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Journal articles on the topic 'Diabetes Mellitus, Beta Cells, ACE2, SARS-CoV-2'
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Nimje, Prajakta D., Vidya Wasnik (Thatere), and Sumeeta Jain. "MANAGEMENT THROUGH AYURVEDIC MEDICATIONS AND LIFESTYLE MODIFICATION (PATHYASEVANA AND YOGASANA) IN A CASE OF POST-COVID COMPLICATION DIABETES MELLITUS (TYPE 2 DM): A SINGLE CASE STUDY." International Ayurvedic Medical Journal 9, no. 10 (2021): 2619–28. http://dx.doi.org/10.46607/iamj5409102021.
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Diabetes is an asymptomatic disease in most people, so there could be a good number of people who may not be aware of their diabetes before they caught COVID-19. Some studies state that in poorly resourced countries, as many as 50% of people with chronic illnesses, such as diabetes, are undiagnosed. Theoretically, COVID-19 can also cause diabetes as the pancreas have ACE2 receptors, which can enable SARS COV2 to enter the pancreatic beta cells, resulting in structural and functional damage. The present study is carried out to know the traditional Ayurvedic treatment for Diabetes Mellitus. For Diabetes Ayurvedic drugs, Pathyasevana and Yogic lifestyle are one of the best choices of management for their prime role in maintaining blood sugar levels and preventing Diabetes. The present study showed a significant effect on associated complaints. Objectives: - To study the effect of Ayurvedic medications and lifestyles modification (Pathyasevana and Yogasana) on Post Covid complications Type 2 Diabetes Mellitus. Materials and Methods: A 33-year-old male, reported to the Government Ayurveda college and hospital, Nagpur. With complaints of loss of appetite, weakness, sweet taste of mouth, mild polydipsia, mild polyurea excessive mental stress, and Insomnia for the last two months. For that, he had taken treatment of allopathic medicine for a few days, but he was not satisfied. He had been given Ayurvedic medications for 3 months. Appropriate modifications were done at diet and lifestyle as per Ayurvedic text. Proper Yoga protocol was provided to him. Fasting and Post Prandial blood sugar levels were measured by an electronic glucometer before and after treatment. Result: - Improvement in subjective and objective symptoms was found. Mild to moderate improvement was noted in weakness, sweet taste of mouth, mild polydipsia, mild polyurea, Insomnia was reduced. Conclusion: - Ayurvedic medicines and lifestyle modifications can be considered as a mainstream treatment in the case of newly diagnosed post covid diabetes mellitus. Keywords: Diabetes Mellitus, Post covid complication, Yogasana, Lifestyle modification.
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Junhai, Gazi Rayeeda, Hasi Rani Saha, and Bidhan Chandra Sarkar. "Prevalence of COVID-19 Among Older People with Type 2 Diabetes Mellitus: A Systematic Review." International Journal of Science and Healthcare Research 7, no. 3 (2022): 273–88. http://dx.doi.org/10.52403/ijshr.20220738.
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Background: On March 11, 2020, the WHO proclaimed the Coronavirus Disease 2019 (COVID-19) pandemic owing to coronavirus-2 (SARS-CoV-2). SARS-CoV-2 is a zoonotic virus that may be spread from bats to humans through airborne droplets and aerosols. SARS-CoV-2 spike protein has a high binding affinity for ACE2 receptors, widely expressed throughout the respiratory system, notably in epithelial lung cells. ACE2 receptors are found in intestinal mucosal, endothelial, heart, renal epithelial as well as cerebral neuronal cells, explaining COVID-19 extrapulmonary symptoms like diarrhea, nausea, vomiting, chest pain, heart failure, renal injury, headache, and confusion. Older persons with type2 diabetes mellitus and hypertension are more susceptible to SARS-CoV-2 infection as drugs by which they are treated promote ACE2 receptor expression. Moreover, comorbidities increase the probability of poor outcomes after infection by the SARS-CoV-2. Research links COVID-19 to hyperglycemia in the elderly with type 2 diabetes. Twenty percent of people with diabetes get severe pneumonia and a septic course from viral infections. Diabetes contributed to sickness severity and fatality in MERS (MERS-CoV). Epidemiological findings in SARS-CoV-2-affected regions, CDC data, and other national health centers and hospitals suggest that individuals with diabetes had a 50% greater chance of dying from COVID-19. Methods: This systematic review involves a critical and reproducible summary of the results of the available publications on COVID-19 and diabetic elderly patients’ topics and questions. Fourteen studies (6 retrospective cohorts, two prospective, two cohorts, one combined retrospective, one observational, one cross-sectional, and one hospital-based study) were included in this systematic review. Results: From all studies, the mean age of older adults with type 2 diabetes mellitus who suffered from COVID-19 was 50 to 89 years. The majority of the studies showed the male predominance of infection. The pooled prevalence of COVID-19 among diabetes mellitus elderly patients was 29.8%. Conclusions: Diabetes patients had a greater COVID-19 prevalence and severity, according to several explanations. Diabetes Mellitus increases the risk of infection due to innate and adaptive immunity deficiencies. Post COVID-19 complications arise due to a lack of equilibrium between pro-inflammatory and anti-inflammatory cytokine networks in type 2 diabetes mellitus, contributing to increased mortality. Therefore, this study necessitates a large investigational study to find out how to boost the immune response against SARS-CoV-2 infection in an equilibrium manner not to produce much inflammatory cytokine in type 2 diabetes mellitus individuals to reduce the risk of developing complications and mortality consequently. Keywords: COVID-19, Diabetes mellitus, Type-2 diabetes, Elderly.
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Kadir, Nursin Abdul, and Ida Parwati. "COVID-19 (Symptomatic Non-Respiratory) with Type 2 Diabetes Mellitus." INDONESIAN JOURNAL OF CLINICAL PATHOLOGY AND MEDICAL LABORATORY 29, no. 1 (2023): 101–6. http://dx.doi.org/10.24293/ijcpml.v29i1.1863.
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COVID-19 is a respiratory infection caused by a new strain of Coronavirus, Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2), which is highly contagious, primarily through respiratory droplets and contact. Typical symptoms include fever, cough, and shortness of breath. Weakness, nausea, and vomiting are often accompanied by respiratory symptoms but are sometimes confusing when these symptoms occur without respiratory symptoms. COVID-19 can affect any age group, are more common in adults and males and increase in patients with comorbidities. One of the most common comorbidities is Diabetes Mellitus (DM). A 40-year-old male patient complained of fever and weakness for three days. Nausea and vomiting since nine days before hospital admission, accompanied by painful swallowing, heartburn, and decreased appetite. History of going out of town and eating with friends 14 days before access to the hospital. 3 3 Laboratory examination results: 6600 leukocytes/mm , 264,000/mm platelets, NLR 2.3, 209 mg/dL of blood glucose, HbA1C 8.6%, SGOT 67 IU/L, SGPT 102 IU/L, IgG SARS-CoV-2 reactive, positive TCM SARS-CoV-2 (N2 Ct 18 and E Ct 20.3), and the duration of negative conversion of RT-PCR SARS-CoV-2 results was 19 days. The SARS-CoV-2 virus not only infects pneumocytes but also gastrointestinal, pancreatic, and endothelial cells via ACE2 receptors in DM patients, causing increased cell wall permeability to foreign pathogens and viral replication in the gastrointestinal lining cells. Subsequent enterocyte invasion causes malabsorption resulting in enteric symptoms. Uncontrolled glycemia conditions can slow viral shedding, so the length of negative conversion of RT-PCR SARS-CoV-2 results is prolonged. Based on the data above, the diagnosis in this patient was COVID-19 (symptomatic non-respiratory) with type 2 DM.
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Casillas Santana, Miguel Angel, Juan Antonio Arreguín Cano, Alejandro Dib Kanán, et al. "Should We Be Concerned about the Association of Diabetes Mellitus and Periodontal Disease in the Risk of Infection by SARS-CoV-2? A Systematic Review and Hypothesis." Medicina 57, no. 5 (2021): 493. http://dx.doi.org/10.3390/medicina57050493.
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The objective of this article was to conduct a systematic review of the literature to contrast the existing evidence regarding the relationship between periodontal disease (PD) and diabetes mellitus (DM) with the possibly increased risk of SARS-CoV-2 infection, as well as to establish a hypothesis that explains the ways in which this interaction could take place. A literature search up from 1 January 2020 to 21 March 2021 was conducted in three electronic databases, namely, PubMed, Web of Science, and Scopus, in order to identify studies on periodontal disease alone or in conjunction with diabetes mellitus, reporting any relation with SARS-CoV-2 infection as a primary outcome. Only articles published in the English language were included. Due to the lack of studies, we decided to collect all the theoretical and clinical evidence suggesting a possible biological pathway evidencing the relationship among PD, DM, and SARS-CoV-2 infection. From a total of 29 articles, 12 were included for final review studies (five reviews, two hypotheses, one Special Issue, one perspective, one commentary, one case–control study, and one case report). In addition, this systematic review article hypothesizes the correlation between PD and type 2 diabetes mellitus (T2DM) by expression of angiotensin-converting enzyme 2 (ACE2) in periodontal tissue and the risk of SARS-CoV-2 infection. T2DM is a metabolic disorder characterized by high blood glucose levels resulting from altered insulin secretion or action. Likewise, periodontitis and T2DM are inflammatory disorders with a bidirectional association, and both diseases have a similar immunomodulatory cascade and cytokine profile. ACE2 is a crucial component of the renin–angiotensin system (RAS) and the key factor of entry in the cells by the new SARS-CoV-2. ACE2 is widely distributed in the lung and kidneys, and interestingly has a great distribution in the oral cavity, principally in the tongue and periodontal tissue. ACE2 in periodontal tissue plays a crucial role between health and disease. Moreover, the ACE2/Ang-(1-7)/MasR axis is downregulated in the dysbiotic and inflammatory periodontal environment. Nevertheless, the balance of ACE2 activity is modified in the context of concurrent diabetes, increasing the expression of ACE2 by the uncontrolled glycemia chronic in T2DM. Therefore, the uncontrolled hyperglycemia possibly increases the risk of developing periodontitis and triggering overexpression of ACE2 in periodontal tissue of T2DM patients, with these events potentially being essential to SARS-CoV-2 infection and the development of mild-to-severe form of COVID-19. In this sense, we would like to point out that the need for randomized controlled trials is imperative to support this association.
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Beliard, Kara A., Mabel Yau, Meredith Wilkes, Christopher Joseph Romero, Elizabeth Wallach, and Robert Rapaport. "SARS-CoV-2 Infection Related Diabetes Mellitus." Journal of the Endocrine Society 5, Supplement_1 (2021): A397. http://dx.doi.org/10.1210/jendso/bvab048.808.
