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Journal articles on the topic 'Respiratory Insufficiency In adulthood'

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Author: Grafiati

Published: 10 December 2022

Last updated: 30 January 2023

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1

Goyal, N., M. Waldrop, and T. Mozaffar. "Unique myopathy presenting in adulthood with proximal muscle weakness and respiratory insufficiency." Neuromuscular Disorders 25 (October 2015): S282. http://dx.doi.org/10.1016/j.nmd.2015.06.346.

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2

El-Maouche, Diala, Courtney J. Hargreaves, Ninet Sinaii, Ashwini Mallappa, Padmasree Veeraraghavan, and Deborah P. Merke. "Longitudinal Assessment of Illnesses, Stress Dosing, and Illness Sequelae in Patients With Congenital Adrenal Hyperplasia." Journal of Clinical Endocrinology & Metabolism 103, no. 6 (March 22, 2018): 2336–45. http://dx.doi.org/10.1210/jc.2018-00208.

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Abstract Context Patients with congenital adrenal hyperplasia (CAH) are at risk for life-threatening adrenal crises. Management of illness episodes aims to prevent adrenal crises. Objective We evaluated rates of illnesses and associated factors in patients with CAH followed prospectively and receiving repeated glucocorticoid stress dosing education. Methods Longitudinal analysis of 156 patients with CAH followed at the National Institutes of Health Clinical Center over 23 years was performed. The rates of illnesses and stress-dose days, emergency room (ER) visits, hospitalizations, and adrenal crises were analyzed in relation to phenotype, age, sex, treatment, and hormonal evaluations. Results A total of 2298 visits were evaluated. Patients were followed for 9.3 ± 6.0 years. During childhood, there were more illness episodes and stress dosing than adulthood (P < 0.001); however, more ER visits and hospitalizations occurred during adulthood (P ≤ 0.03). The most robust predictors of stress dosing were young age, low hydrocortisone and high fludrocortisone dose during childhood, and female sex during adulthood. Gastrointestinal and upper respiratory tract infections (URIs) were the two most common precipitating events for adrenal crises and hospitalizations across all ages. Adrenal crisis with probable hypoglycemia occurred in 11 pediatric patients (ages 1.1 to 11.3 years). Undetectable epinephrine was associated with ER visits during childhood (P = 0.03) and illness episodes during adulthood (P = 0.03). Conclusions Repeated stress-related glucocorticoid dosing teaching is essential, but revised age-appropriate guidelines for the management of infectious illnesses are needed for patients with adrenal insufficiency that aim to reduce adrenal crises and prevent hypoglycemia, particularly in children.

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3

Magnani, Jessie E., and Steven M. Donn. "Persistent Respiratory Distress in the Term Neonate: Genetic Surfactant Deficiency Diseases." Current Pediatric Reviews 16, no. 1 (April 9, 2020): 17–25. http://dx.doi.org/10.2174/1573396315666190723112916.

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: Respiratory distress is one of the most common clinical presentations in newborns requiring admission to a Neonatal Intensive Care Unit (NICU). Many of these infants develop respiratory distress secondary to surfactant deficiency, which causes an interstitial lung disease that can occur in both preterm and term infants. Pulmonary surfactant is a protein and lipid mixture made by type II alveolar cells, which reduces alveolar surface tension and prevents atelectasis. : The etiology of surfactant deficiency in preterm infants is pulmonary immaturity and inadequate production. Term infants may develop respiratory insufficiency secondary to inadequate surfactant, either from exposure to factors that delay surfactant synthesis (such as maternal diabetes) or from dysfunctional surfactant arising from a genetic mutation. : The genetics of surfactant deficiencies are very complex. Some mutations are lethal in the neonatal period, while others cause a wide range of illness severity from infancy to adulthood. Genes that have been implicated in surfactant deficiency include SFTPA1, SFTPA2, SFTPB, SFTPC, and SFTPD (which encode for surfactant proteins A, B, C, and D, respectively); ABCA3 (crucial for surfactant packaging and secretion); and NKX2 (a transcription factor that regulates the expression of the surfactant proteins in lung tissue). : This article discusses the interplay between the genotypes and phenotypes of newborns with surfactant deficiency to assist clinicians in determining which patients warrant a genetic evaluation.

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4

Southam, Brendan R., Adam P. Schumaier, and Alvin H. Crawford. "Spondylocostal Dysostosis: A Literature Review and Case Report with Long-Term Follow-Up of a Conservatively Managed Patient." Case Reports in Orthopedics 2018 (2018): 1–6. http://dx.doi.org/10.1155/2018/1795083.

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Introduction. Patients with spondylocostal dysostosis (SCD) have congenital spine and rib deformities associated with frequently severe thoracic insufficiency and respiratory compromise. The literature is largely composed of case reports and small cohorts, and there is little information regarding adults with this condition. In this report, we describe the natural history of a conservatively treated patient and include quality-of-life issues such as childbearing, athletic participation, and occupational selection. Case Presentation. We present a patient with SCD who was conservatively treated by a single physician from birth for 31 years. Our patient was capable of a reasonably good quality of life through adulthood, including participation in gymnastics and employment. At age 18, she became pregnant and subsequently terminated the pregnancy due to obstetrical concerns for compromised respiration. She has had intermittent respiratory complaints and occasionally experiences dyspnea with exertion, but this only has limited her during certain activities in the past three years. Currently, she takes naproxen for chronic back pain with periodic exacerbations. Discussion. Other cases in the literature have described adult SCD patients who have received nonoperative treatment and achieved a wide range of functional outcomes. This provides some limited evidence to suggest that select patients with SCD may be treated conservatively and achieve a reasonable quality of life. However, close clinical follow-up with these patients is recommended, particularly early on, considering the high rates of infant morbidity and mortality. Chest physiotherapy and early pulmonary care have been associated with favorable outcomes in infancy. Surgery to increase thoracic volume and correct scoliosis has been shown in some cases to improve respiratory function. Treatment depends on the degree of thoracic insufficiency and quality of life. The natural history of SCD remains largely unknown, but some patients are capable of relatively favorable life spans, employment, and participation in athletics.

