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Year : 2021  |  Volume : 34  |  Issue : 1  |  Page : 71-75

Helicobacter pylori infection in the palm and sole of psoriatic patients

1 Department of Dermatology, Andrology and STDs, Faculty of Medicine, Menoufia University, Menoufia, Egypt
2 Department of Medical Biochemistry and Molecular Biology, Faculty of Medicine, Menoufia University, Menoufia, Egypt
3 Dermatology, Andrology and STDs, Menoufia Health Sector, Menoufia, Egypt

Date of Submission18-Aug-2019
Date of Decision30-Sep-2019
Date of Acceptance07-Oct-2019
Date of Web Publication27-Mar-2021

Correspondence Address:
Asmaa M Abousaeida
Shiben El-Kom, Menoufia Governorate
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/mmj.mmj_246_19

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To clarify the role of Helicobacter pylori infection in psoriatic patients with palm and sole affection
Psoriasis is a chronic inflammatory disease that affects 2–3% of the population worldwide. H. pylori infection has been implicated in the pathogenesis of various skin diseases.
Patients and methods
This case–control study was conducted on 40 patients with psoriasis vulgaris and 40 age-matched and sex-matched healthy individuals. All patients were subjected to history taking and complete medical examination. Serum levels of anti-H. pylori immunoglobulin G were measured by enzyme-linked immunosorbent assay technique. Serum levels of anti-H. pylori immunoglobulin G were statistically analyzed in relation to psoriasis area and severity index score.
H. pylori infection was more prevalent among patients who did not manifest palm and sole affection. However, 50% of palm-affected and sole-affected patients were positive for H. pylori infection (P = 0.02).
H. pylori may play a significant role in the development of palmoplantar psoriasis and may provide important clues to assist in the development of new therapeutic strategies for palmoplantar psoriatic patients through its eradication.

Keywords: Helicobacter pylori, palm and sole affection, psoriasis

How to cite this article:
Marae AH, Shehata WA, Azmy R, Abousaeida AM. Helicobacter pylori infection in the palm and sole of psoriatic patients. Menoufia Med J 2021;34:71-5

How to cite this URL:
Marae AH, Shehata WA, Azmy R, Abousaeida AM. Helicobacter pylori infection in the palm and sole of psoriatic patients. Menoufia Med J [serial online] 2021 [cited 2021 Dec 7];34:71-5. Available from: http://www.mmj.eg.net/text.asp?2021/34/1/71/312031

  Introduction Top

Psoriasis is a chronic inflammatory disorder that has a profound impact on a patient's well-being. It is estimated to affect up to 2% of the population worldwide [1]. Psoriasis is an autoimmune skin disease characterized by T-cell-mediated responses most likely a Th1/Th17-induced inflammatory response [2], leading to hyperkeratosis and parakeratosis [3]. It is believed to be triggered by a combination of genetic, epigenetic, and environmental influences and its genetic diversity and epigenetic modifications can be influenced by environmental factors [4]. Environmental factors including smoking, trauma, stressful life events, obesity, diet, drugs, and infections with strong evidence exist for the induction of guttate psoriasis by a preceding tonsillar Streptococcus pyogenes infection, whereas disease exacerbation has been linked with skin and/or gut colonization by Staphylococcus aureus, Malassezia, and Candida albicans [5]. Helicobacter pylori is a microaerophilic, flagellated, curved, Gram-negative bacterium that selectively colonizes the human stomach. Its infection is widespread throughout the world, about 50% of the global human population; with 80% in developing countries and 20–50% in industrialized countries. It is the major cause of gastritis and plays a key role in the development of peptic ulcer and is a risk factor for gastric carcinoma [6]. Several studies have pointed to a possible role of H. pylori infection in the pathogenesis of various skin diseases including chronic urticaria, lichen planus, rosacea, atopic dermatitis, Henoch–Schonlein purpura, recurrent aphthous stomatitis, Sweet's syndrome, Sjögren's syndrome, systemic sclerosis, and alopecia areata [7]. The role of H. pylori in the pathogenesis of extradigestive manifestations is based on the fact that local inflammation caused by the bacterium has systemic effects. The bacterium not only colonizes the gastric mucosa but induces a strong inflammatory response with the release of several cytotoxic substances [8]. Gastric infection with H. pylori is a chronic process that can last for decades and persistent infection induces chronic inflammation and an immune response that can cause lesions both locally and remotely [9]. H. pylori toxins can act as superantigens and thus mediate inflammatory skin lesions that consist predominantly of activated T cells and monocytes. Superantigens bind directly, without antigen processing, to constitutively expressed human leukocyte antigen-DR molecules on professional antigen-presenting cells, such as macrophages or dendritic cells, as well as to cytokine-induced human leukocyte antigen-DR molecules on nonprofessional antigen-presenting cells, such as keratinocytes [10]. H. pylori was shown to induce microvascular dysfunction by interstitial and intravascular cell to cell interactions [11], and H. pylori infection may be significantly associated with increased levels of fibrinogen [12]. Furthermore, it has been shown that platelet activation and aggregation contribute to microvascular dysfunction and inflammatory-cell recruitment associated with H. pylori infection [13]. The aim of this study was to clarify the role of H. pylori infection in psoriatic patients with palm and sole affection.

