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HELICOBACTER PYLORI AND DIABETES MELLITUS
JG SALUJA*, MAHESH AJINKYA**, BHAVNA KHEMANI***, SANJEEV KHANNA+, RAJIV JAIN++
*Head; **Assoc. Prof. of Pathology; ***Chief Pathology Technician, CMPH Medical College and Mumbadevi Homoeopathic Hospital, Vileparle (W), Mumbai 400 056. +Hon. Gastroenterologist, Cooper Hospital. ++Hon. Gastro Surgeon, Maru Hos.
Diabetes mellitus is one of the important causes of dyspepsia. H. pylori is well established cause of many cases of Dyspepsia. The incidence of H. pylori is increased in diabetes mellitus. 40 patients between the age 25-65 years with diabetes and complaining of bloating and epigastric discomfort were included in our study. All the patients were subjected to blood test, Serological test for H. pylori and histopathology study. H. pylori infection is common in diabetics who are not having metabolically controlled hyperglycaemia and these are the individuals who are colonised by H. pylori in gastric antrum. Gastroparesis in diabetes is quite common and confirmed by ultrasonography, peristaltic movements were slow. In our study two cases of this type was managed by cisapride. Because of non competent immune response in diabetic patients the criteria of only doing immunoglobulin levels to diagnose H. pylori infection is not sufficient enough and so a combined biopsy and serological study is warranted in these cases. The conclusion from our study suggest that mainly the immune response in diabetes plays a major role for H. pylori infection.
INTRODUCTION
Diabetes mellitus is one of the important causes of dyspepsia.[1] Disordered GI motor function is now recognized as a major cause of DM Helicobacter pylori is well established cause of many cases of Dyspepsia. The incidence of helicobacter pylori is increased in diabetes mellitus.[2] Delayed gastric emptying and antral dysmotility are important causes of dyspepsia in diabetes. The role of helicobacter pylori infection in diabetic dyspepsia is mainly related to blood glucose concentration. Hyperglycaemia may induce the infection of H. pylori or the silent infection may get reactivated and produce symptoms of dyspepsia in diabetes.
The present study was undertaken to know the precise role of H. pylori in diabetic dyspepsia.
The prospective study was done in Pathology Dept. of Shri Mumbadevi Homoeopathic Hospital between May 1999 and Feb 2000 to know various causes of dyspepsia in diabetes and to determine the possible role of H. pylori infection. All diabetic patients suffering from dyspeptic symptoms were included in the work.
The mechanism of dyspepsia [3] are
a)intestinal motor abnormalities that have decreased antral and/or duodenal contractility in response to a meal. b)unco-ordinated and/or non-propagated duodeno-jejunal motor waves. These motor irregularities are often associated with delays in gastric emptying and therefore it has been understood that the presence of abnormal myoelectrical activity may play an important role in the aetiology of dyspepsia in the diabetes mellitus. Due to this there is recurrent pain or discomfort in epigastrium, bloating, distension, early satiety and nausea.
MATERIAL AND METHODS
40 patients between the age 25-65 yrs. with diabetes and complaining of bloating and epigastric discomfort were included in our study.
Patients with duodenal ulcer, gastrooesophageal reflux disease and gastric malignancy were excluded from the study.
All patients were subjected to blood glucose estimation - fasting and post prandial, glycosylated haemoglobin, Helicobacter pylori.
Gastrointestinal pathology was seen in 22 cases.
TABLE 1 Pathology No. of cases Percentage Gall stones 5 12.5% Fatty liver 4 10.0% Biliary sludge and Cholecystitis 7 17.5% Gastroparesis 2 5.0%
TABLE 2
For presence of Helicobacter pylori antibodiesNo. of cases IgM IgG Percentage 9 Positive Negative 22.7% 16 Negative Positive 40% 1 Positive Positive 2.5% 14 Negative Negative 35%
All the above cases were frankly diabetic and had Glycosylated Hb levels considerably high.