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5

Seliukova, N. Yu. "Long-Term Consequences of the Fetoplacental Insufficiency Influence on the State and Functioning of Different Body Systems in Descendants (Literature Review and Own Research)." Ukraïnsʹkij žurnal medicini, bìologìï ta sportu 5, no. 6 (December 12, 2020): 362–69. http://dx.doi.org/10.26693/jmbs05.06.362.

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The literature review presents the results of processing literature data on one of the topical issues of obstetrics and reproductive medicine - placental insufficiency. According to the World Health Organization, the number of infertile couples is gradually increasing in the world every year. In Ukraine, the frequency of infertile marriages among persons of reproductive age ranges from 12 to 18%. The state of the reproductive system of an adult female is influenced by many factors, from embryonic development to the lifestyle of an adult woman. With an inadequate effect of harmful factors on the fetus, the fetoplacental complex may not react properly, and this is how the symptom complex of disorders arises both on the part of the mother and on the part of the fetus, which is called placental insufficiency, it negatively affects the condition and quality of pregnancy and childbirth. Numerous studies have proven the existence of a connection between the effect of certain factors during pregnancy on the state and functionality of various body systems already in adulthood. It was shown that children who were born from mothers with placental insufficiency suffering from cardiovascular diseases have fewer elastic fibers in the arteries, nephrons in the kidneys. In addition, the pancreas has fewer insulin-producing β-cells and reduced vascularization, as well as altered structure and maturation of the brain, lungs (respiratory distress syndrome) and liver, joint dysplasia, and an imbalance of the immune system. When studying the long-term effects of placental insufficiency, various disorders of physical and mental development are observed, as well as increased somatic and infectious morbidity of newborns and children in the first year of life, in the future it may be the cause of the development of diseases such as arterial hypertension, diabetes mellitus, metabolic syndrome, etc. Conclusion. Our studies have shown the negative impact of placental insufficiency on the reproductive system of adult offspring of rats of two sexes who were born to mothers of two age groups. In particular, the level of testosterone in female offspring was increased against the background of the altered structure of the estrous cycle and the pathological state of ovarian histology. In the male offspring, on the contrary, the total testosterone level decreased, but the histology of the testes and the functional state of the sperm remained unchanged

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Padoan, Rita, Serena Quattrucci, Annalisa Amato, Vincenzo Carnovale, Donatello Salvatore, Marco Salvatore, and Giuseppe Campagna. "The Diagnosis of Cystic Fibrosis in Adult Age. Data from the Italian Registry." Diagnostics 11, no. 2 (February 16, 2021): 321. http://dx.doi.org/10.3390/diagnostics11020321.

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Cystic Fibrosis (CF) registries are an essential resource of epidemiological and clinical data. Although the median age at diagnosis is usually reported in the first months of life, a minority of individuals is diagnosed during adulthood. The aim of this study was to describe demographic, genetic, and clinical characteristics of this subgroup of the Italian CF population by using data from the Italian CF Registry (ICFR). Patients ≥18 years at diagnosis were selected and clinical data at diagnosis were analyzed from the 2012–2018 ICFR data (Cohort A). Subjects with diagnosis ≥18 years were selected from 2018 ICFR dataset (Cohort B) to describe their clinical status. In 2012–18 the incidence of late diagnosis was 18.2%, whereas, in 2018, the prevalence of patients diagnosed ≥18 years was 12.54%. The median age of late diagnosis was 36.2 years, ranging from 19.0 to 68.3. The male patients were diagnosed because of infertility in the 45.9% of cases. Median sweat chloride value (SCL) was 69 mmol/L (range 9–150). F508del mutation accounted for 28.3% of alleles. A wide variability in respiratory function was present with a median percent predicted Forced Expiratory Volume in the first second (ppFEV1) of 90.8% (range 20–147%). Low prevalence of pancreatic insufficiency (25%) and of Pseudomonas aeruginosa (Pa) infection (17%) suggest a mild CF phenotype in the majority of patients. The assessment of the clinical status in the 2018 dataset and the comparison between genders showed a greater nutritional and respiratory impairment in females. Further studies are needed to clarify the importance of a true diagnostic delay or of late onset of CF symptoms.

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7

Delaporta, Polyxeni, Christalena Sofocleous, Stavros Doudounakis, Marina Economou, Emmanouil Kanavakis, and Antonios Kattamis. "Variable Clinical Phenotype and Course In Greek Patients with Shwachman-Diamond Syndrome Carrying Identical SBDS Mutations." Blood 116, no. 21 (November 19, 2010): 4431. http://dx.doi.org/10.1182/blood.v116.21.4431.4431.