  Patients and methods Top

The study was approved by the Ethics Committee of Menoufia Faculty of Medicine; and written prepared consent with justification about the reason, methods, results, and complications was obtained from each participant. This case–control study was conducted at the Dermatology, Andrology, and Sexually transmitted diseases and Medical Biochemistry Departments of Faculty of Medicine, Menoufia University. Forty patients with psoriasis vulgaris with variable degrees of severity and 40 age-matched and sex-matched healthy controls were included in this study.

Inclusion criteria that included patients with psoriasis vulgaris of both sexes did not receive any topical (2 weeks) treatment or systemic (3 months) treatment for psoriasis prior to the study initiation.

Exclusion criteria included patients with other dermatological diseases except psoriasis vulgaris, patients with autoimmune diseases as systemic lupus erythematosus, patients with inflammatory bowel diseases, patients with chronic diseases as chronic renal failure, and patients having infectious conditions at the time of blood sampling such as bacterial infections.

Patients were assessed through full history taking including: personal history, detailed history of psoriasis regarding onset, course and duration of psoriasis, and family history of psoriasis. Complete general examination: detailed dermatological examination for assessment of distribution of psoriatic lesions, scalp affection, nail involvement, joint affection, palm and sole affection, and itching and assessment of psoriasis severity using psoriasis area and severity index (PASI) score [14]. In PASI score, the body is divided into four sections: head (H), arms (A), trunk (T), and legs (L). Each of these areas is scored by itself, and then the four scores are combined into the final PASI score. In each of these areas, the fraction of the total surface area affected was graded on a 0–6 scale where grade 0: 0% of involved area, grade 1: less than 10% of involved area, grade 2: 10–29% of involved area, grade 3: 30–49% of involved area, grade 4: 50–69% of involved area, grade 5: 70–89% of involved area, and grade 6: 90–100% of involved area. For each of the four areas are entered into the formula: 0.1(Eh+Ih+Dh) Ah+0.2(Eu+Iu+Du) Au+0.3(Et+It+Dt) At+0.4(El+Il+Dl) Al to calculate a score from 0 to 72 [15].

Severe psoriasis was defined by a PASI score above 15, intermediate by a PASI between 5 and 15, and mild by a PASI below 5 [16]. Two milliliters of venous blood was withdrawn from every patient under complete aseptic condition; then transferred into a plain tube, centrifuged for 10 min at 4000 rpm using 80-1 Electric Centrifuge from Jiangsu Jinyi Instrument Technology Company (Shanghai, China). The serum obtained was kept frozen at − 20°C till determination of anti-H. pylori immunoglobulin G (IgG) levels which were assayed using the Novalisa Kit, purchased from NovaTec Immunodiagnostica Company (Dietzenbach, Germany) [17].