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Abstract Introduction: SARS-Cov-2 (severe acute respiratory distress syndrome- coronavirus 2) viral infection has a predilection for pancreatic beta cells causing insulin deficiency. Studies from the SARS-CoV outbreak in 2003 highlighted the relationship between SARS-CoV and ACE-2 (angiotensin-converting enzyme 2) receptors in pancreatic islet cells. We describe a pediatric patient who developed Diabetes Mellitus after exposure to the Sars-CoV-2 virus. Case Report: A previously healthy 13-year-old female of Mexican descent was found to be hyperglycemic at her annual visit. The patient endorsed polyuria and polydipsia for 3 weeks, and weight loss for 3months. 3 months prior to presentation, her mother became ill and tested positive for SARS-CoV-2 by PCR analysis. The patient had no SARS-CoV-2 associated symptoms. Her exam was notable for a BMI was in the 78%ile for age with no acanthosis nigricans. She had no family history of diabetes or autoimmune disease. Initial blood glucose was 729 mg/dL, with bicarbonate of 20.6 mEq/L, pH 7.45, and anion gap of 14 mEq/L. Large ketones were present in the urine. Her concomitant C-peptide level of 1.0 ng/ml was low in the setting of hyperglycemia. Her HbA1c was 14.3%. Diabetes-related autoantibodies, celiac, and thyroid antibodies were negative. Her Sars-CoV-2 antibody titer was positive with a negative PCR. The patient was treated with a basal-bolus regimen of subcutaneous insulin at a maximal total daily dose of 0.7 u/kg/day. 5 weeks later, her insulin requirement and HbA1C were both lower; at 0.5 u/kg/day and 9.3% respectively. Discussion: This patient’s symptoms of hyperglycemia started shortly after her exposure to the SARS-CoV-2 virus. She had no features consistent with Type 2 DM. She similarly had no serological evidence of DM related autoimmunity, thus being different from reports of new-onset Type 1 DM with confirmed autoimmunity presenting during the Sars-CoV-2 pandemic. Although Type 1B DM without evidence of humoral islet autoimmunity and monogenic DM could not be fully excluded, we postulate that the patient developed SARS-CoV-2 associated DM given her time course and documented exposure to SARS –CoV-2 with the presence of SARS-CoV antibodies. One similar case has previously been reported By Holstein et al. 1 While we share the lack of direct evidence of causation, we postulate that more patients with similar presentations will be reported during the current pandemic. Reference: 1.Hollstein, T et al. Autoantibody-negative insulin-dependent diabetes mellitus after SARS-CoV-2 infection: a case report [published online ahead of print, 2020 Sep 2]. Nat Metab. 2020;10.1038/s42255-020-00281-8. doi:10.1038/s42255-020-00281-8
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Pramanik, Parthiba, and Purushottam Pramanik. "Diabetes mellitus augments the complications of patients with COVID-19: a review." International Journal of Research in Medical Sciences 8, no. 7 (2020): 2716. http://dx.doi.org/10.18203/2320-6012.ijrms20202925.
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Corona virus disease 2019 (COVID-19) is current pandemic infection caused by RNA virus named severe acute respiratory syndrome coronavirus-2 (SARS Cov-2). The lungs are the organs most affected by COVID-19 and people were died due to severe acute respiratory s syndrome, pneumonia and multi-organs failure. Fatality rate was more, those who suffer in chronic diseases including diabetes mellitus (DM). As COVID-19 pandemic is accelerating , it is important to understand the molecular mechanism through which DM increases the severity related to COVID-19 to able to design more appropriate therapy. The aims of this study was to identify mechanisms through re-analysis of publicly available data by which DM increases susceptibility for COVID-19 infection and/or increase complication for SARS-Cov-2 infection. SARS Cov-2 accesses host cells via membrane bound enzyme, angiotensin converting enzyme-2 (ACE2). This leads to imbalance of vasoprotective and vasodeletorious arms of renin angiotensin system (RAS) with over activity of vasodeletorious arms. Such imbalance of RAS induces alveolar damage, flooding the alveoli and difficulty in breathing. DM augmented the chance of pulmonary infection by impairment of innate immunity and down regulation of ACE2. Hence, diabetic patients of COVID-19 die from multi-organ failure, shock, heart failure, arrhythmias and renal failure along with severe acute respiratory syndrome. Thus it is concluded that DM augments the complications from COVID-19 by enhancing development of RAS imbalance. From view point of public health it is suggested to keep the lung healthy, maintain blood glucose level properly, and intake foods rich in antioxidant and anti-inflammatory agents to prevent and ameliorate the acute effect of COVID-19 in diabetic patients.
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Wicik, Zofia, Ceren Eyileten, Daniel Jakubik, et al. "ACE2 Interaction Networks in COVID-19: A Physiological Framework for Prediction of Outcome in Patients with Cardiovascular Risk Factors." Journal of Clinical Medicine 9, no. 11 (2020): 3743. http://dx.doi.org/10.3390/jcm9113743.
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Background: Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection (coronavirus disease 2019; COVID-19) is associated with adverse outcomes in patients with cardiovascular disease (CVD). The aim of the study was to characterize the interaction between SARS-CoV-2 and Angiotensin-Converting Enzyme 2 (ACE2) functional networks with a focus on CVD. Methods: Using the network medicine approach and publicly available datasets, we investigated ACE2 tissue expression and described ACE2 interaction networks that could be affected by SARS-CoV-2 infection in the heart, lungs and nervous system. We compared them with changes in ACE-2 networks following SARS-CoV-2 infection by analyzing public data of human-induced pluripotent stem cell-derived cardiomyocytes (hiPSC-CMs). This analysis was performed using the Network by Relative Importance (NERI) algorithm, which integrates protein-protein interaction with co-expression networks. We also performed miRNA-target predictions to identify which miRNAs regulate ACE2-related networks and could play a role in the COVID19 outcome. Finally, we performed enrichment analysis for identifying the main COVID-19 risk groups. Results: We found similar ACE2 expression confidence levels in respiratory and cardiovascular systems, supporting that heart tissue is a potential target of SARS-CoV-2. Analysis of ACE2 interaction networks in infected hiPSC-CMs identified multiple hub genes with corrupted signaling which can be responsible for cardiovascular symptoms. The most affected genes were EGFR (Epidermal Growth Factor Receptor), FN1 (Fibronectin 1), TP53, HSP90AA1, and APP (Amyloid Beta Precursor Protein), while the most affected interactions were associated with MAST2 and CALM1 (Calmodulin 1). Enrichment analysis revealed multiple diseases associated with the interaction networks of ACE2, especially cancerous diseases, obesity, hypertensive disease, Alzheimer’s disease, non-insulin-dependent diabetes mellitus, and congestive heart failure. Among affected ACE2-network components connected with the SARS-Cov-2 interactome, we identified AGT (Angiotensinogen), CAT (Catalase), DPP4 (Dipeptidyl Peptidase 4), CCL2 (C-C Motif Chemokine Ligand 2), TFRC (Transferrin Receptor) and CAV1 (Caveolin-1), associated with cardiovascular risk factors. We described for the first time miRNAs which were common regulators of ACE2 networks and virus-related proteins in all analyzed datasets. The top miRNAs regulating ACE2 networks were miR-27a-3p, miR-26b-5p, miR-10b-5p, miR-302c-5p, hsa-miR-587, hsa-miR-1305, hsa-miR-200b-3p, hsa-miR-124-3p, and hsa-miR-16-5p. Conclusion: Our study provides a complete mechanistic framework for investigating the ACE2 network which was validated by expression data. This framework predicted risk groups, including the established ones, thus providing reliable novel information regarding the complexity of signaling pathways affected by SARS-CoV-2. It also identified miRNAs that could be used in personalized diagnosis in COVID-19.
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Pelle, Maria Chiara, Isabella Zaffina, Stefania Lucà, et al. "Endothelial Dysfunction in COVID-19: Potential Mechanisms and Possible Therapeutic Options." Life 12, no. 10 (2022): 1605. http://dx.doi.org/10.3390/life12101605.
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SARS-CoV-2, a novel coronavirus found in Wuhan (China) at the end of 2019, is the etiological agent of the current pandemic that is a heterogeneous disease, named coronavirus disease 2019 (COVID-19). SARS-CoV-2 affects primarily the lungs, but it can induce multi-organ involvement such as acute myocardial injury, myocarditis, thromboembolic eventsandrenal failure. Hypertension, chronic kidney disease, diabetes mellitus and obesity increase the risk of severe complications of COVID-19. There is no certain explanation for this systemic COVID-19 involvement, but it could be related to endothelial dysfunction, due to direct (endothelial cells are infected by the virus) and indirect damage (systemic inflammation) factors. Angiotensin-converting enzyme 2 (ACE2), expressed in human endothelium, has a fundamental role in severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection. In fact, ACE2 is used as a receptor by SARS-CoV-2, leading to the downregulation of these receptors on endothelial cells; once inside, this virus reduces the integrity of endothelial tissue, with exposure of prothrombotic molecules, platelet adhesion, activation of coagulation cascades and, consequently, vascular damage. Systemic microangiopathy and thromboembolism can lead to multi-organ failure with an elevated risk of death. Considering the crucial role of the immunological response and endothelial damage in developing the severe form of COVID-19, in this review, we will attempt to clarify the underlying pathophysiological mechanisms.
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Parrey, Ashaq, Abir aijaz, Mohd Ismail, et al. "New Onset Diabetes and Its Incidence in Severe COVID 19 Disease A Single Centre Study From Kashmir." Journal of Endocrinology and Diabetes 8, no. 2 (2012): 1–4. http://dx.doi.org/10.15226/2374-6890/8/2/001152.
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Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), the novel coronavirus that causes coronavirus disease 2019 (COVID-19), was first reported in Wuhan, China, in December 2019 and has spread worldwide. SARS-CoV-2 is a positivestranded RNA virus that is enclosed by a protein containing lipid bilayer with a single-stranded RNA genome; SARS-CoV-2 has 82% homology with human SARS-CoV, which causes severe acute respiratory syndrome.SARS-CoV-2, virus binds to angiotensinconverting enzyme 2 (ACE2) receptors, which are expressed in key metabolic organs and tissues, including pancreatic beta cells, adipose tissue, the small intestine, and the kidneys. Thus, it is believed that SARS-CoV-2 may cause pleiotropic alterations of glucose metabolism that could complicate the pathophysiology of pre-existing diabetes or lead to new mechanisms of disease. Many studies have made observations that provide support for the hypothesis of a potential diabetogenic effect of Covid-19; in addition it is well-recognized that stress response associated with severe illness have diabetogenic effect. However, whether the alterations of glucose metabolism that occur with a sudden onset in severe COVIOD-19 persist or remit when the infection resolves is unclear. How frequent is the phenomenon of newonset diabetes, and is it classic type 1 or type 2 diabetes or a new type of diabetes. Key words: COVID 19; Prediabetes; Diabetes; Pneumonia.
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Blîndu, Emanuel, Renata Gerculy, Diana Opincariu, Daniel Cernica, and Imre Benedek. "Cessation of Renin-Angiotensin System Antagonists During the SARS-CoV-2 Pandemic – Do We Have the Evidence?" Journal of Interdisciplinary Medicine 5, no. 3 (2020): 105–9. http://dx.doi.org/10.2478/jim-2020-0022.
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AbstractThe aim of this review is to provide a short update on whether treatment with angiotensin-converting enzyme inhibitors (ACEIs) or angiotensin receptor blockers (ARBs) has beneficial or harmful effects in patients infected with SARS-CoV-2. Epidemiological studies have shown that SARS-CoV-2 infects all age groups, presenting a higher incidence in elderly patients with various comorbidities such as hypertension, diabetes mellitus, and cardiovascular diseases. A large proportion of these patients are treated with ACEIs and ARBs. Since it has been demonstrated that SARS-CoV-2 uses angiotensin converting enzyme type 2 (ACE2) as an entry point into host cells, it is important to know whether ACEIs and ARBs could modify the expression of this enzyme, and thus promote the viral infection. Animal studies and a few studies in humans have shown that renin angiotensin system (RAS) inhibitors increase tissue expression of ACE2, but with potentially beneficial effects. In this context, it is imperative to provide appropriate guidance for clinicians and patients. The major cardiology associations across the world have released statements in which they recommend healthcare providers and patients to continue their treatments for hyper-tension and heart failure as prescribed.
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Ivantsova, N. L., A. G. Beliakova, M. I. Dmitrievskaya, A. N. Useinova, V. M. Melnikova, and K. I. Abramova. "PECULIAR PROPERTIES OF USAGE OF DRUGS THAT AFFECT THE RENIN-ANGIOTENSIN SYSTEM IN PATIENTS WITH COVID-19." Crimea Journal of Experimental and Clinical Medicine 11, no. 2 (2022): 75–81. http://dx.doi.org/10.37279/2224-6444-2021-11-2-75-81.
