expected to ameliorate salivary gland function.
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Wormser, Gary P., and Ira Schwartz. "Antibiotic Treatment of Animals Infected with Borrelia burgdorferi." Clinical Microbiology Reviews 22, no. 3 (July 2009): 387–95. http://dx.doi.org/10.1128/cmr.00004-09.
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SUMMARY Despite resolution of the objective manifestations of Lyme disease after antibiotic treatment, a minority of patients have fatigue, musculoskeletal pain, and/or difficulties with concentration or short-term memory of uncertain etiology; these are called post-Lyme disease symptoms or, in more severe cases, post-Lyme disease syndrome or “chronic Lyme disease.” Several recent studies in which Borrelia burgdorferi-infected animals were treated with antibiotic therapy have demonstrated the presence of PCR positivity for B. burgdorferi DNA in the absence of culture positivity. In mice that were treated with antibiotic therapy, residual spirochetes could be taken up by ticks during a blood meal and could be transmitted to SCID mice. These spirochetes are attenuated; their presence is not associated with either inflammation or disease. In this review the methodology and findings of these studies are critically analyzed, and the significance of the results with regard to human Lyme disease is evaluated, with special emphasis on whether these studies provide useful insights into post-Lyme disease syndrome. A serious methodological concern is the failure to consider the pharmacokinetic-pharmacodynamic properties of the antibiotic in choosing the dosage regimen used. We conclude that there is no scientific evidence to support the hypothesis that such spirochetes, should they exist in humans, are the cause of post-Lyme disease syndrome.
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Felger, J. C., S. W. Cole, T. W. W. Pace, F. Hu, B. J. Woolwine, G. H. Doho, C. L. Raison, and A. H. Miller. "Molecular signatures of peripheral blood mononuclear cells during chronic interferon-α treatment: relationship with depression and fatigue." Psychological Medicine 42, no. 8 (December 9, 2011): 1591–603. http://dx.doi.org/10.1017/s0033291711002868.
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BackgroundInterferon-alpha (IFN-α) treatment for infectious disease and cancer causes high rates of depression and fatigue, and has been used to investigate the impact of inflammatory cytokines on brain and behavior. However, little is known about the transcriptional impact of chronic IFN-α on immune cellsin vivoand its relationship to IFN-α-induced behavioral changes.MethodGenome-wide transcriptional profiling was performed on peripheral blood mononuclear cells (PBMCs) from 21 patients with chronic hepatitis C virus (HCV) either awaiting IFN-α therapy (n=10) or at 12 weeks of IFN-α treatment (n=11).ResultsSignificance analysis of microarray data identified 252 up-regulated and 116 down-regulated gene transcripts. Of the up-regulated genes, 2′-5′-oligoadenylate synthetase 2 (OAS2), a gene linked to chronic fatigue syndrome (CFS), was the only gene that was differentially expressed in patients with IFN-α-induced depression/fatigue, and correlated with depression and fatigue scores at 12 weeks (r=0.80,p=0.003 andr=0.70,p=0.017 respectively). Promoter-based bioinformatic analyses linked IFN-α-related transcriptional alterations to transcription factors involved in myeloid differentiation, IFN-α signaling, activator protein-1 (AP1) and cAMP responsive element binding protein/activation transcription factor (CREB/ATF) pathways, which were derived primarily from monocytes and plasmacytoid dendritic cells. IFN-α-treated patients with high depression/fatigue scores demonstrated up-regulation of genes bearing promoter motifs for transcription factors involved in myeloid differentiation, IFN-α and AP1 signaling, and reduced prevalence of motifs for CREB/ATF, which has been implicated in major depression.ConclusionsDepression and fatigue during chronic IFN-α administration were associated with alterations in the expression (OAS2) and transcriptional control (CREB/ATF) of genes linked to behavioral disorders including CFS and major depression, further supporting an immune contribution to these diseases.
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Nham, Tina, Carol Saleh, Derek Chu, Stephanie L. Vakaljan, Jason A. Ohayon, and Deborah M. Siegal. "Refractory urticaria and the importance of diagnosing Schnitzler’s syndrome." BMJ Case Reports 12, no. 4 (April 2019): e228546. http://dx.doi.org/10.1136/bcr-2018-228546.
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A 52-year-old man presented with chronic urticaria that was refractory to standard chronic spontaneous urticaria (CSU) treatment. Over time, he developed systemic symptoms including fatigue, weight loss, arthralgia and bone pain. His laboratory investigations also became significant for microcytic anaemia, neutrophilia and elevated C reactive protein, erythrocyte sedimentation rate and IgE levels, in addition to an IgM monoclonal protein. He achieved only partial remission with typical medications for CSU including omalizumab, cyclosporine and cetirizine. After 6 years, his worsening symptoms and abnormal investigations led to a rare diagnosis of Schnitzler’s syndrome and a trial of the interleukin 1 receptor antagonist, anakinra, which caused a rapid and complete resolution of his symptoms.
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Albers, Eline, Linde N. Nijhof, Emma E. Berkelbach van der Sprenkel, Elise M. van de Putte, Sanne L. Nijhof, and Hans Knoop. "Effectiveness of Internet-Based Cognitive Behavior Therapy (Fatigue in Teenagers on the Internet) for Adolescents With Chronic Fatigue Syndrome in Routine Clinical Care: Observational Study." Journal of Medical Internet Research 23, no. 8 (August 13, 2021): e24839. http://dx.doi.org/10.2196/24839.
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Background Internet-based cognitive behavior therapy (I-CBT) for adolescents with chronic fatigue syndrome/myalgic encephalomyelitis (CFS/ME) has been shown to be effective in a randomized controlled trial (RCT; Fatigue in Teenagers on the Internet [FITNET]). FITNET can cause a significant reduction in fatigue and disability. Objective We aimed to investigate whether FITNET treatment implemented in routine clinical care (IMP-FITNET) was as effective, using the outcomes of the FITNET RCT as the benchmark. Methods Outcomes of CFS/ME adolescents who started IMP-FITNET between October 2012 and March 2018 as part of routine clinical care were compared to the outcomes in the FITNET RCT. The primary outcome was fatigue severity assessed posttreatment. The secondary outcomes were self-reported physical functioning, school attendance, and recovery rates. Clinically relevant deterioration was assessed posttreatment, and for this outcome, a face-to-face CBT trial was used as the benchmark. The attitude of therapists toward the usability of IMP-FITNET was assessed through semistructured interviews. The number of face-to-face consultations during IMP-FITNET was registered. Results Of the 384 referred adolescents with CFS/ME, 244 (63.5%) started IMP-FITNET, 84 (21.9%) started face-to-face CBT, and 56 (14.6%) were not eligible for CBT. Posttreatment scores for fatigue severity (mean 26.0, SD 13.8), physical functioning (mean 88.2, SD 15.0), and full school attendance (mean 84.3, SD 26.5) fell within the 95% CIs of the FITNET RCT. Deterioration of fatigue and physical functioning after IMP-FITNET was observed at rates of 1.2% (n=3) and 4.1% (n=10), respectively, which is comparable to a waiting list condition (fatigue: 1.2% vs 5.7%, χ21=3.5, P=.06; physical functioning: 4.1% vs 11.4%, χ21=3.3, P=.07). Moreover, 41 (16.8%) IMP-FITNET patients made use of face-to-face consultations. Conclusions IMP-FITNET is an effective and safe treatment for adolescents with CFS/ME in routine clinical care.
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Woo, Michael H., and Thomas G. Burnakis. "Infectious Diseases: Interferon Alfa in the Treatment of Chronic Viral Hepatitis B and C." Annals of Pharmacotherapy 31, no. 3 (March 1997): 330–37. http://dx.doi.org/10.1177/106002809703100312.
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Objective To review the indications, efficacy, and toxicity of interferon alfa in the treatment of chronic hepatitis B and C. Data Sources English-language literature pertaining to chronic hepatitis B and C and their management with interferon reported between 1980 and June 1995 was identified through computer searches using MEDLINE and through extensive searching of bibliographies and identified articles. Data Synthesis Two major causes of chronic hepatitis are hepatitis B virus and hepatitis C virus (HBV and HCV). Worldwide, HBV infection is a major cause of cirrhosis and hepatocellular carcinoma, but in the US it is mainly a disease of high-risk groups. In the US, and particularly the southern portion, HCV is more common. Like HBV, HCV also may cause cirrhosis and hepatocellular carcinoma. Except for interferon therapy, the ability to effectively treat chronic hepatitis is limited. Interferon has antiviral, antiproliferative, and immunomodulatory activity. This agent is indicated in patients who have histologic evidence of chronic hepatitis and ongoing viral replication. Thirty percent to 40% of patients with HBV achieve loss of serum HBV e antigen and HBV DNA after treatment with interferon alfa 5 million units/d or 10 million units three times weekly for 16 weeks. Fifty percent of patients with chronic HCV respond to interferon 3 million units three times weekly for 6 months, but half of these relapse within the next 6 months. Prolonged use (18 months) may provide longer term responses in HCV. Adverse effects are common, often dose-dependent, and usually transient. A flu-like syndrome occurs early in the treatment, but fatigue is the most common adverse effect and persists throughout therapy. Long-term interferon treatment has not been extensively evaluated and the impact on survival rates is not known. Conclusions Interferon is the only agent to have shown a consistent therapeutic effect on chronic hepatitis. Response of HBV to interferon is usually sustained, while a recurrence of HCV occurs in 50% of those who initially respond. Despite the benefits of interferon, its adverse effects and impact on hepatitis must be considered before treatment can be freely advocated.
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Bogaevskaya, O. Yu, and S. T. Sokhov. "The risks of injection anesthesia in dentistry." RUDN Journal of Medicine 24, no. 1 (December 15, 2020): 61–68. http://dx.doi.org/10.22363/2313-0245-2020-24-1-61-68.
