Indian Journal of Dermatology
: 2007  |  Volume : 52  |  Issue : 3  |  Page : 138--140

Association of Helicobacter pylori with lichen planus

Hamideh Moravvej1, Homa Hoseini1, Behrooz Barikbin1, Reza Malekzadeh2, Gita Meshkat Razavi1,  
1 Skin Research Center, Department of Dermatology, Shohada Hospital, Shaheed Beheshti Medical University, Shohada Hospital, Tehran, Iran
2 Digestive Disease Research Center, Department of Gastroentrology, Tehran University of Medical Science, Shariati Hospital, Tehran, Iran

Correspondence Address:
Gita Meshkat Razavi
Skin Research Center, Shaheed Beheshti Medical University, Shohada Hospital, Tehran 1989934148


Background : Lichen planus (LP) is a common idiopathic, inflammatory disorder that affects the skin, mucous membranes, nails and hair. Clinical observations and anecdotal reports have suggested a relationship between the exposure to a number of exogenous agents and the development of LP. One of the most important suggested bacterial etiologies is Helicobacter pylori (HP), that is one of the most common bacterial infections in the world, which is also reported to be common in Iran. Objective : This study was performed to evaluate the relation between HP and LP. Materials and Methods: A case control study was conducted with 80 patients with LP to find out a previous history of HP and 80 patients with other skin diseases were examined with urea breath test (UBT) as controls. Results: Sixty-six patients with LP and 49 patients from the controls had positive UBT. There was a significant difference about UBT positive result between these two groups. Conclusion: According to study, these results support a definitive etiological role for HP in LP.

How to cite this article:
Moravvej H, Hoseini H, Barikbin B, Malekzadeh R, Razavi GM. Association of Helicobacter pylori with lichen planus.Indian J Dermatol 2007;52:138-140

How to cite this URL:
Moravvej H, Hoseini H, Barikbin B, Malekzadeh R, Razavi GM. Association of Helicobacter pylori with lichen planus. Indian J Dermatol [serial online] 2007 [cited 2023 Sep 28 ];52:138-140
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Lichen planus (LP), the prototype of lichenoid dermatoses, is an idiopathic inflammatory disease of the skin and mucous membranes. It is characterized by pruritic violaceous papules and plaques with white lines on their surface that favor the extremities. Histologically, a dense band-like lymphocytic infiltrate is observed underlying an acanthotic epidermis with the destruction of basal cell layer and hypergranulosis. [1] Although its etiology and pathogenesis are not fully understood, Lichen planus has been associated with multiple disease processes and agents, such as viral and bacterial infections, autoimmune diseases, medications, vaccinations and dental restorative materials. The incidence of LP varies based on the geographic locale; cutaneous LP has been reported to affect 0.2-1% of the adult population in western countries. [2]

Helicobacter pylori (HP) [3] is one of the most important bacterial etiologies that has been suggested. It is one of the most common bacterial infections, affecting nearly half of the world's population. In addition to its roles in causing gastritis, gastric ulcer, duodenal ulcer and adenocarcinoma of stomach, it has been shown to cause nongastrointestinal disease. [4] This infection is reported to be very common in Iran; the rate up to 90% has been reported from some parts of the country. The rate of infection in the adult population of Tehran is approximately 70%. [5]

Recently, there have been some studies on the possible role of HP infection in the pathogenesis of various extragastric diseases involving dermatologic conditions. [6] The aim of this study was to assess the relation between HP infection and LP in the urban population in Tehran, Iran. Recently, there have been debates regarding the association between HP and various dermatologic conditions. [7],[8],[9],[10],[11]

 Materials and Methods

The study sample consisted of 80 consecutive patients with LP (33 men, 47 women; mean age: 40.9 years) and the control patients were taken from 80 patients with other skin diseases (35 men, 45 women; mean age: 42.7 years). A randomized sample was taken from the patients treated at the Departments of Dermatology between April 2003 and December 2006. Patients who had taken antibiotics within the last 40 days or H 2 blocker within the last 14 days or patients with various skin ulcerative diseases, peptic ulcer, previous treatment for HP or autoimmune diseases were not considered. Diagnosis was based on the typical clinical findings and compatible histopathology.