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Currently, the main task of public health authorities is a developing of coordinated global measures to prepare health systems to deal with the spread of coronavirus infection, an accompanying concern has been identified that is of particular interest to clinicians and researchers about hypertension. Hypertension, coronary artery disease and diabetes mellitus, especially in the elderly, increase susceptibility to SARS-CoV-2 infection. Antihypertensive drugs decrease blood pressure due to dilating blood vessels and decreasing cardiac output. One of the groups of these drugs includes inhibitors of angiotensin-converting enzymes (ACE). Angiotensin-converting enzyme 2 is a specific target for SARS-CoV-2, specially for the S-protein, which is located on its surface, and therefore the relationship of ACE inhibi- tors and the course of the disease plays an important role in treatment, since the penetration process and infection is facilitated by the affinity of the virus S-protein and the human ACE2 receptor. For this reason, the penetration of the virus into the host cells can be facilitated. However, this relationship does not affect the worsening of symptoms and the course of coronavirus infection due to the fact that when the SARS-CoV-2 spike protein (S-protein) binds to ACE2, it is possible to induce the induction of ACE2 shedding from the surface, which also reduces the surface expression of ACE2. The effect of the virus is not only due to binding to ACE2, but also to TMPRSS2. It has been proven that it is be- cause of its binding to TMPRSS2 that it plays a greater role in infection with SARS-CoV-2 than angiotensin-converting enzyme 2. Therefore, it is not advisable to stop taking antihypertensive drugs during coronavirus infection in people with cardiovascular diseases.
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Perlman, Jordan E., and Justin B. Echouffo-Tcheugui. "A Case of Possible SARS-COV-2 Induced Beta-Cell Failure." Journal of the Endocrine Society 5, Supplement_1 (2021): A359—A360. http://dx.doi.org/10.1210/jendso/bvab048.732.
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Abstract Background: There are several known viral triggers of ketosis-prone diabetes, including SARS-1 and HHV-81,2. SARS-COV-2 can bind ACE-2 receptors on the beta-cell causing destruction and acute impairment of insulin secretion3. There is accruing evidence to suggest that COVID-19 infection can worsen preexisting diabetes or induce new disease4. Clinical Case: A 40-year-old Hispanic male presented to the ER complaining of fatigue, polyuria, and polydipsia. A screening COVID-19 PCR was positive but he denied URI symptoms. His admission labs were notable for hyperglycemia (434 mg/dL; n 71–99), metabolic acidosis (pH 7.1 [n 7.35–7.45]; HCO3 3 mmoL/L [n 21–32]), increased anion gap (27 mmoL/L; n < 12) and elevated HbA1c (7.9%; n < 5.7%). The patient’s fructosamine was also high (464 umol/L; n 200–285) and discordant from his HbA1c. There was no evidence of pancreatitis, lactic acidosis, renal impairment or hepatic dysfunction. The patient had no known medical problems, did not drink alcohol to excess, and reported good access to nutrition. He had a strong family history of T2DM, but his BMI (23.3 kg/m2) and lipid panel were normal. The DKA was managed in the medical ICU using fluids and IV insulin per protocol. The patient required 180 units of IV insulin/24-hours (2.5 units/kg/day) to maintain blood glucose 180–250 mg/dL. After 48-hours of IV insulin, he was transitioned to subcutaneous insulin and prescribed multiple daily injections at discharge. There were concerns about possible T1DM and/or glucose toxicity leading to further diagnostics. His GAD-65 (<5 [IU]/mL; n 0–5 [IU]/mL) and IA-2 (<5.4 U/mL; n <5.4 U/mL) antibodies were negative but his c-peptide was suppressed (0.64 ng/mL; n 0.8–3.85). The patient was reevaluated at three months post-discharge. His glycemic control and insulin requirements had improved but repeat c-peptide level was undetectable. He was thought to have beta-cell failure and referred to a diabetologist. Conclusion: This is a case of absolute insulin deficiency persisting for at least three months most likely attributable to acute COVID-19 infection. References: 1. Yang JK, Lin SS, Ji XJ, Guo LM. Binding of SARS coronavirus to its receptor damages islets and causes acute diabetes. Acta Diabetol. 2010;47(3):193–199.2. Sobngwi E, Choukem SP, Agbalika F, et al. Ketosis-prone type 2 diabetes mellitus and human herpesvirus 8 infection in sub-saharan africans. Jama. 2008;299(23):2770–2776.3. Hamming I, Timens W, Bulthuis M, Lely A, Navis G, van Goor H. Tissue distribution of ACE2 protein, the functional receptor for SARS coronavirus. A first step in understanding SARS pathogenesis. J Pathol. 2004;203(2):631–637.4. Bornstein SR, Rubino F, Khunti K, et al. Practical recommendations for the management of diabetes in patients with COVID-19. Lancet Diabetes Endocrinol. 2020;8(6):546–550.
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Rivera Nazario, Ivan Augusto, Arnaldo Nieves Ortiz, Jose Ayala Rivera, et al. "An Atypical Presentation of Hyperosmolar Hyperglycemic State Induced by SARS CoV 2." Journal of the Endocrine Society 5, Supplement_1 (2021): A366—A367. http://dx.doi.org/10.1210/jendso/bvab048.746.
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Abstract Hyperglycemic emergencies such as Diabetic Ketoacidosis (DKA) or Hyperosmolar Hyperglycemic State (HHS) are commonly precipitated by infectious processes. Severe Acute Respiratory Syndrome-Coronavirus 2 (SARS-CoV-2) is a novel infectious process prompting hyperglycemic crisis. SARS-CoV-2 at the level of the lungs affects ACE2 functioning which in turns decrease the B cells proliferation at the pancreas and hinders insulin secretion. Advanced age and comorbidities such as hypertension, cardiovascular disease and diabetes mellitus are considered to be a risk factors for severe illness and mortality between patients with SARS-CoV-2. We present the case of a 39-year-old woman with medical history of uterine fibroma, who presented with complains of general malaise, polyuria and polydipsia of one week evolution, associated with sore throat, subjective fever, dry cough, abdominal pain, nausea and vomiting. Physical examination remarkable for dry oral mucosa, decreased skin turgor, and prolonged capillary refills. Vital signs significant for hypertension, tachycardia, and tachypnea. Laboratory work up remarkable for glucose of 1321 mg/dL, HCO3- of 16 mEq/L, serum osmolality of 333 mOsm/kg, serum ketones positive and HbA1C of 15%. ABG’s showed pH of 7.33, PCO2 of 29.8 and a PAO2 of 158.5 mmHg for a high anion gap metabolic acidosis (AG of 15.3 mEq/L), non-anion gap metabolic acidosis with respiratory alkalosis. Chest X-ray revealed bilateral perihilar, peribronchial cuffing. SARS-CoV-2 PCR testing was positive. Clinical and laboratory workup met criteria for diagnosis of HHS and Diabetes Mellitus de Novo most likely secondary to SARS-CoV-2 infection. Patient was treated with aggressive IV hydration and insulin infusion with resolution of hyperglycemia, ketonemia and symptoms. SARS-CoV-2 infection can precipitate acute metabolic complications in patients with diabetes or unknown diagnosis of diabetes. The effect of the virus could be direct effect on β-cell function. To our knowledge, there are only a few cases reported of HHS precipitated by SARS-CoV-2 infection therefore medical awareness is important for early diagnosis of possible triggering factors such as COVID-19 and early management of patients presenting with new onset hyperglycemic emergencies.
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Zayas, Francisco Jose, Marianne Hernandez-Negron, and Michelle Marie Mangual Garcia. "Development of Diabetes Type 3 After SARS-COV-2 Pancreatic B Cell Injury." Journal of the Endocrine Society 5, Supplement_1 (2021): A373. http://dx.doi.org/10.1210/jendso/bvab048.760.
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Abstract SARS-COV-2 has caused millions of deaths in less than one year, yet little is known about the long-term consequences survivors may suffer. The novel coronavirus uses the ACE2 receptor to infect human cells, allowing it to target organ systems with such receptors including the respiratory, cardiovascular, gastrointestinal and endocrine system. The purpose of this case report is to describe the long-term implications COVID-19 may cause in the endocrine system. A 46-year-old woman was referred to our clinic due to abrupt uncontrolled blood glucose levels ranging from 200-550mg/dL after being infected with COVID-19 for approximately 10 weeks. She has a past medical history of Diabetes Mellitus Type 2 which was diagnosed 3 years ago and was well controlled with diet. Present history reveals polyuria, polydipsia, tiredness and a decreased appetite. Laboratory values show HbA1C 12, negative islet cell antibodies/GAD antibodies, low C-peptide, high TSH, normal FT4 and positive anti-TPO antibodies/thyroglobulin antibodies. The sudden loss of blood glucose control along with low c peptide levels without evidence of autoimmunity support the diagnosis of Pancreatic Diabetes. SARS-COV-2 infection may cause Diabetes Type 3, rendering a patient dependent on insulin use for life. Covid-19 survivors, with or without a previous history of endocrinopathy, should be evaluated for possible long-term sequels of infection as the virus targets tissues throughout the body.
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Cavalcante, Letícia Carla de Lima, Larissa Cristina de Lima Cavalcante, Maria Vitória Menezes Coutinho, Rebeca Montenegro De Lacerda, Rodrigo de Oliveira Arakaki, and Cristiane Monteiro Da Cruz. "Analysis of the infectional profile of diabetic patients infected by COVID 19 in the period of 2020 – 2021 Análise do perfil de infecção dos pacientes diabéticos infectados pela COVID 19 no período de 2020-2021." Brazilian Journal of Health Review 4, no. 5 (2021): 19930–40. http://dx.doi.org/10.34119/bjhrv4n5-119.
Full textAbstract:
The COVID-19 disease has as its etiological agent the SARS-CoV-2, a RNA virus that causes severe respiratory syndrome. Diabetes mellitus is one of the significant risk factors for COVID-19 due to the weakened immune response of these patients and widely distribution of ACE2 in diferent organs. ACE2 is a receptor that antagonizes the RAS system, and is related to the clinical symptoms of COVID 19 .Its expression in the islet cells and exocrine pancreas suggest the susceptibility for SARS-CoV 2 infection in diabetic patients. This stydy analyses the infeccional profile of diabetic patients infeccted by COVID-19 in the city of Maceió. A research was performed in the year of 2020-2021 in english idiom in the database PubMed using the descriptors “ACE receptor” AND “Covid”, “Covid” AND “Diabetes” AND “ ACE receptor” .The criteria of inclusion and exclusion established was the relevance and approach based on the theme to be discussed.It was collected data about confirmed deaths by Covid 19 according to preexisting comorbidities in the city of Maceió – AL shown in the graphics , expressing an average mortality among patients infected by Covid and preexisting Diabetes Mellitus. This study shows a reduction in the percentage of mortality in diabetic patients infected by Covid-19 seen in view of the adoption of measures to restrict the spread of the virus, reducing the numbers of infecion, especially the risk group, in addition to the vaccination campaign which culminated in positive results to the reduction in the mortality in infected diabetics.
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Cavalcante, Letícia Carla de Lima, Larissa Cristina de Lima Cavalcante, Maria Vitória Menezes Coutinho, Rebeca Montenegro De Lacerda, Rodrigo de Oliveira Arakaki, and Cristiane Monteiro Da Cruz. "Analysis of the infectional profile of diabetic patients infected by COVID 19 in the period of 2020 – 2021 Análise do perfil de infecção dos pacientes diabéticos infectados pela COVID 19 no período de 2020-2021." Brazilian Journal of Health Review 4, no. 5 (2021): 19930–40. http://dx.doi.org/10.34119/bjhrv4n5-119.