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The article intends to study the risks of performing injection anesthesia for dentists experiencing chronic fatigue syndrome. Materials and methods used: The survey was conducted from August to November 2019 at various dental clinics of Moscow, with 308 dentists having filled in the questionnaire. Information source: The “Questionnaire on Assessing Injection Security and Chronic Fatigue Syndrome” was offered to dentists from clinics representing different types of ownership and contained 88 questions. Results: 97,14% of the respondents were feeling anxious while performing local anesthesia, yet, regrettably, 14,28% of them had to refer the patient to a dental surgeon for this procedure. 17,14% (n=53) of the 308 respondents noted that they had to confront the patient’s general condition worsening significantly due to a local anesthetic injection prior to the start of dental treatment. The mistakes made mostly had to do with anesthetic choice (26,73%), needle choice (12%), and needle breakage (3,78%). 17,14 per cent of dentists had the experience of confronting grave, even fatal outcomes of anesthesia. The majority of dentists (74,29%) work from 41,2 to 57,7 hours weekly. The risk of developing chronic fatigue syndrome was assessed as high in 11,43% of all cases. Conclusion: Given the absence of prophylaxis in 45,71% of cases related to anesthetic injection and the increased concentration of vasoconstrictor in the anesthetic in 88,57% of all instances, keeping records of complications caused by injection anesthesia is recommended.
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Szrajda, Justyna. "ME/CFS in Adolescents — Study Review." Journal of Neurological and Neurosurgical Nursing 9, no. 2 (June 2020): 76–79. http://dx.doi.org/10.15225/pnn.2020.9.2.5.
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Chronic Fatigue Syndrome (CFS), also called myalgic encephalomyelitis (ME), is a condition characterized by long-term fatigue that is not significantly alleviated during rest and is not caused by previous medical conditions or continuous exercise. Symptoms are quite diverse, but not specific to this disease entity. The most common are: concentration and memory problems, sore throat, swollen lymph nodes, joint pain, sleep disturbances, headache. Moreover, autonomic nervous system functioning and post-exertional malaise examination is considered to be important in diagnosis of adolescent patients with ME/CFS. The presented analysis of research shows that adolescents with ME/CFS urge to be understood and believed regarding an illness that few understood. Continuing education and remaining the social activity in young ME/CFS patients seems to be crucial in maintaining quality of life. ME/ CFS in adolescents might lead to significant problems related to the school absenteeism, poorer quality of life at school, school and academic achievement compared to healthy adolescents. Anxiety might co-occur with ME/CFS in adolescents. Supportive therapy for comorbidities could be considered, if needed. However, there is no established effective treatment for ME/CFS, for which there is urgent need. (JNNN 2020;9(2):76–79) Key Words: ME/CFS, adolescents, Chronic Fatigue Syndrome
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Strand, Elin Bolle, Jesús Castro-Marrero, Ingrid Helland, Jose Alegre, and Anne Marit Mengshoel. "Pain and Depression Are Associated With More Anxiety in ME/CFS: A Cross-Sectional Cohort Study Between Norway and Spain." Clinical Medicine Insights: Psychiatry 11 (January 2020): 117955732094147. http://dx.doi.org/10.1177/1179557320941478.
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Objectives: Lasting, unexplained and high levels of pain may cause anxiety in patients with chronic fatigue syndrome. The objectives of the current study were to test assumptions of the association between pain and anxiety in patients diagnosed with myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) and to clarify the role of depression in this relationship. Methods: Data were collected from 664 participants (age 18-65 years) with 133 ME/CFS patients and 201 healthy controls from Norway and 330 CFS patients from Spain. Binary logistic regression model was applied to test relationships between the included variables in the samples. Results: Both pain and depression made significant direct contributions to the level of anxiety. The strongest risk for higher levels of anxiety was the combination of high levels of depression and high levels of pain in the overall sample (OR = 49.70; P < 0.001), not so much in the Spanish cohort (OR = 11.99; P < 0.0001) and most of all in the Norwegian cohort (OR = 88.21; P < 0.001) sample. Conclusions: It was the combination of high pain levels and high levels of depression that to the greatest extent increased the risk of anxiety in patients with CFS/ME. Whatever diagnostic criterion that is applied, anxiety and depression should be mandatory to assess in the clinical assessments performed for diagnosing the ME/CFS. Approaches addressing anxiety-related pain and treatment of depression should be warranted.
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Fletcher, E. C. "Obstructive sleep apnea and the kidney." Journal of the American Society of Nephrology 4, no. 5 (November 1993): 1111–21. http://dx.doi.org/10.1681/asn.v451111.
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Recent studies of obstructive sleep apnea and its comorbidity with other systemic diseases have stimulated interest in the relationship of apnea to renal disease and hypertension. Polysomnographic sleep studies in patients on dialysis who complain of day-time fatigue or sleepiness reveal significant apnea in up to 73% of those studied. Abnormalities in respiratory controller mechanisms from chronic hypocarbia, metabolic acidosis, and uremic toxins have been blamed for the occurrence of apnea in this setting. Proteinuria and sometimes nephrotic syndrome have been recognized in morbidly obese patients with sleep apnea syndrome. Renal biopsies of such patients have shown glomerulomegaly and focal segmental sclerosis. It is postulated that these lesions may result from increased glomerular filtration and blood flow. Elevated urine output, sodium and chloride excretion, and atrial natriuretic peptide have been well demonstrated in obstructive apnea patients and correct to control levels with treatment of the apnea. Both acute (with each apnea) and chronic daytime blood pressure elevation are frequently observed in sleep apnea patients, and occult sleep apnea is postulated as one possible cause of "primary" hypertension in middle-aged men. In younger patients, such hypertension seems to be more reversible with the elimination of apnea. In older patients, however, the cure of systemic hypertension cannot be guaranteed with the elimination of the apnea, and asymptomatic apnea patients tend not to tolerate the bother and discomfort of apnea treatment with nasal continuous positive airway pressure. Therefore, aside from a careful history regarding sleep symptomatology, polysomnographic studies of clinic populations with primary hypertension to search for apnea as a cause cannot be recommended.
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Lutz, Lena, Johanna Rohrhofer, Sonja Zehetmayer, Michael Stingl, and Eva Untersmayr. "Evaluation of Immune Dysregulation in an Austrian Patient Cohort Suffering from Myalgic Encephalomyelitis/Chronic Fatigue Syndrome." Biomolecules 11, no. 9 (September 14, 2021): 1359. http://dx.doi.org/10.3390/biom11091359.
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Myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) is a severe multi-systemic disease characterized by debilitating fatigue that is not relieved by rest. The causes of the disease are still largely unexplained, and no causative treatment is currently available. Changes in the immune response are considered as fundamental in the development of ME/CFS. Thus, we aimed to evaluate the immunological profile of ME/CFS patients in a retrospective data analysis. As part of the routine workup for ME/CFS patients, a differential blood count, leukocyte subtyping, and quantification of immunoglobulins and IgG subclasses, as well as a complement analysis, was performed. Out of 262 ME/CFS patients, 64.9% had a reduction or deficiency in at least one of the listed immune parameters. In contrast, 26.3% showed signs of immune activation or inflammation. A total of 17.6% of the ME/CFS patients had an unclassified antibody deficiency, with IgG3 and IgG4 subclass deficiencies as the most common phenotypes. Reduced MBL (mannose-binding lectin) levels were found in 32% of ME/CFS patients, and MBL deficiency in 7%. In summary, the present results confirmed the relevance of immune dysfunction in ME/CFS patients underlining the involvement of a dysfunctional immune response in the disease. Thus, immune parameters are relevant disease biomarkers, which might lead to targeted therapeutic approaches in the future.
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Fitzcharles, Mary-Ann, Peter A. Ste-Marie, Don L. Goldenberg, John X. Pereira, Susan Abbey, Manon Choinière, Gordon Ko, et al. "2012 Canadian Guidelines for the Diagnosis and Management of Fibromyalgia Syndrome: Executive Summary." Pain Research and Management 18, no. 3 (2013): 119–26. http://dx.doi.org/10.1155/2013/918216.
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BACKGROUND: Recent neurophysiological evidence attests to the validity of fibromyalgia (FM), a chronic pain condition that affects >2% of the population.OBJECTIVES: To present the evidence-based guidelines for the diagnosis, management and patient trajectory of individuals with FM.METHODS: A needs assessment following consultation with diverse health care professionals identified questions pertinent to various aspects of FM. A literature search identified the evidence available to address these questions; evidence was graded according to the standards of the Oxford Centre for Evidence-Based Medicine. Drafted recommendations were appraised by an advisory panel to reflect meaningful clinical practice.RESULTS: The present recommendations incorporate the new clinical concepts of FM as a clinical construct without any defining physical abnormality or biological marker, characterized by fluctuating, diffuse body pain and the frequent symptoms of sleep disturbance, fatigue, mood and cognitive changes. In the absence of a defining cause or cure, treatment objectives should be patient-tailored and symptom-based, aimed at reducing global complaints and enhancing function. Healthy lifestyle practices with active patient participation in health care forms the cornerstone of care. Multimodal management may include nonpharmacological and pharmacological strategies, although it must be acknowledged that pharmacological treatments provide only modest benefit. Maintenance of function and retention in the workforce is encouraged.CONCLUSIONS: The new Canadian guidelines for the treatment of FM should provide health professionals with confidence in the complete care of these patients and improve clinical outcomes.
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Yakushyna, S. A., L. B. Kisteneva, and S. G. Cheshyk. "Principles of the treatment of chronic Epstein–Barr virus infection and associated diseases." Rossiyskiy Vestnik Perinatologii i Pediatrii (Russian Bulletin of Perinatology and Pediatrics) 64, no. 2 (May 15, 2019): 38–46. http://dx.doi.org/10.21508/1027-4065-2019-64-2-38-46.