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Abstract Abstract 4431 Introduction-Background: Shwachman-Diamond syndrome (SDS) is a rare multi-system genetic disorder mainly characterized by exocrine pancreatic insufficiency, bone marrow failure and skeletal abnormalities. Approximately 90% of patients meeting the clinical diagnostic criteria for SDS have mutations in the SBDS gene, located in chromosome 7q11. No genotype-phenotype correlations have been observed in patients with SDS. Patients and Method: Greek patients with similar SBDS mutations are included in this report. They were selected from the series of patients referred to our unit for SBDS gene molecular analysis due to pancreatic insufficiency and impaired hematopoiesis. Patient 1 presented at birth with respiratory difficulties, hypotonia, anemia, neutropenia and thrombocytopenia. She has congenital anomalies including thoracic dystrophy, digit abnormalities, open foramen ovale and hypertelorism. She was found to have myelodysplasia with a bone marrow clone carrying i(7q) chromosomal abnormality in around 32% of the bone marrow cells. Pancreatic insufficiency was clinically evident even at the age of 5 months. Patient 2 has chronic thrombocytopenia ranging between 40.000/μ L to 147.000/μ L, first presenting at the age of 7 years old. She has metaphyseal dysostosis, flared anterior end of ribs, open foramen ovale and growth hormone deficiency. Her pancreatic insufficiency is present from the age of 16 months. Patient 3 (sister of patient 2) has borderline neutropenia, short stature, metaphyseal dysostosis, open foramen ovale and mild pancreatic insufficiency. Patient 4 has thrombocytopenia since the age of 19 years old. She has stable clonal erythropoesis with a clone carrying the 46,X,del(X)(q24→qter) in 45% of the bone marrow cells. She presents recurrent bacterial infections, particularly bartholinitis. She has mild pancreatic insufficiency. Patient 5 presented with chronic neutropenia and decreaced IgA since the age of 2 months. At the age of 12 months she presented hepatomegaly and elevated liver enzymes. Pancreatic insufficiency initially presented in infancy but improved gradually. Genomic DNA was extracted from peripheral blood lymphocytes and molecular analysis with ECMA (Enzymatic Cleavage Mismatch Analysis), RFLPS and direct sequencing was performed allowing detection and characterization of disease causing mutations. PCR primers were specifically designed to amplify the whole coding region (five exons) and the flanking intron/exon junctions of SBDS gene but not the SBDSP pseudogene. RFLPs used the Bsu36I and AciI enzymes for the detection of the two most common c.183-184 TA>CT and 258+2 T>C mutations respectively. Result: All five patients were compound heterozygotes for 183–184 TA>CT and 258+2 T>C, which are the two most common mutations of SDS. One of those (patient 3) was found to be a mosaic which seems to explain the very mild phenotype, and another (patient 5) presented homozygosity for the 258+2 T>C while carrying the 183–184 TA>CT mutation as well. Patient 1 was successfully transplanted by her HLA-identical sister at the age of 12 months. Her pancreatic insufficiency has not improved and she is still on pancreatic enzyme supplementation. Patient 2 is receiving pancreatic enzyme supplementation and also is currently on growth hormone supplementation. Patients 3 and 4 are not receiving pancreatic enzyme supplementation or granulocyte colony-stimulating factor. Patient 5 is currently receiving only granulocyte colony-stimulating factor. Conclusion: Extreme variability ranging from severe clinical phenotype apparent at birth to close-to- normal phenotype in early adulthood was noted in this small series of Greek patients, carrying similar SBDS mutations. Moreover, gene conversion seems to be a frequent event in the SBDS gene. Further studies to evaluate the heterogeneity and the factors affecting the phenotype/genotype relationship in SDS are warranted. Disclosures: No relevant conflicts of interest to declare.

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Cocanougher, Benjamin T., Lauren Flynn, Pomi Yun, Minal Jain, Melissa Waite, Ruhi Vasavada, Jason D. Wittenbach, et al. "Adult MTM1-related myopathy carriers." Neurology 93, no. 16 (September 20, 2019): e1535-e1542. http://dx.doi.org/10.1212/wnl.0000000000008316.

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ObjectiveTo better characterize adult myotubularin 1 (MTM1)–related myopathy carriers and recommend a phenotypic classification.MethodsThis cohort study was performed at the NIH Clinical Center. Participants were required to carry a confirmed MTM1 mutation and were recruited via the Congenital Muscle Disease International Registry (n = 8), a traveling local clinic of the Neuromuscular and Neurogenetic Disorders of Childhood Section, National Institute of Neurological Disorders and Stroke, NIH and Cure CMD (n = 1), and direct physician referral (n = 1). Neuromuscular examinations, muscle MRI, dynamic breathing MRI, cardiac MRI, pulmonary function tests (PFTs), physical therapy assessments including the Motor Function Measure 32 (MFM-32) scale, and X chromosome inactivation (XCI) studies were performed.ResultsPhenotypic categories were proposed based on ambulatory status and muscle weakness. Carriers were categorized as severe (nonambulatory; n = 1), moderate (minimal independent ambulation/assisted ambulation; n = 3), mild (independent ambulation but with evidence of muscle weakness; n = 4), and nonmanifesting (no evidence of muscle weakness; n = 2). Carriers with more severe muscle weakness exhibited greater degrees of respiratory insufficiency and abnormal signal on muscle imaging. Skeletal asymmetries were evident in both manifesting and nonmanifesting carriers. Skewed XCI did not explain phenotypic severity.ConclusionThis work illustrates the phenotypic range of MTM1-related myopathy carriers in adulthood and recommends a phenotypic classification. This classification, defined by ambulatory status and muscle weakness, is supported by muscle MRI, PFT, and MFM-32 scale composite score findings, which may serve as markers of disease progression and outcome measures in future gene therapy or other clinical trials.