Full textAbstract:
The COVID-19 disease has as its etiological agent the SARS-CoV-2, a RNA virus that causes severe respiratory syndrome. Diabetes mellitus is one of the significant risk factors for COVID-19 due to the weakened immune response of these patients and widely distribution of ACE2 in diferent organs. ACE2 is a receptor that antagonizes the RAS system, and is related to the clinical symptoms of COVID 19 .Its expression in the islet cells and exocrine pancreas suggest the susceptibility for SARS-CoV 2 infection in diabetic patients. This stydy analyses the infeccional profile of diabetic patients infeccted by COVID-19 in the city of Maceió. A research was performed in the year of 2020-2021 in english idiom in the database PubMed using the descriptors “ACE receptor” AND “Covid”, “Covid” AND “Diabetes” AND “ ACE receptor” .The criteria of inclusion and exclusion established was the relevance and approach based on the theme to be discussed.It was collected data about confirmed deaths by Covid 19 according to preexisting comorbidities in the city of Maceió – AL shown in the graphics , expressing an average mortality among patients infected by Covid and preexisting Diabetes Mellitus. This study shows a reduction in the percentage of mortality in diabetic patients infected by Covid-19 seen in view of the adoption of measures to restrict the spread of the virus, reducing the numbers of infecion, especially the risk group, in addition to the vaccination campaign which culminated in positive results to the reduction in the mortality in infected diabetics.
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Komine, Mayumi, Tuba Mussarat Ansary, Md Razib Hossain, Koji Kamiya, and Mamitaro Ohtsuki. "Inflammation Causes Exacerbation of COVID-19: How about Skin Inflammation?" International Journal of Molecular Sciences 23, no. 20 (2022): 12260. http://dx.doi.org/10.3390/ijms232012260.
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COVID-19 is a recently emerged viral infection worldwide. SARS-CoV-2, the causative virus, is believed to have emerged from bat coronaviruses, probably through host conversion. The bat coronavirus which has the highest gene homology to SARS-CoV-2 specifically infects deep forest bats in China whose habitat extends through the Middle East to Southern Europe. Host conversion might have occurred due to the deforestation by humans exposing wild bats to the environment they had never encountered before. SARS-CoV-2 infects cells through two mechanisms: through its receptor ACE2 with the help of enzyme TMPRSS and through membrane fusion with the help of elastases in the inflammatory condition. Obesity, hypertension, diabetes mellitus, and pulmonary diseases cause poor prognosis of COVID-19. Aging is another factor promoting poor prognosis. These diseases and aging cause low-level and persistent inflammation in humans, which can promote poor prognosis of COVID-19. Psoriasis and atopic dermatitis are the major inflammatory skin diseases. These inflammatory skin conditions, however, do not seem to cause poor prognosis for COVID-19 based on the epidemiological data accumulated so far. These mechanisms need to be elucidated.
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Vikulova, O. K., Zamira Zuraeva, L. V. Nikankina, and M. V. Shestakova. "The role of renin-angiotensin system and angiotensin-converting enzyme 2 (ACE2) in the development and course of viral infection COVID-19 in patients with diabetes mellitus." Diabetes mellitus 23, no. 3 (2020): 242–49. http://dx.doi.org/10.14341/dm12501.
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The role of renin-angiotensin system (RAS) in general and angiotensin-converting enzyme 2 (ACE2) in particular in the pathogenesis and course of viral infection caused by SARS-CoV-2 (COVID-19) is of particular interest. This is due not only to the fact that ACE2 is a receptor for the virus the target cells. RAS hyperactivation in patients with arterial hypertension, cardiovascular disease and diabetes mellitus, is considered one of the most important factors for a more severe infection in persons with concomitant pathology. In addition, the effects of PAS blockage with angiotensin converting enzyme inhibitors (ACE inhibitors) and angiotensin II receptor blockers (ARBs) remains one of the most discussed topics in the literature on COVID-19. Thisreview presents the data on the interaction between the virus and the main components of RAS and the factors influencing their expression level, the impact of ACE inhibitors and ARBs therapy on the disease outcome, and presents theperspectives of the treatment with recombinant ACE 2.
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Rida, Rima, Paola Rios, and Alex Manzano. "A Rare Cause of Diabetes: COVID-19." Journal of the Endocrine Society 5, Supplement_1 (2021): A362. http://dx.doi.org/10.1210/jendso/bvab048.737.
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Abstract A Rare Cause of Diabetes: COVID-19 Introduction: Environmental factors like viruses have been described in the mechanism of pancreatic beta cell destruction. Various viruses can trigger autoimmunity in individuals genetically predisposed to diabetes. Severe acute respiratory syndrome coronavirus 2 (SARS CoV-2) has been shown to bind to angiotensin-converting enzyme 2 (ACE 2) which is expressed throughout the body, including pancreatic cells, leading to direct injury of the endocrine pancreas. We report a case of coronavirus infection disease 2019 (COVID-19) causing a new onset of diabetes mellitus presentation with hyperglycemia, polyuria, polydipsia and weight loss. Case Presentation: A 53 year-old, previously healthy, male presented with five days of fever, fatigue, dry cough, dyspnea and diarrhea. On admission he was hypoxic, with a body mass index of 25 kg/m2 and no evidence of insulin resistance on physical exam. He was diagnosed with SARS CoV-2 and admitted for high requirements of oxygen without the need of the intensive care unit. He was treated with tocilizumab, atazanavir, hydroxychloroquine, full dose anticoagulation and azithromycin. Dexamethasone 4 mg every 8 hours was given for three days. During this admission, his fasting glucose was 75–108 mg/dL. Once started on steroids his fasting and prandial glucose was 85–96 mg/dL and 140 mg/dL on one occasion. He was eventually discharged with 2 liters of nasal cannula which he required for one week. One and a half months after, he presented to the emergency department due to a 6 kg weight loss, polyuria, polydipsia, malaise and fatigue. On arrival his glucose was 549 mg/dL, without anion gap or ketones. He had no evidence of new infection and SARS CoV-2 test was negative. He was started on insulin glargine at night and insulin Humalog before each meal with corrections. Hemoglobin A1c was 13.4% with a C-peptide 0.36 ng/mL and glucose of 195 mg/dL at the time of C-peptide test. His antibodies, anti-islet cell antibody, zinc transporter 8 and glutamic acid decarboxylase-65, were negative. He was discharged with basal/bolus regimen and followed up outpatient with Endocrinology. During follow-up, his c-peptide normalized and he was tapered off insulin. Discussion: In 2003, atypical pneumonia caused by SARS CoV-2 was reported to be associated with hyperglycemia in patients without prior history of diabetes. At 3 year follow-up, the patients no longer had diabetes. Moreover, patients with mild SARS CoV-2 during the first day of hospitalization had a higher fasting plasma glucose than patients admitted for other causes of pneumonia. It is known that SARS CoV-2 binds to ACE 2 which downregulates the receptor, leading to impairment of insulin secretion and hyperglycemia. SARS CoV-2 also produces a direct injury in beta pancreatic cells. It is imperative to monitor patients post COVID-19 to evaluate for new onset diabetes and likely resolution.
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Vinciguerra, Mattia, Silvia Romiti, Khalil Fattouch, Antonio De Bellis, and Ernesto Greco. "Atherosclerosis as Pathogenetic Substrate for Sars-Cov2 Cytokine Storm." Journal of Clinical Medicine 9, no. 7 (2020): 2095. http://dx.doi.org/10.3390/jcm9072095.
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The severe acute respiratory syndrome coronavirus 2 (Sars-CoV-2) outbreak is a public health emergency affecting different regions around the world. The lungs are often damaged due to the presence of Sars-CoV-2 binding receptor ACE2 on epithelial alveolar cells. Severity of infection varies from complete absence of symptomatology to more aggressive symptoms, characterized by sudden acute respiratory distress syndrome (ARDS), multiorgan failure, and sepsis, requiring treatment in intensive care unit (ICU). It is not still clear why the immune system is not able to efficiently suppress viral replication in a small percentage of patients. It has been documented as pathological conditions affecting the cardiovascular system, strongly associated to atherosclerotic progression, such as heart failure (HF), coronary heart disease (CHD), hypertension (HTN) and diabetes mellitus (DM), could serve as predictive factors for severity and susceptibility during Sars-CoV-2 infection. Atherosclerotic progression, as a chronic inflammation process, is characterized by immune system dysregulation leading to pro-inflammatory patterns, including interleukin 6 (IL-6), tumor necrosis factor α (TNF-α), and IL-1β. Reviewing immune system and inflammation profiles in atherosclerosis and laboratory results reported in severe COVID-19 infections, we hypothesized a pathogenetic correlation. Atherosclerosis may be an ideal pathogenetic substrate for high viral replication ability, leading to adverse outcomes, as reported in patients with cardiovascular factors. The level of atherosclerotic progression may affect a different degree of severe infection; in a vicious circle, feeding itself, Sars-CoV-2 may exacerbate atherosclerotic evolution due to excessive and aberrant plasmatic concentration of cytokines.
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Kusuma, Victor Perdana, and Deasy Ardiany. "The Pathophysiology and Outcomes of Diabetic Patients with Coronavirus Disease 2019 (COVID-19)." Biomolecular and Health Science Journal 4, no. 2 (2021): 124. http://dx.doi.org/10.20473/bhsj.v4i2.30030.
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Introduction: Coronavirus Disease 2019 (COVID-19) is a respiratory tract infection caused by the SARS-CoV-2 virus, which was announced a pandemic by the World Health Organization (WHO) on March 11, 2020. On March 2, 2020, two confirmed cases of COVID-19 were initially reported in Indonesia. COVID-19 has been reported in 96.2 million people around the world. COVID-19 has already stolen the lives of almost 2 million individuals. Diabetes mellitus patients face an additional challenge with this disease (DM). Several studies have found a link between diabetes mellitus and COVID-19, as well as a bad prognosis for persons with DM and COVID-19. Aim of this study was to learn more about the link between diabetes and COVID-19, as well as the pathophysiology of diabetes.Methods: We searched for articles in PubMed and Google Scholar databases till February 2021, with the following keywords: “SARS-CoV-2”, “COVID-19”, “infection”, “pathogenesis”, “diabetes”Results: Diabetes Mellitus increased the severity and mortality of COVID-19 patients due to mechanisms involving inflammation and immune system activation, increased coagulation activity, oxidative stress, glucotoxicity, endoplasmic reticulum stress, renin-angiotensin-aldosterone system disorders, apoptotic mechanisms, mitochondrial dysfunction, and damage to pancreatic beta cells. COVID-19 infection can also lead to hyperglycemia and new-onset diabetes.Conlusion: Diabetes Mellitus is one of the comorbidities linked to a worse COVID-19 prognosis, according to the findings of this literature study. Furthermore, current research suggests that COVID-19 might cause hyperglycemia or new-onset diabetes, which has a poorer prognosis than COVID-19 patients with pre-existing diabetes.
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Sardu, Celestino, Raffaele Marfella, Francesco Prattichizzo, Rosalba La Grotta, Giuseppe Paolisso, and Antonio Ceriello. "Effect of Hyperglycemia on COVID-19 Outcomes: Vaccination Efficacy, Disease Severity, and Molecular Mechanisms." Journal of Clinical Medicine 11, no. 6 (2022): 1564. http://dx.doi.org/10.3390/jcm11061564.
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Background/Aims: The severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is a positive-stranded single-stranded RNA virus, a member of the subgenus Sarbecovirus (beta-CoV lineage B) and responsible for the coronavirus disease 2019 (COVID-19). COVID-19 encompasses a large range of disease severity, from mild symptoms to severe forms with Intensive Care Unit admission and eventually death. The severe forms of COVID-19 are usually observed in high-risk patients, such as those with type two diabetes mellitus. Here, we review the available evidence linking acute and chronic hyperglycemia to COVID-19 outcomes, describing also the putative mediators of such interactions. Findings/Conclusions: Acute hyperglycemia at hospital admission represents a risk factor for poor COVID-19 prognosis in patients with and without diabetes. Acute and chronic glycemic control are both emerging as major determinants of vaccination efficacy, disease severity and mortality rate in COVID-19 patients. Mechanistically, it has been proposed that hyperglycemia might be a disease-modifier for COVID-19 through multiple mechanisms: (a) induction of glycation and oligomerization of ACE2, the main receptor of SARS-CoV-2; (b) increased expression of the serine protease TMPRSS2, responsible for S protein priming; (c) impairment of the function of innate and adaptive immunity despite the induction of higher pro-inflammatory responses, both local and systemic. Consistently, managing acute hyperglycemia through insulin infusion has been suggested to improve clinical outcomes, while implementing chronic glycemic control positively affects immune response following vaccination. Although more research is warranted to better disentangle the relationship between hyperglycemia and COVID-19, it might be worth considering glycemic control as a potential route to optimize disease prevention and management.