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Epstein – Barr virus, related to herpes viruses, causes infectious mononucleosis during the initial infection; after recovery, the virus persists in the body throughout lifetime. The presence of clinical symptoms and viral load in a patient in 6 months after the infectious mononucleosis disease indicates the formation of chronic active Epstein – Barr viral infection. Hemophagocytic lymphohistiocytosis, posttransplantation lymphoproliferative disease and chronic fatigue syndrome, which has a polyetiological nature, are also associated with the activation of the persistent Epstein – Barr virus. Most of these diseases develop in children due to their physiological immunodeficiency and are accompanied by high mortality – up to 50%. Immune mechanisms, in addition to the virus itself, play a leading role in the pathogenesis of the diseases. The article summarizes all existing approaches to the treatment of chronic Epstein – Barr virus-associated diseases. The authors have analyzed the effectiveness of these approaches on the basis of various published studies. These diseases are treated with etiotropic antiviral drugs – nucleoside analogs, nonspecific immunotherapy, targeted therapy with monoclonal antibody preparations, immune cellular CD8+ therapy. In case of ineffectiveness of these methods, the alternative bone marrow transplantation is used. The article highlightes promising areas for the development of new approaches to the treatment of Epstein – Barr virus-associated diseases.
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Fragkos, Konstantinos, John Barragry, Charisma Fernando, Marco Novelli, Joanna Begent, and Natalia Zárate-Lopez. "Severe eosinophilic colitis caused by neuropathic agents in a patient with chronic fatigue syndrome and functional abdominal pain: case report and review of the literature." Zeitschrift für Gastroenterologie 56, no. 06 (June 2018): 573–77. http://dx.doi.org/10.1055/a-0596-7981.
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AbstractEosinophilic colitis is a rare clinical condition that belongs to the group of eosinophilic gastrointestinal disorders. Its occurrence can be primary or secondary to infection, medications, or autoimmune/hematological conditions. We present a case of a young female adult with severe chronic fatigue syndrome, widespread chronic pain, including functional abdominal pain, who developed severe eosinophilic colitis following successive treatments with gabapentin and pregabalin. On both occasions, symptoms manifested as abdominal pain, diarrhea, and eosinophilia and improved upon discontinuation of the medications. Magnetic resonance imaging of the small bowel demonstrated an ascending colon colitis, and endoscopic investigations confirmed florid colitis mainly in the ascending colon with biopsies demonstrating a dense eosinophilic infiltrate with micro-abscesses. Serum eosinophil counts correlated well with the timing of the agents’ administration. There was no other organ involvement. Symptoms improved upon discontinuation of the drugs and steroid administration. Eosinophilic colitis is an exceptionally rare entity and its mechanism of action is still unclear. Suspicion of eosinophilic colitis should be raised if a patient presents with abdominal pain, diarrhea, and peripheral eosinophilia following treatment with pregabalin or gabapentin.
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Gibson, Pamela Reed, and Amanda Lindberg. "Physicians' Perceptions and Practices Regarding Patient Reports of Multiple Chemical Sensitivity." ISRN Nursing 2011 (September 7, 2011): 1–5. http://dx.doi.org/10.5402/2011/838930.
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Ninety physicians practicing in the state of Virginia USA completed a mail survey regarding Multiple Chemical Sensitivity (MCS). Survey questions addressed demographics; familiarity with MCS; etiology; overlapping conditions; accommodations made for patients and practices regarding evaluation, treatment, and referral. A little over half of respondents were familiar with MCS. Under a third had received any medical training regarding chemical sensitivity, only 7% were “very satisfied” with their knowledge, and 6% had a treatment protocol for the condition. Participants cited a range of etiologies and overlapping conditions including asthma, Reactive Airway Dysfunction Syndrome (RADS), Sick Building Syndrome (SBS), Chronic Fatigues Syndrome (CFS), and Fibromyalgia. Physicians infrequently considered chemicals as a cause of illness when seeing new patients. Evaluation techniques included interviews, blood work, immune profiles, and allergy testing. Interventions recommended included chemical avoidance, alterations in the home environment, diet restrictions, the use of air filters, and referrals to outside specialists.
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Lopez-Mendoza, Javier, Edgar Vargas-Flores, Nicole Mouneu-Ornelas, and Carlos Altamirano-Arcos. "Disease presentation and surgical treatment of patients with foreign-body granulomas and ASIA syndrome: case series." Archives of Plastic Surgery 48, no. 4 (July 15, 2021): 366–72. http://dx.doi.org/10.5999/aps.2020.02152.
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Background The result of illicit polymer injection is chronic inflammation with foreign-body granuloma (FBG) formation. Treatment can be divided into medical and surgical. Some patients develop severe complications with need surgical treatment. This study aims to describe patients who underwent surgical removal of the FBGs and autoimmune/inflammatory syndrome induced by adjuvants (ASIA); additionally, we evaluated the quality of life after surgery.Methods In this retrospective single-center study, the authors examined data of patients who underwent surgical removal of FBG caused by illicit polymer injection for cosmetic purposes and confirmed ASIA from 2015 to 2020 by three different surgical approaches. Descriptive summary statistics were reported on patient demographics, presenting symptoms and clinical examination features, treatment strategies, histopathology reports and quality of life.Results The cohort included 11 female patients with FBGs and ASIA. The most affected anatomical zones were the combination of gluteal region, thighs and legs (40%); and thighs with legs (20%). Main presentation was: skin hyperpigmentation (90.9%), skin induration (63.6%), chronic fatigue (63.6%), and ulcers (36.4%). Surgical modalities consisted of: ultrasonic-assisted liposuction in four patients (36.4%); open en bloc excision and primary closure in four patients (36.4%); and open en bloc excision and microsurgical reconstruction in three patients (27.2%). The postoperative quality of life visual analog scale score was 83.9.Conclusions ASIA treatment represents a challenge for the plastic surgeon. Adequate surgical treatment emphasizing, when possible, the total or near-total resection of the FBG must be performed to improve ASIA evolution.
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Riley, Roger, Asad Khan, Shella Pai, Laura Warmke, Marcus Winkler, and William Gunning. "A Case of Chronic Thrombocytopenia in a 17-Year-Old Female." Laboratory Medicine 50, no. 4 (June 22, 2019): 406–20. http://dx.doi.org/10.1093/labmed/lmz013.
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AbstractStorage pool deficiency (SPD) is a group of rare platelet disorders that result from deficiencies in α-granules, δ-granules, or both. One type of α-SPD is gray platelet syndrome (GPS), caused by mutations in the neurobeachin-like 2 (NBEAL2) gene that results in a bleeding diathesis, thrombocytopenia, splenomegaly, and progressive myelofibrosis. Due to the lack of α-granules, platelets have a gray and degranulated appearance by light microscopy. However, definitive diagnosis of GPS requires confirmation of α-granule deficiency by electron microscopy. Treatment is nonspecific, with the conservative utilization of platelet transfusions being the most important form of therapy. We present a case of a 17-year-old female with a past medical history of thrombocytopenia, first identified at the age of five. Her clinical symptomatology included chronic fatigue, gingival bleeding, bruising, menorrhagia, and leg pain. This report will discuss both the clinical and the pathophysiologic aspects of this rare platelet disorder.
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Jeyakumar, Deepa, Sarmen Sarkissian, Parwiz Siaghani, and Sherif Rezk. "Successful Treatment of Macrophage Activation Syndrome in Chronic Lymphoproliferative Disorder of Natural Killer Cells with Cyclophosphamide." Blood 126, no. 23 (December 3, 2015): 5073. http://dx.doi.org/10.1182/blood.v126.23.5073.5073.
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Abstract Introduction: Chronic natural killer (NK) cell lymphoproliferative disorders comprise a rare subgroup of diseases characterized by proliferation of NK cells with expression of CD3-/CD16+ or CD56+ on flow cytometry. Clinically, these patients present with cytopenias as well as fatigue and B symptoms. The diagnosis can be challenging due to frequent lack of a unique clonal marker. Chronic NK cell lymphoproliferative disorder can be differentiated from NK cell leukemia based on the absence of chronic EBV infection. Macrophage activation syndrome (MAS) can occur in the setting of hematologic malignancies. Due to the rarity of this diagnosis, there are no randomized controlled trials to determine the optimal therapy. We report the case of an elderly gentleman whom we diagnosed with chronic NK cell lymphoproliferative disorder, complicated by transfusion-dependent autoimmune hemolytic anemia, and MAS, and who was successfully treated with oral cyclophosphamide. Case Report: In March 2014, a 75 year old Caucasian male, who was otherwise in good health, had a syncopal episode. Two months earlier, he had reported dyspnea on exertion and cough. He was diagnosed with bronchitis and these symptoms resolved with a course of antibiotics. Cardiac work-up was unremarkable. Complete blood count demonstrated white blood count of 16.8K with 84% lymphocytes, with hemoglobin of 7.8g/dL and platelets of 264K. Lactate dehydrogenase (LDH) was elevated at 615 IU/L, haptoglobin was undetectable, total bilirubin was mildly elevated at 1.5mg/dL and a Coomb's assay was negative. The patient had adequate iron stores with 50% saturation and erythropoietin level was 76.7ug/L. CT of the abdomen/pelvis demonstrated mild splenomegaly of 14cm. CT scan also revealed numerous thoracic-spine soft lesions. Bone marrow biopsy revealed a hypercellular marrow with appropriate trilineage hematopoiesis, erythroid hyperplasia and increased lymphocytes which were CD2+ CD7+ CD16+ and CD 56 negative cells as well as negative for T and B cell markers. This lymphocyte population was identified as NK cells and comprised 16% of his cells. The patient's transfusion dependence did not decrease despite oral prednisone. He transferred to our university medical center. Repeat flow cytometry after one month on prednisone demonstrated an increase to 70% of the lymphocytes. Further, there was a high suspicion for macrophage activation syndrome given his ferritin of 7,358ng/mL, triglycerides of 290mg/dL and interleukin-2 receptor of 7,250pg/mL. There was no evidence of active hemophagocytosis on the bone marrow biopsy. He continued on prednisone 60mg daily, and started on cyclophosphamide 50mg daily. His clinical course over the next several months was complicated by recurrent fevers, night sweats, mental status changes, and hyponatremia. Sepsis was ruled out as a cause of his fevers and his mental status changes were attributed to be secondary to hyponatremia and MAS. Work-up of his hyponatremia revealed syndrome of inappropriate antidiuretic hormone secretion (SIADH). After 2 months of treatment, his sodium level and mental status normalized. His cyclophosphamide was increased to 100mg daily and maintained at that dose. He was then tapered off prednisone. This patient's B symptoms of fevers and night sweats abated after several months of this therapy, and his transfusion dependence and underlying MAS resolved. The patient has been maintained on cyclophosphamide 100mg for 11 months and has shown resolution of his lymphocytosis and normalization of his blood counts. Discussion: Chronic lymphoproliferative disorders of NK cells continue to be a difficult group of diseases to recognize. Moreover, this case was further complicated by MAS based on elevated interleukine-2 receptor, triglycerides and ferritin levels in the setting of B-symptoms and liver enzyme elevations. This constellation of factors has not been previously described in the literature. Due to lack of clonal markers in NK cells, the diagnosis is frequently made by exclusion. The patient has done very well on oral cyclophosphamide and prednisone alone. We present this case to increase provider awareness and hopefully allow for improved diagnosis and treatment options in the future. Disclosures No relevant conflicts of interest to declare.