18 cases had no evidence of gastro-duodenal pathology.
Simultaneously Helicobacter pylori Antibodies were positive.
TABLE 3 Grade Gastritis Helicobacter pylori antibodies IgM IgG IgM+IgG Negative No. % No. % No. % No. % No. % I 9 22.5 9 22.5 — — — — — — II
16 40 — — 16 40 — — — — III 8 20 — — — — — — — — I and II 6 18 — — 6 18 — — — — II and III 1 2.5 — — — — 1 2.5 — —
TABLE 4 Mean plasma glucose value(mg/ml) No. of cases Percentage Less than 140 Nil 0.0% Between 140-160 7 17.5% Between 160-180 2 5.0% Between 180-200 Nil 0.0% Between 200-250 18 45.0% Between 250-300 7 17.5% Between 300-350 6 15.0% More than 350 Nil 0.0%
OGD scopy and antral biopsy were done in all cases.
The grading of gastritis (0-III) depended upon the severity of inflammation of the mucosa and the nature of predominant cell infiltration.
Staining with Giemsa stain revealed helicobacter pylori positivity in 25 cases i.e. in 62.5% cases and H. pylori negative in 15 cases i.e. in 37.5% cases.
Biopsy[4-5] were taken from antrum as well as from body of stomach, because exact history of treatment of dyspepsia was difficult to obtain. In untreated subjects, the gastric antrum is the best site of biopsy whereas biopsy from gastric body should be taken in partially or irrationally treated individual since the Helicobacter pylori later reside in the body of stomach.[6]
Plasma glucose level were carried out by GOD POD method, GHb by ion exchange resins, Helicobacter pylori antibodies by enzyme linked immunoabsorbent assay (ELISA). Helisal Index value below 0.9 EU/ml. considered negative. Greater than 1.1 EU/ml. considered positive.
The Results are calculated as follows:
Mean plasma glucose value (mg/dl)= Fasting + P.P
2
TABLE 5
Glycosylated haemoglobin levels (GHb)GHb levels in % age No. of cases % of cases Less than 7% 8 20.0% Between 7-8% 13 32.5% Between 8-9% 10 25.0% Between 9-10% 6 15.0% Between 10-11% 3 7.5%
TABLE 6
Helicobacter pylori antibodiesIgG IgM Both
IgG + IgMNegative No. of cases 16 9 1 14 % age 40% 22.5% 2.5% 35%
TABLE 7
On BiopsyNo. of cases Percentage Positive 25 62.5% Negative 15 37.5%
DISCUSSION
Jiaden, Chen et al studied electrogastrogram in diabetic subjects in whom nausea, vomiting and abdominal discomfort are common and revealed number of abnormalities including gastric dysrhythmias and diminished post prandial increase in electrogastrogram path.[7-8]
Similar dysrhythmias are observed in H. pylori infection. This myoelectrical change disappears on eradication of H. pylori infection and control of hyperglycaemia.[9-11] Because of ethical reasons, it was not possible to treat for either H. pylori or diabetes mellitus individually.
TABLE 8 No. of patients Percentage H. pylori antibodies
(IgM/IgG/IgM+IgG)Biopsy 21 52.5% Positive Positive 9 22.5% Negative Positive 10 25.0% Positive Negative
Fig.1: Digram of Helicobacter pylori biopsy and antibodies both
H. pylori infection is a common infection in diabetics who are not having metabolically controlled hyperglycaemia and these are individuals who are colonised by H. pylori infection in gastric antrum.[12]
Probably because of chemotactic factors such as tumour, necrotic factor (TNF), interleukins-IL1, IL2, IL8 are present in gastric epithelium. These do not confer protective immunity against H. pylori but induce a number of changes in the gastric epithelium that promote inflammation and epithelial damage. Thus leads to increased risk of aberrant repair giving the picture of gastric atrophy or epithelial cell metaplasia. These are subsets of helper T cells, TH1 and TH2 cells. TH1 cells normally boost cell mediation, immunity to cancer as well as intracellular infection. TH2 cells seem more important in generation of secretory immune response in the mucosa. Paradoxically, during infection with H. pylori, an extra-cellular infection TH1 cells predominate, whereas TH2 cells probably in diabetes may be virtually absent which may account for the persistence of infection. TH1 cell produce cytokines that promote inflammation induce auto-antibody formation and cell mediated damage to epithelium. [13-14]
Hence the immune inflammatory responses observed during infection in diabetics with H. pylori indeed induce auto-immune mediated damage to gastric epithelium.
