HYPERTENSION AND IDENTIFICATION OF TOXIN IN HUMAN URINE AND SERUM FOLLOWING A CLUSTER OF MUSSEL-ASSOCIATED PARALYTIC SHELLFISH POISONING OUTBREAKS

Citation
Bd. Gessner et al., HYPERTENSION AND IDENTIFICATION OF TOXIN IN HUMAN URINE AND SERUM FOLLOWING A CLUSTER OF MUSSEL-ASSOCIATED PARALYTIC SHELLFISH POISONING OUTBREAKS, Toxicon, 35(5), 1997, pp. 711-722
Citations number
35
Categorie Soggetti
Toxicology,"Pharmacology & Pharmacy
Journal title
ISSN journal
00410101
Volume
35
Issue
5
Year of publication
1997
Pages
711 - 722
Database
ISI
SICI code
0041-0101(1997)35:5<711:HAIOTI>2.0.ZU;2-7
Abstract
Following four outbreaks of paralytic shellfish poisoning on Kodiak Is land, Alaska, during 1994, medical records of ill persons were reviewe d and interviews were conducted, Urine and serum specimens were analyz ed at three independent laboratories using four different saxitoxin bi nding assays, High-performance liquid chromatography was used to deter mine the presence of specific toxin congeners, Among 11 ill persons, t hree required mechanical ventilation and one died, Mean peak systolic and diastolic blood pressure measurements were 172 (range 128-247) and 102 (range 78-165) mmHg, respectively, and blood pressure measurement s corresponded with ingested toxin dose, All four different laboratory methodologies detected toxin in serum at 2.8-47 nM during acute illne ss and toxin in urine at 65-372 nM after acute symptom resolution. The composition of specific paralytic shellfish poisons differed between mussels and human biological specimens, suggesting that human metaboli sm of toxins had occurred. The results of this study indicate that sax itoxin analogues may cause severe hypertension. In addition, we demons trate that saxitoxins can be detected in human biological specimens, t hat nanomolar serum toxin levels may cause serious illness and that hu man metabolism of toxin may occur. Clearance of paralytic shellfish po isons from serum was evident within 24 hr and urine was identified as a major route of toxin excretion in humans. (C) 1997 Elsevier Science Ltd.