Clinical Significance of Helicobacter pylori Infection on Psoriasis Severity

Abstract

The aim of the study was to appraise the link between psoriasis and Helicobacter pylori, investigate the influence of H. pylori treatment on psoriasis severity, determine the cutoff value of haptoglobin as a psoriatic biomarker, and determine the most reliable predictor for psoriasis in patients with H. pylori. This study was carried out on 100 adult Saudi participants from the Security Forces Hospital (Riyadh, Kingdom of Saudi Arabia). All participants were allocated into 5 groups (20/group): controls (G1), psoriatic patients (G2), patients with H. pylori (G3), psoriatic patients with untreated H. pylori (G4), and psoriatic patients with treated H. pylori (G5). The study was approved by the ethics committee of Security Forces Hospital, Riyadh, Saudi Arabia. The psoriasis area and severity index (PASI) score, ¹³C-urea breath test (¹³C-UBT), C-reactive protein (CRP), haptoglobin, platelet P-selectin, cluster of differentiation 4/cluster of differentiation 8 (CD4/CD8) ratio, and lymphocyte percentages were recorded. The haptoglobin level was significantly elevated in psoriatic patients compared with G1. In G5, there was significant attenuation in the PASI score, P-selectin, CRP, CD4/CD8 ratio, and lymphocyte percentage compared with G4. There was a significant positive correlation between psoriasis severity and ¹³C-UBT. In addition, ¹³C-UBT and PASI scores were significantly positively correlated with CRP, platelet P-selectin, and percentage of lymphocytes. H. pylori plays a potential role in psoriasis pathogenesis. H. pylori treatment attenuates psoriasis severity. Haptoglobin could be utilized as a psoriatic biomarker with 1.95 g/L as the cutoff value. The most reliable predictor for psoriasis in infected patients with H. pylori is ¹³C-UBT.

Introduction

Psoriasis is one of the most common immune-mediated inflammatory disorders affecting the skin (Boehncke and Schon 2015). It affects ∼125 million people worldwide (International Federation of Psoriasis Associations 2015). Plaque psoriasis is the most common form that manifests as erythematous, gray or silvery white, dry scaly plaques (Kim and others 2015). Dermatologists assess clinical psoriasis severity using the psoriasis area and severity index (PASI) score, which is the gold standard for psoriatic patient classification regarding the severity and extension of the disease (Mesquita and others 2017).

Psoriasis is caused by a complex interplay between adaptive and innate immune responses and genetic and environmental factors. Abnormal differentiation of the epidermis, T cell-mediated keratinocyte proliferation, and dysregulated inflammation are the chief characteristics in its pathogenesis (Varricchi and others 2015; Yong and others 2018). The T helper 17 (Th17) cells secrete a number of inflammatory cytokines, including interleukin-17A (IL-17A), promoting both intralesional angiogenesis and keratinocyte proliferation. The IL-17-producing cluster of differentiation 4 (CD4⁺) T lymphocytes have various helper functions that stimulate the phagocytic capabilities of macrophages, the humoral immune response, and the cytotoxic function of cluster of differentiation 8 (CD8⁺) T lymphocytes (Schadler and others 2019).

Another mediator that may have a role in psoriasis pathogenesis is haptoglobin (Hp), which is a liver-secreted acute-phase protein. It is responsible for binding free hemoglobin and carrying it to the liver for breakdown and iron recycling. The Hp levels are significantly intensified through the acute-phase response of inflammation (Tian and others 2016). Hormonal changes, ultraviolet radiation, trauma, obesity, infections, and immune system changes can cause the development of psoriasis (Steinz and others 2014; El-Boghdady and others 2018).

It has been considered that Helicobacter pylori infection plays a significant role in several extraintestinal pathologies, including metabolic, autoimmune, hematological, cardiovascular, neurological, and skin diseases (Kutlubay and others 2014). This infection is a chronic gastrointestinal infection with a global prevalence of about 4.4 billion individuals (Hooi and others 2017) and about 28% in Saudi Arabia (Hanafi and Mohamed 2013). The H. pylori infection is usually symptomless, but because it is a common cause of peptic ulcer diseases, chronic gastritis, and gastric cancer, symptoms such as nausea, vomiting, and abdominal pain may be observed (Gold and others 2014). Numerous investigation methods are available for H. pylori infection diagnosis with both high specificity and sensitivity, such as the urea breath test (UBT). It is the most popular and accurate noninvasive test for H. pylori infection diagnosis (Garza-González and others 2014).

