A Study of Hepatic Function in Therapeutic Malaria

Fredricks, M. G.

doi:10.1001/jama.1945.02860240021005

Cited by 24 publications

(9 citation statements)

References 9 publications

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“…Follow-up showed that 6 weeks after the malarial attack, liver enlargement had diminished, jaundice Wallace and Diamond (1925), and Fredricks and Hoffbauer (1945). Increased excretion of urobilin and reduction in excretion of azorubin-S was also noted in acute malaria (Maegraith, 1948).…”

Section: Methodsmentioning

confidence: 99%

Hepatic dysfunction in childhood malaria.

Patwari¹,

Aneja²,

Berry³

et al. 1979

Archives of Disease in Childhood

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SUMMARY Hepatic function of 80 children aged under 3 years with Plasmodium vivax malaria were studied during the acute attack and 6 weeks after antimalarial treatment. Raised levels of serum aspartate transaminase (serum AST; SGOT), serum alanine transaminase (serum ALT; SGPT), and alkaline phosphatase were observed in 68 %, 39 %, and 46 % of cases respectively. AST levels were higher than ALT ones and the mean level of both enzymes was much higher in patients with hepatomegaly. The hepatic dysfunction which these observations reflect is transient, as these enzymes were found to be at their normal levels 6 weeks after treatment. A transient derangement of liver function is thus a common feature of childhood malaria, and hepatic dysfunction takes place to a significant degree even in P. vivax malaria.Malaria can bring about the inhibition of certain liver functions even in the absence of normal clinical signs of hepatic insufficiency. While normal liver functions may be restored after termination of the malarial attack, long continued low-grade malarial infection can cause permanent liver damage (Maegraith, 1948). Liver function has been studied in adults suffering from malaria and in experimental animals. Most studies on liver function have been on Plasmodium falciparum malaria, and hepatic dysfunction in Plasmodium vivax malaria has received little attention. Material and methodsChildren attending the outpatient department and those admitted to paediatric wards of this hospital in whom a diagnosis of malaria was confirmed by the presence of malarial parasite in the blood were studied. A detailed history was taken and a clinical examination given and then the following investigations were undertaken: serum bilirubin, serum aspartate transaminase (serum AST; SGOT) and alanine transaminase (serum ALT; SGPT), and alkaline phosphatase. Urine was examined for urobilinogen, bile salts, and bile pigments. Children with jaundice were further investigated for red blood cell morphology, reticulocyte count, and Coombs's Observations. 80 children from one month to 3 years of age were studied. P. vivax was causative in all. Fever was the chief presenting complaint. Clinically, splenomegaly was present in 83 % and hepatomegaly in 68 % of cases. Jaundice was observed in only 8 -7 % of cases; all thejaundiced patients had hepatomegaly.Out of 54 cases with hepatomegaly (group 1) AST was increased in 69%, ALT in 37%, and alkaline phosphatase levels were high in 50%. In 26 cases without hepatomegaly (group 2), 65 % had increased levels of AST, 38% increased ALT, and 38% had increased alkaline phosphatase levels (Table 1).

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Section: Methodsmentioning

confidence: 99%

Hepatic dysfunction in childhood malaria.

Patwari¹,

Aneja²,

Berry³

et al. 1979

Archives of Disease in Childhood

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“…They also noted that jaundice occasionally appears after malaria has been terminated and arsphenamine treatment has been begun. Fredericks and Hoffbauer (2) found that all of 31 patients studied showed from slight to moderate changes in from 1 to all of the liver function tests employed. One patient developed jaundice 43 days after fever therapy and died of hepatic insufficiency.…”

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confidence: 89%

The Occurrence of Jaundice in Therapeutic and Natural Malaria 1

Chalmers¹

1947

J. Clin. Invest.

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“…with (5, 6); previous experiences with this procedure in inoculation malaria have been described (7,8). Urine was analysed for bilirubin with the Harrison strip test (9) and the methylene blue test (10).…”

Section: Subjects and Programmentioning

confidence: 99%

“…The development of a positive Hanger test (cephalin-cholesterol flocculation) in malaria has been reported repeatedly (7,19,24,25). In this test, as in the thymol turbidity test, it is probable that the reactions depend upon changes in the serum proteins and are not, accordingly, specific tests of liver function except in so far as the latter is reflected by qualitative or quantitative changes in the serum proteins.…”

Section: Bilirubin and Urobilinogen In The Urinementioning

confidence: 99%

Experimental Malaria in Man. Ii. Liver Function 1

Keys¹,

Wells²,

Hoffbauer³

et al. 1950

J. Clin. Invest.

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It is generally known that malaria may produce signs of impaired liver function. In studies on experimentally induced malaria in this laboratory (1, 2), special efforts were made in an attempt to obtain information on four aspects of the question as to the effects on the liver: (1) The magnitude and character of the impairment as indicated by the several methods customarily used in the study of liver disease; (2) the time course of change during continuance of the infection; (3) the relationship of the liver function to the body temperature; (4) the recovery course following termination of the malaria with quinine. The present paper summarizes the findings on these points. SUBJECTS AND PROGRAMThe general characteristics of the subjects and the experimental program were described in a preceding paper (2). The 12 volunteer subjects were Conscientious Objectors who were considered to represent well-nourished normal young men in a fair state of physical fitness. Prior to the experiment, emphasis was placed on discovering any indications of previous episodes or history of liver disease. One subject (No. 9) gave a history of illness at the age of 12 which was characterized by an insidious onset with fever, malaise and jaundice of two months' duration, with subsequent full recovery without evidence of residues. Two other subjects had occasionally noted mild indigestion after eating fatty foods. There were no other suggestive points in the histories and no physical abnormalities were found on physical examination. In five subjects the liver could not be palpated. In seven subjects the liver was palpated at the right costal margin on deep inspiration and was apparently of normal texture; the liver was not tender in any of the men.For three weeks before inoculation the subjects were housed and fed in the laboratory on a standard regimen of moderate activity and a standard "good" diet of 3,600 Cal. with (5, 6); previous experiences with this procedure in inoculation malaria have been described (7,8). Urine was analysed for bilirubin with the Harrison strip test (9) and the methylene blue test (10). In a series of control studies it was found that heparinized plasma gave results identical with those obtained on serum for both prompt and total bilirubin and was more satisfactory than either oxalated or citrated plasma. A few trials with freezing plasma and urine samples indicated that subsequent analyses for bilirubin did not agree closely with the results of analyses on the fresh materials so attempts at storage were abandoned. Accordingly, all bilirubin analyses were made on the fresh materials.For the bromsulfalein excretion test a dosage of 5 mg. per kg. of body weight (11) and a 45-minute time interval (12) were employed.Cephalin-cholesterol flocculation was estimated according to Hanger (13), readings being made at 24 and at 48 hours. The thymol turbidity reaction was estimated with Maclagan's method (14).Urobilinogen was estimated with the method of Watson et al. (15,16) in urine samples collected over twohour peri...

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A Study of Hepatic Function in Therapeutic Malaria

Cited by 24 publications

References 9 publications

Hepatic dysfunction in childhood malaria.

Hepatic dysfunction in childhood malaria.

The Occurrence of Jaundice in Therapeutic and Natural Malaria 1

Experimental Malaria in Man. Ii. Liver Function 1

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