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1.
J Clin Endocrinol Metab ; 107(5): 1484-1502, 2022 04 19.
Artículo en Inglés | MEDLINE | ID: mdl-34894254

RESUMEN

PURPOSE: Vitamin D deficiency/insufficiency may increase the susceptibility to coronavirus disease 2019 (COVID-19). We aimed to determine the association between vitamin D deficiency/insufficiency and susceptibility to COVID-19, its severity, mortality, and role of vitamin D in its treatment. METHODS: We searched CINAHL, Cochrane library, EMBASE, PubMED, Scopus, and Web of Science up to May 30, 2021, for observational studies on association between vitamin D deficiency/insufficiency and susceptibility to COVID-19, severe disease, and death among adults, and, randomized controlled trials (RCTs) comparing vitamin D treatment against standard care or placebo, in improving severity or mortality among adults with COVID-19. Risk of bias was assessed using Newcastle-Ottawa scale for observational studies and AUB-KQ1 Cochrane tool for RCTs. Study-level data were analyzed using RevMan 5.3 and R (v4.1.0). Heterogeneity was determined by I2 and sources were explored through prespecified sensitivity analyses, subgroup analyses, and meta-regressions. RESULTS: Of 1877 search results, 76 studies satisfying eligibility criteria were included. Seventy-two observational studies were included in the meta-analysis (n = 1 976 099). Vitamin D deficiency/insufficiency increased the odds of developing COVID-19 (odds ratio [OR] 1.46; 95% CI, 1.28-1.65; P < 0.0001; I2 = 92%), severe disease (OR 1.90; 95% CI, 1.52-2.38; P < 0.0001; I2 = 81%), and death (OR 2.07; 95% CI, 1.28-3.35; P = 0.003; I2 = 73%). The 25-hydroxy vitamin D concentrations were lower in individuals with COVID-19 compared with controls (mean difference [MD] -3.85 ng/mL; 95% CI, -5.44 to -2.26; P ≤ 0.0001), in patients with severe COVID-19 compared with controls with nonsevere COVID-19 (MD -4.84 ng/mL; 95% CI, -7.32 to -2.35; P = 0.0001) and in nonsurvivors compared with survivors (MD -4.80 ng/mL; 95% CI, -7.89 to -1.71; P = 0.002). The association between vitamin D deficiency/insufficiency and death was insignificant when studies with high risk of bias or studies reporting unadjusted effect estimates were excluded. Risk of bias and heterogeneity were high across all analyses. Discrepancies in timing of vitamin D testing, definitions of severe COVID-19, and vitamin D deficiency/insufficiency partly explained the heterogeneity. Four RCTs were widely heterogeneous precluding meta-analysis. CONCLUSION: Multiple observational studies involving nearly 2 million adults suggest vitamin D deficiency/insufficiency increases susceptibility to COVID-19 and severe COVID-19, although with a high risk of bias and heterogeneity. Association with mortality was less robust. Heterogeneity in RCTs precluded their meta-analysis.


Asunto(s)
COVID-19 , Deficiencia de Vitamina D , Adulto , Humanos , Pronóstico , Vitamina D/uso terapéutico , Deficiencia de Vitamina D/complicaciones , Deficiencia de Vitamina D/tratamiento farmacológico , Deficiencia de Vitamina D/epidemiología , Vitaminas/uso terapéutico
2.
J Endocr Soc ; 4(8): bvaa082, 2020 Aug 01.
Artículo en Inglés | MEDLINE | ID: mdl-32728654