Significant local inflammation of the gastric mucosa, which could potentially produce a systemic effect through alteration of systemic inflammatory mediators, is the mechanism proposed by Yong and others (2018) of H. pylori infection causing extragastrointestinal conditions. Few researches have documented that H. pylori seropositivity is related to an elevated level of C-reactive protein (CRP), platelet activation factors, and ILs (De Melo and others 2014; Magen and Delgado 2014). This study was conducted to appraise the link between psoriasis and H. pylori infection, investigate the influence of H. pylori infection treatment on psoriasis severity, determine the cutoff value of haptoglobin as a biochemical marker of psoriasis, and determine the most reliable predictor for psoriasis in infected patients with H. pylori.

Subjects and Methods

Subjects

The current retrospective study was carried out in an adult Saudi population from the Security Forces Hospital (Riyadh, Kingdom of Saudi Arabia). One hundred participants were recruited according to inclusion and exclusion criteria. Participants were allocated into 5 groups of 20 subjects each:

G1: Control group.

G2: Psoriatic patients.

G3: Patients with H. pylori infection.

G4: Psoriatic patients with untreated H. pylori infection.

G5: Psoriatic patients with treated H. pylori infection.

The study was approved by the ethics committee of Security Forces Hospital. Gender, age, their current medication, and PASI score were recorded. However, the PASI score was calculated for all psoriatic patients on the basis of the percent area of skin involved and severity of 3 clinical signs (erythema, induration, and desquamation) on a 0–4 scale (Fredriksson and Pettersson 1978).

Treatment of H. pylori (duration: 7–14 days) included a proton pump inhibitor twice a day at a higher dose or esomeprazole 40 mg by mouth daily, amoxicillin 1 g by mouth bid, and clarithromycin 500 mg by mouth twice daily. The treatment of H. pylori was confirmed by ¹³C-UBT, which was done 6 weeks after treatment. Additionally, gastrointestinal biopsies were performed in some cases to confirm eradication of H. pylori after completion of treatment.

Treatment of psoriasis (according to psoriasis severity) included topical treatment with ± ultraviolet B phototherapy such as calcipotriol and betamethasone dipropionate, 50 μg and 0.5 mg/ointment, or tacrolimus 0.1%, 30-g tube ointment; systemic disease-modifying antirheumatic drugs (DMARDs) such as acitretin 10-mg tab or methotrexate tablet 2.5 mg and injection or cyclosporine 25- and 100-mg capsules; and systemic treatment (Biologics) such as tofacitinib 5-mg tablet or etanercept 25, 50 mg SQ, or ustekinumab 130 mg vial IV, 90 mg prefilled syringe SQ. The majority of patients treated with systemic therapy were males. In G5, all selected patients were treated with antipsoriasis and anti-H. pylori at the same time.

Inclusion criteria

Both genders

Adult Saudi participants

Psoriatic patients

Patients with H. pylori infection.

Exclusion criteria

Patients with other gastric diseases than H. pylori infection

Patients with other autoimmune disorders

Patients with other infections

Patients with inflammatory disease.

Data collection

Between 2014 and 2018, data were collected from medical records of candidate participants. Data on ¹³C-UBT, pancreatic amylase, haptoglobin, CRP, complement component C3 and C4, platelet P-selectin, CD4/CD8 ratio, and percentage of lymphocytes were recorded for all participants.

Statistical analyses

Analyses were carried out using Statistical Package for the Social Sciences (SPSS, V. 21.0). Data are expressed as mean ± standard deviation. Comparisons between different groups were performed using 1-way analysis of variance, followed by the post hoc Bonferroni test to compare individual groups. Pearson's correlation was used to evaluate correlations between the different parameters investigated. The values for sensitivity were plotted against 1-specificity using receiver operating characteristic (ROC) curves. By using a cutoff threshold for each psoriatic biomarker, the diagnostic test (positive versus negative) for psoriasis was defined. To predict psoriasis, the overall accuracy of a biomarker was defined as the average of the specificity and sensitivity. Statistical significance is indicated by P ≤ 0.05.

