Dear editor,
As mentioned in the article in question, the selected control group had 21 volunteers without skin diseases and without gastrointestinal symptoms.1 This group was composed of people with similar socioeconomic status as the patients and who were accompanying those patients during the visits or who had been attended at a neighboring outpatient clinic. We agree that our control group had a small number of participants because of the difficulty in getting healthy people willing to undergo blood collection without any material gain in return.
The methods for the diagnosis of Helicobacter pylori are divided into invasive and non-invasive. In our study, we used the Elisa serological test, a noninvasive method ideal for epidemiological studies, based on the identification of H. pylori-specific IgG antibodies in the patient's serum. However, the has some restrictions. It only detects host exposure to the bacterium, without diagnosing active infection (true infection) (Krogfelt et al., 2005).2 We chose this method due to its reduced cost and the low complexity of accomplishment in relation to other diagnostic methods. We believe that the patient's contact with H. pylori alone is sufficient to trigger the immunological cascade implicated in the pathogenesis of psoriasis. As in our study, Qayoom and Ahmad detected H. pylori antibodies in 40% of psoriasis patients and 10% of control subjects (healthy subjects without gastrointestinal complaints) and concluded that H. pylori plays a causal role in the pathogenesis of psoriasis.3 Similarly, Fathy et al. compared 20 plaque psoriasis patients with 20 healthy volunteers, matched for age and gender, and tested them for H. pilory antibodies using the Elisa test. The mean prevalence of seropositivity in psoriatic patients was significantly higher when compared to controls. Also, the high values correlated with the severity of the disease. They concluded that there is a link between H. pylori and psoriasis and that the bacterium may also influence the pathogenesis of the disease.4
Footnotes
Conflict of interest: None.
Work performed at Dermatology outpatient service at Universidade Federal de Uberlândia (UFU) - Uberlândia (MG), Brazil.
Financial support: None.
REFERENCES
- 1.Mesquita PM, Diogo-Filho A, Jorge MT, Berbert ALCV, Mantese SAO, Rodrigues JJ. Relação da soroprevalência do Helicobacter pylori com a psoríase e sua gravidade. An Bras Dermatol. 2017;92:52–57. [Google Scholar]
- 2.Krogfelt KA, Lehours P, Mégraud F. Diagnosis of Helicobacter pylori infection. Helicobacter. 2005;10:5–13. doi: 10.1111/j.1523-5378.2005.00341.x. [DOI] [PubMed] [Google Scholar]
- 3.Qayoom S, Ahmad QM. Psoriasis and Helicobacter pylori. Indian J Dermatol Venereol Leprol. 2003;69:133–134. [PubMed] [Google Scholar]
- 4.Fathy G, Said M, Abdel-Raheem SM, Sanad H. Helicobacter Pylori Infection: A possible predisposing factor in chronic plaque-type psoriasis. J Egypt Women Dermatol Soc. 2010;7:39–43. [Google Scholar]