Insulinoma--a review of six cases.
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Biomedical subjects
Publications and source records attributed to P Jain.
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It was established that L-glutamine, an aminoacid, has marked anti-inflammatory activity and moderate analgesic activity. The drug was effective orally in suppressing various experimentally induced inflammatory reactions and did not show any gastric irritation in anti-inflammatory doses. It is observed that the anti-inflammatory effect of L-glutamine is not due to counter irritant action. It is suggested that it may partially mediate its anti-inflammatory activity by interfering with the action and/or synthesis of prostaglandins. Its anti-inflammatory activity is comparable to that of phenylbutazone and merits further study.
Guinea-pigs were sensitized with monoaxenic amoebic antigen (Group I), bacterial associate antigen (Group II) and axenic amoebic antigen (Group III). All animals in Group I, 95% in Group II and 70% in group III, developed caecal lesions on intra-caecal inoculation of Entamoeba histolytica trophozoites; 92.8% of control (unsensitized) animals developed lesions in their caeca. Lesions were more severe in sensitized animals than in controls. Hepatic abscesses were found in 7.6% of group I, 11.1% of group II and 7.1% of group III. No animal from the untreated but infected group developed hepatic abscess. It thus appears that specific (amoebic) and non-specific (bacterial) prior sensitization may render the host more susceptible to hepatic amoebic infection.
The virulence of 70 isolates of Entamoeba histolytica was studied in the Wistar strain of albino rat by intracaecal inoculation of amoebae. The results were evaluated by the Neal scoring system, histopathological grading of ulcers and virulence indices. It was found that isolates from acute amoebic cases could infect and produce ulcers in significantly more animals than could the isolates from asymptomatic cyst passers. The virulence indices of isolates from acute cases were also significantly higher as compared to those from asymptomatic cyst passers. However, there was no significant difference between virulence indices of isolates from acute cases and non-dysenteric amoebic colitis. This study also showed that Neal scores failed to correlate with the type of pathology produced by the amoebae in the caecum. It is felt that virulence indices which depend upon the histopathological lesions should also be taken into consideration. The serological response of the patients tended to correlate with the virulence indices of isolates but only minimally. The results thus contradict a common belief amongst clinicians that higher levels of anti-amoebic antibodies reflect severe disease, as compared to low levels of antiamoebic antibodies.
Amoebic antigen prepared from axenic Entamoeba histolytica (NIH:200 strain) grown at 37 degrees C in TPS I medium was chromatographed on a Sephadex G-200 column. Three fractions (F-I, F-II, F-II) were obtained, the molecular weights of which ranged from 650,000 to 1,450. Fractions were concentrated by lyophilization and antisera against each fraction and whole antigen were raised in rabbits. Partially purified fractions were used in various serological tests and their reactivities were compared with whole amoebic antigen. Main haemagglutinating and precipitating activities were confined to Fraction I, which had 14% of total protein and the highest molecular weight (650,000). 5 micrograms/ml of protein contained in this fraction gave antibody titres comparable to those obtained with whole antigen with 40 micrograms/ml or protein. Other fractions, although they had precipitin activity, lacked haemagglutinating activity. The protective efficacies of these fractions are being investigated in our laboratory.
Axenic amoebic antigen was chromatographed on Sephadex G-200. Two peaks divided into three fractions were obtained which were concentrated by lyophilization. Guinea-pigs were given a series of subcutaneous injections of crude Entamoeba histolytica antigen and its chromatographic fractions mixed with Freund's complete adjuvant. After three immunizing doses, the animals were challenged with intracaecal injection of a virulent isolate of amoebae (Strain No. H-25) and were killed seven days later. The antibody response was studied by indirect haemagglutination (IHA) and counter-current immunoelectrophoresis (CIEP) before intracaecal inoculation and at the time of killing. Fraction I, which had the highest molecular weight, stimulated high levels of antibodies in guinea-pigs and showed 92% protection. Only one animal of 12 inoculated had gross lesions and these were very mild. The caecal contents of three of the 11 animals without gross lesions were positive for amoebae but no tissue invasion was observed. Partial protection was observed with other antigens--30% with whole amoebae, 18% with Fraction II and 30% with Fraction III. In most there were multiple ulcers of the deep penetrating type and amoebae either penetrating and invading the muscular layer or the lytic process extending up to the muscular layer. In one animal, immunized with whole amoebic antigen, multiple hepatic lesions were also observed and trophozoites of E. histolytica were demonstrated histologically.
Guinea-pigs were immunzied with a low grade amoebic infection, either intracaecally or intramesenterically. The immunized animals were challenged with a virulent strain of Entamoeba histolytica. Some of the animals, immunized via the intracaecal route were challenged repeatedly. 10 to 30% of immunized animals developed caecal lesions compared with 92.8% of non-immunized animals. The percentage of protection in animals challenged repeatedly was greater than in those challenged once. Neither immunized nor non-immunized guinea-pigs developed hepatic abscesses. It appears that prior low grade infection could lead to resistance to subsequent amoebic challenge.
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Cell-mediated immune response (CMIR) and humoral antibody response was studied in fifteen patients with amoebic liver abscess, five patients with amoebic colitis and fifteen patients with non-amoebic diseases which served as unexposed controls. CMIR as judged by macrophage migration inhibition factor (MIF) test was altered in amoebic patients and more so in amoebic liver abscess patients; it was normal in unexposed controls. This altered CMIR reverted back to normal levels within five to seven days after the initiation of drug therapy. There was no clear-cut correlation between CMIR and humoral antibody response although by and large the degree of macrophage migration inhibition and humoral antibody titres were high in patients with amoebic liver abscess. It is thus felt that CMIR is altered in amoebic patients during the acute phase and is independent of humoral antibody response.
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