Goiters and hypothyroidism are well-known patient complications of the use of lithium for treatment of bipolar disease. However, the occurrence of lithium-induced hyperthyroidism is a more rare event. Many times, the condition can be confused with a flare of mania. Monitoring through serial biochemical measurement of thyroid function is critical in patients taking lithium. Hyperthyroidism induced by lithium is a condition that generally can be controlled medically without the patient having to discontinue lithium therapy, although in some circumstances, discontinuation of lithium therapy may be indicated. We report on a patient case of lithium-associated hyperthyroidism that resolved after discontinuation of the medication.

The differentiation between primary or tertiary (both hypercalcemic) and secondary (normocalcemic) hyperparathyroidism requires the identification of hypercalcemia. Calcium in the blood exists as bound, complexed and ionized fractions. Calcium sensors on parathyroid cells interact only with the ionized fraction (about 50% of the total calcium concentration). Many formulas using albumin, total protein or phosphate to correct or adjust total calcium to reflect the level of ionized calcium may be accurate only within a limited range. In addition, they can introduce errors based on inaccuracies in the measurement of these other metabolites. Clinical conditions, mainly those illnesses affecting acid-base balance, can alter the proportions of bound and free calcium. How and when the blood samples are drawn can alter the level of total calcium. Prolonged standing or prolonged venous stasis causes hemoconcentration, increasing the bound fraction. Preceding exercise can also affect blood calcium levels. Ingestion of calcium supplements or calcium-containing nutrients can cause transient elevations in blood calcium levels lasting several hours, leading to unnecessary further testing. Fasting total calcium levels may be sufficient for monitoring progress. However, for diagnostic purposes, fasting ionized calcium levels should be used. Therefore, for an isolated high total calcium level, we recommend obtaining a repeat fasting total and ionized calcium measurement before further investigations. Hypercalcemia may be diagnosed if there are persistent or frequent total or, preferably, ionized calcium levels >3 SD above the mean of the normal range or if there are progressively rising levels.

Hypercalcemia as a complication of carcinoid tumors is extremely rare. Accordingly, we report the case of a 55-year-old male with metastatic carcinoid tumor and hypercalcemia, which corrected when the patient was treated with octreotide for symptomatic relief of watery diarrhea. The etiology of the hypercalcemia is presumed to be a neoplastic expression of fibroblast growth factor-23, which was found to be inappropriately high-to-normal when other factors such as parathyroid hormone, calcitonin and vitamin D were appropriately low or low-to-normal.

Resistant hypertension is defined as blood pressure uncontrolled to guideline levels despite the use of ≥3 antihypertensive medications. When evaluating patients with resistant hypertension, it is important to consider issues such as blood pressure measurement technique, lifestyle, other comorbid conditions and medications, and the white coat effect. To this point, potential contributing factors include obstructive sleep apnea, excess alcohol intake, and use of blood pressure-elevating medications, such as nonsteroidal anti-inflammatory drugs, sympathomimetics, certain anorexic agents, and oral contraceptives. Secondary causes of hypertension are common in patients with resistant hypertension and appropriate screening tests should be performed as suggested by signs, symptoms, and laboratory abnormalities. In this regard, there is increasing evidence that hyperaldosteronism is common in the resistant hypertensive patient group. Pharmacologic therapy in patients with resistant hypertension is centered on drug combinations that have different mechanisms of action, including diuretics, which are essential in maximizing antihypertensive effects. The role of mineralocorticoid receptor antagonists is expanding, especially in patients with the metabolic syndrome, where aldosterone excess is increasingly recognized as an etiology of resistant hypertension. Finally, when appropriate, specialist referral may be necessary to appropriately assess and treat these patients.