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Bogdan, Raluca Daniela, Roxana Elena Bohiltea, and Adrian Ioan Toma. "Respiratory Follow Up of the Premature Neonates—Rationale and Practical Issues." Journal of Clinical Medicine 11, no. 6 (March 21, 2022): 1746. http://dx.doi.org/10.3390/jcm11061746.

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The aim of the review was to present the state of knowledge about the respiratory pathology in former premature neonates (children that were born preterm—before 37 weeks of gestation—and are examined and evaluated after 40 weeks corrected age) other than chronic lung disease, in order to provide reasons for a respiratory follow-up program for this category of patients. After a search of the current evidence, we found that premature infants are prone to long-term respiratory consequences due to several reasons: development of the lung outside of the uterus, leading to dysmaturation of the structures, pulmonary pathology due to immaturity, infectious agents or mechanical ventilation and deficient control of breathing. The medium- to long-term respiratory consequences of being born before term are represented by an increased risk of respiratory infections (especially viral) during the first years of life, a risk of recurrent wheezing and asthma and a decrease in pulmonary volumes and airway flows. Late preterm infants have risks of pulmonary long-term consequences similar to other former premature infants. Due to all the above risks, premature neonates should be followed in an organized fashion, being examined at regular time intervals from discharge from the maternity hospital until adulthood—this could lead to an early detection of the risks and preventive therapies in order to improve their prognosis and assure a normal and productive life. The difficulties related to establishing such programs are represented by the insufficient standardization of the data gathering forms, clinical examinations and lung function tests, but it is our belief that if more premature infants are followed, the experience will allow standards to be established in these fields and the methods of data gathering and evaluation to be unified.

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Levytskyi, A. F., V. O. Rogozinskyi, M. M. Dolianytskyi, and L. V. Duda. "Halo-gravity traction in the treatment of complex spinal deformities in children with respiratory dysfunctions." Paediatric Surgery. Ukraine, no. 3(72) (September 29, 2021): 10–14. http://dx.doi.org/10.15574/ps.2021.72.10.

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HGT is a safe technique as the world literature describes complications in the form of loosening of the pins or superficial infections of the skin around the pins, which are not significant and do not pose a threat to the patient’s life. Purpose – to improve the results of the ventilation function of the lungs in patients with complex spinal deformities through the preliminary use of halo gravity traction and to introduce an effective and safe method for the treatment of complex spinal deformities in children with respiratory dysfunctions. Materials and methods. 64 children with complex spinal deformities (>100°) were treated in the orthopedic and traumatology department of the Okhmatdet NSPU using halo gravity traction during the period from 2003 until 2018. Of these, 38 are boys and 26 are girls. The average age of the patients was 11.6 years. The average Risser score was 3.8 (P>0.01). Results. According to the data of spirography performed, 46% of patients had moderate ventilation disorders and 54% – severe ventilation disorders (FVC<60% – grade 3 and 4 of ventilation failure). Mixed type disorders were recorded in 83% of patients, and restrictive type disorders in 17% (8/48) of children. After HGT, there was an improvement in pulmonary function indicators: an increase in FVC from 63.19% to 71.77% and FEV1 from 54.71% to 65.46%, Tiffeneau-Pinelli index – from 74.59% to 85.33%. Compared with the initial level of indicators, the improvement in FVC was 13.6% after HGT and 14.6% in dynamics during the year, and FEV1 – 19.6% and 21.6%, respectively. The results obtained indicate a significant improvement in the ventilation function of the lungs, especially due to the degree of FEV1 increase, which correlates with the degree of improvement in performance, mortality and life prognosis. Conclusions. The use of HGT makes it possible to improve the results of the final correction of spinal deformity, which in turn significantly improves the ventilation function of the lungs, which in turn helps to reduce the risks of mortality due to pulmonary insufficiency in adulthood. The choice of the appropriate methods of surgical correction for complex deformity of the spine is a prerequisite for successful treatment and the achievement of three-dimensional correction of the spine to maximally approximate its parameters to the physiological norm. The indication for halo gravity traction is a rigid scoliotic deformity of the spine with a deformity angle (>100°). This study was conducted in accordance with the principles of the Helsinki Declaration. The research protocol was approved by the Local Ethics Committee of the institutions mentioned in the work. Informed parental agreement was obtained for the research. No conflict of interests was declared by the authors. Key words: spinal deformity, respiratory dysfunctions, halo-gravity traction.

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11

Storek, Jan, Ansamma Joseph, German Espino, Monja A. Dawson, Daniel C. Douek, Keith M. Sullivan, Mary E. D. Flowers, et al. "Immunity of patients surviving 20 to 30 years after allogeneic or syngeneic bone marrow transplantation." Blood 98, no. 13 (December 15, 2001): 3505–12. http://dx.doi.org/10.1182/blood.v98.13.3505.

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Abstract The duration of immunodeficiency following marrow transplantation is not known. Questionnaires were used to study the infection rates in 72 patients surviving 20 to 30 years after marrow grafting. Furthermore, in 33 of the 72 patients and in 16 donors (siblings who originally donated the marrow) leukocyte subsets were assessed by flow cytometry. T-cell receptor excision circles (TRECs), markers of T cells generated de novo, were quantitated by real-time polymerase chain reaction. Immunoglobulin G2 (IgG2) and antigen-specific IgG levels were determined by enzyme-linked immunosorbent assay. Infections diagnosed 15 years after transplantation occurred rarely. The average rate was 0.07 infections per patient-year (one infection every 14 years), excluding respiratory tract infections, gastroenteritis, lip sores, and hepatitis C. The counts of circulating monocytes, natural killer cells, B cells, CD4 T cells, and CD8 T cells in the patients were not lower than in the donors. The counts of TREC+ CD4 T cells in transplant recipients younger than age 18 years (at the time of transplantation) were not different from the counts in their donors. In contrast, the counts of TREC+ CD4 T cells were lower in transplant recipients age 18 years or older, even in those with no history of clinical extensive chronic graft-versus-host disease, compared with their donors. The levels of total IgG2 and specific IgG against Haemophilus influenzae and Streptococcus pneumoniae were similar in patients and donors. Overall, the immunity of patients surviving 20 to 30 years after transplantation is normal or near normal. Patients who received transplants in adulthood have a clinically insignificant deficiency of de novo–generated CD4 T cells, suggesting that in these patients the posttransplantation thymic insufficiency may not be fully reversible.

