ABSTRACT
A 59-year-old woman was found unresponsive at home. Initial neurologic examination revealed aphasia and right-sided weakness. Laboratory results demonstrated a serum calcium level of 17.3 mg/dL (corrected serum calcium for albumin concentration was 16.8 mg/dL). Extensive workup for intrinsic aetiology of hypercalcemia was unrevealing. Further discussion with family members and investigation of the patient's home for over-the-counter medications and herbal supplements revealed chronic ingestion of calcium carbonate tablets. CT angiogram of the brain revealed multifocal intracranial vascular segmental narrowing, which resolved on a follow-up cerebral angiogram done 2 days later. These findings were consistent with reversible cerebral vasoconstriction syndrome.Appropriate blood pressure control with parenteral agents, calcium channel blockade with nimodipine and supportive care therapies resulted in significant improvement in neurologic status. By discharge, patient had near-complete resolution of neurologic symptoms.
Subject(s)
Antacids , Brain , Calcium Carbonate , Hypercalcemia , Vasospasm, Intracranial , Female , Humans , Middle Aged , Antacids/poisoning , Brain/diagnostic imaging , Calcium Carbonate/poisoning , Calcium Channel Blockers/therapeutic use , Cerebral Angiography , Computed Tomography Angiography , Hypercalcemia/chemically induced , Hypercalcemia/complications , Magnetic Resonance Imaging , Nimodipine/therapeutic use , Vasospasm, Intracranial/diagnostic imaging , Vasospasm, Intracranial/drug therapy , Vasospasm, Intracranial/etiology , Vasospasm, Intracranial/physiopathologyABSTRACT
BACKGROUND: The carcinogenic effect of betelnut chewing leading to oral cancer is well known. Betelnut chewing may also affect the autonomic nervous system. In this report, we present another potential hazard of betelnuts, milk-alkali syndrome. CASE REPORT: Two patients who had chewed a large quantity of betelnuts developed hypercalcemia, metabolic alkalosis, and renal insufficiency. They ingested a large amount of calcium carbonate from a local special paste used for betelnut preparation, the main ingredient of which is ground oyster shell. The symptoms and metabolic abnormalities disappeared promptly after abstinence from betelnut chewing and administration of saline solution. Improvement of renal function was observed in both patients. Analysis of the calcium content of the paste suggested that the patients might have ingested 9 g and 6 g of calcium carbonate per day, respectively. CONCLUSION: This is the first report of milk-alkali syndrome not caused iatrogenically, but by recreational usage of oyster shell preparations of betelnuts.