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Keating, Elizabeth M., Ryan M. Antiel, Karen E. Weiss, Dustin Wallace, Seth J. Antiel, Philip R. Fischer, Ashley N. Junghans-Rutelonis, and Cynthia Harbeck-Weber. "Parental Perceptions of Pediatric Pain and POTS-Related Disability." Clinical Pediatrics 56, no. 13 (December 8, 2016): 1185–92. http://dx.doi.org/10.1177/0009922816681137.
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Adolescents with postural orthostatic tachycardia syndrome (POTS) often have pain and functional impairment. This study evaluated how parental attributions of children’s symptoms relate to child functional impairment. Adolescents with chronic pain and clinical symptoms suggestive of autonomic dysfunction (fatigue, dizziness, nausea) that attended a multidisciplinary chronic pain clinic completed measures of depression, anxiety, and functioning (n = 141). Parents of 114 of these patients completed the Parent Pain Attribution Questionnaire (PPAQ), a measure indicating the extent they believe physical and psychosocial factors account for their child’s health condition. Patients were retrospectively grouped as to whether or not they had significant POTS on tilt table testing (n = 37). Greater parental attribution to physical causes was associated with increased levels of functional disability whether patients had POTS ( r = 0.45, P = .006) or not ( r = 0.25, P = .03). These results suggest that providers should advocate a more comprehensive family-oriented rehabilitative approach to treatment.
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Chatelet, Valerie, Veronique Fremeaux-Bacchi, Maxence Ficheux, Thierry Lobbedez, and Bruno Hurault-Deligny. "Efficacy of Eculizumab in a Plasmatherapy-Dependent Patient with Atypical Hemolytic Uremic Syndrome with C3 Mutation Following Plasmatherapy Withdrawal." Blood 112, no. 11 (November 16, 2008): 4579. http://dx.doi.org/10.1182/blood.v112.11.4579.4579.
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Abstract Atypical hemolytic uremic syndrome (aHUS) is a rare microangiopathic hemolytic anemia characterized by chronic intravascular hemolysis, consumptive thrombocytopenia, microvascular glomerular thrombosis and acute renal failure. Atypical HUS develops as the result of unregulated complement activation either through genetic abnormalities in one or more complement proteins or more rarely the development of autoantibodies to complement factor H. Complement dysregulation has been shown to cause cause subendothelium exposure and activation of platelets resulting in a chronic proinflammatory and prothrombotic state. The prognosis for aHUS is poor as 25% of patients die during acute phases of the disease and 50% progress to end-stage-renal disease. In addition, the majority of renal transplants result in loss of the graft. Plasmatherapy (PT), either plasmapheresis, plasma infusion, or both, is currently used in an attempt to control complement activation and thereby reduce the thrombotic microangiopathy (TMA) and declining renal function, but this therapy is cumbersome and not effective in all patients. Eculizumab, an antibody targeting complement C5, blocks activation of terminal complement and generation of the proinflammatory and prothrombotic molecules C5a and C5b-9. In previous studies eculizumab significantly blocked complement-mediated hemolysis in patients with paroxysmal nocturnal hemoglobinuria, subsequently reducing thrombotic events and improving renal function. In this study, we report the first case of eculizumab treatment in a patient with recurrent aHUS after renal transplantation who refused further PT. The patient is a 42-year-old female diagnosed with a familial form of aHUS with a C3 mutation leading to a binding defect between C3b and the complement control molecules factor H and membrane cofactor protein. The patient showed reduced serum levels of C3c (670 mg/L) suggesting C3 consumption. The patient had received 2 previous renal transplants, the last of which was performed in 2004; aHUS recurred after each transplant and required PT. In March 2007 the patient experienced an acute episode of aHUS and received 2 intensive PT sessions (60 treatments over 9 mos) to resolve the recurrence. In April 2008, the patient presented with septicemia and acute renal failure and was hospitalized for 10 days. In May 2008 her platelet count dropped to 170 ×109/L, haptoglobin became undetectable (< 0.15 g/L), and schistocytes increased to 3.7% suggesting an acute TMA exacerbation, confirmed by renal biopsy. Plasmatherapy was initiated with a course of high dose steroids and IV immunoglobulins. The administration of frequent PT treatments (16 treatments over 5 weeks) resulted in an improvement in the ongoing TMA. However, despite intensive PT, the patient continued to suffer from severe fatigue and daily episodes of diarrhea and chose to discontinue this therapy. As a result, disease deterioration was observed (see 10 Days of No PT in Table). The clinical deterioration established the need for an alternative treatment to reduce TMA and stabilize renal function. PT (3 treatments) was performed as a bridging treatment to eculizumab. Treatment with eculizumab was initiated 4 days following the last PT. The patient received a meningococcal vaccine 4 days prior to treatment with eculizumab and then prophylactic antibiotics (ciprofloxacin) after the vaccination. The patient received 4 doses of eculizumab, 900 mg IV approximately every 7 days, and then 1200 mg 7 days later, and is scheduled to receive chronic dosing at 1200 mg every 14 days. Platelet count, hemolysis and renal function were monitored. After one month of eculizumab treatment, and without concomitant PT, platelet count increased (range from 227 to 284 ×109/L), schistocytes decreased to 0.8% and haptoglobin increased to within normal limits (1.5 g/L; see “Ecu Dose 5”). Levels of C3c fluctuated between 420 and 690 mg/L, creatinine levels were stable and no further episodes of diarrhea were reported. In summary, the data suggest that chronic blockade of complement C5 with eculizumab maintained renal function and reduced platelet consumption and hemolysis without PT in a patient with aHUS previously dependent on frequent PT. Based on these results clinical trials are warranted to confirm the activity of eculizumab for the treatment of patients with recurrent aHUS that are dependent on PT.
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Sai Susmitha, Rebba, Saidu Harshini, Thanmayee Thunga, Sivani Vathyam, Satheesh S. Gottipati, and P. Srinivasa Babu. "A STUDY ON THE DETAILED DESCRIPTION OFFIFTH DISEASE& MYSTERY REGARDING THE NON-PHARMACOLOGICAL TREATMENT OFFIFTH DISEASE." International Journal of Advanced Research 9, no. 08 (August 31, 2021): 532–37. http://dx.doi.org/10.21474/ijar01/13301.
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Fifth disease is a mild rash illness, caused due to parvovirus B19. This will be mainly seen in children compare to adults. Other names for this include: ErythemaInfectiosum (EI), Slapped cheek syndrome. Epidemics of erythema infectiosum mainly occurs in late winter or early spring. Tests for this include specific parvovirus B19 IgM antibody. IgM antibodies usually founds within 7 to 10 days of virus exposure, the remain measures are from 2 to 3 months after exposure to virus. Symptoms mainlyincludes rash, headache, fatigue, low-grade fever. However,there is no vaccine or medicine that prevent parvovirus B19 infection. Adults who have symptoms of joint pain and swelling may need rest, to alter their activities. Andtake Nonsteroidal anti-inflammatory drugs like Aspirin, Ibuprofen, or Naproxen sodium. Patients who are suffering with chronic parvovirus arthritis occasionally benefit from drugs such as hydroxychloroquine and corticosteroids and also, they want to avoid dairy products, Sweets and sugar. They want to increase their fluid intake and vitamin c supplements to improve their immune system.
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Wadekar, Abhijit, Sanyukta Hepat, Anamika Giri, and Sourya Acharya. "Wernicke’s Encephalopathy with Normal Neuroimaging - Suspect and Treat - A Case Report." Journal of Evolution of Medical and Dental Sciences 10, no. 33 (August 16, 2021): 2867–69. http://dx.doi.org/10.14260/jemds/2021/584.
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Wernicke’s encephalopathy (WE) is an unrecognized nutritional deficiency which often goes unnoticed. WE is clinically often composed of a triad including nystagmus, ophthalmoplegia and altered mental status. Although this triad practically is present only in a handful of cases1 it is also described as an acute neuropsychiatric presentation of thiamine deficiency. Early diagnosis and prompt treatment are of utmost importance here as it can prevent chronic brain damage which is often the end effect of thiamine deficiency. Wernicke’s encephalopathy is most commonly found in patients with chronic alcoholism, less frequent in non-alcoholic patients. In non-alcoholic patients, Wernicke’s encephalopathy might develop due to erosion of upper portion of gastrointestinal tract or secondary to intractable vomiting, inadequate dietary intake or malabsorption. Other causes include malignancies (gastric cancer, leukaemia, lymphoma), hyperemesis, anorexia, thyroid conditions.1,2 Wernicke’s encephalopathy is caused due to thiamine (B1) deficiency. B1 is a water-soluble vitamin which acts as a co-factor for carbohydrate metabolism. It is also important for neuronal cell function.2 This vitamin can’t be synthesised in the human body and thus dietary intake play a very important role. Symptoms of thiamine deficiency Include - Nystagmus, ataxia, encephalopathy, mental confusion. Early onset includes symptoms like: - headache, irritability, fatigue and abdominal discomfort. Prophylactic thiamine supplementation forms a major treatment for patients at risk for developing refeeding syndrome (RFS). RFS is an underdiagnosed condition which is characterised by potential shift in the fluid and electrolytes.