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Stanishevska, N. V. "Modern concept of biological identification of selenoproteins." Regulatory Mechanisms in Biosystems 9, no. 4 (October 19, 2018): 553–60. http://dx.doi.org/10.15421/021883.

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Humans possess 25 selenoproteins, approximately half of which are enzymes (selenoenzymes) required for preventing, regulating, or reversing oxidative damage, while others participate in providing calcium metabolism, thyroid hormone maintenance, protein synthesis, cytoskeletal structure etc. This review examines the latest evidences of the biological effects of selenoproteins according to the method of complex analysis of the material. Selenoprotein P promotes insulin resistance in type 2 diabetes, mediates myocardial ischemic-reperfusion injuries and provides protection against disease by reducing chronic oxidative stress. Selenoprotein T is expressed at the endoplasmic reticulum membrane in all cells during development, but is confined to endocrine tissues in adulthood, controls homeostasis of glucose and prevents neurodegeneration by reducing oxidative stress factors. Expression of selenoprotein K is required for efficient Ca2+ flux into melanoma cancer cells, tumour growth and metastasic potential depend on SelK but it suppresses human choriocarcinoma cells. SelK also serves to maintain the normal physiological functions of skeletal muscle. Selenoprotein N deficiency, caused by mutations in the human gene, promotes myopathy characterized by muscle weakness, spinal rigidity, respiratory insufficiency. Sel N participates in normal physiology of skeletal and smooth muscle tissues. Selenoprotein M is located in the endoplasmic reticulum, characterized by high expression in the brain, antioxidative, neuroprotective activity and regulates intracellular Ca2+ levels. Also, the overexpression of SelM was detected in human hepatocellular carcinoma. Selenoprotein S is mentioned as a regulator of ER stress and inflammatory processes. Selenoprotein F controls cell proliferation by the impact on G1period of the cell cycle. Moreover, it is implicated in the pathogenesis of some types of cancer. The Sel F deficiency reduces the migration and invasive ability of the cells. Knockdown of selenoprotein W in rodents leads to increased release of Ca2+, causes oxidative ultramicroscopic injuries of the endoplasmic reticulum and mitochondria ultrastructure, which in turn increases the levels of inflammatory factors. Selenoprotein H is involved in redox regulation, in tumourogenesis. Knockdown of selenoprotein H decreases cellular differentiation and increases proliferation and migration of cells. Selenoproteins U, V, I, O, R are recently identified and their functions are not clearly known. The data analyzed in the review help determine promising directions in the study of the selenoproteins.

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YOKOYAMA, Tetsuro. "Respiratory insufficiency." Nihon Naika Gakkai Zasshi 79, no. 9 (1990): 1134–43. http://dx.doi.org/10.2169/naika.79.1134.

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Haapaniemi, Emma M., Meri Kaustio, Helka Nurkkala, Merja Helminen, Satu Mustjoki, Einarsdottir Elisabet, Sahu Biswajyoti, et al. "Dominant NFKB1 Mutations Cause Antibody Deficiency and Autoinflammatory Episodes." Blood 126, no. 23 (December 3, 2015): 206. http://dx.doi.org/10.1182/blood.v126.23.206.206.

