Phenindione Jaundice

Hargreaves, Tom; Howell, Mauricio Vargas

doi:10.1136/hrt.27.6.932

Cited by 7 publications

(2 citation statements)

References 13 publications

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“…Many of the patients with mitral valve disease had received phenindione for varying periods of time before operation. Hargreaves and Howell (1965) have described three cases of jaundice of a hypersensitivity type due to phenindione, noting that only 12 previous cases have been reported. They also found that it interfered with the conjugation of bilirubin in vitro.…”

Section: Pre-operative Evidence Of Liver Dysfunctionmentioning

confidence: 99%

Early jaundice after open-heart surgery

Lockey¹,

McIntyre²,

Ross³

et al. 1967

Thorax

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Two hundred and thirty-two patients subjected to open-heart surgery have been analysed regarding early post-operative jaundice. The overall incidence of jaundice was 13%, being 55% where the mitral valve and 5% where the aortic valve was predominantly involved. Only one out of 59 patients in whom a congenital lesion was repaired became jaundiced. Hyperbilirubinaemia without jaundice was common. The biochemical pattern of the jaundice was singularly constant, the most striking feature being the rise in serum bilirubin level. The highest value occurred between the second and tenth post-operative days. At total levels less than about 4 mg. /100 ml. the unconjugated fraction usually equalled or exceeded the conjugated. The alkaline phosphatase was normal in the first post-operative week but was sometimes slightly raised in the second, when the bilirubin levels were usually falling. The S.G.P.T. was normal or very slightly raised. Bilirubinuria was present. Centrilobular congestion with no evidence of extrahepatic biliary obstruction was found at post-mortem examination, and liver biopsy in three very severely jaundiced patients revealed only intrahepatic cholestasis. Pre-operative evidence of liver dysfunction was found in 13 patients who subsequently became jaundiced. Twelve had lesions predominantly affecting the mitral valve. Haemolysis, heart failure, and infection probably all played a part, and the effect of operation per se on liver function has been discussed. Drugs and viral hepatitis do not seem implicated in our patients. Maintenance of lower venous pressures in the post-operative period and the use of less blood reduced both the incidence and severity of jaundice.

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Section: Pre-operative Evidence Of Liver Dysfunctionmentioning

confidence: 99%

Early jaundice after open-heart surgery

Lockey¹,

McIntyre²,

Ross³

et al. 1967

Thorax

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show abstract

“…69 Phenindione-induced jaundice often follows the onset of a rash and pyrexia, though typically not until the fifth week of treatment, 70 and eosinophilia is a common association. 71 Although Churchill's jaundice developed earlier than five weeks, there does not appear to have been an alternative cause for the jaundice. Although Type I (mild) halothane-induced hepatotoxicity is marked by mild transient increases in serum transaminase activities, it is not characterised by jaundice and usually occurs 1–2 weeks after halothane exposure.…”

Section: Discussionmentioning

confidence: 99%

Sir Winston Churchill KG: hip fracture in Monte Carlo (‘Remember, I want to die in England’) on 28 June 1962, femoral vein thrombosis and jaundice in London

Vale

Scadding

2019

J R Soc Med

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Drug-Induced Cholestasis

Zimmerman

Lewis

1987

Medical Toxicology

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Intrahepatic cholestasis, defined as arrested bile flow, mimics extrahepatic obstruction in its biochemical, clinical and morphological features. It may be due to hepatocyte lesions of which there are three types, termed canalicular, hepatocanalicular and hepatocellular, respectively; or it may be due to ductal lesions at the level of the cholangiole or portal or septal ducts. Defective bile flow due to hepatic lesions reflects abnormal modification of the ductular bile. Defective formation of canalicular bile may involve bile acid-dependent or independent flow. It appears to result most importantly from defective secretion of bile acid-dependent flow secondary to defective uptake from sinusoidal blood, defective transcellular transport and defective secretion; or from regurgitation of secreted bile via leaky tight junctions. An independent defect in bile acid-independent flow is less clear. Defective flow of bile along the canaliculus may reflect increased viscosity and impaired canalicular contractility secondary to injury of the pericanalicular microfibrillar network. Impaired flow beyond the canaliculus may result from ductal injury. Sites of lesions that contribute to cholestasis include the sinusoidal and canalicular plasma membrane, the pericanalicular network and the tight junction and, less certainly, microtubules and microfilaments and Golgi apparatus. A number of drugs that lead to cholestasis have been found to lead to injury at one or more of these sites. Other agents (alpha-naphthylisothiocyanate, methylenedianiline, contaminated rapeseed oil, paraquat) lead to ductal injury resulting in cholestasis. Reports of inspissated casts in ductules (benoxaprofen jaundice) and injury to the major excretory tree (5-fluorouridine after hepatic artery infusion) have led to other forms of ductal cholestasis. Most instances of drug-induced cholestasis present as acute, transient illness, although important chronic forms also occur. The clinical features include the reflection of the cholestasis (pruritus, jaundice), systemic manifestations and extrahepatic organ involvement. While nearly all classes of medicinal agents include some that can lead to cholestasis, there are differences among the various categories. Phenothiazines and related antipsychotic and 'tranquillizer' drugs characteristically lead to cholestatic hepatic injury. The tricyclic antidepressants may lead to cholestatic or hepatocellular injury.(ABSTRACT TRUNCATED AT 400 WORDS)

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Phenindione Jaundice

Cited by 7 publications

References 13 publications

Early jaundice after open-heart surgery

Early jaundice after open-heart surgery

Sir Winston Churchill KG: hip fracture in Monte Carlo (‘Remember, I want to die in England’) on 28 June 1962, femoral vein thrombosis and jaundice in London

Drug-Induced Cholestasis

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