Psoriasis and helicobacter pylori

Introduction

Most studies indicate that once psoriasis appears as an early localized disease, it persists throughout life, manifesting itself at unpredic[Table - 1]ntervals.[1] Spontaneous remissions do occur with varying frequencies. Several factors are now .accepted, as of importance in provoking a fresh episode of psoriasis or in exacerbating pre-existing disease. Recently, it has been suggested that H. pylori infection of gastric mucosae may be one of the organisms capable of triggering psoriasis.[2]

Helicobacter pylori, a gram-negative curved or spiral bacterium discovered in 1983, resides in the gastric mucosa. Although symptomatic gastritis eventually develops in only 30% of infected persons, it is believed to be the major cause of chronic gastritis as well as gastric and duodenal ulcers.[3]

H. pylori infects 50% of the worlds population and at least 25% of the US population.[3] Socioeconomic status is believed to be the major risk factor for childhood acquisition of life long infection with H. pylori .[4] As the standard of living improves, the incidence of infection with H. pylori declines. In developing countries such as India, the prevalence rate is over 80% by age of 20 years.[5] Enzyme-linked immunosorbent assay (ELISA) tests used in these studies have sensitivity and specificity of 93 to 95%.[3] Charles in a study of 33 psoriatic patients found H. pylori antibodies in 9 (27%) patients only.

In our state, both acid peptic disease and psoriasis are common. Thus it was thought relevant to conduct the present study to determine if antibodies to H. pylori could be found in a significant number of patients with psoriasis but without known gastro intestinal complaints.

Materials and Methods

We studied a select group of 50 clinically typical psoriatic patients without any GIT complaints, who presented to the Department of Dermatology, SMHS Hospital, Srinagar. Healthy individuals without any gastrointestinal complaints were taken as controls. Patients taking antibiotics or medications for upper gastrointestinal problems were excluded from the study. Informed consent was obtained in all cases.

After obtaining a thorough history, a complete physical and dermatological examination was performed. Attention was given to the type of psoriasis and area of involvement. The "rule of nines" method was used for assessing the total area of involvement. Patients with surface areainvolvement of < 20% were categorized ′mild′, 20% to 40% as moderate and> 40% as severe psoriasis.

Besides routine investigations, H. pylori serology was done in both groups using ′UBIMAGIWELTM, enzyme immunoassay; It is microbial ELISA. The walls of the well are coated with purified Helicobacter pylori antigen.

The Ig G value of anti-Helicobacter pylori in each patient was obtained as follows:-

The test was considered valid when optical density (OD) value of reagent blank was less that 0.20, the O.D. value of calibrator was 0.60 o more and the Eu/ml (Enzyme units/ml) values o negative and positive control was within the rang printed on the labels. The test was considered negative when EU/MI was < 60, equivocal whet 30-40 and positive when more than 40.

The results were analyzed using chi square test.

Results

Among the study group of 50 psoriatic patients the distribution of sex was male 56% (28 / 50) and females 44% (22/50). The age range from 5-60 years. 29 (58) patients had ′mild′, 1 (36%) had ′moderate′ and 3 (6%) had ′severe psoriasis. 20 (40%) patients in the psoriatic group [Table - 1] and 5 (10%) patients in the control group [Table:2] demonstrated H. pylori antibodies. [Table:3] and [Table:4] show H. pylori serology in various types and severity of psoriaris.

Statistical analysis using chi-square test showed a significant difference (p< 0.05) in the H. pylori seropositivity between the two groups. These data support a causal role of H pylori in the poathogenesis of psoriasis.

Discussion

In the current study, 20 (40%), psoriatic patients and 5 (10%) patients of control group demonstrated H. pylori antibodies. Although the seropositivity of both the group is within the expected prevalence range, there is a statistically significant difference in the seropositivity of two groups. The low seropositivity in both the groups when compared to general population may be explained by the fact that we excluded patients with known upper gastrointestinal complaints from the study. Although our study supports a causal role of H. pylori in the pathogenesis of psoriasis, a large scale study is needed to confirm the findings.