Results

Demographic characteristics and PASI score in different groups

Table 1 presents the demographic characteristics and PASI scores in different groups. There was no significant difference in age of patients between different groups. The score of PASI was statistically significantly increased in the group of psoriatic patients with untreated H. pylori infection compared with the psoriatic group. On the other hand, psoriatic patients with treated H. pylori infection showed a significant decrease in the PASI score compared with psoriatic patients with untreated H. pylori infection.

Table 1.

Demographic Characteristics of Patients and the Score of Psoriasis Area and Severity Index in Different Groups (n = 100)

Parameters	Groups
Parameters	G1	G2	G3	G4	G5
N	20	20	20	20	20
Age (years)	34 ± 5.42	35 ± 4.37	34 ± 2.40	35.4 ± 2.46	34.7 ± 6.17
Gender
Male	4 (20)	4 (20)	2 (10)	16 (80)	16 (80)
Female	16 (80)	16 (80)	18 (90)	4 (20)	4 (20)
PASI score	NA	33 ± 2.45	NA	43.9 ± 4.36^a	31.8 ± 7.32^b

Results are expressed as a number (percentage), mean ± SD. G1: control group. G3: patients with Helicobacter pylori infection. G5: psoriatic patients with treated H. pylori infection. P ≤ 0.05 was considered significant.

Significant difference from psoriatic patients (G2).

Significant difference from psoriatic patients with untreated H. pylori infection (G4).

N, number of subjects; NA, not applicable; PASI score, psoriasis area and severity index score; SD, standard deviation.

Biomarkers of H. pylori infection in different groups

Table 2 displays the results of biomarkers of H. pylori infection in all groups. The results showed that the levels of ¹³C-UBT in the group of psoriatic patients with untreated H. pylori infection were significantly increased compared with patients infected with H. pylori. However, psoriatic patients with treated H. pylori infection showed a statistically significant decrease in ¹³C-UBT levels compared with G3 and G4. The levels of pancreatic amylase were significantly elevated in groups 3, 4, and 5 compared with groups 1 and 2. Furthermore, psoriatic patients in the eliminated H. pylori infection group showed a significant attenuation in pancreatic amylase levels compared with patients with H. pylori infection and psoriatic patients with untreated H. pylori infection.

Table 2.

Biomarkers of Helicobacter pylori Infection in Different Groups (n = 100)

Parameters	Groups
Parameters	G1	G2	G3	G4	G5
¹³C-Urea breath test	Nil	Nil	17.6 ± 2.17	20.8 ± 2.04^c	4.2 ± 2.65^a,b
Pancreatic amylase (U/L)	16.0 ± 3.74	17.0 ± 3.74	34.0 ± 6.93^c,d	33.5 ± 1.23^c,d	28.0 ± 4.08^a –d

Results are expressed as mean ± SD. G5: psoriatic patients with treated H. pylori infection. P ≤ 0.05 was considered significant.

Significant difference from patients with H. pylori infection (G3).

Significant difference from psoriatic patients with untreated H. pylori infection (G4).

Significant difference from the control group (G1).

Significant difference from psoriatic patients (G2).

Psoriatic and inflammatory biomarkers in different groups

Table 3 presents the results for psoriatic and inflammatory biomarkers. The levels of haptoglobin statistically significantly declined in patients with H. pylori infection compared with G2. On the other hand, its levels were significantly higher in all psoriatic patients (G2, G4, and G5) compared with G1. In G5, after the treatment of H. pylori infection, the haptoglobin levels were significantly elevated compared with patients with H. pylori infection, but significantly diminished compared with psoriatic patients. The levels of CRP were significantly elevated in all groups compared with G1. In psoriatic patients infected with H. pylori, its levels were statistically significantly amplified compared with G2 and G3. On the other hand, the CRP levels were statistically significantly attenuated in psoriatic patients with treated H. pylori infection compared with G4.