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Lee, Seung, Coby Palmares, Niko Koutsoukos, J. Brice Weinberg, Trisa Palmares, Alice Song, Harold Song, et al. "Ruxolitinib Used to Treat Hypereosinophilic Syndrome." Blood 128, no. 22 (December 2, 2016): 5500. http://dx.doi.org/10.1182/blood.v128.22.5500.5500.
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Abstract Introduction: Hypereosinophilic syndrome (HES) is a rare hematologic disorder in which the eosinophils proliferate and infiltrate and damage multiple organs. Without treatment, the condition is fatal, usually due to cardiac dysfunction, particularly left ventricular dysfunction. Causes of reactive eosinophilia include allergic and hypersensitivity reactions, drug allergies, cytokine therapy (recombinant human interleukin), cutaneous disorders, connective tissue diseases, collagen vascular disorders, parasitic infections, immunodeficiency disorders, sarcoidosis, and neoplasms, such as Hodgkin's and non-Hodgkin's lymphoma (B- and T-cell), acute lymphoplastic leukemia, chronic myeloproliferative disorders. Jakafi is approved for myelodysplastic syndrome (MDS) and is effective in reducing splenomegaly. The medication is off-label for HES. This report demonstrates the successful treatment of HES with ruxolitinib. Methods: Case report Results: A 77 year-old Asian male presented with sudden onset pruritus. There was no history of drug allergy or scabies. Past medical history included hypertension, benign prostatic hypertrophy, and early glaucoma. He had shingles 3 times in his 50's on his thorax. Past surgical history included vasectomy, laser iridotomies, and pterygectomies. His medications included losartan, doxazosin and silodosin, amlodipine, carvedilol, and multi-vitamins. He was a retired pediatrician who was actively involved in gardening, carpentry, roller-blading, swimming, and walking his dogs. The patient first presented to his primary care physician, who offered a psychosomatic explanation for his symptoms. A CBC with a differential demonstrated elevated eosinophils of 36%. He was referred to an allergist, who started oral prednisone. There was some relief. He was given interferon. This resulted in fatigue and purple fingernails and no improvement in the pruritus, so interferon was discontinued. He was referred to a dermatologist who prescribed hydroxyzine and fluocinolone cream. This provided minimal relief. He saw a 2nd dermatologist who performed a skin biopsy, which was negative. The patient was referred to an oncologist. Bone marrow biopsy revealed a slight hypercellularity of 30-40% and increased eosinophilia of 16%. There was no evidence of leukemia, lymphoma, or MDS. Cytogenetic testing revealed the following: 46XY, del 9 (q13q22). Kappa/Lambda ratio was slightly elevated at 4.15. KIT mutation by PCR, T-cell clonality by PCR, and FISH panel were negative. Immunoglobulin testing revealed: IgA 140, IgG 1317, IgM 65, and IgE 358. The patient also saw an infectious disease specialist. HIV, ANA, serum tryptase, LDH, Vitamin B12,urine protein electrophoresis, parasitic work-up (trichinella, toxocara, strongyloides) was negative. Echocardiogram demonstrated an ejection fraction of 62%. The patient continued to have chronic pruritus with sleeplessness. In desperation, he attempted to discontinue his prostate medications in hopes that his condition was a simple allergy to medications, but this resulted in urinary retention with fever, sepsis, and anasarca, necessitating urgent antibiotic treatment. Although the patient was negative for the FIP1L1-PDGFRA mutation, a trial of imatinib (tyrosine kinase inhibitor) was given. Not surprisingly, there was no improvement in his symptoms or condition. The patient's symptoms worsened, so oral prednisone was increased from 20 to 80 mg. There was no improvement in his symptoms. Additional testing was obtained, revealing a JAK 2 kinase mutation. He was prescribed ruxolitinib 20 mg po bid. By the 3rd day, he could sleep a full night without pruritus. His prednisone was tapered; by one month, he had tapered off of his prednisone. He developed mild neutropenia, so ruxolinitib was decreased. He noted that when he missed even one dose of his ruxolitinib, the pruritus would recur. Most recent labs (4 years after initial presentation) revealed normal eosinophils of 2%. He had mild anemia and thrombocytosis, which were stable. Conclusions: This is the first case of HES treated with ruxolitinib. The patient had side effects from the standard treatments (prednisone, interferon, imatinib). Newer treatments should be available to patients who had documented HES to prevent delay in treatment and increased morbidity. Ruxolitinib is a potential treatment for HES who are intolerant of other treatments. Disclosures No relevant conflicts of interest to declare.
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Deshpande, Shubhangi V., Varsha Y. Godbole, and Archana D. Asher. "Pancytopenia: the perspective from Western Gujarat, India." International Journal of Advances in Medicine 6, no. 3 (May 24, 2019): 731. http://dx.doi.org/10.18203/2349-3933.ijam20192083.
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Background: Pancytopenia is one of the common laboratory findings in patients presenting to us with varied clinical presentations. Risks of untreated Pancytopenia are high causing anxiety to treating doctors and patients alike. It also involves long list of investigations including a very painful marrow biopsy, life-threatening complications and treatment involves multiple blood component therapy. A total of 101 cases of pancytopenia over a period of 1 year were analysed retrospectively to find i) commonest presenting symptoms ii) commonest cause of pancytopenia, response to treatment iii) Depending on the cause, to consider if any measures can be taken for preventionMethods: Cross sectional study of 101 admitted patients of Pancytopenia on the basis of information extracted from the case sheets. The data was analyzed and presented as frequencies and Percentages.Results: Out of 101 cases analysed, 53 (52.47%) were females 48 (47.52%) patients males. Fatigue 74 patients (73.2%) was the commonest presenting symptom followed by fever 33 (32.6%), breathlessness 13 (12.87%) and bleeding 4(3.8%). Vitamin B12 deficiency 58 (57.6%) patients showed and was the commonest cause of pancytopenia. Infections in 24 (23.7%) like malaria16 (15.6%), dengue 5 (4.96%), PLHA 1(0.96%) and hepatitis B 2 (1.96%) was the second common cause in present study. Recovery of pancytopenia was prompt in Malaria Dengue. HIV, Hepatitis B viral infection showed persistent pancytopenia with hypoplastic marrow. Chronic liver disease portal hypertension splenomegaly accounted for 9 (8.9%) patients. Drug induced marrow suppression due to ongoing treatment for underling disease resulted in pancytopenia in 4 (3.96%) patients. Aplastic anaemia in3 (2.9%), myelodysplastic syndrome 2 (1.9%) and acute leukaemia 1 (0.96%) were the less common causes.Conclusions: Commonest symptom on presentation were related more to anaemia than to neutropenia and thrombocytopenia. megaloblastic anaemia due to Vitamin B12 deficiency was the leading reversible cause of pancytopenia in present study followed by infections like Malaria Dengue. Gujarat, India being predominantly vegetarian state, local dietary habits are thought to be responsible for inadequate B12 daily consumption, hence we suggest fortifying the daily diet with B12 supplementation at a larger scale just like iodisation of salt to counter iodine deficiency.
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Siracusa, Rosalba, Rosanna Di Paola, Salvatore Cuzzocrea, and Daniela Impellizzeri. "Fibromyalgia: Pathogenesis, Mechanisms, Diagnosis and Treatment Options Update." International Journal of Molecular Sciences 22, no. 8 (April 9, 2021): 3891. http://dx.doi.org/10.3390/ijms22083891.
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Fibromyalgia is a syndrome characterized by chronic and widespread musculoskeletal pain, often accompanied by other symptoms, such as fatigue, intestinal disorders and alterations in sleep and mood. It is estimated that two to eight percent of the world population is affected by fibromyalgia. From a medical point of view, this pathology still presents inexplicable aspects. It is known that fibromyalgia is caused by a central sensitization phenomenon characterized by the dysfunction of neuro-circuits, which involves the perception, transmission and processing of afferent nociceptive stimuli, with the prevalent manifestation of pain at the level of the locomotor system. In recent years, the pathogenesis of fibromyalgia has also been linked to other factors, such as inflammatory, immune, endocrine, genetic and psychosocial factors. A rheumatologist typically makes a diagnosis of fibromyalgia when the patient describes a history of pain spreading in all quadrants of the body for at least three months and when pain is caused by digital pressure in at least 11 out of 18 allogenic points, called tender points. Fibromyalgia does not involve organic damage, and several diagnostic approaches have been developed in recent years, including the analysis of genetic, epigenetic and serological biomarkers. Symptoms often begin after physical or emotional trauma, but in many cases, there appears to be no obvious trigger. Women are more prone to developing the disease than men. Unfortunately, the conventional medical therapies that target this pathology produce limited benefits. They remain largely pharmacological in nature and tend to treat the symptomatic aspects of various disorders reported by the patient. The statistics, however, highlight the fact that 90% of people with fibromyalgia also turn to complementary medicine to manage their symptoms.
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Araja, Diana, Uldis Berkis, Asja Lunga, and Modra Murovska. "Shadow Burden of Undiagnosed Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS) on Society: Retrospective and Prospective—In Light of COVID-19." Journal of Clinical Medicine 10, no. 14 (July 6, 2021): 3017. http://dx.doi.org/10.3390/jcm10143017.
