Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0036572 (seizures)
 80,221 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Cantharidin, known popularly as Spanish fly, has been used for millennia as a sexual stimulant. The chemical is derived from blister beetles and is notable for its vesicant properties. While most commonly available preparations of Spanish fly contain cantharidin in negligible amounts, if at all, the chemical is available illicitly in concentrations capable of causing severe toxicity. Symptoms of cantharidin poisoning include burning of the mouth, dysphagia, nausea, hematemesis, gross hematuria, and dysuria. Mucosal erosion and hemorrhage is seen in the upper gastrointestinal (GI) tract. Renal dysfunction is common and related to acute tubular necrosis and glomerular destruction. Priapism, seizures, and cardiac abnormalities are less commonly seen. We report four cases of cantharidin poisoning presenting to our emergency department with complaints of dysuria and dark urine. Three patients had abdominal pain, one had flank pain, and the one woman had vaginal bleeding. Three had hematuria and two had occult rectal bleeding. Low-grade disseminated intravascular coagulation, not previously associated with cantharidin poisoning, was noted in two patients. Management of cantharidin poisoning is supportive. Given the widespread availability of Spanish fly, its reputation as an aphrodisiac, and the fact that ingestion is frequently unwitting, cantharidin poisoning may be a more common cause of morbidity than is generally recognized. Cantharidin poisoning should be suspected in any patient presenting with unexplained hematuria or with GI hemorrhage associated with diffuse injury of the upper GI tract.
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PMID:Poisoning from "Spanish fly" (cantharidin). 876 16

A case of a young woman who suffers from refractory epilepsy in the form of Rasmussen encephalitis and acute intermittent porphyria is presented. The patient developed refractory partial seizures with progressive hemispheric atrophy in the first decade. Both her serum and cerebrospinal fluid contained significantly elevated levels of anti-GluR3B antibodies. Her serum also contained anti-NR2A antibodies (directed against the N-methyl-D-aspartate receptor). Seven years later, acute intermittent porphyria was diagnosed as she developed an acute episode of abdominal pain, dark urine, and hyponatremia. For several years, all attempts to discontinue porphyrinogenic antiepileptic drugs such as phenobarbital and valproate resulted in seizure worsening. During a major acute intermittent porphyria crisis, brain edema and coma developed, allowing the discontinuation of phenobarbital. On recovery, atrophy of the right hemisphere ensued. Several etiologic hypotheses are presented. Double insults, porphyria, and an autoimmune process are suggested for the development of Rasmussen encephalitis in this patient. The authors recommend testing for porphyria in cases of Rasmussen encephalitis and other intractable seizures.
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PMID:Acute intermittent porphyria, Rasmussen encephalitis, or both? 1760 16