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Abstract The NFkB signaling pathway is a master regulator of the immune response. Recently, dominant mutations in NFKB2 have shown to cause antibody deficiency with adrenal insufficiency. We investigated two families with antibody deficiency and autoinflammatory features, with onset in teenage years and early adulthood (Fig. 1 and Table 1). In family 1, all patients available to study presented with respiratory tract infections and B cell dysfunction marked by hypogammaglobulinemia, poor antibody response to vaccines, or low switched memory B cell counts. Several experienced recurrent episodes of aphthous mucositis in upper gastrointestinal and genital area, sometimes accompanied by abdominal pain, monoarthritis, or fever with elevated inflammatory markers (peripheral blood leukocytes >10x106 cells/ml, C reactive protein >100 mg/L). A lesional biopsy revealed lymphocytic small cell vasculitis reminiscent of Behcet's disease. In family 2, all patients presented with respiratory tract infections, hypogammaglobulinemia, and poor vaccine responses. Based on the pedigrees, we assumed autosomal dominant inheritance. For family 1, we performed genotyping and linkage analysis coupled with whole genome sequencing to pinpoint the causative variant. Linkage analysis showed a 15.4 Mb haplotype on chr4 segregating with the phenotype in all affected individuals. When focusing our search on novel, heterozygous variants negatively affecting conserved residues, we identified only one variant in this genomic location, localizing to NFKB1 gene (p.H67R). In family 2, we exome sequenced one affected individual and filtered the data for novel heterozygous variants negatively affecting conserved residues. This resulted in 17 variants, out of which the I553M NFKB1 variant was considered the best candidate. Several functional analyses showed that the mutations had a negative impact on NFKB1 function. The H67R variant increased NFKB1 affinity to NEMO and delayed protein entry to nucleus, when assessed by affinity purification mass spectrometry and immunofluorescence microscopy. The mutation also decreased NFKB1 transcriptional activity, when expressed together with an NFkB-responsive luciferase reporter, and showed a neomorphic DNA binding pattern on chromatin immunoprecipitation-sequencing. Furthermore, the cell growth was hampered when the mutant NFKB1 was overexpressed in cultured HEK293 cells. The I553M showed a similar negative effect on cultured cell proliferation. Furthermore, the I553M variant negatively affected serine S907 and S893 phosphorylation, leading to defective posttranslational processing of the full-length NFKB1 upon TNF stimulation. To conclude, we show that hypogammaglobulinemia and Behcet's disease-like autoinflammatory syndrome can be caused by mutations in NFKB1. This suggests that a subset of Behcet's disease cases may be of monogenic origin, and highlights the role of NFkB complex in B cell maturation and innate immune regulation. Table 1. Patient characteristics Patient 1 2 3 4 5 6 7 8 9 10 11 12 Age 55 43# 25 29 40 30 37 7 10 60# 61 32 Sex F M F F F F M F M M F M Mutation status H67R ND H67R H67R H67R H67R H67R H67R H67R ND I553M I553M Immunodeficiency Infections URTI RTI URTI - URTI URTI URTI URTI - RTI RTI RTI Antibody deficiency Hypogammaglobulinemia, SAD ND Hypogammaglobulinemia, SAD - IgG subclass deficiency, SAD Hypogammaglobulinemia, SAD Hypogammaglobulinemia, SAD Hypogammaglobulinemia Hypogammaglobulinemia Hypogammaglobulinemia Hypogammaglobulinemia, SAD SAD Immunoglobulin replacement + - + - - + + - - - + - Immune dysregulation Febrile attacks - + + + - - + + - - - - Complex aphtae Mouth, genitalia ND Mouth, genitalia Mouth, genitalia - Mouth Esophagus Mouth, esophagus - - - - Arthritis Monoarthritis - Monoarthritis Monoarthritis - - - - - - Oligoarthritis - Gut disease Periodic abdominal pain, chronic idiopathic diarrhea ND Periodic abdominal pain, microscopic colitis Periodic abdominal pain - - - Periodic abdominal pain - ND Chronic idiopathic diarrhea Coeliac disease Other - Hyperinflammatory response and death after gallbladder surgery - Iritis, Hyperinflammatory response to tooth excision Kidney tumor - Rudimentary left kidney - - - Astma, hypothyreosis - URTI, upper respiratory tract infections; RTI, respiratory tract infections including recurrent pneumonia; SAD, Specific antibody deficiency; ND, No data; #Death age Figure 1. Family pedigrees. Figure 1. Family pedigrees. Disclosures Mustjoki: Sigrid Juselius Foundation: Research Funding; Signe and Ane Gyllenberg Foundation: Research Funding; the Finnish Cancer Societies: Research Funding; Novartis: Honoraria, Research Funding; Academy of Finland: Research Funding; Finnish Cancer Institute: Research Funding; Pfizer: Honoraria, Research Funding; Bristol-Myers Squibb: Honoraria, Research Funding. Saarela:Roche: Honoraria.

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15

KIRA, SHIRO. "Respiratory organ.Chronic respiratory insufficiency." Nihon Naika Gakkai Zasshi 80, no. 3 (1991): 458–61. http://dx.doi.org/10.2169/naika.80.458.

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16

Pearl, Ronald G. "Posttraumatic Respiratory Insufficiency." Anesthesia & Analgesia 74, no. 6 (June 1992): 787???789. http://dx.doi.org/10.1213/00000539-199206000-00001.

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BARZILAY, EITAN, AMIRAM LEV, MILAD IBRAHIM, and CARLOS LESMES. "Traumatic respiratory insufficiency." Critical Care Medicine 15, no. 2 (February 1987): 118–21. http://dx.doi.org/10.1097/00003246-198702000-00007.

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18

OKUBO, TAKAO. "Respiratory insufficiency and fatigue of respiratory muscles." Nihon Naika Gakkai Zasshi 83, no. 9 (1994): 1621–26. http://dx.doi.org/10.2169/naika.83.1621.

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19

Kosov, М. N. "Respiratory insufficiency in premature children." Journal of obstetrics and women's diseases 51, no. 2 (April 14, 2002): 62–65. http://dx.doi.org/10.17816/jowd90409.

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Pathology of respiratory system plays a significant role in morbidity and mortality of premature neonates and it means that searching of new and remodeling of existing methods to diagnose and treat respiratory insufficiency (RI) is of particular importance. We evaluated a new method of an early preclinical diagnosis of RI based on using of capnography assessment of end- tidal CO2 concentration, which makes possible to propose a leading pathophysiological mechanism of RI. Using of the gradient between end-tidal and capillary CO2 concentrations helps to predict development of serious ventilation-perfusion mismatch when it exceeds 2O mm Hg. So, in the treatment of RI in neonates individualized therapy should be used, based on the assessment of the leading pathophysiological mechanism.

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20

Kuru, Satoshi. "Respiratory Insufficiency in Myotonic Dystrophy." Japanese Journal of Rehabilitation Medicine 59, no. 2 (February 18, 2022): 156–60. http://dx.doi.org/10.2490/jjrmc.59.156.

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21

Chervin, Ronald D., and Christian Guilleminault. "Diaphragm Pacing for Respiratory Insufficiency." Journal of Clinical Neurophysiology 14, no. 5 (September 1997): 369–77. http://dx.doi.org/10.1097/00004691-199709000-00003.