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Khaydarova, F. A., N. U. Alimova, A. V. Alieva, A. S. Sadykova, and M. D. Aripova. "Impact of COVID-19 infection on the development of type 1 diabetes mellitus in children and adolescents." Diabetes mellitus 25, no. 1 (2022): 21–26. http://dx.doi.org/10.14341/dm12785.
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Children did not escape the COVID-19 pandemic. Although, in general, the course of viral infection in children is mild, the question of the long-term effects of COVID-19 on a child and adolescent, in particular, on pancreatic beta cells, remains unclear.Аim: Тo study the characteristics of children with diabetes mellitus identified after COVID-19 infection.Materials and methods: This article presents the preliminary results obtained from children and adolescents hospitalized at the RSSPMCE clinic with the newly diagnosed diabetes mellitus after COVID infection, as well as a systematic review of 61 clinical cases (case series study).Results: Of the 120 children hospitalized at the RSSPMCE clinic with newly diagnosed diabetes, 15 were diagnosed with diabetes after COVID-19 infection, all in a state of diabetic ketoacidosis. Only 20% of children knew about the previous COVID-19 infection, the course of the disease was mild, in 80% of children the infection was asymptomatic. At the time of diabetes onset, all children had a high level of HbA1c - above 10%, a low level of vitamin D, high levels of antibodies to SARS-CoV-2 (IgG), and the need for insulin was above the average.Conclusion: The SARS CoV-2 virus could be the direct cause of the development of diabetes mellitus in children, even with the asymptomatic course of the viral infection. However, the question remains about the exact classification of diabetes after COVID-19 in children. It is necessary to inform the population about the first signs and symptoms of diabetes mellitus in order to timely consult a doctor for the diagnosis of diabetes mellitus.
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McCord, Joe M., Brooks M. Hybertson, Adela Cota-Gomez, Kara P. Geraci, and Bifeng Gao. "Nrf2 Activator PB125® as a Potential Therapeutic Agent against COVID-19." Antioxidants 9, no. 6 (2020): 518. http://dx.doi.org/10.3390/antiox9060518.
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Nrf2 is a transcription factor that regulates cellular redox balance and the expression of a wide array of genes involved in immunity and inflammation, including antiviral actions. Nrf2 activity declines with age, making the elderly more susceptible to oxidative stress-mediated diseases, which include type 2 diabetes, chronic inflammation, and viral infections. Published evidence suggests that Nrf2 activity may regulate important mechanisms affecting viral susceptibility and replication. We examined gene expression levels by GeneChip microarray and by RNA-seq assays. We found that the potent Nrf2-activating composition PB125® downregulates ACE2 and TMPRSS2 mRNA expression in human liver-derived HepG2 cells. ACE2 is a surface receptor and TMPRSS2 activates the spike protein for SARS-CoV-2 entry into host cells. Furthermore, in endotoxin-stimulated primary human pulmonary artery endothelial cells, we report the marked downregulation by PB125 of 36 genes encoding cytokines. These include IL-1-beta, IL-6, TNF-α, the cell adhesion molecules ICAM-1, VCAM-1, and E-selectin, and a group of IFN-γ-induced genes. Many of these cytokines have been specifically identified in the “cytokine storm” observed in fatal cases of COVID-19, suggesting that Nrf2 activation may significantly decrease the intensity of the storm.
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JC, Ekezie, and Haddad D. "New Onset Type-1 Diabetes Mellitus in a Toddler with Sars-Cov-2 Infection Presenting In Diabetic Ketoacidosis: A Case Report." New Medical Innovations and Research 2, no. 5 (2021): 01–03. http://dx.doi.org/10.31579/2767-7370/022.
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Introduction: Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), though mostly sparing the lungs in children, has been found to affect other organs including the endocrine pancreas. Type 1 diabetes mellitus (T1DM) may occur through direct negative effects of the virus on beta-cell function leading to diminished insulin production. Diabetic ketoacidosis (DKA) is a known and life-threatening complication of T1DM. Case presentation: This is a case of a 3-year-old previously healthy male who presented with 4 days history of fever, with malaise and hyperpnea for one day. Review of systems was notable for increased thirst and urination, nausea, vomiting, fatigue, and visible weight loss for 4 days. Initial investigations done showed elevated blood glucose, ketonuria, increased anion gap metabolic acidosis, and positive SARS-CoV-2 polymerase chain reaction (PCR). He was immediately commenced on intravenous fluids and insulin with progressive improvement and was discharged on hospital day 6. Conclusion: Coronavirus disease-2019 (COVID-19) has impacted children most profoundly with the new post-infectious multi-inflammatory syndrome, however, it is important to remember that primary coronavirus infection is still a threat to pediatric patients, for example, and its cytotoxic effects on the pancreatic beta cells that may lead to T1DM. We, therefore, recommend that caregivers, parents, and medical professionals should have a high index of suspicion when children present with symptoms consistent with a diagnosis of T1DM during the COVID-19 pandemic so that diagnosis can be made promptly and therefore DKA prevented.
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Evi Awwaliyah, Hotimah, and Michio Shimabukuro. "Clinical characteristics and mortality associated with COVID-19 in islamic hospital of Jemursari, Surabaya, Indonesia: A hospital-based retrospective cohort study." Bali Medical Journal 11, no. 3 (2022): 1202–6. http://dx.doi.org/10.15562/bmj.v11i3.3541.
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Introduction: According to WHO, the COVID-19 epidemic a public health emergency came to international attention in March 2020, and the pandemic quickly spread around the world. This disease is caused by the novel coronavirus SARS-CoV-2, which may enter human target cells via angiotensin-converting enzyme 2 (ACE2). This study aimed to assess the risk factors associated with poor prognosis among COVID-19 patients in the Islamic Hospital of Jemursari, Surabaya, Indonesia. Methods: This study was a retrospective cohort study that used patients hospitalized with COVID-19 at the Islamic Hospital of Jemursari, Surabaya as a study subject. Patients of all ages who enter the hospital and were confirmed with a positive real-time polymerase chain reaction (RT-PCR) result for SARS-CoV-2 were inclusion criteria of this study. Results: We included 554 COVID-19-positive patients with the highest age at 26-35 years old as much as 26.72%, followed by the second highest at 36-45 years old at 20.86%. In addition, from all the patients in this study, it was found that the most patients were 281 male and 273 female. Characteristics of comorbidities in COVID-19 patients, where type 2 diabetes mellitus is the most comorbid factor 88.89% in recovered COVID-19 patients and 11.11% in patients who have died. In addition, hypertension is also the second most comorbid 96.55% of Covid-19 patients. Conclusion: Based on this study, the independent risk factors related to critical outcomes among COVID-19 cases include old age, males, diabetes mellitus, cardiac-related disease history, and the presence of two or more comorbidities. In future research, we suggest designing a unique multi-item scale system to prognosticate COVID-19 patients.
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Babenko, A. Yu, and M. Yu Laevskaya. "Diabetes mellitus and COVID-19. How are they connected? Current strategy of fight." "Arterial’naya Gipertenziya" ("Arterial Hypertension") 26, no. 3 (2020): 304–11. http://dx.doi.org/10.18705/1607-419x-2020-26-3-304-311.
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Infectious epidemic of COVID-19 caused by the new coronavirus is characterized by severe course in patients with diabetes mellitus, which presents another noninfectious pandemic accelerating for last decades. Today, according to the International Diabetic Federation data, there are 463 million patients with diabetes mellitus in the world. The burden of the COVID-19 epidemic is largely explained by a frequent combination of these two pathologies. From the previous flu epidemics and already available data of the current epidemic, diabetes mellitus and obesity are considered to be the predictors of more severe course of COVID-19 and mortality. On the other hand, SARS-CoV-2 can aggravate diabetes mellitus, via direct damage of pancreatic beta cells and the liver injury, resulting in higher insulin resistance. We discuss the mechanisms underlying the relation between coronavirus infection and diabetes mellitus and consequences of their mutual influence. Also the article reviews potential strategies of personalized therapy in COVID-19. Timely control and maintenance of individualized target glycemic level is the cornerstone of successful prevention of COVID-19 complications. Disease severity defines strategy of treatment and the choice of antihyperglycemic therapy.
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Kara, Mehmet, and Ilhami Celik. "Effect of clinical progress in antihypertensive medications among COVID-19 patients." Medical Science and Discovery 9, no. 10 (2022): 593–98. http://dx.doi.org/10.36472/msd.v9i10.829.
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Objective: Many chronic diseases, such as hypertension, diabetes, and coronary heart disease, paving the way for the disease to progress unfavorably in Covid-19. Angiotensin-converting enzyme inhibitors (ACEIs) and angiotensin-2 receptor blockers (ARBs) can upregulate ACE2 receptors (which SARS-COV-2 uses to enter the host cell) or protect against infection by limiting the effects of Angiotensin 2. This study aimed to reveal the impact of antihypertensive drugs on the hospital staying, and mortality in Covid-19 patients followed in the hospital. Methods and Results: One hundred patients were randomly selected with hypertension, diabetes mellitus and coronary artery disease hospitalized in Kayseri City Training and Research Hospital due to Covid-19 infection. Patients were grouped as taking ACEIs and ARBs group and not taking ACEIs and ARBs group. There were no differences among the groups in terms of the frequency of chronic disease and treatment modalities. The length of the hospital stays, bedding into the Intensive Care Unit (ICU), and mortality rates were higher in the group without ACEIs or ARBs. Mortality was significantly lower among patients who used ACEIs and ARBs (P=0.00, P=0.02, respectively) and incredibly high among beta-blocker users (P=0.00). It was found that the advanced age, male gender and use of beta-blockers were associated with mortality. Conclusion: Although antihypertensive medications are allegedly associated with increased mortality rates, the risk of mortality has not been detected in people taking ACEIs and ARBs. Further studies involving a greater number of patients are needed.
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Martinez, Alfonso Hoyos, Kelly Anne Hicks, Tracy Patel Moorjani, Jennifer Bell, and Yuezhen Lin. "A Case of Autoantibody Negative Pediatric Diabetes Mellitus With Marked Insulin Resistance Concomitant With COVID-19: A Novel Form of Disease?" Journal of the Endocrine Society 5, Supplement_1 (2021): A690—A691. http://dx.doi.org/10.1210/jendso/bvab048.1406.