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Background: Myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) is a poorly understood, complex, multisystem disorder, with severe fatigue not alleviated by rest, and other symptoms, which lead to substantial reductions in functional activity and quality of life. Due to the unclear aetiology, treatment of patients is complicated, but one of the initial problems is the insufficient diagnostic process. The increase in the number of undiagnosed ME/CFS patients became specifically relevant in the light of the COVID-19 pandemic. The aim of this research was to investigate the issues of undiagnosed potential ME/CFS patients, with a hypothetical forecast of the expansion of post-viral CFS as a consequence of COVID-19 and its burden on society. Methods: The theoretical research was founded on the estimation of classic factors presumably affecting the diagnostic scope of ME/CFS and their ascription to Latvian circumstances, as well as a literature review to assess the potential interaction between ME/CFS and COVID-19 as a new contributing agent. The empirical study design consisted of two parts: The first part was dedicated to a comparison of the self-reported data of ME/CFS patients with those of persons experiencing symptoms similar to ME/CFS, but without a diagnosis. This part envisaged the creation of an assumption of the ME/CFS shadow burden “status quo”, not addressing the impact of COVID-19. The second part aimed to investigate data from former COVID-19 patients’ surveys on the presence of ME/CFS symptoms, 6 months after being affected by COVID-19. Descriptive and analytical statistical methods were used to analyse the obtained data. Results: The received data assumed that the previously obtained data on the ME/CFS prevalence of 0.8% in the Latvian population are appropriate, and the literature review reports a prevalence of 0.2–1.0% in developed countries. Regarding the reciprocity of ME/CFS and COVID-19, the literature review showed a lack of research in this field. The empirical results show quite similar self-esteem among ME/CFS patients and undiagnosed patients with longstanding disease experience, while former COVID-19 patients show a significantly lower severity of these problems. Notably, “psychological distress (anxiety)” and “episodic fatigue” are significantly predominant symptoms reported by former COVID-19 patients in comparison with ME/CFS patients and undiagnosed patients prior to the COVID-19 pandemic. The results of our analysis predict that the total amount of direct medical costs for undiagnosed patients (out-of-pocket payments) is more than EUR 15 million p.a. (in Latvia), and this may increase by at least 15% due to the consequences of COVID-19. Conclusions: ME/CFS creates a significant shadow burden on society, even considering only the direct medical costs of undiagnosed patients—the number of whom in Latvia is probably at least five times higher than the number of discerned patients. Simultaneously, COVID-19 can induce long-lasting complications and chronic conditions, such as post-viral CFS, and increase this burden. The Latvian research data assume that ME/CFS patients are not a high-risk group for COVID-19; however, COVID-19 causes ME/CFS-relevant symptoms in patients. This increases the need for monitoring of patients for even longer after recovering from COVID-19′s symptoms, in order to prevent complications and the progression of chronic diseases. In the context of further epidemiological uncertainty, and the possibility of severe post-viral consequences, preventive measures are becoming significantly more important; an integrated diagnostic approach and appropriate treatment could reduce this burden in the future.
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DRYDEN, M. S., K. SAEED, S. OGBORN, and P. SWALES. "Lyme borreliosis in southern United Kingdom and a case for a new syndrome, chronic arthropod-borne neuropathy." Epidemiology and Infection 143, no. 3 (May 9, 2014): 561–72. http://dx.doi.org/10.1017/s0950268814001071.
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SUMMARYThis series of serologically confirmed Lyme disease is the largest reported in the UK and represents 508 patients who presented to one hospital in the South of England between 1992 and 2012. The mean rate of borreliosis throughout this period was 9·8/100 000 population, much higher than the reported national rate of 1·7/100 000. The actual rate increased each year until 2009 when it levelled off. Patients clinically presented with rash (71%), neurological symptoms (16%, of whom half had VII cranial nerve palsies), arthropathy (8%), pyrexia (5%), cardiac abnormalities (1%) or other manifestations (<1%). Twenty percent of patients had additional non-specific symptoms of fatigue, myalgia, and cognitive changes. Serological diagnosis was with a two-tiered system of ELISA and immunoblot. There was a marked seasonal presentation in the summer months and in the first and sixth decades of life. A third of patients gave a clear history of a tick bite. The median interval between tick bite and clinical symptoms was 15 days [interquartile range (IQR) 9–28 days], with a further interval of 14 days to clinical diagnosis/treatment (IQR 2–31 days). Most cases were acquired locally and only 5% abroad. Patients responded to standard antibiotic therapy and recurrence or persistence was extremely rare. A second group of patients, not included in the clinical case series, were those who believed they had Lyme disease based on a probable tick bite but were seronegative by currently available validated tests and presented with subjective symptoms. This condition is often labelled chronic Lyme disease. These patients have a different disease from Lyme disease and therefore an alternative name, chronic arthropod-borne neuropathy (CAN), and case definition for this condition is proposed. We suggest that this chronic condition needs to be distinguished from Lyme disease, as calling the chronic illness ‘Lyme disease’ causes confusion to patients and physicians. We recommend research initiatives to investigate the aetiology, diagnosis and therapy of CAN.
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Granan, Lars-Petter, Silje Endresen Reme, Henrik Børsting Jacobsen, Audun Stubhaug, and Tone Marte Ljoså. "The Oslo University Hospital Pain Registry: development of a digital chronic pain registry and baseline data from 1,712 patients." Scandinavian Journal of Pain 19, no. 2 (April 24, 2019): 365–73. http://dx.doi.org/10.1515/sjpain-2017-0160.
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Abstract Background and aims Chronic pain is a leading cause to years lived with disability worldwide. However, few of the interventions used in pain medicine have proven efficacy, and evidence from the existing studies may not be valid for the general pain population. Therefore, it is of utmost need that we describe chronic pain conditions in their most relevant aspects, their various guises, as well as the real world outcomes of our clinical interventions. The most obvious and crude way to make these assessments are through large registries where patient characteristics, treatment characteristics (including but not limited to what, when, how often and by whom), treatment outcomes and patient outcomes are scrutinized and recorded. Methods and results This article describes in detail the design and baseline data of the comprehensive Oslo University Hospital Pain Registry (OPR). OPR is the local registry of the largest university and interdisciplinary outpatient pain clinic in Norway. Data registration started in October 2015, and approximately 1,000 patients are assessed and treated at the clinic each year. During the first 2 years of running the OPR (through September 2017), a total of 1,712 patient baseline reports were recorded from 2,001 patients. Clinicians enter data about relevant treatments and interventions, while patients provide self-reported data on aspects related to pain and pain management. The patients complete an electronic registration immediately before their first consultation at the outpatient pain clinic. The baseline questions of the OPR cover: Basic demographics; The Modified Oswestry Disability Index to assess general function; A pain drawing to assess pain location; Questions regarding the temporal aspects of pain; Six 0–10 Numeric Rating Scales to assess pain intensity and bothersomeness; The EQ-5D-5L to measure health-related quality of life; The Hopkins Symptom Check List-25 to assess psychological distress; A single question about self-rated health; The general self-efficacy scale to assess the patient’s perceived self-efficacy; The Bodily Distress Syndrome checklist to assess functional disorders; The Injustice Experience Questionnaire to assess whether the patients experience injustice; Chalder Fatigue Questionnaire to assess fatigue; The Insomnia Severity Index to assesses the levels of insomnia symptoms; The Pain Catastrophizing Scale to measure pain catastrophizing and exaggerated negative orientation toward pain stimuli and pain experience; And the SF36v2 to assess patients’ self-report of generic health and wellbeing. The baseline data show that chronic pain patients have a high degree of negative impact in all aspects of their lives. Conclusions and implications The OPR is the most comprehensive pain registry for multidisciplinary and interdisciplinary outpatient pain clinics in Norway. Detailed design of the registry and key baseline data are presented. Registries are of great value in that they enable real world effectiveness outcomes for patients with chronic pain conditions. The OPR can thus serve as a model for similar initiatives elsewhere. The OPR cohort may also serve as a historical control in future studies, both with experimental and observational design.
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Baby, Merilyn, Deepa Badrinath Murthy, Melissa Kaori Litao, Gail Shust, and Bina Cherryl Shah. "Exogenous Cushing’s Syndrome, Hypogonadism and Diabetes Secondary to Megestrol Acetate." Journal of the Endocrine Society 5, Supplement_1 (May 1, 2021): A700. http://dx.doi.org/10.1210/jendso/bvab048.1425.
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Abstract Introduction: Megestrol acetate (MA) is a synthetic progestin that is often prescribed for anorexic patients with HIV due to its effects on weight gain and appetite stimulation. It can cause several endocrine/metabolic abnormalities. Chronic use of MA can cause exogenous Cushing’s Syndrome (ECS) and iatrogenic adrenal insufficiency (AI) due to its stronger affinity for the glucocorticoid receptor (GR). It can also cause gonadotropin suppression, diabetes and hyperprolactinemia. We present a case of a young woman with perinatal HIV/AIDS that developed ECS secondary to MA treatment in the setting of fatigue, rapid weight gain and irregular menses. Case: A 19 year old female with perinatal HIV/AIDS (CD4<200) was treated with MA (200mg/day for 5 months) for anorexia and weight loss. On exam she was pre-hypertensive (BP 138/62), obese (BMI 43.07, SDS +2.25; weight 114kg, SDS +2.34) with increased fat deposition over upper back and abdominal striae, excessive weight gain (21.5 kg in 5 months) suggestive of ECS. She had menarche at 13 years of age and had regular menses until starting MA, upon which she developed oligomenorrhea. A random serum cortisol level was <0.5ug/dl at 1pm with a low ACTH <1.5pg/ml and DHEAS of 13.4ug/dl. Her FSH was 3.4 mIU/L and LH 0.82 mIU/L, estradiol was <2pg/dl and total testosterone <2.5ng/dl consistent with secondary hypogonadism. Liver/kidney function, prolactin and lipid profile were normal. HbA1c increased from 5.3 to 6.4% in 8 months so she was started on metformin. ECS with AI, central hypogonadism and diabetes were all attributed to MA therapy. MA was discontinued gradually over two weeks. Stress dosing of glucocorticoids were advised as needed. Results: Gradual recovery of HPA axis was noted after discontinuation of MA. Two months after taper, serum ACTH level rose to 2.5pg/ml but AM cortisol level remained low at <0.5ug.dl. Her HPA axis showed partial recovery by 5 months with ACTH level of 53.2pg/ml and AM cortisol level of 5.5ug/dl. By 8 months after discontinuing MA therapy, AM cortisol was 9.3ug/dl, suggesting complete HPA axis recovery. Her HPG axis also normalized by 8 months with FSH 6.6 mIU/L and LH of 14.6 mIU/L, estradiol 32pg/dl with regular menses. Metformin was discontinued at 4 months due to hypoglycemia and HbA1C of 5.7%. Subsequently, euglycemia was achieved (HbA1C of 5.4%) within 9 months. BMI was stable (BMI 43.07, SDS +2.25; weight 114kg, SDS +2.34). Conclusion: Multiple endocrine abnormalities may occur due to MA therapy due to its affinity to bind with glucocorticoid and progesterone/androgen receptors. ECS and AI are known to occur with various forms of glucocorticoid use, but rarely can be seen with MA therapy. HPA axis, HPG axis and metabolic parameters should be evaluated and monitored carefully during MA therapy.
