Introduction: Vitamin D deficiency and chronic obstructive pulmonary disease (COPD) are both world-wide health problems. Vitamin D has known to be important in infectious pathologies. However, there are conflicting results in the role of vitamin D in COPD exacerbation. This study was design to evaluate the prevalence of vitamin D deficiency among patients with COPD exacerbation in relation with surrogate markers of exacerbation and long-term mortality in hospitalized patients with COPD.
Materials And Methods: 117 hospitalized COPD patients were included between January 2010 to June 2013. Information was obtained through the patients' records and the electronic database of the hospital. The patients who had on vitamin D and/or calcium therapy, and who were suspected of asthma were excluded from the study.
Result: The study included 117 patients and none of them were on vitamin D replacement on entry. The mean age was 67.95 ± 9.8 years. The number of male/female patients was 104/13. The mean forced expiratory volume in one second in percent predicted (FEV1%) was 39.97 ± 18.45. One hundred fifteen patients had vitamin D deficiency whereas only two patients had vitamin D ≥ 30 ng/dL. Seventy nine (69.5%) of the patients had severe vitamin D deficiency (< 10 ng/dL). The percentage of frequent exacerbators, patients who had microorganism growth and the median duration of hospital stay, mean FEV1 and survival did not differ between the group of vitamin D < or ≥ 10 ng/dL. There was no meaningful correlation of vitamin D level and any of the surrogate markers of exacerbation.
Conclusions: Severe vitamin D deficiency is heavily prevalent in Turkish COPD patients. However, it did not have an association on exacerbation and long term survival.
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Cureus
December 2024
Family Medicine, Najran Armed Forces Hospital, Najran, SAU.
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Department of Renal Medicine, Westmead Hospital, Westmead, New South Wales, Australia.
Fracture is an under-recognized but common complication of diabetes mellitus, with an incidence approaching twofold in type 2 diabetes mellitus (T2DM) and up to sevenfold in type 1 diabetes mellitus (T1DM) compared with that in the general population. Both T1DM and T2DM induce chronic hyperglycaemia, leading to the accumulation of advanced glycosylation end products that affect osteoblast function, increased collagen crosslinking and a senescence phenotype promoting inflammation. Together with an increased incidence of microvascular disease and an increased risk of vitamin D deficiency, these factors reduce bone quality, thereby increasing bone fragility.
View Article and Find Full Text PDFPediatr Hematol Oncol
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Department of Pediatrics - Division of Pediatric Hematology, Universidade Federal de São Paulo, Sao Paulo, Brazil.
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Department of Medicine, Washington University School of Medicine, St. Louis, MO, USA; Department of Medicine, VA Medical Center, St. Louis, MO, USA; Department of Cell Biology and Physiology, Washington University School of Medicine, St. Louis, MO, USA. Electronic address:
Targeting optimal glycemic control based on hemoglobin A1c (A1c) values reduces but does not abolish the onset of diabetic kidney disease and its progression to chronic kidney disease (CKD). This suggests that factors other than the average glucose contribute to the residual risk. Vitamin D deficiency and frequent episodes of acute hyperglycemia (AH) are associated with the onset of albuminuria and CKD progression in diabetes.
View Article and Find Full Text PDFAnn Endocrinol (Paris)
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Department of Endocrinology, Diabetes and Metabolic Diseases, Angers University Hospital, Reference Center for Rare Thyroid and Hormone Receptor Diseases, 49933 Angers cedex 09, France; Univ Angers, Inserm, CNRS, MITOVASC, Equipe CarMe, SFR ICAT, F-49000 Angers, France. Electronic address:
Primary hyperparathyroidism is treated surgically. Postoperatively, close monitoring of blood calcium levels is necessary to detect any hypocalcemia. Postoperative PTH assays can be performed within 24 hours to identify patients who will not develop permanent hypoparathyroidism.
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