Hyperinsulinemia and urinary calcium excretion in calcium stone formers with idiopathic hypercalciuria.

CONTEXT: Calcium stone formers with idiopathic hypercalciuria (IH) are known to exhibit an exaggerated postprandial rise in urine calcium excretion compared with non-stone-forming individuals, and insulin has been proposed to mediate this difference. OBJECTIVE: Our objective was to investigate the impact of hyperinsulinemia on urine calcium excretion in IH compared with non-stone-forming controls. PARTICIPANTS AND SETTING: Ten IH patients and 22 control non-stone-forming subjects (8 lean and 14 overweight and obese) participated at the University of Texas Southwestern Clinical and Translational Research Center. DESIGN: After stabilization on a fixed metabolic diet, subjects underwent a hyperinsulinemic-euglycemic clamp. Fasting 2-hour urine specimens were collected before and during the clamp. MAIN OUTCOME MEASURES: Changes in fractional calcium excretion (F(E)Ca) during the clamp were compared between the 3 groups of subjects (IH, overweight/obese controls, and lean controls). Insulin sensitivity was measured by glucose disposal rate. RESULTS: IH had significantly higher 24-hour urine calcium excretion than controls, and exhibited similar age, body mass index, and insulin sensitivity as overweight/obese controls. The hyperinsulinemic-euglycemic clamp resulted in a significant increase in serum insulin with no significant changes in serum calcium and glucose. This was accompanied by a small increase in F(E)Ca, with no significant differences between the 3 groups. There was no correlation between insulin sensitivity and 24-hour urine calcium or the change in F(E)Ca during the hyperinsulinemic clamp. CONCLUSIONS: The rise in urine calcium associated with euglycemic hyperinsulinemia was small and not statistically different between IH and non-stone-forming controls. Insulin is therefore unlikely to play a significant pathogenetic role in IH.

Ectopic atypical parathyroid lipoadenoma: a rare cause of severe primary hyperparathyroidism.

Parathyroid lipoadenomas are a rare and benign variant of parathyroid adenomas that are defined morphologically by an abundance of fat cells. They may be functional with secretion of parathyroid hormone or nonfunctional. We present a case of a parathyroid lipoadenoma in a patient presenting with clinical manifestations of severe primary hyperparathyroidism. Unusual features in this case included the ectopic location of the lipoadenoma in the mediastinum, the significant size of 6.6 × 3.4 cm, and weight of 30.1 g. In addition to the large size of this generally benign type of parathyroid neoplasm, histologic findings included focal band-forming fibrosis compatible with the diagnosis of an atypical parathyroid adenoma. In conclusion, this case illustrates a difficult case of an ectopic functioning parathyroid lipoadenoma with chronic sequelae due to severe hyperparathyroidism.

Benign adrenal adenomas secreting excess mineralocorticoids and glucocorticoids.

OBJECTIVE: To recognize that benign adrenal adenomas can co-secrete excess aldosterone and cortisol, which can change clinical management. METHODS: We reviewed the clinical and histological features of an adrenal tumor co-secreting aldosterone and cortisol in a patient. Biochemical testing as well as postoperative immunohistochemistry was carried out on tissue samples for assessing enzymes involved in steroidogenesis. RESULTS: A patient presented with hypertension, hypokalemia, and symptoms related to hypercortisolism. The case demonstrated suppressed renin concentrations with an elevated aldosterone:renin ratio, abnormal dexamethasone suppression test results, and elevated midnight salivary cortisol concentrations. The patient had a right adrenal nodule with autonomous cortisol production and interval growth. Right adrenalectomy was carried out. Postoperatively, the patient tolerated the surgery, but he was placed on a short course of steroid replacement given a subnormal postoperative serum cortisol concentration. Long-term follow-up of the patient showed that his blood pressure and glucose levels had improved. Histopathology slides showed positive staining for 3ß-hydroxysteroid dehydrogenase, 11ß-hydroxylase, and 21 hydroxylase. CONCLUSION: In addition to the clinical manifestations and laboratory values, the presence of these enzymes in this type of tumor provides support that the tumor in this patient was able to produce mineralocorticoids and glucocorticoids. The recognition of patients with a tumor that is co-secreting aldosterone and cortisol can affect decisions to treat with glucocorticoids perioperatively to avoid adrenal crisis. LEARNING POINTS: Recognition of the presence of adrenal adenomas co-secreting mineralocorticoids and glucocorticoids.Consideration for perioperative and postoperative glucocorticoid use in the treatment of co-secreting adrenal adenomas.