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Abstract Background: SARS-CoV-2 uses the angiotensin-converting enzyme 2 (ACE2) receptor to enter human cells. This receptor is avidly expressed in the pancreatic islets, suggesting the virus may target β-cell function. 17% of adults with COVID-19 have evidence of pancreatic injury. There is a direct relation between insulin resistance and COVID-19 severity and mortality with patients with higher insulin resistance presenting with higher inflammatory response. Fulminant type 1 diabetes (fT1D) has abrupt onset of symptoms with insulinopenia without evidence of autoimmunity, usually preceded by viral illness. Clinical case: A 12-year-old Hispanic male presented with a week history of polyuria, polydipsia, headache, and fatigue but no weight loss, fever, cough, anosmia, or diarrhea. Laboratory testing revealed new onset diabetes with DKA with HbA1C 11.3%, blood pH 7.04, glucose 381 mg/dL, C-peptide 0.6 ng/mL, β-hydroxybutyrate 8.2 mmol/L, and a positive nasopharyngeal PCR for SARS-CoV-2 but no elevation of inflammatory markers (CRP, ESR and ferritin). There was evidence of mild pancreatic injury (lipase 179 U/L, n:15-110 U/L), and all autoantibodies for autoimmune diabetes were negative. He was pubertal (Tanner 3), non-obese (BMI Z score -0.3) and without acanthosis nigricans. Past medical and family history were non-contributory. He was treated with IV insulin at 0.1 u/kg/h until DKA resolved within 24 h then transitioned to subcutaneous insulin at 1 u/kg/day. He did not have signs of systemic inflammatory response, need for respiratory support, or glucocorticoids but had persistent hyperglycemia prompting an increase of insulin dosing and resumption of IV insulin. His insulin requirements continued to increase up to 4 u/kg/d with sustained hyperglycemia indicative of an exceptional state of insulin resistance. On Day 6 of admission metformin was initiated, on Day 9 insulin requirements declined and he was discharged on an insulin regimen close to 1.5 u/kg/d. Eventually metformin was discontinued on Day 20 after diagnosis without rebound in insulin requirements. On Day 28 he had improved glycemic control (HbA1c 8.8%) at insulin doses more appropriate for his age and pubertal status (0.9 u/kg/d). Clinical lessons: We report a case of autoantibody negative diabetes with pancreatic injury and marked insulin resistance unrelated to systemic inflammatory response associated with COVID-19. The clinical presentation was reminiscent of fT1D with the exception of exceptional insulin resistance. This is perhaps a novel form of diabetes mellitus not otherwise classified. Although the pathophysiology remains obscure, it is plausible that it is mediated by direct islet injury. Notably, there was a discordance between the severity of illness and insulin resistance suggesting an intrinsic effect of SARS-CoV-2 on glucose hemostasis.
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Alqaisi, Sura, and Ali Rahman. "ODP649 COVID-19 Induced Diabetic Ketoacidosis Which Unmasked Latent Autoimmune Diabetes In Adult." Journal of the Endocrine Society 6, Supplement_1 (2022): A346—A347. http://dx.doi.org/10.1210/jendso/bvac150.721.
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Abstract Latent autoimmune diabetes in adults (LADA)" is a kind"of autoimmune diabetes" that progresses slowly. Numerous studies have termed LADA type 1.5 diabetes because it is often associated with antibodies against insulin-producing pancreatic cells. In contrast to type 1 diabetes, patients with LADA may go six months without insulin following diagnosis. Individuals with LADA are often well beyond the age of 30. Because they develop symptoms later than patients with type 1 diabetes and because their pancreases initially generate some insulin, persons with LADA are sometimes misdiagnosed as having type 2 diabetes. Individuals with LADA have a lower BMI and a better metabolic profile than patients with type 2 diabetes. The majority of individuals with LADA are diagnosed after the age of 30, exhibit detectable islet antibodies — most often to glutamic acid decarboxylase (GAD65) — and advance more rapidly on insulin than those with Type 2 diabetes. COVID-19 is a pandemic virus produced by the SARS-CoV-2 virus. The researchers discovered that this virus may damage"insulin-producing cells in the pancreas in a variety of ways. It may cause direct harm to the pancreatic beta cells required for normal insulin production since SARS-CoV-2 has a spike protein that binds to the target cell's receptor. Recent research established that angiotensin-converting enzyme-2 (ACE2) functions as a functional receptor for the SARS-CoV-2 S-protein, promoting viral entry into target cells, most notably the lung, ileum, and various other cardiovascular, renal, gastrointestinal, and pancreatic organs". It"has been shown that overexpression of ACE2 mRNA in the pancreas causes islet cell destruction and acute beta cell malfunction, manifesting as new-onset diabetes in healthy persons or increasing hyperglycemia or ketoacidosis in diabetic patients." A 37-year-old male with no major previous medical history except than COVID-19 infection seven months before admission arrived at the emergency department complaining of two days of nausea, vomiting, and stomach discomfort. He has also advocated for polyuria, polydipsia, and accidental weight loss after contracting COVID-19. His vital signs were abnormal for a heart rate of 124 beats per minute". "His BMI was 24, he had an unremarkable physical examination, and he had no substantial family history". "His laboratory values were as"follows: Na 135 mEq/L, K 3.2 mEq/L, Cl 108 mEq/L, HCO3 10 mEq/L, Anion Gap 17, Glucose 500 mg/dl, Hemoglobin A1C 13%. His urine analysis revealed ketones, TG 120 mg/dl, LDL 60 mg/dl, and HDL 50 mg/dl. The patient was diagnosed with diabetic ketoacidosis, admitted to the intensive care unit, and began on an insulin drip, intravenous fluid hydration, and potassium supplements. "After" one night, his anion gap was closed then bridged with the use of five units of Lantus. Further testing indicated that the laboratory tested positive for Glutamic Acid Decarboxylase antibodies (GAD65) at a concentration of 2U/ml (1 U/ml) and C-Peptide at a value of "0.4 ng/ml (0.8-3 ng/ml). The patient met the Immunology of Diabetes Society's (IDS) criteria for LADA diagnosis: adult-onset, islet cell autoantibody, and initial insulin independence. The patient was finally sent home with Insulin and a referral to an Endocrinologist, and at his three-month follow-up visit, he reports that his symptoms have improved, he has gained some weight, and his A1C is 6.9 percent. Due to the similarities between many kinds of diabetes and LADA, it may be difficult to determine which type a patient has. Type 1 diabetes often manifests early in life, before the age of 30, with positive autoantibodies and the need for insulin treatment. While patients diagnosed with type 2 diabetes after the age of 30 are often obese, lack autoantibodies, and react favorably to lifestyle changes and oral hypoglycemic medications. However, since LADA manifests late in life, it has features of both type 1 and types 2 diabetes. Typically, the patient has a low BMI and initially reacts somewhat to lifestyle changes and oral hypoglycemic medications but eventually develops insulin resistance. Presentation: No date and time listed
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Wasilewska, Inga, Jakub Rezmer, and Łukasz Świątek. "Diabetes mellitus and COVID-19: current state of knowledge." Journal of Education, Health and Sport 12, no. 8 (2022): 1170–75. http://dx.doi.org/10.12775/jehs.2022.12.08.101.
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Introduction: Diabetes mellitus is a chronic metabolic disease characterized by disturbances in carbohydrate metabolism. Long-term high blood glucose levels can lead to a variety of serious complications and organ failure. Diabetic patients are particularly at risk of the severe course of COVID-19. Objective: The study aimed to investigate the relationship between diabetes and COVID-19. The literature available in the PubMed database was used to carry out a systematic review of the literature. The meta-analyzes from 2021 and 2022 were used for the analysis, with the inclusion of the phrases "DIABETES" and "COVID-19" in the title. A brief description of the state of knowledge: Diabetes does not increase the incidence of COVID-19, but the risk of severe disease is higher in patients with diabetes compared to the non-diabetic population. This is especially true of patients with uncontrolled glycaemia. SARS-CoV-2 disrupts the carbohydrate metabolism, can damage pancreatic beta cells and, in this mechanism, induce diabetes or cause the progression of pre-existing diabetes. There is an increased incidence of COVID-19 complications, including acute respiratory distress syndrome and death in patients with diabetes. Conclusions: Diabetic patients are at a higher risk of the severe course and rapid progression of COVID-19. Important in COVID-19 therapy is glycemic control and monitoring the percentage of glycosylated hemoglobin, CRP and D-dimers. The modification of the current treatment may be necessary. In patients who have undergone COVID-19, attention should be paid to the possibility of induction of diabetes or dysregulation of carbohydrate metabolism in patients suffering from diabetes previously.
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Yatskov, I. A., V. A. Beloglazov, and E. I. Ryapova. "Lipopolysaccharide and ARDS caused by new coronavirus infection: hypotheses and facts." Medical Immunology (Russia) 24, no. 1 (2022): 7–18. http://dx.doi.org/10.15789/1563-0625-laa-2229.
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This review presents data from the literature that provide insight into the role of the lipopolysaccharide (LPS) of the Gram-negative bacteria in pathogenesis of acute respiratory distress syndrome (ARDS) caused by the novel SARS-CoV-2 coronavirus infection. ARDS is a syndrome of severe respiratory failure, an acutely occurring diffuse inflammatory lesion of lung tissue that develops as a nonspecific reaction to various direct (aspiration, inhalation of toxic gases), and systemic (sepsis, polytrauma) damaging factors and leading to development of acute respiratory failure (ARF), due to impaired structure of the lung parenchyma, disturbances in vascular permeability, decreased area of ventilated lung tissue. ARDS from coronavirus infection appears to have worse outcomes than ARDS from other causes. Mortality from typical ARDS at the intensive care units and hospitals is 35.3% and 40.0%, respectively, while the lethality rates for COVID-19-associated ARDS, ranged from 26% to 61.5%. Among patients who underwent artificial ventilation of the lungs, the mortality rates can range from 65.7% to 94%. Risk factors for poor outcomes include, e.g., older age, presence of concomitant diseases such as hypertension, cardiovascular disease and diabetes mellitus; decreased number of lymphocytes, kidney injury, and increased D-dimer levels. Death with ARDS in COVID-19 occurs as a result of respiratory failure (53%), respiratory failure combined with heart failure (33%), myocardial damage and circulatory failure (7%), or death from an unknown cause. A large number of studies show that bacterial LPS is directly or indirectly involved in all pathogenetic links of ARDS caused by the SARS-CoV-2 virus, i.e., worsening the course of inflammatory lung diseases due to decreased level of angiotensin-converting enzyme 2 (ACE2); increasing generation of reactive oxygen species (ROS) via NADPH oxidase and subsequent inactivation of endothelial nitric oxide synthase (eNOS) and decreasing bioavailability of endothelial NO, thus leading to endothelial dysfunction; interacting with proteins of surfactants. SP-A and SP-D, promoting early destruction of the cellular monolayers and lowering surface tension, interact with soluble CD14 receptor, which also has a pro-inflammatory effect on epithelial and endothelial cells, leading to p38MAPK activation via TLR4 receptors, causing degradation of IêBá protein and subsequent translocation of p65 NF-êB into the nucleus, thus inducing transcription of IL-6 and adhesion molecules (ICAM-1, VCAM-1 and E-selectin), and, as shown by Petruk et al. (2020), causing direct binding to the viral S protein in combination with LPS, thus enhancing activation of nuclear factor-kappa B (NF-êB) in monocytic THP-1 cells and cytokine responses in mononuclear blood cells. These pathophysiological mechanisms require further in-depth study in order to understand the nature of changes that occur in the patients with new SARS-CoV-2 infection.
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Schiaffini, Riccardo, Andrea Campana, Annalisa Deodati, Emanuela Peschiaroli, Maria Francesca Lanzillotta, and Alessandra Fierabracci. "SARS-CoV-2 infection as possible downstream disease precipitator in autoantibody-positive insulin-dependent diabetes mellitus: a case report." Italian Journal of Pediatrics 48, no. 1 (2022). http://dx.doi.org/10.1186/s13052-022-01226-5.
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Abstract Background SARS-CoV-2 causes lesions, in addition to lung, in endocrine organs such as the pancreas through ACE2 receptor. Recently the relationship between SARS-CoV-2 exposition and the incidence or evolution of clinical autoimmune diabetes has attracted the attention of diabetologists. Case presentation We report the analysis of the clinical history of a child diagnosed for insulin-dependent diabetes mellitus (Type 1 diabetes) at the time a paucisymptomatic COVID-19 infection occurred, followed by well-controlled metabolic status. As opposite to previous findings SARS-CoV2 did not cause ketosis and ketoacidosis. Polydipsia was reported a few months and weight loss 4 weeks before SARS- CoV-2 infection suggesting that SARS-CoV-2 could not be the trigger of Type 1 diabetes in this patient. Conclusions SARS-CoV-2 in this patient was an unexpected event in the course of disease. We advance the hypothesis that the SARS-CoV-2 infection, even if paucisymptomatic could have acted in the present case report as a hypothetical downstream precipitating factor; whilst the inciting triggering event of the autoimmune disease, as confirmed by the presence of circulating autoantibodies, could have occurred even before, as generally assumed for this category of disorders. The precipitating mechanism could have been the acute interaction between virus and the ACE receptor on the beta cells, at the time that hyperglycemia and glycosuria were ascertained, and HbA1c levels confirmed a metabolic dysregulation over the previous 3 months in absence of ketoacidosis.
