Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0149521 (chronic pancreatitis)
 7,199 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The incidence of post-transplant diabetes mellitus was evaluated retrospectively in 901 consecutive renal transplant recipients. Thirty-two (3.6%) patients developed diabetes mellitus requiring drug therapy. 18 of 32 became hyperglycaemic within 3 months of transplantation. Post-transplant diabetes mellitus occurred in 24 of 628 (3.8%) patients treated with conventional therapy consisting in azathioprine and prednisone, and in 8 of 273 (2.9%) patients receiving cyclosporin A (CsA) in addition (triple therapy). To identify predisposing factors 32 non-diabetic patients matched for age, sex, number of graft, immunosuppressive protocol, and graft function at onset of diabetes were used as case controls. Thirteen of 32 patients with diabetes mellitus and 5 of 32 control patients had abnormal glucose tolerance pretransplant (P less than 0.025). HLA-B8 was significantly more frequent in patients with post-transplant diabetes mellitus than in control patients (9 of 29 vs 2 of 31, P less than 0.02). Twelve (38%) patients became diabetic during or immediately after anti-rejection therapy with intravenous pulse prednisone. Four diabetic patients experienced chronic pancreatitis pre-transplant. Family history of diabetes mellitus, bodyweight, number of rejection episodes, and immunosuppressive drug doses were similar in both groups. Actuarial patient and graft survival was not significantly different in diabetic patients and controls, although 10-year data tended to be better in controls. Thus, post-transplant diabetes mellitus was not a frequent complication in patients sometimes predisposed by an impaired glucose tolerance pre-transplant and was triggered by pulse prednisone therapy in 38%.
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PMID:Post-transplant diabetes mellitus in renal allograft recipients: a matched-pair control study. 211 51

Inappropriate expression of HLA Class II (D/DR) molecules has been detected in the target cells of most autoimmune diseases including Type I (insulin-dependent) diabetes. The possibility that this phenomenon is due to the action of lymphocytes or some of their products has been investigated by analysing in vitro the modulation of HLA products in Beta cells. Monolayer cultures from 25 human pancreatic glands were supplemented with alpha-interferon (IFN), beta-IFN or gamma-IFN, interleukin 2 (IL-2) and supernatants from activated lymphocytes. In addition, lectins and a variety of other hormones, biological products and chemicals were tested. Major histocompatibility complex (MHC) expression was assessed by double immunofluorescence technique using monoclonal antibodies to non-polymorphic determinants of Class I and Class II molecules and the pancreatic cells were identified by antibodies to islet hormones and other cytoplasmic antigens. gamma-IFN and lectins produced a parallel enhancement of HLA-A,B,C expression in islet, exocrine/ductal cells and fibroblasts. HLA-D/DR was inducible in all pancreatic cell types, except endocrine islet cells which did not produce Class II molecules in response to any of the stimuli including supernatants from activated lymphocytes. Exocrine/ductal cells from glands of patients with chronic pancreatitis spontaneously expressed Class II products, but islet cells were devoid of any detectable D/DR. These data are consistent with recent observations which have indicated that in the 'diabetic' pancreas inappropriate Class II expression in the Beta cells occurs independently of the presence of lymphocytes infiltrating the islets, and make it necessary to postulate that other factors are responsible for the Class II induction in Beta cells in human Type I diabetes.
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PMID:Differential expression and regulation of MHC products in the endocrine and exocrine cells of the human pancreas. 309 71

HLA-A and B antigens were studied in 88 Caucasoids with chronic pancreatitis resident in the Manchester area. In the subgroup of 52 patients with alcohol-related chronic pancreatitis HLA-B21 was significantly increased in frequency compared with 344 local controls (Pc = 0.0128). In the non-alcoholic sub-group of 36 patients, the incidence of HLA-A1 was significantly higher than in controls (Pc = 0.0021); whilst HLA-B8 was present in 38.8% of patients and 27.9% of controls. When these data are amalgamated with data from Lyon (France), the antigen HLA-A1 is significantly associated with non-alcoholic chronic pancreatitis.
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PMID:Chronic pancreatitis, HLA and autoimmunity. 316 7

