ABSTRACT
BACKGROUND: Vitamin D deficiency is the most common nutritional deficiency worldwide in all ages. Prolonged and severe vitamin D deficiency can result in secondary hyperparathyroidism and osteomalacia. Vitamin D deficiency can be caused by various factors included here institutionalisation, malabsorption, inadequate exposure to sunlight etc. Osteomalacia is a disorder of decreased mineralisation of newly formed osteoid at sited of bone turnover, which can be manifested with symptoms such as diffuse body aches and pain. Muscles weakness from vitamin D deficiency causes difficulty in walking, developing proximal myopathy. Nearly 30-50% of all age groups are Vitamin D deficient worldwide. CASE PRESENTATION: We report a case of 51-years-old woman, with a religious garment, with slowly progressing weakness of the proximal limb muscles, extreme fatigue, chest and lower spine pain, paresthesia, depression, difficulties in walking and waddling gait. On whole-body bone scintigraphy diffuse metabolic changes were present, and in DXA osteoporosis was shown due to severe vitamin D deficiency and secondary hyperparathyroidism. Treatment with high doses of vitamin D and calcium replacement improved clinical manifestation of osteomalacia for few months. Absent of waddling gait with no pain was evident due to the better muscle and bone performance after the treatment. CONCLUSION: Suspicious cases for osteomalacia in population wearing a religious garment and those that are not adequately exposed to the sunlight, laboratory evaluation should include measurement of 25 (OH) vitamin D, PTH, calcium, alkaline phosphatase and performing of DXA in order such cases do not get undiagnosed.
ABSTRACT
Several studies have demonstrated the decreased insulin resistance (IR) in persons with type 2 diabetes mellitus (T2DM) treated with glimepiride. Those suggest this might be associated with observed higher concentrations of adiponectin. We assessed if there is a difference in IR and metabolic syndrome components between glimepiride and glibenclamide treatment as well as adiponectin concentration in T2DM. Our research observed 20 T2DM patients treated with glibenclamid and 20 switched to glimepiride (n = 20) treatment for 24 weeks. Anthropometric measurements and laboratory analysis were performed at the beginning and at the end of treatment while IR was accessed by homeostasis model assessment of insulin resistance (HOMA-IR). The glimepiride group revealed better glycaemic control compared to glibenclamide group. Moreover, the adiponectin concentration increased (23.9 ± 17.3 to 29.1 ± 12.2 ng/mL, p = 0.087) whereas it decreased in the glibenclamide group (34.3 ± 22.6 to 20.3 ± 11.3 ng/mL, p = 0.011) following 24 weeks of treatment. The serum adiponectin and HOMA-IR were inversely correlated within the group of glibenclamide (r = -0.667, p = 0.009). The present study demonstrates that glimepiride might have beneficial effect on IR compared to glibenclamide, as suggested. However, this observation needs further study investigation among other formulations of SU.