H. pylori infection does not alter the extent of gastro-intestinal injury in patients consuming NSAID. H. pylori possibly prevent the decrease in mucosal prostaglandin levels which is pathway of NSAID induced gastroduodenal injury. [15] As diabetics are also high consumers of NSAID for various reasons (e.g. Osteoarthritis etc.), this statement assumes greater relevance.
In our study the next important cause of dyspepsia was Cholelithiasis fatty liver.[16]
Gastroparesis in diabetes is quite common and it was confirmed by ultrasonographic study, peristaltic movements were slow.[17] In our study two cases of this type was managed by cisapride.
Because of non competent immune response in diabetic patients the criteria of only doing immunoglobulin level to diagnose H. pylori infection is not sufficient enough and so a combined biopsy and serological study is warranted in these cases.
The conclusion from above study suggests that the immune response in diabetes plays a major role for Helicobacter pylori infection.
There are few clinical study observations that in spite of normal immune competence the H. pylori is persistent in diabetes. This warrants further detailed study of H. pylori in relation to immune system and mental behaviour of diabetic patients.
ACKNOWLEDGEMENT
We sincerely thank Dr. SK Goel, Dean of CMPH Medical College and Superintendent of Mumbadevi Homoeopathic Hospital for giving permission to publish the Data.
REFERENCES
1.Chen JDZ, et al. American Journal of Gastroenterology 1994; 22 : 423-31.
2.K McQuid. Dyspepsia in text book of Gastroenterology Sleissenger and Fordtran eds WB Saunder Company 6th edition. 1998; 1 : 105-17.
3. Tally NJ. A critique of therapeutic trials in Helicobacter pylori infection as a cause of gastritis, duodenal ulcer dyspepsia. A systemic overview. Can Medical Association Journal 1994; 150-77.
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5.Kosunen TM, et al. Diagnostic value of decreasing IgG, IgA, IgM antibody titres after eradication of Helicobacter pylori. Lancet 1992; 339 : 893-5.
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8.Jiaden Chen, Richard W. McCallum Current status and future development of Electrogastrogram motility. Clinical prescriptives in Gastroenterology 1998; 5 (issue 2) : 15-18.
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12.Sharma MP. The pathogenesis of Helicobacter pylori induced peptic ulcer Mediwave. 1999; 17-20.
13.Fuachere JL, et al. Immunological Aspects etc., Curr opin Gastroenterology 1995; 11 : 12-34.
14.Shumoyama T. Crabtree, Bacterial factors and immune pathogenesis in H. pylori infection. Gut 1998; 43 (Suppl 1) : 52-55.
15.Hudson N. Balsitis effect of H. pylori colonization on gastric mucosa eicasonoid synthesis in patients taking NSAIDs. Gut 1993; 34 : 748-51.
16.Thirumalachri KS, Venkatshwaria K. Dyspepsia in Diabetes - Endoscopic and Ultrasound study NOVO Nordisk Diabetes update proceeding. 1999; 279-82.
17.Giuseppe Riezzo, et al. Gastric emptying and Myoelectrical activity in children with non ulcer dyspepsia. Motility Vol. 5 4-7. Clinical Prescriptives in Gastroenterology.
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