Since immunological and hereditary factors may be important in chronic pancreatitis, histocompatibility antigens of classes I and II were studied in 50 British Caucasian patients, after exclusion of insulin-dependent diabetics for whom HLA associations are recognised. Chronic pancreatitis was defined by at least two independent criteria, and only subjects with alcohol-related and idiopathic disease were included. In 22 patients (21 male), weekly ethanol intake had chronically exceeded 100 g (usually substantially so); the remaining 28 had idiopathic chronic pancreatitis (ICP). Twenty patients (40%) had autoantibodies, in 11 (22%) to gastric parietal cells. Nine of those with ICP (three male) had parietal cell antibody, more than expected for the age/sex distribution. There were overall increased frequencies of HLA Cw5 and B44. In ICP there were increased frequencies of HLA A25 and Cw1, and a decreased frequency of B7. In patients with alcohol-related disease there were increased frequencies of Cw5 (50.0% vs control 15.9%), B44 (54.5% vs 29.4%), and DR4 (61.1% vs 33.6%). The increased frequency of Cw5 in alcohol-related disease alone remained significant after correction (p less than 0.05). A hypothesis that hereditary and possibly immunological factors may contribute to the aetiology of chronic pancreatitis is supported.
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PMID:HLA antigens in chronic pancreatitis. 368 17

Immunostaging was performed in patients with chronic pancreatitis of different etiologic groups. Immune responifveness was assessed by immunoglobulin serum levels, non specific autoantibody formation, C3 levels, antistreptolysin reaction, antibody titer against Toxoplasma gondii, E. coli, Herpes simplex-, Mumps- and Cytomegalovirus and screening for soluble immune-complexes (PEG precipitation assay), number of T- and B-lymphocytes, lymphocyte responsiveness to PHA, PPD, tetatoxoid and mumps-antigen in a whole blood assay, skin testing with candidin, trichophytin, tuberculin and streptokinase and HLA-typing. In some cases we found a depressed cell-mediated immune responsiveness. Patients were divided into two groups based on this main finding. Cellular hyporesponsiveness was correlated to the severity of the disease and a high incidence of HLA-B5 but not to any etiologic factor of the disease.
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PMID:[Immunostaging of patients with chronic pancreatitis. I. A study of humoral and cell-mediated immunity (author's transl)]. 645 Nov 61

HLA A and B antigens in 46 patients with chronic pancreatitis were studied in Japan. Patients were divided into the two groups according to the etiology of the disease: one was chronic idiopathic pancreatitis (18 cases) and the other was chronic alcoholic pancreatitis (28 cases). One hundred twenty unrelated subjects were also examined as control. HLA B5 was detected in 14 of 18 cases of chronic idiopathic pancreatitis, which was significantly higher statistically than in control (P less than 0.001, corrected P less than 0.05). In contrast, no HLA antigens of locus A and B were found which had a relationship to chronic alcoholic pancreatitis. These results suggest that some genetic factors may be implicated in the development of chronic idiopathic pancreatitis and differing from that of alcoholic pancreatitis.
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PMID:HLA antigens in chronic idiopathic pancreatitis compared with chronic alcoholic pancreatitis. 724 84

HLA A, B and C antigens were determined in 128 patients with chronic pancreatitis in Japan. Patients were divided into two groups, chronic alcoholic and chronic idiopathic, from two parts of Japan, the eastern and the western part, with control subjects in each region. A significantly higher frequency of B5 was demonstrated among chronic idiopathic pancreatitis and of B13 among chronic alcoholic pancreatitis in the eastern part, and no definite findings were obtained in the western part of Japan. On the other hand, the frequency of BW 54 was lower among chronic alcoholic pancreatitis in both parts of Japan, but the corrected p value for this antigen was not statistically significant. These facts suggest that 'HLA antigens in chronic pancreatitis have some racial and regional differences.
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PMID:HLA antigen and chronic pancreatitis in Japan. 727 3