Table 3.

Psoriatic and Inflammatory Biomarkers in Different Groups (n = 100)

Parameters	Groups
Parameters	G1	G2	G3	G4	G5
Haptoglobin (g/L)	0.4 ± 0.10	3.1 ± 0.86^a	0.3 ± 0.07^b	1.4 ± 0.43^a–c	2.4 ± 0.93^a–d
C-reactive protein (mg/L)	1.9 ± 0.33	23.8 ± 2.40^a	21.9 ± 2.88^a	37.8 ± 4.54^a –c	22.1 ± 2.38^a,d
Platelet P-selectin (ng/mL)	21.1 ± 1.48	119.8 ± 6.23^a	134.4 ± 3.48^a,b	141.8 ± 8.28^a,b	122.3 ± 10.07^a,c,d

Results are expressed as mean ± SD. G5: psoriatic patients with treated H. pylori infection. P ≤ 0.05 was considered significant.

Significant difference from the control group (G1).

Significant difference from psoriatic patients (G2).

Significant difference from patients with H. pylori infection (G3).

Significant difference from psoriatic patients with untreated H. pylori infection (G4).

Furthermore, the current data revealed that levels of platelet P-selectin were significantly higher in all groups than G1. In addition, platelet P-selectin levels in G3 and G4 were significantly higher than in psoriatic patients after treatment of H. pylori infection in G5.

Immunity-related biomarkers in different groups

With regard to C3, its level was higher in G2, G3, and G5 than in the control group. C4 levels were significantly elevated in all groups compared with G1 (Table 4). The CD4/CD8 ratio was significantly higher in G2, G4, and G5 than in G1. This ratio significantly diminished after treatment of H. pylori infection in G5 compared with G2 and G4. Finally, the lymphocyte percentages were statistically significantly elevated in G2, G3, and G4 compared with G1. In psoriatic patients with eliminated H. pylori infection, the lymphocyte percentages were significantly lower than that in both G2 and G4.

Table 4.

Immunity-Related Biomarkers in Different Groups (n = 100)

Parameters	Groups
Parameters	G1	G2	G3	G4	G5
C3 (g/L)	0.9 ± 0.08	1.3 ± 0.12^a	1.3 ± 0.28^a	1.2 ± 0.22	1.6 ± 0.40^a –c
C4 (g/L)	0.170 ± 0.043	0.398 ± 0.052^a	0.36 ± 0.063^a	0.418 ± 0.048^a	0.407 ± 0.129^a
CD4/CD8 ratio	1.9 ± 0.28	3.9 ± 0.63^a	2.0 ± 0.36^b	3.4 ± 0.67^a,d	2.6 ± 0.61^a –c
Lymphocytes (%)	17.7 ± 3.9	28.6 ± 2.52^a	23.1 ± 1.71^a,b	33.0 ± 6.53^a,d	20.7 ± 4.19^b,c

Results are expressed as mean ± SD. G5: psoriatic patients with treated H. pylori infection. P ≤ 0.05 was considered significant.

Significant difference from the control group (G1).

Significant difference from psoriatic patients (G2).

Significant difference from psoriatic patients with untreated H. pylori infection (G4).

Significant difference from patients with H. pylori infection (G3).

CD, cluster of differentiation.

Correlation of ¹³C-UBT and PASI score with other biomarkers

There was a significant positive correlation (r = 0.648, P ≤ 0.01) between psoriasis severity (PASI score) and H. pylori infection biomarker (¹³C-UBT). In addition, ¹³C-UBT and PASI scores were significantly positively correlated with CRP, platelet P-selectin, and percentage of lymphocytes in G4 and G5, as presented in Table 5.

Table 5.

Correlation of ¹³C-Urea Breath Test and Psoriasis Area and Severity Index Score with Other Biomarkers in G4 and G5

Biomarkers	¹³C-Urea breath test	C-reactive protein (mg/L)	Platelet P-selectin (ng/mL)	Lymphocytes (%)
¹³C-urea breath test	—	0.551^a	0.685^a	0.492^b
PASI score	0.648^a	0.710^a	0.461^b	0.416^b

Results are expressed as correlation coefficients (r).

