Thyroid: an unusual hideout for sarcoidosis.

OBJECTIVE: To present a case of dysphagia secondary to a progressively increasing nontoxic multinodular goiter caused by sarcoidosis. METHODS: We summarize the clinical presentation and pertinent pathology in a patient with sarcoidosis involving the thyroid gland. A review of literature regarding this topic is also presented. RESULTS: A 54-year-old man was noted to have asymptomatic nontoxic thyromegaly. Biopsy of right thyroid nodule was benign while the biopsy from the isthmus nodule was nondiagnostic. He presented with acute onset of dysphagia two months later and the work-up for gastrointestinal causes was negative. Chest imaging showed left-sided lymphadenopathy, and biopsy of a lymph node showed sarcoidosis. Two years after the initial presentation a repeat biopsy of the isthmus nodule was again reported as nondiagnostic. Because he had persistent dysphagia, he underwent total thyroidectomy with resolution of dysphagia. Histopathological examination of the thyroid revealed non necrotizing granulomas consistent with sarcoidosis. CONCLUSION: This case brings to light this uncommon etiology of a nontoxic multinodular goiter. Involvement of the thyroid gland by sarcoidosis is very rare. It has been reported in 4.2 to 4.6% of patients with sarcoidosis. In patients with pulmonary or extrapulmonary sarcoidosis and associated thyromegaly, possible involvement of the thyroid by this process should be considered.

Clinical potential of sodium-glucose cotransporter 2 inhibitors in the management of type 2 diabetes.

BACKGROUND: The kidney plays an important role in glucose metabolism, and has been considered a target for therapeutic intervention. The sodium-glucose cotransporter type 2 (SGLT2) mediates most of the glucose reabsorption from the proximal renal tubule. Inhibition of SGLT2 leads to glucosuria and provides a unique mechanism to lower elevated blood glucose levels in diabetes. The purpose of this review is to explore the physiology of SGLT2 and discuss several SGLT2 inhibitors which have clinical data in patients with type 2 diabetes. METHODS: We performed a PubMed search using the terms "SGLT2" and "SGLT2 inhibitor" through April 10, 2012. Published articles, press releases, and abstracts presented at national and international meetings were considered. RESULTS: SGLT2 inhibitors correct a novel pathophysiological defect, have an insulin-independent action, are efficacious with glycosylated hemoglobin reduction ranging from 0.5% to 1.5%, promote weight loss, have a low incidence of hypoglycemia, complement the action of other antidiabetic agents, and can be used at any stage of diabetes. They are generally well tolerated. However, due to side effects, such as repeated urinary tract and genital infections, increased hematocrit, and decreased blood pressure, appropriate patient selection for drug initiation and close monitoring after initiation will be important. Results of ongoing clinical studies of the effect of SGLT2 inhibitors on diabetic complications and cardiovascular safety are crucial to determine the risk-benefit ratio. A recent decision by the Committee for Medicinal Products for Human Use of the European Medicines Agency has recommended approval of dapagliflozin for the treatment of type 2 diabetes as an adjunct to diet and exercise, in combination with other glucose-lowering medicinal products, including insulin, and as a monotherapy for metformin-intolerant patients. Clinical research also remains to be carried out on the long-term effects of glucosuria and other potential effects of SGLT2 inhibitors, especially in view of the observed increase in the incidence of bladder and breast cancer. SGLT2 inhibitors represent a promising approach for the treatment of diabetes, and could potentially be an addition to existing therapies.

Type 2 diabetes, glycemic control, and continuous positive airway pressure in obstructive sleep apnea.

BACKGROUND: Sleep-disordered breathing (SDB) is a prevalent condition associated with significant comorbidities, including hypertension, obesity, cardiovascular disease, and insulin resistance. It has been previously shown that the severity of insulin resistance is related to the severity of SDB. METHODS: Using a 72-hour continuous glucose monitoring system, we studied changes in interstitial glucose levels and measured hemoglobin A1c levels in 25 patients with type 2 diabetes mellitus before and after continuous positive airway pressure (CPAP) treatment for SDB. RESULTS: With a mean +/- SD CPAP treatment period of 83 +/- 50 days, the mean +/- SD 1-hour postprandial glucose values were significantly reduced for breakfast (191 +/- 68 mg/dL to 130 +/- 41 mg/dL [10.6 +/- 3.8 mmol/L to 7.2 +/- 2.3 mmol/L]), lunch (196 +/- 70 mg/dL to 138 +/- 49 mg/dL [10.9 +/- 3.9 mmol/L to 7.7 +/- 2.7 mmol/L]), and dinner (199 +/- 66 mg/dL to 137 +/- 48 mg/dL [11.0 +/- 3.7 mmol/L to 7.6 +/- 2.7 mmol/L]). In the 17 patients with a baseline hemoglobin A1c level greater than 7%, there was a significant reduction in hemoglobin A1c level (9.2% +/- 2.0% to 8.6% +/- 1.8%). Furthermore, in subjects who used CPAP for more than 4 h/d, the reduction in hemoglobin A1c level was significantly correlated with days of CPAP use. There was no such correlation in subjects who used CPAP for 4 h/d or less. CONCLUSIONS: These findings suggest that SDB is pathophysiologically related to impaired glucose homeostasis, and that CPAP can be an important therapeutic approach for diabetic patients with SDB.

Cushing's syndrome from ectopic production of corticotropin by a metastatic gastrinoma.

OBJECTIVE: To present a case of a young woman with new-onset diabetes mellitus resistant to insulin attributable to Cushing's syndrome caused by ectopic production of corticotropin by a metastatic gastrinoma. METHODS: We summarize the clinical presentation and the pertinent laboratory values in a patient with Cushing's syndrome. A review of the literature regarding ectopic production of corticotropin by gastrinomas is also presented. RESULTS: A 26-year-old woman with dehydration, severe hyperglycemia, and hypokalemia was seen in consultation. The patient required large doses of insulin to control plasma glucose, and further work-up confirmed the presence of Cushing's syndrome caused by ectopic production of corticotropin from a metastatic gastrinoma. CONCLUSION: This case is unusual in that the patient was relatively young and the clinical presentation of Cushing's syndrome was dominated by uncontrolled diabetes, insulin resistance, and hypokalemia. At the time of this diagnosis, the patient already had evidence of multiple liver metastatic lesions from a pancreatic gastrinoma. The rapid occurrence of difficult-to-treat diabetes and hypokalemia should raise the suspicion of Cushing's syndrome from ectopic production of corticotropin. In fact, patients with metastatic pancreatic tumors and poorly controlled diabetes with hypokalemia should undergo evaluation for Cushing's syndrome, even in the absence of the typical stigmas, because of rapid development of the disease and high levels of corticotropin.