Statistical analysis

The gathered data were structured, tabulated, and statistically analyzed using a personal computer with the statistical package of social sciences, version 20, for Windows (SPSS Inc., Chicago, Illinois, USA) and MedCalc 13 for Windows (MedCalc Software BVBA, Ostend, Belgium), where the following statistics were applied: Student's t test was used to assess the difference between the studied parameters in the two groups: Mann–Whitney U test and Pearson's correlation (r) were used to evaluate the relation between the studied parameters in the same group and probability. P value is considered to be statistically significant if less than 0.05.

  Results Top

Clinical data of cases and controls are shown in [Table 1]. Among the studied 40 cases, there was 10 cases presented with palmoplantar psoriasis (PPP), half of them were positive to H. pylori infection and this result was statistically significant (P = 0.02) [Table 2] and [Figure 1].
Table 1: Age and sex among cases and controls (n=80)

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Table 2: Relation between prevalence of Helicobacter pylori infection and palm and sole affection in cases (n=40)

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Figure 1: Relation between anti-Helicobacter pylori immunoglobulin G titer and palm and sole affection.

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In palm-affected and sole-affected patients the titer of anti-H. pylori IgG levels was 32.1 ± 27 as a mean ± SD value while in palm and sole free patients mean ± SD value was 45.5 ± 20.5 but this difference was statistically insignificant (P = 0.1) [Table 3].
Table 3: Relation between the mean of anti-Helicobacter pylori immunoglobulin G titer and palm and sole affection in the studied psoriatic patients

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Also, there was a significant relation between means of anti-H. pylori IgG titer nail involvement (P = 0.05) [Table 4] and [Figure 2].
Table 4: Relation between the mean of anti-Helicobacter pylori immunoglobulin G titer and nail involvement in the studied psoriatic patients

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Figure 2: Relation between the mean of anti-Helicobacter pylori immunoglobulin G titer and nail involvement in the studied cases.

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  Discussion Top

Psoriasis is a chronic, noncontagious, inflammatory disease that affects skin and joints. In the skin, it is characterized by erythematous-squamous plaques, affecting mainly extensor surfaces of the limbs and scalp [18]. H. pylori infection has been suggested as a culprit of various extragastrointestinal disorders. It is debatable whether H. pylori infection exacerbates or triggers the pathogenesis of psoriasis [19]. H. pylori causes a chronic low level inflammation of the stomach lining and is strongly linked to the development of duodenal and gastric ulcers as well as gastric cancer [20]. H. pylori could conceivably produce effects elsewhere by altering the levels of systemic inflammatory mediators [21]. Although the infection is noninvasive, it triggers a marked local inflammatory response and a systemic immune response [22]. Epidemiological and experimental data point to a strong relation of H. pylori infection on the development of many extragastric diseases; H. pylori antigens activate cross-reactive T cells and induce the production of autoantibodies [23]. H. pylori might be a triggering factor in psoriasis. Prolonged interaction between the bacterium and host immune mechanisms makes H. pylori a possible infectious agent for triggering autoimmunity [9]. In the current study, H. pylori infection was less prevalent among patients who manifested palm and sole affection (87%) in palm and sole free patients versus (50%) in patients with palm and sole affection (P = 0.02). This may be attributable to the low number of patients who presented with palm and sole affection among current sample size [10 (25%) cases]. PPP is a clinical variant of psoriasis that affects the palms of the hands and the soles of the feet present in 3–4% of psoriatic patients and has multiple features as hyperkeratotic plaques, cracks, and small pustules [24]. Hübner and Tenbaum [25] described a case of a 35-year old man, presenting symptoms consistent with PPP and the presence of H. pylori infection was confirmed by 13C-urea breath test. Complete remission of lesions in palms and soles was obtained after eradication of H. pylori with amoxicillin (1 g twice daily) and clarithromycin (500 mg twice daily) for 7 days, in association with omeprazole (20 mg twice daily) for 4 weeks. They concluded that PPP may be an abnormal immunologic reaction to a variety of bacterial or viral infections and H. pylori infection could have triggered PPP in their patient. Another study was done by Rodriguez et al. [26] on a 38-year old nonsmoking woman, with a history of dyspepsia admitted to a hospital with 3 years of an evolving pustular eruption on her palms and soles. Several treatments, including systemic and topical corticosteroids, dapsone and colchicine, had been ineffective. 13C-urea breath test was performed and the presence of H. pylori was confirmed and a punch biopsy from the palmar pustules revealed intraepidermal pustule formation, with a subcorneal neutrophilic infiltrate, compatible with PPP. Amoxicillin (1 g, twice daily) and clarithromycin (500 mg, twice daily) were given for 8 days, in association with omeprazole (20 mg, once daily) for 1 month. Cutaneous lesions disappeared within 3 weeks. Four weeks after treatment a new 13C-urea breath test was repeated and eradication of H. pylori could be confirmed. Four years after this treatment, the clinical signs of PPP had not returned. They concluded that PPP may be an abnormal immunologic reaction to a variety of infections and H. pylori infection could have triggered PPP in their patient. In the current study, there was also a statistically significant relation between the mean of anti-H. pylori IgG and nail affection (P = 0.05). It may be attributed to the fact that nail psoriasis is often associated with an inflammation at the insertion points of tendons and ligaments giving rise to enthesitis. Thus, nail lesions were believed to represent an abnormal response to tissue stressing of the integrated nail joint apparatus rather than being due to autoimmunity. The nail and joint disease may be linked to tissue-specific factors including tissue biochemical stressing and microtrauma that lead to the activation of aberrant innate immune responses and thus H. pylori IgG titer can be used as a predictor of nail affection in psoriatic patients [27].

