Background Prospective comparative studies on the effects of various antidiabetic agents on bone metabolism are limited. This study aimed to assess changes in bone mass and biochemical bone markers in postmenopausal patients with type 2 diabetes mellitus (T2DM).
Methods This prospective, multicenter, open-label, comparative trial included 264 patients with T2DM. Patients who had received a metformin, or sulfonylurea/metformin combination (Group 1); a thiazolidinedione combination (Group 2); a dipeptidyl peptidase-4 inhibitor (gemigliptin) combination (Group 3); or an sodium-glucose cotransporter 2 inhibitor (empagliflozin) combination (Group 4) were prospectively treated for 12 months; bone mineral density (BMD) and bone turnover marker (BTM) changes were evaluated.
Results The femoral neck BMD percentage changes were −0.79%±2.86% (Group 1), −2.50%±3.08% (Group 2), −1.05%±2.74% (Group 3), and −1.24%±2.91% (Group 4) (P<0.05). The total hip BMD percentage changes were −0.57%±1.79% (Group 1), −1.74%±1.48% (Group 2), −0.75%±1.87% (Group 3), and −1.27%±1.72% (Group 4) (P<0.05). Mean serum BTM (C-terminal type 1 collagen telopeptide and procollagen type 1 amino-terminal propeptide) levels measured during the study period did not change over time or differ between groups.
Conclusion Significant bone loss in the femoral neck and total hip was associated with thiazolidinedione combination regimens. However, bone loss was not significantly associated with combination regimens including gemigliptin or empagliflozin. Caution should be exercised during treatment with antidiabetic medications that adversely affect the bone in patients with diabetes at a high risk of bone loss.
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Graves' disease is one of the common autoimmune diseases, and it has been controlled by such antithyroid drugs as propylthiouracil (PTU) or methimazole. There are a number of side effects, including agranulocytosis, skin rash, hepatotoxicity, fever, arthralgia and a lupus-like syndrome during treatment. PTU has been recently observed to be associated with the development of antineutrophil cytoplasmic antibody (ANCA) positive vasculitis, and this can cause diffuse alveolar hemorrhage. A 32-year-old woman with Graves' disease had been treated with PTU for 4 years, and she had experienced intermittent hemoptysis for 2 weeks before she visited the hospital. Both myeloperoxidase and proteinase 3 ANCA were positive without other organ systems being involved. She was diagnosed with PTU-induced vasculitis. Cessation of PTU and administration of corticosteroids improved the clinical manifestations.
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Cushing's disease is the most common cause of endogenous Cushing's syndrome caused by the excessive secretion of adrenocorticotropic hormone (ACTH) by pituitary ACTH-secreting tumors. The tumors are usually microadenomas (< 10 mm in diameter). Macroadenomas are rare, and corticotroph hyperplasia and carcinomas are extremely rare. Patients with these tumors exhibit an increase in plasma ACTH and cortisol levels, elevated urinary excretion of cortisol and adrenocortical steroid metabolites, evidence of altered negative feedback of cortisol and disturbances in neuroendocrine regulation. The diagnosis of Cushing's disease can be challenging in patients with renal failure the presence of abnormal plasma cortisol, poor gastrointestinal tract absorption of dexamethasone and altered functioning of the hypophyseal-pituitary-adrenal axis have been reported in end-stage renal disease, and the urinary cortisol increment method is not reliable in these patients. The prevalence of renal cell carcinoma in patients on dialysis is higher than in the general population. We recently treated a patient with Cushing's disease and end-stage renal disease as a result of renal cell carcinoma. The diagnosis was made by laboratory evaluation of plasma and radiological examination. Here we report a case of Cushing's disease with a review of the medical literature.
Lymphocytic hypophysitis, an inflammatory disease of the pituitary gland that is often associated with pregnancy, is caused by autoimmune destruction of the pituitary gland evidenced by diffuse inflammatory cell infiltration of the pituitary gland and some kinds of detectable autoantibodies. We report a case of lymphocytic hypophysitis in a 31-year-old woman presenting with severe hypoglycemia and hyponatremia after delivery. Hormonal study revealed panhypopituitarism and magnetic resonance imaging with enhancement showed the bulging contour of the right side pituitary gland with an ill-defined mass-like lesion and nodular thickening of the stalk. The patient's symptoms and biochemical data improved greatly with replacement of L-thyroxine and glucocorticoid. Partial recovery of panhypopituitarism was also seen. The follow-up tests revealed dramatic resolution of the pituitary lesion.
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Pheochromocytoma is usually associated with a combination of various clinical manifestations caused by the overproduction of catecholamines. It is frequently accompanied by impaired glucose tolerance operating through 2-and-adrenergic mechanisms. A 41-year-old-woman was admitted to the hospital because of poorly-controlled diabetes mellitus and hypertension. She had suffered intermittent paroxysmal attacks of headache and chest discomfort and had been treated intermittently over a 2 year period for diabetes mellitus and hypertension. At admission, the levels of serum epinephrine, norepinephrine urinary excretion of total metanephrine, and VMA were all abnormally elevated. Adrenal CT showed a well-defined, homogenous mass in the right adrenal region and the tumor was diagnosed as pheochromocytoma. After tumor resection, the increased blood level of catecholamines, the urinary excretion of total metanephrine, and VMA were normalized, as was the hyperglycemia state. Diabetes mellitus of the patient was considered permanently resolved after tumor removal by the result of glucose tolerance in 75g oral glucose tolerance test.