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Akkuş, Gamze. "Newly-onset Autoimmune Diabetes Mellitus triggered by Covid 19 infection: A case based review." Endocrine, Metabolic & Immune Disorders - Drug Targets 22 (October 4, 2022). http://dx.doi.org/10.2174/2666145415666221004111511.
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Abstract: The devastating global pandemic Coronavirus disease 2019 (Covid 19) which was isolated in China in January 2020 is responsible for outbreak of pneumonia and other multisystemic complications. The clinical picture of the infection has an extreme variability: it goes from asymptomatic patients or mild forms with fever, cough, fatigue and loss of smell and taste, to severe cases ending up in the intensive care unit (ICU). This is due to possible cytokine storm that may lead to multi organ failure, septic shock, or thrombosis. Severe Acute Respiratory Syndrome coronavirus 2 (SARS-CoV -2) which is the virus that causes Covid 19, binds to angiotensin-converting enzyme 2 (ACE2) receptors, which are expressed in key metabolic organ and tissues including pancreatic beta cells, adipose tissue, the small intestine and the kidneys. Therefore it is possible to state tht newly-onset diabetes is triggered by Covid 19 infection. Although there have been many hypotheses which clarify the potential diabetogenic effect of Covid 19, only few observations were reported during this pandemic. Two male patients who were admitted to us with devastating hyperglycemia symptoms were diagnosed as type 1/autoimmune diabetes mellitus within 3 months following Covid 19 infection. Autoantibodies and decreased C peptide levels were detected in these patients. We speculated that autoimmune insulitis and pancreatic beta-cell destruction might be triggered by Covid 19 infection through several mechanisms. Our purpose is to raise awareness on the possible link between SARS-CoV-2 and newly onset type 1 diabetes mellitus. Further studies are needed to determine a more definitive link between the two clinical entities.
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Steenblock, Charlotte, Stefanie Richter, Ilona Berger, et al. "Viral infiltration of pancreatic islets in patients with COVID-19." Nature Communications 12, no. 1 (2021). http://dx.doi.org/10.1038/s41467-021-23886-3.
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AbstractMetabolic diseases are associated with an increased risk of severe COVID-19 and conversely, new-onset hyperglycemia and complications of preexisting diabetes have been observed in COVID-19 patients. Here, we performed a comprehensive analysis of pancreatic autopsy tissue from COVID-19 patients using immunofluorescence, immunohistochemistry, RNA scope and electron microscopy and detected SARS-CoV-2 viral infiltration of beta-cells in all patients. Using SARS-CoV-2 pseudoviruses, we confirmed that isolated human islet cells are permissive to infection. In eleven COVID-19 patients, we examined the expression of ACE2, TMPRSS and other receptors and factors, such as DPP4, HMBG1 and NRP1, that might facilitate virus entry. Whereas 70% of the COVID-19 patients expressed ACE2 in the vasculature, only 30% displayed ACE2-expression in beta-cells. Even in the absence of manifest new-onset diabetes, necroptotic cell death, immune cell infiltration and SARS-CoV-2 viral infection of pancreatic beta-cells may contribute to varying degrees of metabolic dysregulation in patients with COVID-19.
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Lazartigues, Eric, Mirza Muhammad Fahd Qadir, and Franck Mauvais-Jarvis. "Endocrine Significance of SARS-CoV-2’s Reliance on ACE2." Endocrinology 161, no. 9 (2020). http://dx.doi.org/10.1210/endocr/bqaa108.
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Abstract The current COVID-19 pandemic is the most disruptive event in the past 50 years, with a global impact on health care and world economies. It is caused by severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2), a coronavirus that uses angiotensin-converting enzyme 2 (ACE2) as an entry point to the cells. ACE2 is a transmembrane carboxypeptidase and member of the renin-angiotensin system. This mini-review summarizes the main findings regarding ACE2 expression and function in endocrine tissues. We discuss rapidly evolving knowledge on the potential role of ACE2 and SARS coronaviruses in endocrinology and the development of diabetes mellitus, hypogonadism, and pituitary and thyroid diseases.
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Shao, Shiying, Qin Yang, Ruping Pan, Xuefeng Yu, and Yong Chen. "Interaction of Severe Acute Respiratory Syndrome Coronavirus 2 and Diabetes." Frontiers in Endocrinology 12 (October 6, 2021). http://dx.doi.org/10.3389/fendo.2021.731974.
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Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is causing a worldwide epidemic. It spreads very fast and hits people of all ages, especially patients with underlying diseases such as diabetes. In this review, we focus on the influences of diabetes on the outcome of SARS-CoV-2 infection and the involved mechanisms including lung dysfunction, immune disorder, abnormal expression of angiotensin-converting enzyme 2 (ACE2), overactivation of mechanistic target of rapamycin (mTOR) signaling pathway, and increased furin level. On the other hand, SARS-CoV-2 may trigger the development of diabetes. It causes the damage of pancreatic β cells, which is probably mediated by ACE2 protein in the islets. Furthermore, SARS-CoV-2 may aggravate insulin resistance through attacking other metabolic organs. Of note, certain anti-diabetic drugs (OADs), such as peroxisome proliferator-activated receptor γ (PPARγ) activator and glucagon-like peptide 1 receptor (GLP-1R) agonist, have been shown to upregulate ACE2 in animal models, which may increase the risk of SARS-CoV-2 infection. However, Metformin, as a first-line medicine for the treatment of type 2 diabetes mellitus (T2DM), may be a potential drug benefiting diabetic patients with SARS-CoV-2 infection, probably via a suppression of mTOR signaling together with its anti-inflammatory and anti-fibrosis function in lung. Remarkably, another kind of OADs, dipeptidyl Peptidase 4 (DPP4) inhibitor, may also exert beneficial effects in this respect, probably via a prevention of SARS-CoV-2 binding to cells. Thus, it is of significant to identify appropriate OADs for the treatment of diabetes in the context of SARS-CoV-2 infections.
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Al-kuraishy, Hayder M., Ali I. Al-Gareeb, M. Alblihed, Susana G. Guerreiro, Natália Cruz-Martins, and Gaber El-Saber Batiha. "COVID-19 in Relation to Hyperglycemia and Diabetes Mellitus." Frontiers in Cardiovascular Medicine 8 (May 20, 2021). http://dx.doi.org/10.3389/fcvm.2021.644095.
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Coronavirus disease 2019 (COVID-19), triggered by the severe acute respiratory syndrome-coronavirus 2 (SARS-CoV-2), may lead to extrapulmonary manifestations like diabetes mellitus (DM) and hyperglycemia, both predicting a poor prognosis and an increased risk of death. SARS-CoV-2 infects the pancreas through angiotensin-converting enzyme 2 (ACE2), where it is highly expressed compared to other organs, leading to pancreatic damage with subsequent impairment of insulin secretion and development of hyperglycemia even in non-DM patients. Thus, this review aims to provide an overview of the potential link between COVID-19 and hyperglycemia as a risk factor for DM development in relation to DM pharmacotherapy. For that, a systematic search was done in the database of MEDLINE through Scopus, Web of Science, PubMed, Embase, China National Knowledge Infrastructure (CNKI), China Biology Medicine (CBM), and Wanfang Data. Data obtained underline that SARS-CoV-2 infection in DM patients is more severe and associated with poor clinical outcomes due to preexistence of comorbidities and inflammation disorders. SARS-CoV-2 infection impairs glucose homeostasis and metabolism in DM and non-DM patients due to cytokine storm (CS) development, downregulation of ACE2, and direct injury of pancreatic β-cells. Therefore, the potent anti-inflammatory effect of diabetic pharmacotherapies such as metformin, pioglitazone, sodium-glucose co-transporter-2 inhibitors (SGLT2Is), and dipeptidyl peptidase-4 (DPP4) inhibitors may mitigate COVID-19 severity. In addition, some antidiabetic agents and also insulin may reduce SARS-CoV-2 infectivity and severity through the modulation of the ACE2 receptor expression. The findings presented here illustrate that insulin therapy might seem as more appropriate than other anti-DM pharmacotherapies in the management of COVID-19 patients with DM due to low risk of uncontrolled hyperglycemia and diabetic ketoacidosis (DKA). From these findings, we could not give the final conclusion about the efficacy of diabetic pharmacotherapy in COVID-19; thus, clinical trial and prospective studies are warranted to confirm this finding and concern.
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"COVID-19 y su asociación con los inhibidores de la enzima convertidora de angiotensina y los antagonistas de los receptores para angiotensina II." Revista de la Facultad de Medicina 63, no. 4 (2020): 30–34. http://dx.doi.org/10.22201/fm.24484865e.2020.63.4.05.
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Worldwide, over 7 million people have been infected due to the pandemic of COVID-19. The comorbidities associated to this disease are: hypertension, diabetes mellitus, obesity, obstructive pulmonary disease (COPD), cardiovascular disease, chronic renal failure, smoking, immunosuppression, and hypertension. Angiotensin-converting enzyme 2 (ACE2) is the functional receptor for SARS-CoV-2. This virus has an S protein that recognizes ACE2 as its receptor to enter the cell. ACE2 is a plasmatic protein expressed in alveolar cells type I, II, fibroblasts, endothelial cells and macrophages. Treatment with inhibitors of the angiotensin-converting enzyme (ACEi) or the receptor antagonist for angiotensin II (ARBs) notably increase the expression of ACE2. Therefore, in patients with these pathologies and treated with these medicines, the risk of developing the COVID-19 in a severe and fatal way could be increased. In Mexico, the major mortality due to COVID-19 is related to hypertension, diabetes mellitus, obesity and being over 65 years of age. Therefore, we suggest that during the SARS-CoV-2 pandemic, patients with hypertension treated with ACEi or ARBs, should receive alternative treatments such as L-type Ca2+ channel blockers (amlodipine) that have not been associated with ACE2 until now. Key words: COVID-19; SARS-CoV-2; captopril; losartan hypertension."
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Nouri-Keshtkar, Marjan, Sara Taghizadeh, Aisan Farhadi, et al. "Potential Impact of Diabetes and Obesity on Alveolar Type 2 (AT2)-Lipofibroblast (LIF) Interactions After COVID-19 Infection." Frontiers in Cell and Developmental Biology 9 (July 8, 2021). http://dx.doi.org/10.3389/fcell.2021.676150.
Full textAbstract:
Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), a new emerging respiratory virus, caused evolving pneumonia outbreak around the world. In SARS-Cov-2 infected patients, diabetes mellitus (DM) and obesity are two metabolic diseases associated with higher severity of SARS-CoV-2 related complications, characterized by acute lung injury requiring assisted ventilation as well as fibrosis development in surviving patients. Different factors are potentially responsible for this exacerbated response to SARS-CoV-2 infection. In patients with DM, base-line increase in inflammation and oxidative stress represent preexisting risk factors for virus-induced damages. Such factors are also likely to be found in obese patients. In addition, it has been proposed that massive injury to the alveolar epithelial type 2 (AT2) cells, which express the SARS-CoV-2 receptor angiotensin-converting enzyme 2 (ACE2), leads to the activation of their stromal niches represented by the Lipofibroblasts (LIF). LIF are instrumental in maintaining the self-renewal of AT2 stem cells. LIF have been proposed to transdifferentiate into Myofibroblast (MYF) following injury to AT2 cells, thereby contributing to fibrosis. We hypothesized that LIF’s activity could be impacted by DM or obesity in an age- and gender-dependent manner, rendering them more prone to transition toward the profibrotic MYF status in the context of severe COVID-19 pneumonia. Understanding the cumulative effects of DM and/or obesity in the context of SARS-CoV-2 infection at the cellular level will be crucial for efficient therapeutic solutions.