  Conclusion Top

H. pylori may play a significant role in the development of PPP and may provide important clues to assist in the development of new therapeutic strategies for PPP patients through its eradication.

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Conflicts of interest

There are no conflicts of interest.

  References Top

Langham S, Langham J, Goertz HP, Ratcliffe M. Large-scale, prospective, observational studies in patients with psoriasis and psoriatic arthritis: a systemic and critical review. BMC Med Res Methodol 2011; 11:32.  Back to cited text no. 1
Coimbra S, Figueiredo A, Castro E, Rocha-Pereira P, Santos-Silva A. The roles of cells and cytokines in the pathogenesis of psoriasis. Int J Dermatol 2012; 51:389–398.  Back to cited text no. 2
Nestle FO, Kaplan DH, Barker J. Psoraisis. N Engl J Med 2009; 361:496–509.  Back to cited text no. 3
Seldin MF. The genetics of human autoimmune disease: a perspective on progress in the field and future directions. J Autoimmun 2015; 64:1–12.  Back to cited text no. 4
Fry L, Baker BS. Triggering psoriasis: the role of infections and medications. Clin Dermatol 2007; 25:606–615.  Back to cited text no. 5
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.  Back to cited text no. 6
Gravina A, Federico A, Ruocco E, Schiavo A, Masarone M, Tuccillo C, et al. Helicobacter pylori infection but not small intestinal bacterial overgrowth may play a pathogenic role in rosacea. United European Gastroenterol J 2015; 3:17–24.  Back to cited text no. 7
Testerman TL, Morris J. An updated view of Helicobacter pylori pathogenesis, diagnosis and treatment. World J Gastroentrol 2014; 20:12781–12808.  Back to cited text no. 8
Magen E, Delgado JS. Helicobacter pylori and skin autoimmune diseases. World J Gastroenterol 2014; 20:1510–1516.  Back to cited text no. 9
Leung DY, Hauk P, Strrickland I, Travers JB, Norris DA. The role of superantigens in human diseases: therapeutic implications for the treatment of skin diseases. Br J Dermatol 1998; 53:17–29.  Back to cited text no. 10
Kurose I, Granger DN, Evans DJ Jr, Doloros G, Graham DY, Masayuki DC, et al. Helicobacter pylori-induced microvascular protein leakage in rats: role of neutrophils, mast cells, and platelets. Gastroenterology 1994; 107:70–79.  Back to cited text no. 11
Zito F, Di Castelnuovo A, D'Orazio A, Negrini R, De Lucia D, Donati MB, et al. Helicobacer pylori infection and the risk of myocardial infarction: role of fibrinogen and its genetic control. Thromb Haemost 1999; 82:14–18.  Back to cited text no. 12
Elizalde JI, Gomez J, Panes J, Lozano M, Casadevall M, Ramirez J, et al. Platelet activation in mice and human Helicobacter pylori infection. J Clin Invest 1997; 100:996–1005.  Back to cited text no. 13