RESUMEN

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) virus has spread across the globe rapidly causing an unprecedented pandemic. Because of the novelty of the disease, the possible impact on the endocrine system is not clear. To compile a mini-review describing possible endocrine consequences of SARS-CoV-2 infection, we performed a literature survey using the key words Covid-19, Coronavirus, SARS CoV-1, SARS Cov-2, Endocrine, and related terms in medical databases including PubMed, Google Scholar, and MedARXiv from the year 2000. Additional references were identified through manual screening of bibliographies and via citations in the selected articles. The literature review is current until April 28, 2020. In light of the literature, we discuss SARS-CoV-2 and explore the endocrine consequences based on the experience with structurally-similar SARS-CoV-1. Studies from the SARS -CoV-1 epidemic have reported variable changes in the endocrine organs. SARS-CoV-2 attaches to the ACE2 system in the pancreas causing perturbation of insulin production resulting in hyperglycemic emergencies. In patients with preexisting endocrine disorders who develop COVID-19, several factors warrant management decisions. Hydrocortisone dose adjustments are required in patients with adrenal insufficiency. Identification and management of critical illness-related corticosteroid insufficiency is crucial. Patients with Cushing syndrome may have poorer outcomes because of the associated immunodeficiency and coagulopathy. Vitamin D deficiency appears to be associated with increased susceptibility or severity to SARS-CoV-2 infection, and replacement may improve outcomes. Robust strategies required for the optimal management of endocrinopathies in COVID-19 are discussed extensively in this mini-review.

3.
BMC Nephrol ; 19(1): 319, 2018 11 09.
Artículo en Inglés | MEDLINE | ID: mdl-30413156

RESUMEN

BACKGROUND: Infective complications following percutaneous renal biopsy are rare, even among immunocompromised. However it is important to be vigilant about such complications, to detect them early and prevent morbidity and mortality. We report a case of retroperitoneal abscess with extension to subcutaneous plane after a renal biopsy. CASE PRESENTATION: A 42-year-old female with long standing cutaneous lupus underwent renal biopsy for evaluation of nephrotic range proteinuria. She was on high dose prednisolone complicated with steroid induced hyperglycaemia. Eight weeks after the biopsy she presented with left flank pain, malaise and fever. There was a tender subcutaneous induration over the biopsy site. Contrast CT abdomen showed a retroperitoneal abscess with subcutaneous extension along the path of the biopsy needle. This was successfully treated with surgical drainage and broad-spectrum antibiotics. CONCLUSIONS: Infections and abscess formation are rare but serious complications of renal biopsy. Immunocompromised state is a potential risk factor. Possible mechanisms and measures for prevention and early detection of this rare complication are discussed.


Asunto(s)
Absceso Abdominal/diagnóstico por imagen , Absceso Abdominal/etiología , Riñón/patología , Tejido Subcutáneo/diagnóstico por imagen , Absceso Abdominal/metabolismo , Adulto , Biopsia/efectos adversos , Femenino , Humanos , Espacio Retroperitoneal/diagnóstico por imagen , Tejido Subcutáneo/metabolismo
4.
BMC Infect Dis ; 18(1): 367, 2018 08 06.
Artículo en Inglés | MEDLINE | ID: mdl-30081818

RESUMEN

BACKGROUND: Aspergillosis is a serious infection particularly affecting the immunodeficient host. Its co-infection with tuberculosis and cytomegalovirus has not been reported before. Embolic events are well recognized with aspergillous endocarditis and aortitis. Splenic abscess is a rare serious complication of disseminated aspergillosis and is difficult to treat. We report the first case of multiple embolic events and splenic abscess in a patient with pulmonary aspergillosis and cytomegaloviral and tuberculous co-infection, without endocarditis or aortitis. CASE PRESENTATION: Thirty-year-old male presented with fever and non-productive cough while on glucocorticoids for glomerulonephritis. He was found to have pulmonary aspergillosis and subsequently developed bilateral lower limb and cerebral fungal emboli and fungal abscess in the spleen. He had IgM and B cell deficiency and cytomegalovirus (CMV) and tuberculous co-infections. He recovered after prolonged course of antimicrobials, splenectomy and cessation of glucocorticoid therapy which also lead to the resolution of immune deficiencies. CONCLUSION: This report illustrates rare combination of B and T cell suppressive effects of glucocorticoids leading to co-infections with CMV, Mycobacterium tuberculosis and Aspergillus and systemic fungal embolization from pulmonary aspergillosis.


