Specific precipitating factor in an acute psychosis.
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Several factors are hypothesized to precipitate or exacerbate type III hyperlipoproteinemia (HLP) in humans. Among such factors are those that directly overload remnant lipoprotein production or disrupt removal pathways, including an increased ratio of apolipoprotein (apo) E2 to normal apoE, overproduction of apoB-containing lipoproteins, and decreased LDL receptor activity. Hypolipidemic apoE2-transgenic mice bred onto an apoE-null background had dramatically higher plasma total cholesterol (192 +/- 26 mg/dL for males, 203 +/- 40 mg/dL for females) and triglyceride (295 +/- 51 mg/dL for males, 277 +/- 58 mg/dL for females) levels than apoE2 mice with endogenous mouse apoE. Thus, eliminating normal apoE in the presence of apoE2 (thereby increasing the relative abundance of the defective ligand) can convert a hypolipidemic to a hyperlipidemic phenotype. Hypolipidemic apoE2 transgenic mice overexpressing human apoB had moderate remnant accumulation compared with apoE2-only or apoB-only transgenic mice, indicating that overproduction of apoB-containing lipoproteins in the presence of apoE2 can augment remnant production. Hypolipidemic apoE2 transgenic mice bred-onto an LDL receptor-null background had markedly higher plasma total cholesterol (288 +/- 51 mg/dL for males, 298 +/- 73 mg/dL for females) and triglyceride (356 +/- 72 mg/dL for males, 317 +/- 88 mg/dL for females) levels than apoE2-only mice, and remnant accumulation increased even in apoE2 mice with a heterozygous LDL receptor-knockout background (compared with apoE2-only mice), suggesting that reducing or eliminating a major receptor-mediated remnant-removal pathway in the presence of apoE2 can also precipitate a hyperlipidemic phenotype. In all cases where either lipoprotein remnant production or removal pathways were severely stressed, increased remnant accumulation was apparent. As judged by the chemical characteristics of the remnant lipoproteins, the lipoprotein phenotype was quite similar to that of human type III HLP, especially in the apoE2-expressing mice with no endogenous apoE or LDL receptors, and thus these mice represent improved models of the disorder.
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The records of 92 asthmatics who underwent mechanical ventilation were reviewed. In seven patients (8%) the severe attack was precipitated by a non-steroidal anti-inflammatory drug (NSAID); one of these patients died. Five of the cases had a history of asthmatic attacks provoked by NSAIDs; whilst in two the severe attack requiring mechanical ventilation was the first manifestation of NSAID-intolerance. In two patients the NSAID had been prescribed by their physicians. Another aspirin-intolerant patient, a general practitioner, self-administered a NSAID. The sudden attack in another patient was precipitated by a preparation which contains aspirin and is usually recommended for indigestion. In the fatal case the attack was provoked by a capsule containing aspirin, which had been given by a herbalist. Unlike other reports, we found that NSAID-intolerance is a frequent provoking factor in severe acute asthma requiring mechanical ventilation. Inadequate investigation of precipitating factors in asthmatics with severe sudden attacks is a possible reason why this phenomenon is underreported.
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The present study tested the assertion that there exists exclusively in persons with senile cataracts a serum factor capable of precipitating with gamma crystallin extract from bovine lens. The results of this work do not support this assertion without the imposition of rigid specifications regarding test solution concentrations and observation time. Among the 84 subjects tested, 2 individuals had posterior subcapsular cataracts. The precipitates resulting from incubation with serum from these individuals were similar to those resulting from incubations with serum from senile cataract patients. The present study did not confirm the existence of exclusive serum factors capable of precipitating with gamma crystallin extract in patients with senile cataracts.
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