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Ugurlu, S., T. Civi Karaaslan, Z. Toker Dincer, and E. Tarakci. "AB0715 THE PREVALENCE OF FIBROMIYALGIA IN PATIENTS WITH FAMILIAL MEDITERRANEAN FEVER AND THE RELATIONSHIP BETWEEN FATIGUE AND QUALITY OF LIFE." Annals of the Rheumatic Diseases 80, Suppl 1 (May 19, 2021): 1389.1–1389. http://dx.doi.org/10.1136/annrheumdis-2021-eular.1288.
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Background:Familial Mediterranean Fever (FMF) can cause various muscle diseases. Because it is a chronic auto inflammatory disease, painful trigger points may be encountered in the examination due to a decrease in the pain threshold (1-3).Objectives:The aim of this study was to determine the prevalence of Fibromiyalgia in patients with FMF, at the same time to identify the relationship between fatigue and quality of life.Methods:Sixtyseven patients (38 female, 29 male) with FMF were enrolled in the study. They were diagnosed with FMF based on the Livneh diagnostic criteria (4). Fibromyalgia involvement of the patients was evaluated according to the Fibromyalgia Impact Questionnaire (FIQ). Patients with diagnose with other chronic disease were excluded. Fatigue Severity Scale (FSS) was used to evaluate fatigue. Quality of life was evaluated with Short Form-36 (SF-36).Results:Respectively, the mean age, disease duration and body mass index were 34.46±12.69 years, 12.66±7.86 years and 24.96±5.42 kg/m2. In addition, 65% of the patients had no rheumatic disease in their family history. The mean of scores of FIQ was 38.66±25.14, the mean of FSS was 38.07±17.56, the mean of SF-36-PCS was 45.55±10.54 and SF36-MCS was 30.93±17.39. Patients were categorized as mild (n=28), moderate (n=24) and severe (n=15) affected according to their FİQ score. The relationships of scores of FIQ, FSS and SF-36 were demonstrated Table 1.Conclusion:Fibromyalgia symptoms can be seen in FMF. According to our results, it has been shown that patients with moderate and severe symptoms have increased fatigue levels and decreased quality of life. In the light of these results, we can say that also the fibromyalgia symptom of patients with FMF should be considered in the treatment.References:[1]Sari, Ismail; Birlik, Merih; Kasifoglu, Timucin. Familial Mediterranean fever: an updated review. European journal of rheumatology, 2014, 1.1: 21.[2]Alayli G, Durmus D, Ozkaya O, Sen HE, Genc G, Kuru O. Frequency of juvenile fibromyalgia syndrome in children with familial Mediterranean fever: effects on depression and quality of life. Clin Exp Rheumatol 2011; 29: S127-32.[3]Langevitz P, Buskila D, Finkelstein R, Zaks N, Neuman L, Sukenik S, et al. Fibromyalgia in familial Mediterranean fever. J Rheumatol 1994; 21: 1335-7.[4]Bashardoust, Bahman. Familial Mediterranean fever; diagnosis, treatment, and complications. Journal of nephropharmacology, 2015, 4.1: 5.Table 1.The correlations of FIQ, FSS and SF-36 scores.FSSSF-36 PCSSF-36 MCSFIQ-mildmean±sd23.78±14.8853.34±7.0140.98±13.73r0.595**-0.014-0.551**p0.0010.9440.002FIQ-moderatemean±sd45.75±10.8341.09±8.8938.13±9.19r0.053-0.379-0.145p0.8060.0680.498FIQ-severemean±sd52.46±10.1138.13±9.1920.32±15.68r0.622*-0.548*-0.268p0.0130.0350.333-Pearson CorrelationDisclosure of Interests:None declared
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Russell, I. Jon. "Fibromyalgia Syndrome: New Developments in Pathophysiology and Management." CNS Spectrums 13, S5 (March 2008): 4–5. http://dx.doi.org/10.1017/s1092852900026766.
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Fibromyalgia syndrome (FMS) is a common, chronically painful condition that is still seeking a home among the clinical professions. It is characterized by moderately severe soft-tissue pain and allodynia, which suggests a role for one group of specialists, but its pathogenesis is in the nociceptive machinery of the central nervous system, which defines the territory of other specialties. Comorbidities such as insomnia, cognitive dysfunction, depression, anxiety, recurrent headaches, dizziness, fatigue, morning stiffness, dysesthesia, irritable bowel syndrome, and irritable urethra logically invoke input from practitioners from almost every field of medicine.The precipitating causes of FMS may vary among individuals, but a mechanism underlying the painful symptoms involves central sensitization leading to an amplified perception of pain. As a result, this condition is recognized as the human model for chronic widespread allodynia. Biological abnormalities that are detected in most patients by objective methods include dysfunctional sleep (polysomnography), central sensitization (functional magnetic resonance imaging), temporal summation (windup, second pain), and facilitation of nociception (elevated spinal fluid levels of substance P, deficient biogenic amines that fail to maintain descending inhibition, and, in primary FMS, elevated spinal fluid levels of nerve growth factor).Treatment of FMS is symptomatic and multimodal, including education, physical modalities, and medications that target central neural pathways. Rehabilitation goals include improved physical function, social adaptation, emotional balance, and a better quality of life. Several series of placebo-controlled clinical trials have made available new medications with unique therapeutic mechanisms. Thus, it can be predicted that the next 10 years will see validation of a clinical case definition, more interest in the underlying pathogenesis, a better understanding of how medical care should be adapted to subgroup variations, new medications with specific domain indications, mechanism-directed polypharmacy, characterization of the genetic predisposition, and more emphasis on preventable inciting events.
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Rauf, Abdur, Tareq Abu-Izneid, Ahmed Olatunde, Anees Ahmed Khalil, Fahad A. Alhumaydhi, Tabussam Tufail, Mohammad Ali Shariati, et al. "COVID-19 Pandemic: Epidemiology, Etiology, Conventional and Non-Conventional Therapies." International Journal of Environmental Research and Public Health 17, no. 21 (November 4, 2020): 8155. http://dx.doi.org/10.3390/ijerph17218155.
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Coronavirus disease 2019 (COVID-19), which reported in an outbreak in 2019 in Wuhan, Hubei province, China, is caused by the SARS-CoV-2 virus. The virus belongs to the beta-coronavirus class, along with the Middle East Respiratory Syndrome coronavirus and Severe Acute Respiratory Syndrome coronavirus. Interestingly, the virus binds with angiotensin-converting enzyme-2 found in host cells, through the spike (S) protein that exists on its surface. This binding causes the entry of the virus into cells of the host organism. The actual mechanism used by the COVID-19 virus to induce disease is still speculative. A total of 44,322,504 cases, a 1,173,189 death toll and 32,486,703 recovery cases have been reported in 217 countries globally as of 28 October 2020. Symptoms from the infection of the virus include chest pain, fever, fatigue, nausea, and others. Acute respiratory stress syndrome, arrhythmia, and shock are some of the chronic manifestations recorded in severe COVID-19. Transmission is majorly by individual-to-individual through coughing, sneezing, etc. The lack of knowledge regarding the mechanism of and immune response to the virus has posed a challenge in the development of a novel drug and vaccine. Currently, treatment of the disease involves the use of anti-viral medications such as lopinavir, remdesivir, and other drugs. These drugs show some efficacy in the management of COVID-19. Studies are still on-going for the development of an ideal and novel drug for treatment. In terms of natural product intervention, Traditional Chinese Medicines (TCM) have been employed to alleviate the clinical manifestation and severity of the disease and have shown some efficacy. This review presents an updated detailed overview of COVID-19 and the virus, concerning its structure, epidemiology, symptoms and transmission, immune responses, and current interventions, and highlights the potential of TCM. It is anticipated that this review will further add to the understanding of COVID-19 and the virus, hence opening new research perspectives.
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Ooi, Soo Liang, Sok Cheon Pak, Peter S. Micalos, Emily Schupfer, Catherine Lockley, Mi Houn Park, and Sung-Joo Hwang. "The Health-Promoting Properties and Clinical Applications of Rice Bran Arabinoxylan Modified with Shiitake Mushroom Enzyme—A Narrative Review." Molecules 26, no. 9 (April 27, 2021): 2539. http://dx.doi.org/10.3390/molecules26092539.
