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Role of Helicobacter pylori in common rosacea subtypes: A genotypic comparative study of Egyptian patients.

J Dermatol. 2012 Oct 5;

Authors: El-Khalawany M, Mahmoud A, Mosbeh AS, Abd Alsalam F, Ghonaim N, Abou-Bakr A

Helicobacter pylori was incriminated as an etiological factor of rosacea. However, there is still controversy about this association. We conducted a comparative study in order to assess the role of H. pylori in rosacea patients who had dyspeptic symptoms. The study included 68 patients and 54 controls. Screening for H. pylori was performed and positive cases were referred for gastric endoscopy. The inflammatory response and bacterial density were evaluated in gastric biopsy. H. pylori vacA alleles, cagA and iceA genotypes were assessed by polymerase chain reaction. We found that 49 rosacea (72%) and 25 controls (46.3%) were infected with H. pylori. Thirty-one rosacea cases were papulopustular (PPR) while 18 were erythematotelangiectatic (ETR). Gastric ulceration was higher in PPR cases (38.7%) than ETR (11.1%) and controls (12%). A significant inflammatory reaction was observed more in PPR cases (74.2%) compared with 44.4% in ETR (P = 0.04) and 44% in controls (P = 0.02). Analysis of H. pylori genotypes revealed that vacA s1m1 was more identified in PPR cases (54.8%) compared with 22.2% in ETR (P = 0.03) and 16% in controls (P = 0.003). There was a significant elevation of cagA/vacA s1m1 positivity in PPR cases. After the eradication regimen of H. pylori, a significant improvement (P < 0.05) was observed in 15 out of 27 PPR cases (55.6%) compared with three out of 17 ETR (17.6%). We concluded that H. pylori has a significant role in rosacea patients who had dyspeptic symptoms. The PPR type is more influenced by H. pylori and this is regarded as being because of certain virulent strains that increase the inflammatory response in gastric mucosa and also in cutaneous lesions.

PMID: 23039081 [PubMed - as supplied by publisher]

http://www.ncbi.nlm.nih.gov/PubMed/23039081?dopt=Abstract = URL to article

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