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Hypergastrinaemia in Cirrhosis of Liver

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Hypergastrinaemia in Cirrhosis of Liver Gut: first published as 10.1136/gut.17.9.700 on 1 September 1976. Downloaded from Gut, 1976, 17, 700-708 Hypergastrinaemia in cirrhosis of liver SHIU KUM LAM From the Department ofMedicine, University of Hong Kong, Queen Mary Hospital, Hong Kong SUMMARY The basal acid output (BAO), post-pentagastrin acid output (MAO), fasting and post- prandial gastrin levels in 40 patients with proven cirrhosis of the liver were compared with those in 20 normal controls. The mean BAO and MAO were significantly lower than normal, the mean fasting gastrin level was significantly higher than normal, and the postprandial gastrin response was significantly increased and prolonged. These differences were still significant even when the patients were divided into cryptogenic and alcoholic subgroups. A significant inverse relationship between MAO and the integrated gastrin response to meal was observed both in the normal controls and in the cirrhotic patients. The MAO and integrated gastrin response of the cirrhotic patients did not correlate with the degree of liver function impairment. In five cirrhotic patients fasting and postprandial gastrin levels were unchanged after splenorenal shunt operation. A more consistent abnormality of the gastric mucosa as assessed by endoscopy and biopsies appeared to be mucosal congestion with occasional atrophic gastritis. The severity of mucosal abnormality, however, was unrelated to the degree of hypoacidity. These results indicate, firstly, that the hypergastrinaemia in cirrhotic patients is a reflection of gastric hypoacidity and bears no direct relationship to hepatic dysfunction. Secondly, the gastric hypoacidity does not accrue solely from mucosal abnormality. It is suggested that this hypoacidity may result from the presence of excessive amounts of cir- culating acid-inhibiting intestinal peptides, which the diseased liver fails to metabolise. http://gut.bmj.com/ Anincreased incidence of pepticulceration inpatients lated serum gastrin response is such that, in duodenal with cirrhosis of the liver had been observed by ulceration, both secretions are on average higher many authors (Schnitker and Hass, 1934; Welbourn, than normal, whereas, in gastric ulceration, the 1952; Palmer and Brick, 1953; Swisher et al., 1955; relationship is an inverse one, there being a high on September 27, 2021 by guest. Protected copyright. Fainer and Halsted, 1955; Hallen and Kroorc, 1963; fasting serum gastrin reflecting a low acid output. Patek, 1963; Tabaqchali and Dawson, 1964; In this study, the relationship of acid and gastrin Bergman and van der Linden, 1965; Jackson et al., release in cirrhotic patients was examined, and an 1965; Orloff et al., 1969; Resnick et al., 1969; attempt was made to correlate the findings with the Jackson et al., 1971; Phillips et a!., 1975), but severity of disturbance of liver function and the disputed by some (Ratnoff and Patek, 1942; Lipp morphology of the gastric mucosa. In addition, and Lipsitz, 1952; Doll, 1952; Sullivan et al., 1954). the effect of a portosystemic shunting operation on The pathogenesis for the apparent increase in acid and gastrin release was also studied. frequency is unknown. It is unrelated to gastric hyperacidity, since acid secretion in cirrhotic Methods patients has been shown to be abnormally low (Scobie and Summerskill, 1954; Ostrow et al., 1960; PATIENTS Schmidt and Martini, 1969) or to be normal (Tabaq- Forty patients, 35 males and five females, with ages chali and Dawson, 1964). ranging from 24 to 65 years (mean 52-1 years) were It is now generally accepted (Grossman, 1974) studied. The presence of cirrhosis was confirmed by that the relationship between pentagastrin or needle biopsies of the liver in 35 patients and at histamine stimulated acid output and food stimu- necropsy in the remaining five patients who died 'This study is supported by research grant no 158-295 of the between one and seven months after the study. In University of Hong Kong. the latter five patients needle biopsy of the liver was Received for publication 4 June 1976 not performed at the time of the study because of 700 Gut: first published as 10.1136/gut.17.9.700 on 1 September 1976. Downloaded from Hypergastrinaemia in cirrhosis ofliver 701 persistent coagulation abnormalities. In 27 of the aged from 19 to 65 years (mean = 46-2 years). cirrhotic patients, no cause of cirrhosis could be Informed consent was obtained from all. determined and, for the purpose of this study, they were designated cryptogenic cirrhotics. The morpho- GASTRIC ACID OUTPUT logical features were those of post-necrotic scarring, The basal acid output (BAO) and the maximum as had been previously described (Cook et al., 1963). acid output (MAO) after an intramuscular injection Among these, 16 were considered by the radiologists of pentagastrin (6 ,ug/kg body weight) was measured to have a small-sized liver and nine to have a