Excretion of Coproporphyrin in Hepatic Disease

Nesbitt, Samuel

doi:10.1001/archinte.1943.00210040042005

Cited by 5 publications

(1 citation statement)

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“…During acute episodes of hepatic insufficiency the urine volume and coproporphyrin excretion both decline. The same author (161) has demonstrated the urinary excretion of coproporphyrins I and III by patients with hepatic damage or obstruction during maintenance on a porphyrin-free diet. These compounds, which arise during the synthesis of hemoglobin, had been recovered previously from the urine of healthy persons, but in these persons they could have had a dietary origin since the subjects were not on a meat-free diet.…”

Section: Biliary System and Bilementioning

confidence: 97%

Liver and Bile

Freeman¹

1946

Annu. Rev. Physiol.

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Chicago, Illinois 169Annu. Rev. Physiol. 1946.8:169-198. Downloaded from www.annualreviews.org Access provided by Michigan State University Library on 02/03/15. For personal use only.Quick links to online content Further ANNUAL REVIEWS Annu. Rev. Physiol. 1946.8:169-198. Downloaded from www.annualreviews.org Access provided by Michigan State University Library on 02/03/15. For personal use only.LIVER AND BILE 171 carbon was recovered in the expired air in a sixteen hour period. The distribution of the nitrogen of glycine was followed byShemin & Rittenberg (10), who fed the heavy nitrogen as glycine to rats and followed its concentration in various tissue proteins.Their results indicate that half the total protein nitrogen of the liver is replaced every seven days, and that 10 per cent of the liver glycine nitrogen is replaced daily by glycine from other sources.Treadwell, Tidwell & Grafa (11) found that rats maintained on a high fat, low protein diet had a significantly higher liver glycogen than when the diet was high in both fat and protein.The animals with fatty livers (low protein) had an increased glycogenolysis during fasting and decreased glycogenesis following glucose administration. Soskin (12) has recently reviewed the general role of the liver in regulating the blood sugar level and emphasized the diabetic type of sugar tolerance curve associated with impaired liver function.The hepatic reserve of glycogen in children has been estimated by Mirsky & Nelson (13) by determining the sugar excretion, hypoglycemia, and ketosis provoked by phlorhizin administration.A loss of 15 to 20 gm. of sugar by a normal child leads to hypo glycemia_and ketonemia. Younger children were found to have less glycogen reserve. Dziewiatkowski & Lewis (14) found that glycogen depletion occurs in young well-fed rats four hours after administration of menthol or sodium tertiary butyl acetate. Since these compounds are excreted as glycuronates, it appears probable that glycogen is used as a source for glycuronate syn thesis. This relation between glycuronates and glycogen may account for the results reported by Ottenberg and collaborators (15), who found a low glycuronate excretion after borneol ad ministration, not only by patients with liver disease but by patients with other diseases as well.Other aspects of liver metabolism.-Dounce has described an improved method for isolating the intact cell nuclei of rat liver (16). The following enzymes were found in the nuclei: arginase, cytochrome oxidase, esterase, lactic acid dehydrogenase, alkaline and acid phosphatase. The total lipid content of the nuclei was between 10.5 and 11.0 per cent. A heat labile enzyme that cata lyzes the decarboxylation of oxalacetic acid was shown by Evans and associates (17) to be present in a c�ll-free extract of pigeon liver. WQQdwa r q (18) found that liver tumors produced by Annu. Rev. Physiol. 1946.8:169-198. Downloaded from www.annualreviews.org Access provided by Michigan State University Library on 02/03/15. For personal use only.

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Section: Biliary System and Bilementioning

confidence: 97%

Liver and Bile

Freeman¹

1946

Annu. Rev. Physiol.

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Aplastic Anemia and Its Association With Hemochromatosis

ZELTMACHER¹

1945

Arch Intern Med

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Porphyria

Schwarz¹

1954

AMA Arch Intern Med

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PORPHYRIA is considered to be an "inborn error" in the metabolism of the porphyrins.* Many of its clinical manifestations are neurologic or psychiatric or both. Indeed, it does not seem to be unusual to have the metabolic disorder discovered only after the neuropsychiatric symptoms have developed. This imposes a responsibility on the part of the physician to be alert to the possibility of such a process in appropriate neurologic and psychiatric cases and to be acquainted with the symptoms and signs produced by this disorder of pyrrole metabolism. For this reason, we wish to report three cases illustrating the different clinical features of the disease and the neuropathologic changes observed in two of them. REPORT OF CASESCase 1.\p=m-\N.T., a Negro girl, aged 17, was admitted to the hospital on April 9, 1944, complaining of vomiting and pain in the right side of her abdomen. These symptoms had developed quite suddenly on April 5 and had persisted so that she had been sent into the hospital with a diagnosis of "acute appendicitis" or some "acute inflammatory disease" in the "pelvis." For about a year before this, she was said to have had recurrent attacks of abdominal pain, but they were never so severe or so prolonged as the present attack. She also claimed to have had a similar pain, but milder, on the second or third day of her menstruation. Before the present illness, she had had some nocturia, and since the onset she had experienced painful, difficult urination.Her mother, father, three brothers, and three sisters were apparently healthy. The physical examination on admission revealed the abdomen to be soft and relaxed. There was tenderness on deep pressure over the whole abdomen, more marked in the right lower quadrant. Peristalsis was felt to be decreased. The neurologic examination was essentially negative at this time.On admission, the temperature was 99.4 F., pulse rate 98 per minute, and respiratory rate 24 per minute. The blood pressure on April 12 was 145/105. Laboratory Studies on Admission.-Erythrocytes were 4,130,000 per cubic millimeter of blood and leucocytes 13,550; of the latter 77% were neutrophiles, 21% were lymphocytes, and 2% were monocytes. The urine was red-brown in color and showed a specific gravity of 1.035, a slight trace of albumin, no sugar, a negative benzidine test, no erythrocytes, and 5 to 8 leuko¬ cytes per high-power field. The sedimentation rate was 40 mm. in an hour.

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Excretion of Coproporphyrin in Hepatic Disease

Cited by 5 publications

References 20 publications

Liver and Bile

Liver and Bile

Aplastic Anemia and Its Association With Hemochromatosis

Porphyria

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