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Rice bran arabinoxylan compound (RBAC) is derived from defatted rice bran hydrolyzed with Lentinus edodes mycelial enzyme. It has been marketed as a functional food and a nutraceutical with health-promoting properties. Some research has demonstrated this rice bran derivative to be a potent immunomodulator, which also possesses anti-inflammatory, antioxidant, and anti-angiogenic properties. To date, research on RBAC has predominantly focused on its immunomodulatory action and application as a complementary therapy for cancer. Nonetheless, the clinical applications of RBAC can extend beyond cancer therapy. This article is a narrative review of the research on the potential benefits of RBAC for cancer and other health conditions based on the available literature. RBAC research has shown it to be useful as a complementary treatment for cancer and human immunodeficiency virus infection. It can positively modulate serum glucose, lipid and protein metabolism in diabetic patients. Additionally, RBAC has been shown to ameliorate irritable bowel syndrome and protect against liver injury caused by hepatitis or nonalcoholic fatty liver disease. It can potentially ease symptoms in chronic fatigue syndrome and prevent the common cold. RBAC is safe to consume and has no known side effects at the typical dosage of 2–3 g/day. Nevertheless, further research in both basic studies and human clinical trials are required to investigate the clinical applications, mechanisms, and effects of RBAC.
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Moskovko, S. P., G. S. Moskovko, M. I. Andriievska, and Ya V. Spivak. "PECULIARITIES OF COMORBID PAIN SYNDROME AND COGNITIVE DYSFUNCTION IN PATIENTS WITH MULTIPLE SCLEROSIS." Актуальні проблеми сучасної медицини: Вісник Української медичної стоматологічної академії 20, no. 4 (December 30, 2020): 216–24. http://dx.doi.org/10.31718/2077-1096.20.4.216.
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In this paper, we reviewed scientific sources on multiple sclerosis, analyzed the latest data on the peculiarities of cognitive dysfunction and comorbid pain syndrome in patients with multiple sclerosis. Multiple sclerosis belongs to the group of chronic progressive demyelinating diseases with a predominant lesion of the central nervous system. It affects over 2.5 million people worldwide and is considered as one of the most disabling neurological disorders. Symptoms range from physical ones including loss of vision, spasticity, bladder and bowel dysfunction, problems with walking and balance, fatigue and pain, to mental problems such as cognitive impairment, depression, and anxiety. Comorbid conditions have a significant impact on the quality of life of patients with multiple sclerosis. This evokes considerable scientific interest, since their presence can cause a delay in diagnosis, change the progression of neurological deficits, reduce physical activity and increase the severity of symptoms of the underlying disease. One of the most common comorbid conditions associated with multiple sclerosis is pain. The prevalence of pain syndrome ranges from 29% to 86%. Patients can consider pain as one of the first symptoms of multiple sclerosis. Moreover, in the treatment and diagnosis of multiple sclerosis, in most cases, the state of cognition is missed or neglected, but it always accompanies the patients in the form of cognitive disorders of varying severity. Cognitive function is understood as the most complex mechanism by which the process of rational cognition of the environment and interaction with it is carried out. Both a series of cognitive tests for multiple sclerosis and an MRI evaluation of gray matter atrophy can help to assess the state of cognition. Also, an additional diagnostic method is transcranial magnetic stimulation, with which it is possible to create a model for mapping the cerebral cortex using evoked motor potentials. Thus, the analysis of the literature has shown that the issues of the influence of comorbidity and cognitive dysfunction on the course of multiple sclerosis, the relationship of the onset of multiple sclerosis with comorbid conditions, and the correlation of neurological deficit with the cognitive ability of patients are not studied completely yet.
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Mathias, Priyanka M., and Eric J. Epstein. "IATROGENIC CUSHING SYNDROME IN AN HIV-INFECTED PATIENT SECONDARY TO CONCOMITANT THERAPY WITH GENVOYA AND EPIDURAL TRIAMCINOLONE." AACE Clinical Case Reports 6, no. 5 (September 2020): e217-e220. http://dx.doi.org/10.4158/accr-2020-0138.
Full textAbstract:
Objective: We report the first known case of Cushing syndrome and secondary adrenal insufficiency in a patient with concomitant use of epidural triamcinolone and Genvoya® (elvitegravir 150 mg/cobicistat 150 mg/emtricitabine 200 mg/tenofovir alafenamide 10 mg) for the human immunodeficiency viruses (HIV). The prompt recognition of this drug-drug interaction is critical to avoid adverse outcomes when glucocorticoids are used with anti-retroviral treatment containing cobicistat, a potent cytochrome P450 3A (CYP3A4) inhibitor. Methods: The patient was evaluated by determining morning serum cortisol concentrations, the serum cortisol response to cosyntropin, and a urine synthetic glucocorticoid panel that is capable of measuring triamcinolone. We also employed the Naranjo Nomogram for Causality as well as a Drug Interaction Probability scale to assess medication-related adverse effects. Long term outcome was assessed by measuring morning serum cortisol and adrenocorticotropic hormone levels. Results: A 76-year-old female with HIV on Genvoya® presented with fatigue, weight loss, and hyperglycemia. She had received multiple epidural triamcinolone injections for chronic back pain before her presentation. We hypothesized that the patient’s presentation of Cushing syndrome and adrenal insufficiency was caused by the inhibition of triamcinolone metabolism by cobicistat. The patient’s antiretroviral therapy was changed to a regimen without cobicistat. She was started on maintenance hydrocortisone to prevent an adrenal crisis. A repeat urine glucocorticoid panel, within 3 days of the patient’s HIV regimen being changed, showed a significant decrease in triamcinolone levels. Conclusion: It is essential to avoid drugs that include cobicistat when administering glucocorticoids that are metabolized via the CYP3A4 pathway due to the risk of developing Cushing syndrome and secondary adrenal insufficiency.
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Fleming, Patrick, Maggie Cheung, and David Sokol. "Complement-Mediated Thrombotic Microangiopathy: A Murky Presentation of a Rare Disease Entity." Blood 132, Supplement 1 (November 29, 2018): 5005. http://dx.doi.org/10.1182/blood-2018-99-119893.
Full textAbstract:
Abstract Complement-mediated thrombotic microangiopathy (TMA), also known as atypical hemolytic uremic syndrome (aHUS) is a rare, hereditary, progressive, life-threatening disorder caused by a disruption in regulation of the alternative pathway of the complement system. Eculizumab, a terminal complement inhibitor, has emerged as a first-line therapy, however data are limited to small case series (Brocklebank et al., 2017). Here, we present a diagnostically challenging case of complement-mediated TMA, who received eculizumab therapy with excellent hematologic response. A 68-year-old female with history of possible Sjogren's syndrome, migraine disorder, chronic fatigue syndrome, inflammatory colitis, hypertension, and poor medical follow up presented with 6-day history of severe fatigue, hematochezia, decreased urine output, dyspnea with exertion and anginal chest pain. 2 weeks prior, patient endorsed "flu-like" illness and had diffuse myalgias without fevers. Further history revealed ibuprofen usage of 800-1200 mg/day for several years. Shortly after admission, patient became severely agitated and confused with an attempt to elope from hospital. During diagnostic workup, labs were significant for hemoglobin 5.6 g/dL, platelets 57,000/uL, serum creatinine 6.6 mg/dL, BUN 101 mg/dL. Peripheral smear showed schistocytes and tear drop cells, low platelets without clumping, and hypochromic normocytic red cells. LDH of 2152 U/L, haptoglobin <34 mg/dL, and GI PCR was panel negative for E. coli O157 and Shiga-like toxin producing E. coli. She was presumed to have thrombotic thrombocytopenic purpura (TTP) as she presented with 4 of the 5 characteristic pentad, including microangiopathic hemolytic anemia, acute renal failure, thrombocytopenia, and severe neurologic findings. Patient received several PRBC transfusions, five plasma exchange treatments, hemodialysis and corticosteroids. She had initial improvement in platelet count and decrease in LDH with plasma exchange, however plateaued by day 5. Further testing revealed low complement C3 level of 51 mg/dL, low complement C4 level of 22.7 mg/dL, and pre-PLEX ADAMSTS13 level of 93%, suggesting complement-mediated TMA as the correct diagnosis. Patient was subsequently transferred to tertiary care center for initiation of eculizumab. Genetic testing was completed, notable for decreased Factor H and a heterozygous missense mutation in complement factor H of uncertain significance, only having been previously reported in a single patient with aHUS (Fremeaux-Bacci et al., 2013). She achieved excellent hematologic response with eculizumab evidenced by improved platelet count, haptoglobin, decreased LDH, however she unfortunately remained dialysis-dependent. Thrombotic microangiopathy (TMA) syndromes are overlapping entities which can be categorized by primary vs secondary etiology. Primary syndromes include TTP (hereditary or acquired), Shiga-toxin mediated HUS, drug-induced TMA and complement mediated TMA. Secondary causes include pregnancy-associated (pre-eclampsia/HEELP syndrome), malignancy, systemic infection, severe hypertension, autoimmune disorders like SLE, and complications from organ transplantation. When evaluating a patient with suspected TMA, it is important to correctly categorize their disease to guide appropriate treatment. Complement-mediated TMA results from a hereditary deficiency of regulatory proteins that restrict activation of alternative complement pathway. These proteins include complement factor H (CFG) and its related proteins (CFHRs), membrane cofactor protein (MCP), CFI. Instead, it may result from an autoantibody inhibiting CFH of CFI. The consequence of this up-regulation is uncontrolled damage to vascular endothelium and renal cells, which manifests as a characteristic pentad. In our case, a CFH gene mutation was identified and history revealed a flu-like illness preceding her hospitalization. It is plausible that this illness may have served as a "second-hit" via complement-amplification. (Asif et al., 2017). Alternatively, in this patient with history of inflammatory colitis and reported Sjogren's syndrome, subclinical autoimmune disorder may also have served as a trigger. This case presentation serves as a reminder to not overlook the "zebra" that is complement-mediated TMA, to allow for prompt initiation of eculizumab therapy. Figure. Figure. Disclosures No relevant conflicts of interest to declare.