Urinary Excretion of Coproporphyrin Isomers I and Iii and Δ‐aminolaevulic Acid in Normal Pregnancy and Obstetric Hepatosis

Koskelo, Pentti; Toivonen, Ilkka

doi:10.3109/00016346809157485

Cited by 7 publications

(3 citation statements)

References 9 publications

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“…With impairment of hepatic excretory function there is an increase in the total coproporphyrins excreted in urine with a rise in the proportion of the I isomer (3). This change in the pattern of coproporphyrin excretion has been found in postnecrotic cirrhosis, obstructive jaundice, hepatitis, pregnancy, and after the administration of oral contraceptive agents (3,5,9). In the Dubin-Johnson syndrome (5, 6) a similar but greater increase in the proportion of the I isomer in urine is described (up to 90% of the total).…”

Section: Discussionmentioning

confidence: 50%

“…In liver disease and in acquired or genetic disturbances characterized by reduced hepatic excretory function, there is an increase in the total uriReceived for publication 10 May 1972 and in revised form 14 July 1972. nary excretion of coproporphyrins (3)(4)(5)(6)9), but with a concomitant shift in the isomer ratio towards a predonminance of the type I compound. A series of experiments were undertaken in this study to characterize the hepatic transport process for the two coproporphyrin isomers in order to define the possible mechanism for the unequal distribution of the isomers in urine and bile during normal and impaired hepatic function.…”

Section: Introductionmentioning

confidence: 99%

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Coproporphyrin I and III excretion in bile and urine

Kaplowitz¹,

Javitt²,

Kappas³

1972

J. Clin. Invest.

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A B S T R A C T The excretion of coproporphyrin isomers I and III was studied in the rat. Both isomers were found to bind equally to rat plasma and liver cytosol in vitro and to disappear from plasma at equal rates after single injections in vivo. During equimolar infusions of isomers into bile fistula animals, both the I and III isomers were excreted in bile in a concentration ratio of 2: 1, respectively. Pretreatment of animals with ethinylestradiol or simultaneous infusions of phenoldibromophthalein disulfonate caused a reduction in total hepatic excretion with no change in the 2: 1 ratio in bile. As hepatic excretion fell, excretion of both isomers in urine rose, with an increase in the proportion of the I isomer. The findings mimic those reported to occur in man and can be explained by inhibition of a common carrier which requires a stereospecific configuration that statistically favors the hepatic transport of the symmetrical coproporphyrin I isomer.

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Section: Discussionmentioning

confidence: 50%

Section: Introductionmentioning

confidence: 99%

Coproporphyrin I and III excretion in bile and urine

Kaplowitz¹,

Javitt²,

Kappas³

1972

J. Clin. Invest.

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“…Both isomers are produced primarily in liver and bone marrow and are found normally in urine and feces [12]. Coproporphyrin excretion in urine has been studied in adults [2,3,[8][9][10][11]181, but not in infants or amniotic fluid.…”

Section: Introductionmentioning

confidence: 99%

Coproporphyrin Excretion in Amniotic Fluid and Urine from Premature Infants: A Possible Maturation Defect

Wolkoff

Arias

1974

Pediatr Res

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ExtractCoproporphyrin analysis was performed on urine from 17 male and 7 female premature infants (birth wt 1.5-4.5 kg, average 1.7 kg). Six specimens of amniotic fluid obtained before elective abortion induced by saline solution infusion were also examined. Normal adult control subjects excreted 24.6y0 5.6y0 of total coproporphyrin as coproporphyrin I. Twenty-three premature infants excreted 59.4y0 A 17.3%as coproporphyrin I, significantly higher amounts than control subjects (P < 0.001).Coproporphyrin I excretion in six specimens of amniotic fluid was 84.9y0 '0 fo.470, significantly higher than in urine from adults and premature infants ( P < 0.001). SpeculationThese results raise the possibility of a similar hepatic excretory defect in porphyrin metabolism in the developing fetus and in the Dubin-Johnson syndrome. I n the fbrmer, the defect is developmental; in the latter, it is lifelong and is present in obligate heterozygotes. Uroporphyrinogen I11 cosynthetase normally catalyzes conversion of porphobilinogen to isomer I11 rather than isomer I porphyrins.Developmental deficiency of this enzyme may be responsible for the observed pattern of coproporphyrin isomers seen in the fetus and neonate.

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