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22

Fishman, A. P. "THE ROADS TO RESPIRATORY INSUFFICIENCY." Annals of the New York Academy of Sciences 121, no. 3 (December 16, 2006): 657–61. http://dx.doi.org/10.1111/j.1749-6632.1965.tb14235.x.

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23

Saaresranta, Tarja, Pa¨ivi Polo-Kantola, Kerttu Irjala, Hans Helenius, and Olli Polo. "Respiratory Insufficiency in Postmenopausal Women." Chest 115, no. 6 (June 1999): 1581–87. http://dx.doi.org/10.1378/chest.115.6.1581.

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24

KUNO, Kenshi. "Management of chronic respiratory insufficiency." Nihon Naika Gakkai Zasshi 80, no. 9 (1991): 1491–98. http://dx.doi.org/10.2169/naika.80.1491.

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25

HALL, John C., Richard A. Tarala, and Jane L. HALL. "Respiratory insufficiency after abdominal surgery." Respirology 1, no. 2 (June 1996): 133–38. http://dx.doi.org/10.1111/j.1440-1843.1996.tb00022.x.

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26

van Berkel, M., H. Dik, J. W. van der Meer, and J. Versteeg. "Acute respiratory insufficiency from psittacosis." BMJ 290, no. 6480 (May 18, 1985): 1503–4. http://dx.doi.org/10.1136/bmj.290.6480.1503.

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27

Wheatley, T., and G. R. Park. "Acute respiratory insufficiency from psittacosis." BMJ 291, no. 6487 (July 6, 1985): 53–54. http://dx.doi.org/10.1136/bmj.291.6487.53-b.

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28

Winter, J. H., D. Lyon, J. P. Vance, R. D. Stevenson, and C. D. Forbes. "Acute respiratory insufficiency from psittacosis." BMJ 291, no. 6487 (July 6, 1985): 54. http://dx.doi.org/10.1136/bmj.291.6487.54.

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29

ISHIHARA, KYOSUKE. "Respiratory insufficiency Advances in diagnosis and treatments. II. Treatments of respiratory insufficiency. 3. Pharmacotherapy." Nihon Naika Gakkai Zasshi 88, no. 1 (1999): 63–69. http://dx.doi.org/10.2169/naika.88.63.

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30

HIRATA, KAZUTO. "Respiratory insufficiency Advances in diagnosis and treatments. II. Treatment of respiratory insufficiency. 4. Exercise therapy." Nihon Naika Gakkai Zasshi 88, no. 1 (1999): 70–76. http://dx.doi.org/10.2169/naika.88.70.

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YONEDA, TAKAHIRO. "Respiratory insufficiency Advances in diagnosis and treatments. II. Treatment of respiratory insufficiency. 8. Nutritional management." Nihon Naika Gakkai Zasshi 88, no. 1 (1999): 94–99. http://dx.doi.org/10.2169/naika.88.94.

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YOSHIDA, MINORU. "Respiratory insufficiency. Advances in diagnosis and treatment. 2. Treatment. 2. Physical therapy for respiratory insufficiency." Nihon Naika Gakkai Zasshi 79, no. 6 (1990): 743–50. http://dx.doi.org/10.2169/naika.79.743.

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33

Serra Soler, Guillermo, María Soledad Gogorza Pérez, Ana Jiménez Portilla, and Vicente Pereg Macazaga. "Primary adrenal insufficiency due to X-linked adrenoleukodystrophy diagnosed in adulthood." Endocrinología, Diabetes y Nutrición (English ed.) 64, no. 8 (October 2017): 458–59. http://dx.doi.org/10.1016/j.endien.2017.10.007.

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34

İNKAYA, Ahmet Çağkan, Ebru ORTAÇ ERSOY, Serpil ÖCAL, and Serhat ÜNAL. "HIV Positive Patient with Respiratory Insufficiency." Flora the Journal of Infectious Diseases and Clinical Microbiology 21, no. 4 (March 1, 2016): 182–85. http://dx.doi.org/10.5578/flora.20955.

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35

Chanatry, Brian J., and Andrew Gettinger. "Progressive respiratory insufficiency after cesarean section." Critical Care Medicine 23, no. 1 (January 1995): 204–7. http://dx.doi.org/10.1097/00003246-199501000-00032.

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36

Harvald, Bent, Lise Hendriksen, and Lene Høy. "Alkalosis in Patients with Respiratory Insufficiency." Acta Medica Scandinavica 180, no. 5 (April 24, 2009): 513–18. http://dx.doi.org/10.1111/j.0954-6820.1966.tb02864.x.

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37

Zifko, U., B. G. Young, and C. F. Bolton. "Electrophysiological monitoring in neurological respiratory insufficiency." Journal of Neurology, Neurosurgery & Psychiatry 62, no. 3 (March 1, 1997): 299–300. http://dx.doi.org/10.1136/jnnp.62.3.299.

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38

Hickey, S. A., G. R. Ford, J. N. G. Evans, J. A. Patrick, and G. T. Spencer. "Tracheostomy closure in restrictive respiratory insufficiency." Journal of Laryngology & Otology 104, no. 11 (November 1990): 883–86. http://dx.doi.org/10.1017/s0022215100114240.