Asunto(s)
Infecciones por Citomegalovirus/tratamiento farmacológico , Terapia de Inmunosupresión/efectos adversos , Aspergilosis Pulmonar/tratamiento farmacológico , Enfermedades del Bazo/microbiología , Tuberculosis/tratamiento farmacológico , Absceso Abdominal/tratamiento farmacológico , Absceso Abdominal/microbiología , Absceso Abdominal/cirugía , Adulto , Antiinfecciosos/uso terapéutico , Linfocitos B/inmunología , Linfocitos B/patología , Coinfección , Embolia/microbiología , Embolia/terapia , Fiebre/etiología , Glucocorticoides/efectos adversos , Humanos , Síndromes de Inmunodeficiencia/microbiología , Masculino , Aspergilosis Pulmonar/complicaciones , Embolia Pulmonar/microbiología , Esplenectomía , Enfermedades del Bazo/tratamiento farmacológico , Enfermedades del Bazo/cirugía , Tuberculosis/microbiología
5.
J Clin Lipidol ; 12(2): 447-454, 2018.
Artículo en Inglés | MEDLINE | ID: mdl-29429894

RESUMEN

BACKGROUND: Dyslipidemia is a major risk factor for cardiovascular disease. Prevalence patterns and determinants of dyslipidemia in Sri Lanka are unkown. OBJECTIVES: We aimed to determine the prevalence and correlates of dyslipidemia among Sri Lankan adults. METHODS: A nationally representative sample was recruited by multistage random cluster sampling in Sri Lanka Diabetes and Cardiovascular Study, a cross-sectional study. Data collected by an interviewer-administered questionnaire, physical examination, anthropometric measurements lipid analysis from take 12-hour fasting blood samples were used. RESULTS: Among 4451 participants 60.5% were women and mean age was 46 years. Mean (standard deviation) total cholesterol (TC), high-density lipoprotein cholesterol (HDLC), low-density lipoprotein cholesterol (LDLC), triglycerides (TGs), and TC/HDLC levels were 206.7 mg/dL (±43.5), 46.8 mg/dL (±10.6), 135.5 mg/dL (±37.6), 121.7 mg/dL (±66.8), and 4.6 (±1.1), respectively. Women had higher mean TC, HDLC, LDLC, and TG values compared to men across all age groups. Mean TC, LDLC, and TGs increased with age in both genders; 77.4% of participants had some form of dyslipidemia. Low HDLC was the commonest type (49.6%) of dyslipidemia. Increasing age, female sex, living in urban sector, high body mass index, central obesity, diabetes, hypertension, insufficient physical activity, and smoking were associated with having some form of dyslipidemia. CONCLUSION: Three in four Sri Lankan adults have some form of dyslipidemia. Physical inactivity, obesity, hypertension, and diabetes are the leading modifiable risk factors.


Asunto(s)
Enfermedades Cardiovasculares/sangre , Diabetes Mellitus/sangre , Dislipidemias/sangre , Adulto , Enfermedades Cardiovasculares/diagnóstico , Enfermedades Cardiovasculares/epidemiología , Colesterol/sangre , HDL-Colesterol/sangre , LDL-Colesterol/sangre , Estudios Transversales , Diabetes Mellitus/diagnóstico , Diabetes Mellitus/epidemiología , Dislipidemias/diagnóstico , Dislipidemias/epidemiología , Femenino , Humanos , Masculino , Persona de Mediana Edad , Prevalencia , Factores de Riesgo , Sri Lanka/epidemiología , Triglicéridos/sangre
6.
BMC Rheumatol ; 2: 37, 2018.
Artículo en Inglés | MEDLINE | ID: mdl-30886987

RESUMEN

BACKGROUND: Autoimmune disorders are known to produce false positives in serological tests for infections. Aetiological association between infections and autoimmunity, increased susceptibility to infectious and autoimmune disorders with immune dysregulation and non-specific polyclonal expansion of B cells with autoimmunity may cause confusion in diagnosis and patient management. We report a patient with Adult Onset Still's Disease (AOSD) presenting with rising melioidosis antibody titres that caused diagnostic confusion. CASE PRESENTATION: A forty-nine-year-old female presented with prolonged fever, sore-throat, large joint arthritis, lymphadenopathy, hepatomegaly and transient rash. She had elevated inflammatory markers and a rising melioidosis antibody titre. The patient responded poorly to prolonged course of appropriate antimicrobials but showed rapid and sustained improvement with glucocorticoids. CONCLUSION: Positive melioidosis serology could have been due to a co-infection or false positive antibody reaction due to non-specific B cell expansion or an indicator of true infection that triggered the immune dysregulation to develop AOSD.

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