From the present review it appears that insulin-dependent diabetes is a common finding in chronic pancreatitis, and impaired secretion of insulin from beta-cells of the pancreatic islets is essential for the development of this form of secondary diabetes. Judged from a positive correlation between insulin secretory capacity and stimulated pancreatic enzyme output, beta-cell function may decrease in parallel with exocrine pancreatic function. However, in patients with insulin-dependent diabetes secondary to chronic pancreatitis beta-cell function was preserved to a greater extent and glucoregulation was better than in comparable Type 1 (insulin-dependent) diabetic patients. Immunological phenomena and associations with certain HLA-alleles characterizing Type 1 diabetes mellitus were not found in insulin-dependent diabetes secondary to chronic pancreatitis. This may contribute to the slower destruction of the beta-cells in chronic pancreatitis than encountered in Type 1 diabetes. The small number of chronic pancreatitis patients who developed totally absence of endogenous insulin production still have some alpha-cell function during i.v. arginine and meal stimulation. However, insulin-induced hypoglycemia and insulin withdrawal did not stimulate glucagon secretion in the secondary diabetic patients in contrast to comparable Type 1 diabetics. Nevertheless, blood glucose counterregulation is intact in the secondary diabetics due to preserved catecholamine secretion. Furthermore, ketonemia develops during dissipation of insulin, in spite of absence of increased glucagon secretion, emphasizing the role of insulin dissipation for the development of ketoacidosis in this form of diabetes. The suggested increased susceptibility to severe hypoglycemia and less tendency to development of ketonemia may further be influenced by altered insulin sensitivity, nutritional factors and concomitant hepatic failure in diabetes secondary to chronic pancreatitis. Pancreatic polypeptide secretion was absent in chronic pancreatitis without endogenous insulin production. Pancreatic polypeptide secreting cells thus seem to be at least as vulnerable as the beta-cells to the destructive processes characterizing chronic pancreatitis, whereas glucagon secreting alpha-cells preserve secretory capacity to a greater extent than PP-cells and beta-cells. No data, however, favour the view that absent pancreatic polypeptide secretion has any major effect on the glucoregulation in diabetes secondary to chronic pancreatitis. Increased plasma concentration of somatostatin was found in patients with insulin-dependent diabetes secondary to chronic pancreatitis. The source of somatostatin in the patients is unknown, but somatostatin may contribute to a reduction in overall blood glucose level in patients without endogenous insulin secretion due to inhibition of glucagon secretion.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Diabetes mellitus secondary to chronic pancreatitis. 849 94

Immunogenetic examination comprising determination of erythrocyte antigens (ABO systems and resus-factor) and leukocytes (HLA system) using hemagglutination and compliment-dependent cytotoxicity, respectively, was performed for 138 patients with chronic recurrent pancreatitis, 52 patients with chronic pancreatitis and 456 healthy subjects. Analysis of relations between the above antigens, the disease risk, clinical and laboratory parameters, readings of ultrasound histogram and the efficacy of treatment helped discover not only provoking and protecting genes, but also some pathogenetic mechanisms involved in genetic predisposition. These findings may be used in the choice of treatment policy and to upgrade the significance of prognosis of principal forms of chronic pancreatitis.
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PMID:[Immunogenetic aspects of pathogenesis, prognosis and treatment of the main forms of chronic pancreatitis]. 899 7

132 chronic pancreatitis patients were studied for humoral immunity components and HLA antigens distribution. Antibodies to pancreatic tissue, insulin, o-DNA, d-DNA, n-DNA, ds-RNA were recognized in 44.5, 21.8, 41.8, 29.1, 20.9, 19.1% of chronic pancreatitis patients, respectively. Most pronounced immunological shifts occurred in aggravation of the disease. HLA-antigen typing was indicative of more frequent incidence in chronic pancreatitis patients of antigens HLA A1, B8, B27, Cw1 and less frequent occurrence of antigens A2, Cw4. The results evidence nonuniform etiology and pathogenesis of chronic pancreatitis.
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PMID:[Humoral immunity and the distribution of HLA antigens in patients with chronic pancreatitis]. 913 12


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