title: [Metabolic acidosis and hypoglycemia during calcium hopantenate administration--report on 5 patients].
abstract: Calcium hopantenate (HOPA) has been widely used as an activator of cerebral metabolism in Japan. However, several cases of acute encephalopathy during HOPA administration were recently reported, which were characterized by marked metabolic acidosis and hypoglycemia. The encephalopathy in these patients was named Reye-like syndrome because of the similarity to Reye's syndrome in children. The purposes of this presentation are to report on 5 patients with acute encephalopathy developing during HOPA administration, to summarize their symptoms and clinical courses, and to discuss the pathogenesis of metabolic acidosis and hypoglycemia. Initial characteristics of the clinical course in all patients were loss of appetite, nausea and vomiting, followed by unconsciousness. Laboratory examinations revealed marked metabolic acidosis, severe hypoglycemia, hyperlactacidemia, leukocytosis, ketonuria, and increased Ht and BUN. A few days after development of the initial symptoms, mild renal and liver dysfunction, and elevation of serum amylase were observed in all patients. Hyperlactacidemia was present in 4 in the initial period. Blood concentration of HOPA was 2.131 micrograms/ml in patient 1 (8-10 hours after final administration), and 10.7 micrograms/ml in patient 5 (24 hours after final administration). These values are extremely high, because usually HOPA concentration is almost negligible 7 hours after the drug is taken. As the pathogenesis of acute encephalopathy due to HOPA administration, the failure of fatty acid beta-oxidation has been proposed by some investigators. However, the serum concentrations of CoA, pantothenic acid and carnitine during the initial stage were not reduced in our patients. Furthermore, it is very difficult to explain the severe hypoglycemia in terms of the beta-oxidation theory.(ABSTRACT TRUNCATED AT 250 WORDS)
authors.forename: S
authors.initials: S
authors.lastname: Ohsuga
authors.forename: H
authors.initials: H
authors.lastname: Ohsuga
authors.forename: T
authors.initials: T
authors.lastname: Takeoka
authors.forename: A
authors.initials: A
authors.lastname: Ikeda
authors.forename: Y
authors.initials: Y
authors.lastname: Shinohara
mesh_terms: D000140:Acidosis, Lactic / Q000139:chemically induced* / Q000378:metabolism; D000368:Aged; D000369:Aged, 80 and over; D005260:Female; D006801:Humans; D007003:Hypoglycemia / Q000139:chemically induced* / Q000378:metabolism; D008297:Male; D010205:Pantothenic Acid / Q000009:adverse effects / Q000031:analogs & derivatives*; D012202:Reye Syndrome / Q000139:chemically induced / Q000378:metabolism; D005680:gamma-Aminobutyric Acid / Q000009:adverse effects / Q000031:analogs & derivatives*
chemical_list: C016030:pantogab; D010205:Pantothenic Acid; D005680:gamma-Aminobutyric Acid