A questionnaire was used to interview the 80 patients with LP and the 80 patients in the control group with various skin diseases who were visiting the outpatient clinic (the only inclusion criterion was to match the sex and age distribution of both the groups). The data regarding ulcerative and autoimmune diseases were based on the medical history obtained from all the patients. Active HP infection was assessed using the 14C-urea breath test as described elsewhere. Patients were excluded if they had a comorbid condition, were younger than 18 years, pregnant or lactating. [12]

The statistical analysis was performed using SPSS software. The Chi-square test and student's t-test were used to examine the difference in HP prevalence among the different patient groups.


Data on the frequency of positive findings and titers in patients with LP and controls are summarized in the [Table 1]. The urea breath test (UBT) positivity rate (UBT titer greater than 50) in LP group was 66 (82.5%) out of 80 patients and in the control it was 49 (61.25%) out of 80 patients. The mean titer in patients with LP was 202.2 and in the control it was 105.1. There were marked differences between the patients with LP and those in the control. The difference between the patients with LP and the control were statistically significant ( P=0.0001).


LP is a unique, common inflammatory disorder that affects the skin, mucous membranes, nails and hair. Although its etiology and pathogenesis are not fully understood, LP has been associated with multiple disease processes and agents, such as viral and bacterial infections, autoimmune diseases and medications. Studies investigating a possible role for the bacterial infection in the etiology of LP were limited and have not supported a definitive etiologic role for HP. [1],[2],[3]

Helicobacter pylori infection can be diagnosed by noninvasive methods or by the endoscopic biopsy of the gastric mucosa; the selection of the appropriate test depends on the clinical settings. The noninvasive methods are the urea breath test, serologic test and stool antigen assays. The UBT relies on the abundant, HP-derived urease activity in the stomach; it qualitatively detects the active infection with sensitivity and specificity that is greater than 90%. The test is indicated for initial diagnosis of the infection and for the follow-up of eradication therapy. [13]

A high prevalence of HP in Iran lead us to assess the relationship between HP and LP. [14] Several studies have reported the relationship between HP and LP. Dauden E [7] conducted a study in which 61 patients with LP were subjected to UBT; 75.4% showed positive UBT with a mean titer of 35.46 and 74.1% of their controls showed positive UBT with a mean titer of 21.50, which shows no statistically significant differences between the patients and their controls. In another study by Riggio, [8] detected HP in recurrent aphthous and oral lichen planus (OLP) by polymerase chain reaction (PCR) in 28 patients with aphthous; 3 patients showed positive PCR for the DNA of HP and in 20 patients with OLP did not show positive PCR for the DNA of HP. Further, Shimayama [9] studied regarding the association of HP with oral mucosal ulcerative disorder: 12 cases of recurrent aphthous stomatitis (RAS), 3 cases of erosive LP and 7 cases of herpes simplex virus (HSV). Serum IgG antibodies were examined against HP in all cases. All the RAS and LP cases were culture negative for HP, while two cases of HSV were positive. The two culture-positive cases were also seropositive for the HP antigen. Vanio E [10] conducted a study on the peptic ulcer and HP in 78 patients with LP and 57 controls and obtained the difference between the patients with LP and controls; however, the difference was not statistically significant.

In our study, active HP infection was found in 82.5% of the patients with LP and 61.25% of the patients in control group; the difference was statistically significant. Our hypothesis is that HP could be at least the provoking factor behind LP, particularly as a chronic infecting agent maintaining LP. There is found evidence in favour of this hypothesis. However, the etiology of LP is probably multifactorial and the possibility still remains that HP may trigger LP in certain individuals. An autoimmune mechanism has been suggested in LP, and HP has been associated with autoimmune processes in susceptible patients. In our study, we found the evidently higher prevalence of HP in patients with LP than those in the control group.

Based on the results of our study, we consider the pathogenic role of HP in LP to be highly probable. The differences in the UBT titer of patients with LP vs that of controls and the high frequency and titer of the UBT positivity that depends on LP and not on the other skin diseases are probably related to the autoimmune processes. Further investigation for the eradication of HP in LP patients with positive UBT is required for a definite conclusion.


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