Hepatotoxic Drugs Causing Porphyria in Man and Animals*

Schmid, Rudi

doi:10.1111/j.1749-6632.1963.tb57100.x

Cited by 9 publications

(5 citation statements)

References 36 publications

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“…Overproduction of all haem precursors might reflect an exaggerated but normal response to porphyrinogenic drugs [7,37] such as the barbiturates, which accelerate their own biotransformation by stimulating the synthesis of the microsomal haemoprotein, cyto chrome P-450 [2, 11, 17, 25]. In this situation it would be rational to treat the patient with methods designed to suppress haem and porphyrin biosynthesis.…”

Section: Variegate Porphyria (Vp)mentioning

confidence: 99%

Enzymatic Defects in Hepatic Porphyria

Pimstone¹,

Blekkenhorst²,

Eals³

1973

Enzyme

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Section: Variegate Porphyria (Vp)mentioning

confidence: 99%

Enzymatic Defects in Hepatic Porphyria

Pimstone¹,

Blekkenhorst²,

Eals³

1973

Enzyme

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“…However, probably PCT may occur as a merely acquired disease. This is suggested by the outbreak of hepatic cutaneous porphyria in Turkey, probably caused by the ingestion of hexachlorobenzene (10). This porphyria generally occurred in children and adolescents but otherwise showed a great resemblance to PCT.…”

Section: Discussionmentioning

confidence: 99%

Porphyria Cutanea Tarda—a Genetic Disease?

Dehlin

Enerbäck

Lundvall

1973

Journal of Internal Medicine

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Abstract. The siblings of patients with clinically manifest porphyria cutanea tarda (PCT) have been investigated by chemical analysis of urinary and faecal porphyrin excretion and by fluorescence microscopical examination of smears from fine needle biopsy specimens of the liver. Four families and one alcoholic and one non‐alcoholic control group were studied. In two families red porphyrin fluorescence was demonstrated in 5 out of 15 asymptomatic siblings, and one sibling who refused liver biopsy was found to have a clinically manifest PCT. In the two other families no porphyrin abnormality could be demonstrated in the 7 asymptomatic siblings. In the control group comprising 36 non‐alcoholic subjects no porphyrin fluorescence could be demonstrated, but in the alcoholic control group of 59 subjects liver porphyrin fluorescence was found in two. Alcoholic abuse was common in the two families in which several members had porphyrin abnormalities indicating latent PCT. In the group of alcoholics liver porphyrin fluorescence was uncommon. Hence the present results indicate that PCT might be a genetic disease.

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“…HCB has also been associated with mass poisoning of humans, presenting with symptoms of porphyria (CAM & NIGOWSYAN 1963). The porphyrinogenic action of chronic HCB treatment in rats is well documented (SCHMID 1973: LISSNER et al 1975, although a precise mechanism for this effect remains to be established. Short-time feeding (7-10 days) of rats with a 0.2 olo HCB-containing diet leads to a 2-4 fold increase in liver microsomal cytochrome P-450 with a concomitant shift in the carbon monoxide-difference spectrum towards 448 nm ( STONARD & NENOV 1974;STONARD 1975).…”

Section: Discussionmentioning

confidence: 99%

Hexachlorobenzene Induction of 2,4‐Diaminoanisole Mutagenicity in Vitro

Dybing¹,

Aune²

1977

Acta Pharmacologica et Toxicologica

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Hexachlorobenzene (HCB)‐pretreatment of rats leads to an increase in liver microsomal 2,4‐diaminoanisole activation to a mutagen after a dose of 10 mg/kg intraperitoneally and to an increase in ethylmorphine N‐demethylase after a dose of 50 mg/kg intraperitoneally. 2,4‐Diaminoanisole mutagenicity was increased 24 hrs after HCB‐pretreatment, whereas ethylmorphine N‐demethylase first increased after 48 hrs. There is a sex difference in the inducing effects of HCB on ethylmorphine N‐demethylase, but not on 2,4‐diaminoanisole mutagenicity. HCB‐pretreatment also leads to increases in 2,4‐diaminoansiole mutagenicity in the kidneys, but not in the lungs or in foetal liver.

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Hepatotoxic Drugs Causing Porphyria in Man and Animals*

Cited by 9 publications

References 36 publications

Enzymatic Defects in Hepatic Porphyria

Enzymatic Defects in Hepatic Porphyria

Porphyria Cutanea Tarda—a Genetic Disease?

Hexachlorobenzene Induction of 2,4‐Diaminoanisole Mutagenicity in Vitro

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