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|Year : 1977 | Volume
| Issue : 3 | Page : 112-117
Malabsorption in cirrhosis of the liver
RV Patwardhan, BD Pimparkar, JM Mehta, UK Sheth
Department of Medicine and Pharmacology, Seth G. S. Medical College and K.E.M. Hospital, Parel, Bombay-400 012., India
R V Patwardhan
Department of Medicine and Pharmacology, Seth G. S. Medical College and K.E.M. Hospital, Parel, Bombay-400 012.
Source of Support: None, Conflict of Interest: None
Gastrointestinal function of absorption has been studied in twenty biopsy proved cases of cirrhosis of the liver. The gastrointestinal function was assessed by means of glucose and lactose tolerance tests and by fecal fat, d-Xylose and Co 57 B 12 excretion tests. Steatorrhoea and lactose intolerance are common in cirrhotics. The etiopathogenesis of this malabsorption in cirrhotics is discussed and appears multifactorial in origin.
|How to cite this article:|
Patwardhan R V, Pimparkar B D, Mehta J M, Sheth U K. Malabsorption in cirrhosis of the liver. J Postgrad Med 1977;23:112-7
| :: Introduction|| |
Although, Bright  in 1836 commented that "the evacuation of fatty matter, more or less mingled with feces accompanied the complete retention of bile", it is not commonly realised that steatorrhoea is a common feature of chronic liver disease. Hence, we undertook a study to assess the gastrointestinal function in biopsy proved cases of cirrhosis of liver.
| :: Material and Methods|| |
Twenty biopsy proved cases of cirrhosis of liver were studied. All were males, ranging in age from 19 to 60 years. A detailed history and a good clinical examination, with special emphasis on symptoms suggestive of malabsorption and liver cell dysfunction was recorded on a special proforma. Sixteen patients gave history of alcoholism while five patients had a history of jaundice. The duration of disease was more than 3 years in 75% of cases. Each subject had had routine investigations such as, hemogram, E.S.R., stool and urine analysis, estimation of blood urea nitrogen, serum amylase, and serum electrolytes.
X-ray chest and plain X-ray abdomen, particularly to rule out either pulmonary tuberculosis and/or pancreatic calcification, and,/or calculus cholecystitis, were also taken.
Liver function was assessed by various biochemical liver function tests and by liver biopsy. Serum bilirubin was estimated by the method of Malloy and Evelyin,  serum alkaline phosphatase by the method of King and Armstrong,  S.G.O.T. and S.G.P.T. by the method of Reitman and Frankel,  and Prothrombin time by Quick's one stage method. Total serum proteins were estimated by the method of Phillips et al,  whereas electrophoretic pattern was done by the method of Koiw and Gronwall.  The results of gastric secretory function in chronic liver disease are published separately and hence are not included in this paper.
The intestinal absorption of carbohydrates was tested by lactose and glucose tolerance tests, the blood glucose being estimated by the method of Folin and Wu  and d-Xylose excretion test by the method of Roe and Rice,  as modified by Santini et al  Fecal fat was estimated by the method of Van de Kamer et a1  and Co57 B 12 absorption by the method of Schilling.  The gastrointestinal mucosal pattern and motility were studied by barium meal follow through X-rays, supplemented whenever necessary by barium enema X-rays.
| :: Results|| |
[Table 1] shows the symptomatology. As expected, swelling of feet, distention of abdomen, weight loss, oedema, ascites, anaemia, muscle wasting, hepatosplenomegaly, and obvious venous collaterals were the most common symptoms and signs.
[Table 2] shows hemoglobin and serum protein values. The mean ± S.D. values for hemoglobin, and serum albumin were significantly lower while those for gamma globulins were significantly higher than those in normal controls. Serum bilirubin was elevated in 4 patients, serum alkaline phosphatase in 2; serum enzymes, (S.G.P.T. & S.G.O.T.), in 6; while prothrombin time was prolonged in all cases. Patients who were icteric had no evidence of obstructive jaundice either clinically or radiological ly.
All patients had had barium meal follow through X-rays, [Table 3]. These were normal in 8 patients. Somewhat delayed motility and coarsening of the mucosa were the most common findings. Less than 25% of the cases showed dilatation, fragmentation, or segmentation. [Table 4] and [Table 5] show the results of absorption studies. All patients had normal Co 57 B 12 absorption. Although two patients had abnormal d-Xylose excretion, the mean 5 hour urinary excretion of d-Xylose in cirrhotics was within normal limits. Eighty per cent of patients with cirrhosis had flat lactose tolerance test, and the mean ± S.D., as well as the maximal rise over the fasting levels after a lactose load was also significantly lower in cirrhotics. Glucose tolerance test, on the other hand, was flat in only 2, (10%), diabetic in 8 (40%), while it was normal in 10 patients (50%). The mean maximum rise over the fasting level after a glucose load was within normal limits in cirrhotics. The mean daily fat excretion was significantly high and 65%, of cirrhotics had steatorrhoea.
| :: Discussion|| |
Steatorrhoea in the presence of obstructive or hepatocellular jaundice has been confirmed repeatedly. , Some correlation has been demonstrated between the depth of jaundice and the degree of steatorrhoea by Gross et al , .It would be reasonable to assume that the liver with its diverse functions in the metabolism of absorbed food-stuffs, when diseased would contribute to the development of malabsorption. However, it is perhaps less widely recognised that steatorrhoea may be a feature of an unicteric liver disease where major obstruction to the biliary tract can be excluded. ,,,,,, Earlier case reports included only those cases that had well marked malabsorption. Later unselected case series by many workers have reported an overall incidence of steatorrhoea in 50% of the patients with cirrhosis or chronic liver disease. This study reveals an incidence of 65%. The mechanism or etiopathogenesis of this steatorrhoea in liver disease is not certain and is considered to be related to the associated mal- or under-nutrition, associated portal hypertension and ascites, decreased synthesis of bile acids by cirrhotic liver, or increased deconjugation of bile acids in the intestine from bacterial overgrowth.
All subjects showed normal Co 57 B 12 absorption while only two patients (10%) had malabsorption of d-Xylose. Forty per cent of our cirrhotics showed diabetic glucose tolerance curve, whereas, it was flat in only 2, (10%). Thus, the findings of normal absorption of Co 57 B 12 d-Xylose and glucose with increased incidence of diabetes in cirrhotics, and normal barium meal X-rays findings are similar to those reported by others.
Nearly 80% of our cirrhotics showed lactose intolerance. Lactose intolerance in cirrhotics has not been commonly reported. The etiopathogenesis of this intolerance is also not certain. It could probably be due to associated bacterial overgrowth. However, this needs to be confirmed by further studies which are n progress. Thus, the evidence from his and other studies suggests that mal-absorption in chronic liver disease is common and is multi-factorial in origin.
| :: Acknowledgement|| |
We wish to thank the Dean, Seth G.S. Medical College and K.E.M. Hospital for allowing the facilities to carry out this research project and to publish the report.
| :: References|| |
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[Table 1], [Table 2], [Table 3], [Table 4], [Table 5]