Overdose with calcium channel blockers (CCBs) may lead to serious complicat
ions. CCBs act by blocking calcium entry into the cell, thus lowering intra
cellular calcium ([Ca2+](i)). [Ca2+](i) during CCB overdose has not yet bee
n reported. We measured [Ca2+](i) in lymphocytes of a patient with acute ve
rapamil overdose with a complex clinical picture. A 59-year-old woman was a
dmitted after a suicidal ingestion of 7200 mg of a sustained-release verapa
mil preparation. She presented with hypotension, complete atrioventricular
block, stupor, hypokalemia, and hyperglycemia. Acute oliguric renal failure
, acute pancreatitis, and the adult respiratory distress syndrome further c
omplicated her medical course. Treatment was supportive and she recovered c
ompletely. Intracellular calcium ([Ca2+](i)) was measured in the patient's
lymphocytes using a spectrofluorometer with the calcium-sensitive dye Fura-
2-acetoxymethyl ester. Thirty nine hours after the ingestion, [Ca2+](i) was
low at 52 nM (compared with 80 nM in a healthy control subject). Lymphocyt
ic [Ca2+](i) did not respond to stimulation with phytohemagglutinin (PHA).
Fourteen days after the verapamil overdose, after the patient had recovered
completely, lymphocytic [Ca2+](i) was still low at 55 nM. At this time, th
ere was an incomplete response to PHA in the lymphocytes. Three months afte
r the ingestion, [Ca2+](i) was normal, with a normal response to PHA. Verap
amil overdose may run a complex clinical course, but fu II recovery is to b
e hoped for with full supportive care. Cellular intoxication, as reflected
by low lymphocytic [Ca2+](i), is prolonged and lags behind the clinical rec
overy by weeks.