A Case Report Showing Association between Vitamin D, HbA1C and Frozen Shoulder in Type II Diabetes Patient

The major and most well-known function of vitamin D is to maintain calcium and phosphorus homeostasis and promote bone mineralization. Vitamin D insufficiency has long been suspected as a risk factor for type 1 diabetes based on animal and human observational studies [1] More recently, there is accumulating evidence to suggest that altered vitamin D and calcium homeostasis may also play a role in the development of type 2 DM. Vitamin D replenishment improves glycaemia and insulin secretion in patients with type 2 diabetes with established hypovitaminosis D, thereby suggesting a role for vitamin D in the pathogenesis of type 2 diabetes mellitus. The presence of vitamin D receptors (VDR) and vitamin D–binding proteins (DBP) in pancreatic tissue and the relationship between certain allelic variations in the VDR and DBP genes with glucose tolerance and insulin secretion have further supported this hypothesis [2-4] Hyperglycemia may accelerate non-enzymatic glycosylation and abnormal collagen deposition in periarticular connective tissues, which alters the structural matrix and mechanical properties of these tissues leading to diffuse arthrofibrosis. [5,6] As a result patients’ quality of life may decrease and they may be debilitated by cheiroarthropathy, frozen shoulder etc [7,8]. This study is also an evidence for the same.