Non-parathyroid hypercalcemia associated with paraffin oil injection in 12 younger male bodybuilders: a case series.

INTRODUCTION: Injection of paraffin oil to augment muscles size is a troubling phenomenon known to cause a foreign body reaction with formation of granulomas. In a few case reports, long-term side effects have been reported in terms of hypercalcemia and renal failure. METHODS: We identified a case series of 12 male bodybuilders presenting with non-parathyroid hypercalcemia who previously had injected paraffin oil to increase muscles size. RESULTS: At admission, all patients had moderate-to-severe hypercalcemia with suppressed PTH levels and impaired renal function. Calcitriol levels were within the normal range or slightly elevated. Follow-up measurements showed marked hypercalciuria with nearly normal levels of bone turnover markers. A correlation was found between levels of peptidyl dipeptidase and calcitriol (R = 0.812, P = 0.050). Treatment with antiresorptive agents seemed less effective than glucocorticoids, which resulted in a significantly lowering of ionized calcium levels and improved renal function, although no patients were cured by this treatment. Immunosuppression with azathioprine or mycophenolate may have a glucocorticoid-saving effect. One patient had surgery with removal of affected muscle tissue, without any apparent effect on plasma calcium levels. CONCLUSION: The hypercalcemia and associated hypercalciuria seems to be due to an intestinal hyperabsorption of calcium. It remains to be elucidated, whether an increased calcitriol synthesis within granulomas is the only (main) mechanism by which intestinal calcium absorption is increased. Glucocorticoids seem most appropriate as the first choice for treatment. Bodybuilders should be warned against use of intramuscular oil injections (and other substances), as this may have severe adverse health consequences.

Systematic genetic screening in a prospective group of Danish patients with pheochromocytoma.

Recent guidelines recommend consideration of genetic screening in all newly diagnosed patients with pheochromocytoma. Patients diagnosed with pheochromocytoma in the Region of Southern Denmark during 2006-2013 without previously recognized monogenetic etiology were offered genetic screening for mutations in the VHL, RET, SDHB, SDHC, and SDHD genes. A total of 41 patients were included, and genetic data were available in 35. In four of the 35 patients, a pathogenic variant was identified prior to the diagnosis of pheochromocytoma (von Hippel-Lindau disease, n=2; neurofibromatosis type 1, n=2). The patients carrying a genetic mutation were all younger than 45 years at time of diagnosis of pheochromocytoma, two patients presented with bilateral tumors, and one patient had a positive family history of pheochromocytoma. Genetic screening of the remaining 31 patients did not identify any mutations. The sporadic cases had a median age of 58 years (range 33-80 years). Three of 31 sporadic cases (ages 60, 69, and 76 years at time of diagnosis) presented with bilateral adrenal tumors, one patient had multiple adrenal tumors in both adrenal glands, and no patients had a positive family history of pheochromocytoma. Of the 31 patients, 24 (68.6%) were diagnosed with pheochromocytoma due to evaluation of an adrenal incidentaloma. In conclusion, monogenetic etiology was identified in four of 35 (11.4%) patients diagnosed with pheochromocytoma.

Optical coherence tomography plaque characterization in a patient with ST segment elevation myocardial infarction after cocaine intake.

A 28-year old man presented to the Emergency Department with malaise after cocaine intake. After arrival he developed retrosternal chest pain and the electrocardiogram showed ST segment elevations in V1-V2 and ST segment depressions in V5-V6. An acute coronary angiogram revealed a focal non-occlusive lesion with thrombus in the left anterior descending artery. Supplementary optical coherence tomography (OCT) detected plaque erosion with adherent thrombus to be the responsible underlying pathophysiological mechanism. The patient received an effective antithrombotic regimen. Repeat angiogram with additional OCT one month later documented thrombus resolution and complete restoration of the previously eroded coronary vascular surface area.