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Okoduwa, Stanley I. R., Daniel H. Mhya, Idongesit A. Enang, and Akinbobola O. Salawu. "Diabetes Mellitus and COVID-19: Possible Interactions and Mechanisms in Comorbid Patients." Journal of Health Science and Medical Research, October 27, 2022. http://dx.doi.org/10.31584/jhsmr.2022904.
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Beginning in December 2019 and still ongoing, coronavirus disease 2019 (COVID-19) infections have posed a public health challenge worldwide. There have been reports of diabetes mellitus (DM) as one of the most prevalent comorbidities in patients with COVID-19. Although the interactions and possible mechanisms of this association have not been fully established, the existence of DM is believed to aggravate the adverse effects of COVID-19 infection. Hence, the need for this paper. Findings from other studies have shown different possible mechanisms of how COVID-19 and DM aggravate the severity of each other. Among the hypothetical mechanisms reported between COVID-19 and DM in this paper are: COVID-19 causes complications of DM through the following: (1) Destruction of β-cells in the pancreas by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection. (2) Cytokine storm generation which mediates tissue inflammation resulting in organ damage and (3) The use of corticosteroid drugs which have been found to be highly diabetogenic. Similarly, DM facilitates internalizing of SARS-CoV-2 symptoms through increasing expression of angiotensin-converting enzyme 2 (ACE2) and the furin protein, viral load, entrance and replication of SARS-CoV-2, glycosylation, and compromising of the immune response that worsens COVID-19. Having a clear understanding of the biochemical mechanisms of interactions between COVID-19 and DM may be useful for future research of agents targeted as therapeutic remedies for managing patients with diabetes infected with COVID-19 and vice versa.
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Najafi, Reza, Nahid Mamizadeh, Seyed Hossein Hosseini, Sima Roushenas, and Leila Bazhdan. "A challenging case of COVID-19: a COVID-19 positive adolescent presented with severe diabetic ketoacidosis, resistant hypertension." BMC Endocrine Disorders 22, no. 1 (2022). http://dx.doi.org/10.1186/s12902-022-00979-8.
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Abstract Background Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is a virus which causes COVID-19. It binds to the angiotensin-converting enzyme 2 (ACE2) receptors, expressed in key metabolic organs and tissues, including pancreatic beta cells, adipose tissue, the small intestine, and kidneys. This condition has been linked to a variety of additional symptoms, including acute encephalopathy, changes in consciousness, and even gastrointestinal bleeding. Case presentation In this study, we have reported a 13-year-old boy, 69 kg, with SARS-COV-2 infection. In this case, multiple systems, including the endocrine, renal, pulmonary, gastrointestinal, and nervous systems, were affected. Conclusions It is speculated that different manifestations of COVID-19 can be seen in clinical settings, and practitioners should be more cautious not to miss the chimeric characteristics of COVID-19 infection.
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Alizadeh, Shaban, Reza Afrisham, Yasaman Jadidi, et al. "Gastrointestinal, liver, pancreas, oral and psychological long-term symptoms of COVID-19 after recovery; A review." Mini-Reviews in Medicinal Chemistry 23 (November 16, 2022). http://dx.doi.org/10.2174/1389557523666221116154907.
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Abstracts: Due to the importance of control and prevention of COVID-19-correlated long-term symptoms, the present review article has summarized what has been currently known regarding the molecular and cellular mechanisms linking COVID-19 to important long-term complications including psychological complications, liver and gastrointestinal manifestations, oral signs as well as even diabetes. COVID-19 can directly affect the body cells through their Angiotensin-converting enzyme 2 [ACE-2] to induce inflammatory responses and cytokine storm. The cytokines cause the release of reactive oxygen species [ROS] and subsequently initiate and promote cell injuries. Another way, COVID-19-associated dysbiosis may be involved in GI pathogenesis. In addition, SARS-CoV-2 reduces butyrate-secreting bacteria and leads to the induction of hyperinflammation. Moreover, SARS-CoV-2-mediated endoplasmic reticulum stress induces de novo lipogenesis in hepatocytes, which leads to hepatic steatosis and inhibits autophagy via increasing mTOR. In pancreas tissue, the virus damages beta-cells and impairs insulin secretion. SARS-COV-2 may change the ACE2 activity by modifying ANGII levels in taste buds which leads to gustatory dysfunction. SARS-CoV-2 infection and its resulting stress can lead to severe inflammation that can subsequently alter neurotransmitter signals. This, in turn, negatively affects the structure of neurons and leads to mood and anxiety disorders. In conclusion, all the pathways mentioned earlier can play a crucial role in the disease's pathogenesis and related comorbidities. However, more studies are needed to clarify the underlying mechanism of the pathogenesis of the new coming virus.
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Schipani, Elena, Andrea Cozzi, Giuseppe Salvatore Murgida, et al. "New-onset type 1 diabetes mellitus triggered by SARS-CoV-2 infection in a patient with Hashimoto thyroiditis: a case report." Italian Journal of Medicine, January 25, 2021. http://dx.doi.org/10.4081/itjm.2021.1387.
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New onset type 1 diabetes mellitus is an uncommon but possible complication triggered by SARSCoV- 2 infection. Metabolic inflammation supported by cytokine storm leading to pancreatic beta cells destruction is the most probable link between COVID-19 and diabetes. Here, we describe the case of a 51-year-old female suffering from Hashimoto thyroiditis, who came to our attenction for new onset polyuria-polydipsia syndrome associated to hyperglycemia after a mild form of COVID- 19 recognized two months before and already recovered. Type 1 diabetes was diagnosed.
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Roeroe, Pomantow A. L., Bisuk P. Sedli, and Octavianus Umboh. "Faktor Risiko Terjadinya Coronavirus Disease 2019 (Covid-19) pada Penyandang Diabetes Melitus Tipe 2." e-CliniC 9, no. 1 (2021). http://dx.doi.org/10.35790/ecl.v9i1.32301.
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Abstract: Coronavirus Disease 2019 (COVID-19) is an infectious disease caused by SARS-CoV-2 and has been declared as a pandemic by WHO in March 11, 2020. This disease is an additional problem in people with type 2 diabetes mellitus (T2DM). Several studies have shown that diabetes is a risk factor for COVID-19. This study was aimed to determine the risk factors for the occurrence of Coronavirus Disease 2019 (COVID-19) in T2DM patients. This was a literature review study using several journal databases, namely Google Scholar, PubMed, and Science Direct. Literature searching was performed by using the PICOS method and the analysis was carried out qualitatively The results obtained 10 literatures reporting that T2DM would increase the severity and mortality of COVID-19 patients related to elderly age, obesity, chronic systemic inflammation, increased coagulation activity, potential direct damage to the pancreas, changes in expression of ACE2 receptors, dysregulation of the number, activity of immune cells, alveolar dysfunction, and endothelial dysfunction. There was not yet strong evidence regarding discontinuation or continuation of various diabetes drugs in COVID-19 patients, but insulin remains the recommended agent for blood glucose control. In conclusion, T2DM increases the severity and mortality rate of COVID-19 patients Keywords: diabetes mellitus; COVID-19; risk factors Abstrak: Coronavirus Disease 2019 (COVID-19) merupakan salah satu penyakit infeksi yang disebabkan oleh SARS-CoV-2 dan telah ditetapkan sebagai pandemi oleh WHO pada 11 Maret 2020. Penyakit ini menjadi masalah tambahan bagi penyandang diabetes melitus tipe 2 (DMT2). Beberapa penelitian menunjukkan bahwa diabetes merupakan salah satu faktor risiko terjadinya COVID-19. Penelitian ini bertujuan untuk mengetahui faktor risiko terjadinya COVID-19 pada penyandang DMT2. Jenis penelitian ialah literature review menggunakan laporan penelitian dari beberapa database jurnal, yaitu google scholar, PubMed, dan ClinicalKey. Pencarian artikel menggunakan metode PICOS dan analisis dilakukan secara kualitatif. Hasil penelitian mendapatkan 10 laporan penelitian yang melaporkan bahwa DMT2 meningkatkan tingkat keparahan dan mortalitas pasien COVID-19 akibat adanya mekanisme terkait dengan usia lanjut, obesitas, peradangan sistemik kronis, peningkatan aktivitas koagulasi, potensi kerusakan langsung pankreas, perubahan ekspresi reseptor ACE2, disregulasi jumlah dan aktivitas sel imun, disfungsi alveolar, dan disfungsi endotel. Belum terdapat bukti kuat mengenai penghentian atau pelanjutan berbagai obat diabetes pada pasien COVID-19, tetapi insulin tetap menjadi obat yang disarankan untuk mengontrol glukosa darah. Simpulan penelitian ini ialah DMT2 meningkatkan tingkat keparahan dan mortalitas dari pasien COVID-19.Kata kunci: diabetes melitus tipe 2 (DMT2), COVID-19, faktor risiko
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Patel, Sanyamee, Prashilkumar Patel, Ayushi Mehta, Ishan Patel, Shubham Thakor, and Om Lumbhani. "incidence of myocarditis and pericarditis in post COVID-19 unvaccinated patients." International journal of health sciences, July 31, 2022, 11743–51. http://dx.doi.org/10.53730/ijhs.v6ns5.11049.
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Background and Aim: Viral infections have also been associated with the presence of autoimmune diseases such as systemic lupus disease, rheumatoid arthritis, and diabetes mellitus. SARS-CoV-2 gains entry into human cells by binding its spike protein to the membrane protein angiotensinconverting enzyme 2 (ACE2). It has recently been reported that the incidence of myocarditis and pericarditis is increased in COVID-19 patients during the acute illness. However; whether or not myocarditis and pericarditis after the recovery period are a part of the long COVID-19 syndrome is yet unknown. Hence, we studied the incidence of myocarditis and pericarditis in COVID-19 patients after recovering from the acute infection. Material and Methods: We retrieved records of all adult patients (age ≥ 18 years) who had a documented positive COVID-19 PCR test (n = 500) for the period of 1 year. A control group was created from a cohort of adult patients with at least one negative COVID-19 From this pool of patients, the control cohort was created by 3:1 matching of age (±2 years) and gender. Total 1000 patients in control group were selected.
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Saheb Sharif-Askari, Fatemeh, Narjes Saheb Sharif-Askari, Shirin Hafezi, et al. "Upregulation of interleukin-19 in saliva of patients with COVID-19." Scientific Reports 12, no. 1 (2022). http://dx.doi.org/10.1038/s41598-022-20087-w.
Full textAbstract:
AbstractCytokines are major players in orchestrating inflammation, disease pathogenesis and severity during COVID-19 disease. However, the role of IL-19 in COVID-19 pathogenesis remains elusive. Herein, through the analysis of transcriptomic datasets of SARS-CoV-2 infected lung cells, nasopharyngeal swabs, and lung autopsies of COVID-19 patients, we report that expression levels of IL-19 and its receptor, IL-20R2, were upregulated following SARS-CoV-2 infection. Of 202 adult COVID-19 patients, IL-19 protein level was significantly higher in blood and saliva of asymptomatic patients compared to healthy controls when adjusted for patients’ demographics (P < 0.001). Interestingly, high saliva IL-19 level was also associated with COVID-19 severity (P < 0.0001), need for mechanical ventilation (P = 0.002), and/or death (P = 0.010) within 29 days of admission, after adjusting for patients’ demographics, diabetes mellitus comorbidity, and COVID-19 serum markers of severity such as D-dimer, C-reactive protein, and ferritin. Moreover, patients who received interferon beta during their hospital stay had lower plasma IL-19 concentrations (24 pg mL−1) than those who received tocilizumab (39.2 pg mL−1) or corticosteroids (42.5 pg mL−1). Our findings indicate that high saliva IL-19 level was associated with COVID-19 infectivity and disease severity.