Hypercalcemia and soft tissue calcification owing to sarcoidosis: the sunlight-cola connection.

Hypercalcemia occurs in sarcoidosis because of 1,25-dihydroxyvitamin D production by pulmonary alveolar macrophages. Long-standing hypercalcemia and hypercalciuria may cause such complications as nephrocalcinosis, nephrolithiasis, and soft tissue calcification, which can be at least partially reversible with treatment. Here we present a 43-year-old African-American man with diffuse soft tissue calcifications and acute kidney injury owing to sarcoidosis-induced hypercalcemia, probably exacerbated by sun exposure and phosphorus intake in the form of dietary cola drinks. Soft tissue calcifications resolved and kidney function improved significantly with hydration and glucocorticoid therapy. We discuss the pathophysiology of the hypercalcemia of sarcoidosis and current treatment options.

Refractory hypocalcemia following near-total thyroidectomy in a patient with a prior Roux-en-Y gastric bypass.

Patients undergoing malabsorptive weight-loss procedures are at increased risk of calcium and vitamin D deficiency. Thyroidectomy carries the risk of both immediate and long-term hypocalcemia. Here we describe a patient who underwent Roux-en-Y gastric bypass (RYGB) and subsequent near-total thyroidectomy and then developed refractory hypocalcemia. Serum calcium reached a nadir of 6.1 mg/dl despite aggressive therapy with oral and IV calcium, calcitriol (1,25(OH)(2)D(3)), and IV magnesium sulfate. One year later, the patient has permanent hypoparathyroidism and requires very high doses of calcium, vitamin D, and calcitriol to prevent symptomatic hypocalcemia. Providers should be aware that malabsorption of calcium and vitamin D after RYGB may complicate patient management after thyroidectomy.

Diagnostic confusion attributable to spurious elevation of both total thyroid hormone and thyroid hormone uptake measurements in the setting of autoantibodies: case report and review of related literature.

OBJECTIVE: To review the effect of thyroid autoantibodies on thyroid function assays and to present a case in which thyroid autoantibodies resulted in spurious assay readings for both total thyroid hormone levels and thyroid hormone uptake measurements. METHODS: We present a detailed case, including serial laboratory data, and review the relevant literature. RESULTS: A 61-year-old man with a history of autoimmune disease presented for evaluation of abnormal results of thyroid function tests. The patient had been treated for hypothyroidism with levothyroxine and was noted to have an elevated total thyroxine (T4) level in the setting of a low total triiodothyronine (T3) value and a mildly elevated thyrotropin concentration. He had been referred for evaluation of a presumed deiodinase deficiency that impaired conversion of T4 to T3. During treatment with levothyroxine, these test results were confirmed, and the patient was also found to have an elevated T4 uptake. These findings were initially thought to be due to an excess of transthyretin; however, more extensive testing revealed that the patient had an autoantibody to T4 that interfered with the assays for both T4 and T4 uptake. CONCLUSION: Autoantibodies to both T3 and T4 have been described. Such antibodies are not uncommon in patients with thyroid disease. On rare occasions, these antibodies may cause spurious assay readings and obscure the diagnosis. To our knowledge, this is the first report in which both the total T4 level and the T4 uptake were elevated because of the presence of autoantibodies. Thyroid hormone autoantibodies must be considered when clinicians encounter patients with unexplained abnormal results of thyroid function tests.