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AbstractA retrospective study is presented of 31 patients who required ventilatory support via a tracheostomy for periods of one month to 27 years whilst in a tertiary referral centre for the care of patients with restrictive respiratory insufficiency. All patients underwent closure of a long-standing tracheostomy. Post-operative follow-up periods of up to 16 years are documented. The indications for and the complications of tracheostomy closure in patients with severe chronic restrictive respiratory insufficiency requiring long-term respiratory support are discussed. It is concluded that the benefits of operative tracheostomy closure outweigh the disadvantages in this unusual type of patient.

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39

Puri, Prem. "Urinoma drainage for neonatal respiratory insufficiency." Journal of Pediatric Surgery 26, no. 1 (January 1991): 119. http://dx.doi.org/10.1016/0022-3468(91)90478-c.

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40

&NA;. "Respiratory insufficiency from dapsone-induced methemoglobinemia." AIDS 5, no. 11 (November 1991): 1392–93. http://dx.doi.org/10.1097/00002030-199111000-00023.

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41

Hoffer, F. A., W. D. Winters, A. B. Retik, and S. A. Ringer. "Urinoma drainage for neonatal respiratory insufficiency." Pediatric Radiology 20, no. 4 (March 1990): 270–71. http://dx.doi.org/10.1007/bf02019664.

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42

KAWAKAMI, YOSHIKAZU. "Respiratory organ. Countermeasures for chronic respiratory insufficiency---recent progress." Nihon Naika Gakkai Zasshi 79, no. 3 (1990): 392–95. http://dx.doi.org/10.2169/naika.79.392.

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OTA, YASUYO. "Respiratory organ.3.Respiratory insufficiency and oxygen inhalation therapy." Nihon Naika Gakkai Zasshi 81, no. 3 (1992): 427–30. http://dx.doi.org/10.2169/naika.81.427.

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44

KIMURA, KENTARO. "Respiratory insufficiency Advances in diagnosis and treatments. II. Treatment of respiratory insufficiency. 7. Home respiration therapy." Nihon Naika Gakkai Zasshi 88, no. 1 (1999): 89–93. http://dx.doi.org/10.2169/naika.88.89.

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45

TOMITA, TOMOYUKI. "Respiratory insufficiency : the advances of diagnosis and treatment. 2. Treatment. 1. Respiratory insufficiency and oxygenation therapy." Nihon Naika Gakkai Zasshi 79, no. 6 (1990): 738–42. http://dx.doi.org/10.2169/naika.79.738.

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46

KONNO, KIMIO. "Respiratory insufficiency : the advances of diagnosis and treatment. 2. Treatment. 5. Management of chronic respiratory insufficiency." Nihon Naika Gakkai Zasshi 79, no. 6 (1990): 762–70. http://dx.doi.org/10.2169/naika.79.762.

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47

KIDA, KOZUI. "Respiratory insufficiency Advances in diagnosis and treatments. II. Treatment of respiratory insufficiency. 2. Comprehensive rehabilitation for respiration." Nihon Naika Gakkai Zasshi 88, no. 1 (1999): 57–62. http://dx.doi.org/10.2169/naika.88.57.

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48

KUNO, KENSHI. "Respiratory insufficiency. Advances in diagnosis and treatment. 2. Treatment. 8. The treatment of respiratory insufficiency during sleep." Nihon Naika Gakkai Zasshi 79, no. 6 (1990): 782–86. http://dx.doi.org/10.2169/naika.79.782.

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49

Chevalier, Robert L., Barbara A. Thornhill, and Alice Y. Chang. "Unilateral ureteral obstruction in neonatal rats leads to renal insufficiency in adulthood." Kidney International 58, no. 5 (November 2000): 1987–95. http://dx.doi.org/10.1111/j.1523-1755.2000.00371.x.

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50

Ni, Yuan, Dan Xu, Feng Lv, Yang Wan, Guanlan Fan, Wen Zou, Yunxi Chen, Linguo Pei, Jing Yang, and Hui Wang. "Prenatal ethanol exposure induces susceptibility to premature ovarian insufficiency." Journal of Endocrinology 243, no. 1 (October 2019): 43–58. http://dx.doi.org/10.1530/joe-19-0063.

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Prenatal ethanol exposure (PEE) adversely affects the offspring reproductive system. We aimed to confirm the susceptibility to premature ovarian insufficiency (POI) in female PEE offspring and elucidate its intrauterine programming mechanism. The pregnant Wistar female rats were intragastrically administered with 4 g/kg × day of ethanol from gestational day (GD) 9 to 20. Offspring reproductive parameters were detected on GD20, postnatal week (PW) 6 and PW12. The PEE foetuses showed a decreased number of oocytes, increased ovarian cell apoptosis and upregulated expression levels of ovarian insulin-like growth factor 1 (IGF1) signalling pathway and steroidogenic enzymes. The proportion of atretic follicles in adult rats was increased, while the number of anti-Müllerian hormone-positive antral follicles was decreased. The serum oestradiol (E2) levels were decreased, but the follicle stimulation hormone levels were elevated. The ovarian Igf1 signalling pathway was transformed from activation during puberty to relative inhibition in adulthood, and the expression levels of ovarian steroidogenic enzymes were inhibited in adulthood. Furthermore, we treated the human granulosa cell line KGN with different ethanol concentrations (15, 30, 60, 120 mM) and found that the expression of IGF1 signalling pathway components, 3β-HSD and P450arom, as well as the production of E2, was increased. After IGF1 siRNA transfection, P450arom expression and E2 production were downregulated. These results suggest that PEE induces POI susceptibility in adult females, which may be caused by over-activation of the foetal ovarian Igf1 signalling pathway and steroidogenesis under PEE, resulting in accelerated early development of folliculogenesis and depletion of primordial follicles.

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