Langley RG, Ellis CN. Evaluating psoriasis with psoriasis area and severity index, psoriasis global assessment, and lattice system physician's global assessment. J Am Acad Dermatol 2004; 51:563–569.  Back to cited text no. 14
Jacobson CC, Kimball AB. Rethinking the psoriasis area and severity index: the impact of area should be increased. Br J Dermatol 2004; 151:381–387.  Back to cited text no. 15
Bergmann C, Strohbuecker L, Lotfi R, Sucker A, Joosten I, Koenen H, et al. High mobility group bo×1 is increased in the sera of psoriatic patients with disease progression. J Eur Acad Dermatol Venereol 2016; 30:435–441.  Back to cited text no. 16
Marshall BJ, Gilman RH. Helicobacter pylori infections. In Richard LG, David HW, Peter FW, eds. Tropical infectious diseases: principles, pathogens and practice. 2nd ed. Philadelphia: Churchill Livingstone; 2006. 300–309.  Back to cited text no. 17
Mesquita PM, Diogo AF, Jorge MT, Berbert AL, Mantese SA, Rodrigues JJ. Relationship of Helicobacter pylori seroprevalence with the occurrence and severity of psoriasis. An Bras Dermatol 2017; 92:52–57.  Back to cited text no. 18
Yong WC, Upala S, Sanguankeo A. Association between psoriasis and Helicobacter pylori infection: a systematic review and meta-analysis. Indian J Dermatol 2018; 63:193–200.  Back to cited text no. 19
Blaser MJ. Who are we? Indigenous microbes and the ecology of human diseases. EMBO Rep 2006; 7:956–960.  Back to cited text no. 20
Gasbarrini A, Franceschi F, Gasbarrini G, Pola P. Extraintestinal pathology associated with Helicobacter infection. Eur J Gastroenterol Hepatol 1997; 9:231–233.  Back to cited text no. 21
Mobley HL. H. pylori factors associated with disease development. Gastroenterology 1997; 113:21–28.  Back to cited text no. 22
Ram M, Barzilai O, Shapira Y, Anaya JM, Tincani A, Stojanovich L, et al. Helicobacter pylori serology in autoimmune diseases- fact or fiction? Clin Chem Lab Med 2013; 51:1075–1082.  Back to cited text no. 23
Huizen J. What's to know about palmoplantar psoriasis? Medical News Today; 2018. Available at: www.medicalnewstoday.com/articles/314742.php. [Last accessed on 2019 Jul 17].  Back to cited text no. 24
Hübner A, Tenbaum S. Complete remission of palmoplantar psoriasis through Helicobacter pylori eradication: a case report. Clin Exp Dermatol 2008; 33:339–340.  Back to cited text no. 25
Rodriguez M, Cabrera A, Bustinduy M, Guimera F, Dorta S, Escoda M, et al. Palmoplantar pustulosis associated with gastric Helicobacter pylori infection. Clin Exp Dermatol 2002; 27:720–720.  Back to cited text no. 26
McGonagle D, Tan AL, Benjamin M. The nail as a musculoskeletal appendage-implications for an improved understanding of the link between psoriasis and arthritis. Dermatology 2009; 218:97–102.  Back to cited text no. 27


  [Figure 1], [Figure 2]

  [Table 1], [Table 2], [Table 3], [Table 4]


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