Samantha L. Margulies

Vitamin D deficiency in patients with intestinal malabsorption syndromes – think in and outside the gut

There is a very high prevalence of vitamin D deficiency, which is defined by a serum level of 25‐hydroxyvitamin D [25(OH)D] of lower than 20 ng/mL, in all populations of the world. Unfortunately, the prevalence of vitamin D deficiency in patients with intestinal malabsorption syndromes, including cystic fibrosis (CF), celiac disease (CD), short bowel syndrome and inflammatory bowel disease (IBD), is higher than that in the general population, indicating the presence of disease‐specific causative factors. In this review, we aimed to present clinical findings to highlight the roles of insufficient exposure to sunlight and inflammation in the development of vitamin D deficiency in patients with intestinal malabsorption syndromes. Furthermore, we aimed to present experimental evidence that supported a role of vitamin D deficiency in the pathogenesis of IBD. Finally, we reviewed clinical intervention strategies aiming to normalize vitamin D status in and even to improve the conditions of patients and to discuss certain issues that needed to be addressed in future research.

Deficiencies of vitamin D in patients with intestinal malabsorption syndromes: Think in and outside of the gut

There is a very high prevalence of vitamin D deficiency, which is defined by a serum level of 25‐hydroxyvitamin D [25(OH)D] of lower than 20 ng/mL, in all populations of the world. Unfortunately, the prevalence of vitamin D deficiency in patients with intestinal malabsorption syndromes, including cystic fibrosis (CF), celiac disease (CD), short bowel syndrome and inflammatory bowel disease (IBD), is higher than that in the general population, indicating the presence of disease‐specific causative factors. In this review, we aimed to present clinical findings to highlight the roles of insufficient exposure to sunlight and inflammation in the development of vitamin D deficiency in patients with intestinal malabsorption syndromes. Furthermore, we aimed to present experimental evidence that supported a role of vitamin D deficiency in the pathogenesis of IBD. Finally, we reviewed clinical intervention strategies aiming to normalize vitamin D status in and even to improve the conditions of patients and to discuss certain issues that needed to be addressed in future research.

Teaching and learning of medical biochemistry according to clinical realities: A case study.

To foster medical students to become physicians who will be lifelong independent learners and critical thinkers with healthy skepticism and provide high‐quality patient care guided by the best evidence, teaching of evidence‐based medicine (EBM) has become an important component of medical education. Currently, the teaching and learning of biochemistry in medical schools incorporates its medical relevance and applications. However, to our knowledge there have been no reports on integrating EBM with teaching and learning medical biochemistry. Here, we present a case study to illustrate the significance of this approach. This case study was based on a biochemistry/nutrition question in a popular board review book about whether a homeless alcoholic man is at risk of developing a deficiency of vitamin E. The possible answers and explanation provided in the book raised a question about the correct answer, which provided us with an opportunity to adapt the philosophy and certain basic EBM principles to find evidence for the clinical applicability of a commonly taught biochemistry topic. The outcome of this case study not only taught us how to conduct an EBM exercise to answer a specific patient question, but also provided us with an opportunity for in‐depth teaching and learning of the medical relevance of a specific biochemistry topic based on the best clinical evidence obtained from a systematic research of medical literature.

Engaging Medical Students in Problem-Based Search and Study of the Biomedical Literature.

1Department of Biochemistry and Molecular Medicine, The George Washington University School of Medicine and Health Sciences, Washington DC, USA 2Department of Obstetrics, Gynecology and Reproductive Sciences, Yale School of Medicine, New Haven, USA 3Department of Emergency Medicine, University of Pennsylvania School of Medicine, Philadelphia, USA 4Walter Reed National Military Medical Center, Bethesda, USA 5MedStar Harbor Hospital, Baltimore, USA 6The George Washington University School of Medicine and Health Sciences, Washington DC, USA

Vitamin D Deficiency in Patients with Pancreatitis: Is Vitamin D ReplacementRequired?

Clinical findings have shown that approximately 40% of patients with pancreatitis, acute or chronic, have severe vitamin D deficiency; this can reach up to 60% of patients with chronic pancreatitis. These findings raise an important question: Is vitamin D deficiency a cause or a result of pancreatitis? The answer(s) to this question is clinically important given that high oral doses of vitamin D supplementation are widely prescribed for individuals with vitamin D deficiency. Considering that there is active conversion of 25(OH)D3 to 1,25(OH)2D3 by activated macrophages in tissues undergoing inflammation, that elevation of the blood levels of 1,25(OH)2D3 levels can cause hypercalcemia, that hypercalcemia can precipitate pancreatitis, that excessive use of vitamin D supplementation can cause acute pancreatitis and that sarcoidosis causes elevated blood levels of 1,25(OH)2D3, hypercalcemia and acute pancreatitis, it is reasonable to consider both 25(OH)D3 and 1,25(OH)2D3 as negative acute-phase reactants, specifically in the context of the pathogenesis of pancreatitis. Thus, down-regulation of blood levels of 25(OH)D3 and 1,25(OH)2D3 in patients with pancreatitis appears to be a protective mechanism to prevent the development hypercalcemia, which would exacerbate the pancreatitis. Therefore, it is reasonable to consider that vitamin D replacement treatment may produce more harm than benefit for patients with pancreatitis.