HELICOBACTER PYLORI AND DIABETES MELLITUS

HELICOBACTER PYLORI AND DIABETES MELLITUS

Authors: A. sUTA*, M. MOTOCU*, L. DONGOLO**, J. SZAKADATI**, C. BRISC*, L. FAUR*, V. PORUMB*,

*Faculty of Medicine and Pharmacy-University of Oradea

** Faculty of Medicine and Pharmacy-University of Budapesta (Semmelweis Egyetem Altalanos Orvostudomanyi Kar, I.Klinika)

Diabetes mellitus (DM) is one of the important causes of dyspepsia. Helicobacter pylori (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 hyperglycemia 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. 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. 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.[1] Delayed gastric emptying and antral dysmotility are important causes of dyspepsia in diabetes. The role of helicobacter pylori infection in diabetic dyspepsi 737j97h a 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 Clinical Emergency Hospital of Oradea and I.sz. Klinika Budapesta between May 2006 and Feb 2007 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 [2] 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 etiology 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 TABLE 2

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

TABLE 4

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 positive in 25 cases i.e. in 62.5% cases and H. pylori negative in 15 cases i.e. in 37.5% cases. Biopsy[3-4] 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

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.

TABLE 5 Glycosylated haemoglobin levels (GHb)

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.[5-6]

Similar dysrhythmias are observed in H. pylori infection. This myoelectrical change disappears on eradication of H. pylori infection and control of hyperglycaemia.[7-9] Because of ethical reasons, it was not possible to treat for either H. pylori or diabetes mellitus individually.

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.

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.

Hence the immune inflammatory responses observed during infection in diabetics with H. pylori indeed induce auto-immune mediated damage to gastric epithelium.

Gastroparesis in diabetes is quite common and it was confirmed by ultrasonographic study, peristaltic movements were slow. In our study two cases of this type was managed by domperidone.

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.

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