normal- in the conventional manner in all the 60 study sized liver on hepatic scintiscanrning. In the remain- subjects (Baron, 1973). The acid content in the ing 13 patients with cirrhosis a clear history of gastric juice was estimated by an automatic titrator excessive alcohol consumption was present. Usually (Radiometer, Copenhagen, type TTT II). more than half a catty double distilled rice wine a day or its equivalent (about 100 g ethanol) was SERUM GASTRIN consumed, and these patients were considered to On a separate day after an overnight fast, a 19 g have alcoholic cirrhosis. Ten of the patients in this butterfly needle was inserted into an antecubital group had an abnormally large liver and three a vein of the study subject and kept patent by a slow normal-sized liver on hepatic scintiscanning. The infusion of normal saline. After two fasting blood patients were not allowed to take any alcohol for at samples were taken at - 15 minutes and zero time, least seven days before the study. No peptic ulcer each subject ingested a standard protein meal in the stomach or duodenum was demonstrated in composed of 50 g protein, 40 g fat, and 40 g carbo- any one patient by barium study, endoscopy, at hydrate. Additional blood samples were taken at subsequent surgery and/or at necropsy. Blood urea 15, 30, 45, 60, 90, and 120 minutes. In 19 cirrhotic and creatinine were below 7 mmol/l and 125 ,umol/l patients and 10 normal controls, additional blood respectively at the time of the study in all patients. samples were collected at 150, 180, 210, and 240 Gastrointestinal bleeding occurred in 12 patients, minutes after the meal. Each sample was stored and for these a period of at least six weeks was immediately at 4°C. The serum from all samples allowed before performing the study. When ascites were extracted by centrifugation immediately at the was present, this was ameliorated as far as possible end of the test and stored at - 20°C for subsequent using diuretics until the attending physician was radioimmunoassay of gastrin. satisfied that no further improvement would be http://gut.bmj.com/ likely. RADIOIMMUNOASSAY OF SERUM GASTRIN The details of the assay have been previously LIVER FUNCTION SCORE reported (Byrnes et al., 1976; Lam and Lai, 1976). The liver function of each patient was scored, The antiserum used had been raised in rabbit against using a modification of Child's classification (Child, gastrin I and If extracted from pig antra using the 1964). Five points were given for previous stage I method of Gregory and Tracy (1964) and conjugated and II encephalopathy, 10 points if the encephalo- to egg albumin. The association constant of the on September 27, 2021 by guest. Protected copyright. pathy had been stage III or IV (staging by Adams antiserum was 5-2 and 1011 I/mol. Sensitivity of the and Foley, 1955). Five points were given when assay was down to 2-4 pmol/l (5 pg/ml) of serum ascites were present, 10 points if this was poorly using synthetic human gastrin I (Imperial Chemical controlled. Two and a half points were given when Industries) as standard. Cross-reaction by chole- serum bilirubin was between 25-7-51.3 mmol/l, cystokinin was 2 x 10-4 on a molar basis. Within 5 points if this was over 51-3 mmol/l. Two and a half and between assay coefficients of variation were points were given when serum albumin was between 6-2 % and 13% respectively. In each individual the 25 and 30 g/l, 5 points when this was less than integrated gastrin response from zero time to 120 25 g/l. A patient could thus in theory score a maxi- minutes after the meal (£ GO-120) was calculated mum of 30 points. Each patient was then graded as from the area under the gastrin response curve having mild (score 0-10), moderate (score 11-20), within the two-hour period. Similarly the integrated and severe (score 21-30) liver function impairment. gastrin response between 120 minutes and 240 minutes after the meal (£ G120-240) was calculated CONTROLS in those subjects who had blood taken up to four These were carefully selected from among healthy hours after the meal. medical and nursing staffs and patients in the general medical wards who had recovered from an unrelated GASTRIC MUCOSAL MORPHOLOGY condition and who were otherwise healthy. There Twenty-eight of the cirrhotic patients (20 crypto- were 20 such subjects, 16 males and four females, genic and eight alcoholic) consented to the carrying Gut: first published as 10.1136/gut.17.9.700 on 1 September 1976. Downloaded from 702 Shniu Kum Lam Table 1 Acid output and meal stimulated gastrin response in cirrhosis and controls (mean ± SEM) No. Basal acid output Maximum acidoutput X GO-120 E G120-240 (mmol/h) (nmollmin/l) (nmol/min/l) (mmol/h) (mmol/h/kg) Normal 20 2-3 ± 0-3 13-6 1 1 0-27 0-02 54 + 04 5 3 ± 0-8 (10 subjects) CirrhoFsi Cryptogenic 27 1-0 ± 0 4 6-7 i 15 0-13 0-03 8-2 0-8 Alcoholic 13 0 7 ± 0-4 6-7 + 1-8 0-13 ± 003 8-7 1-0 Total 40 0 9 ± 0 3 6-7 1-2 013 0-02 8-4 07 8-4 ± 0 9 (19 subjects) p < 0 01 for all comparisons between normal and cirrhosis.
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