P ≤ 0.01.

P ≤ 0.05.

Correlation between different biomarkers

A significant positive correlation (r = 0.423, P ≤ 0.05) between pancreatic amylase and PASI score was observed, as presented in Fig. 1a. However, Fig. 1b shows a significant negative correlation (r = −0.629, P ≤ 0.01) between ¹³C-UBT and haptoglobin in G4 and G5.

FIG. 1.

Correlations between the different biomarkers investigated in psoriatic patients with untreated Helicobacter pylori infection (G4) and psoriatic patients with treated H. pylori infection (G5). (a) Pancreatic amylase and PASI score. (b) ¹³C-UBT and haptoglobin. *P ≤ 0.05; **P ≤ 0.01. ¹³C-UBT, ¹³C-urea breath test; PASI, psoriasis area and severity index; r, correlation coefficient.

ROC analysis for haptoglobin, ¹³C-UBT, and pancreatic amylase

Regarding the ROC curve, the area under the curve (AUC) was 0.781 for haptoglobin. In addition, the best cutoff value for haptoglobin as a biochemical marker of psoriasis was 1.95 g/L. Furthermore, the AUC for ¹³C-UBT and pancreatic amylase was 0.920 and 0.843, respectively. Therefore, ¹³C-UBT is the most significant predictor for psoriasis in patients with H. pylori infection. The best cutoff values for ¹³C-UBT and pancreatic amylase were 18.5 and 30 μ/L, respectively (Fig. 2).

FIG. 2.

ROC curve for (a) haptoglobin, (b) ¹³C-UBT, and (c) pancreatic amylase. The arrow denotes the best cutoff point. AUC, area under the curve; ROC, receiver operating characteristic.

Discussion

Psoriasis, a systemic, chronic immune-mediated disorder, is characterized by abnormal differentiation of the epidermis and keratinocyte hyperproliferation as an outcome of a complex interplay between genetic, adaptive, and innate immune responses (Varricchi and others 2015). The results of the work by Hägg and others (2017) are in agreement with the current data, which showed that the PASI score was statistically significantly increased in the group of psoriatic patients with untreated H. pylori infection (80% males) compared with the psoriatic group (80% females), and the majority of patients treated with systemic therapy were males. Psoriasis care is affected by several factors, including gender. In a survey study, female psoriatic patients were 1.47 times more likely to seek self-care compared with males (Bhutani and others 2013).

Additionally, the present work revealed that CD4/CD8 ratios and percentages of lymphocytes were significantly higher in psoriatic patients (G2) and psoriatic patients with untreated/treated H. pylori infection (G4 and G5) than G1. The C3 and C4 levels increased in all groups compared with G1. This result was confirmed by a significant positive correlation between PASI scores and percentages of lymphocytes. Psoriasis induces a dysregulated inflammation mediated by tumor necrosis factor alpha (TNF-α) and dendritic and T cells. Dendritic cells produce IL-12 and IL-23 to stimulate IL-17-generating CD4⁺ T lymphocytes that have various helper functions that activate the phagocytic capabilities of macrophages, the humoral immune response, and the cytotoxic function of CD8⁺ T lymphocytes.

The CD8⁺ T cells may also play a crucial role in psoriasis pathogenesis by toxic chemokine production (Lowes and others 2014). The release of cytokines promotes intralesional angiogenesis, keratinocyte proliferation, and antigen-independent activation of T lymphocytes (Bartsch and others 2015). The present work is consistent with the observation of Rocha-Pereira and others (2004) who presented that C3 and C4 increased with the severity of psoriasis.

Furthermore, the present study recorded that the haptoglobin level was significantly increased in all psoriatic patients (G2, G4, and G5) compared with G1. The CRP level was significantly higher in all groups compared with the control group. In psoriatic patients with untreated H. pylori infection, its level statistically significantly increased compared with G2 and G3. Furthermore, results showed that the levels of platelet P-selectin were significantly increased in all groups compared with G1. These data were confirmed by a significant positive correlation of the PASI score with CRP and platelet P-selectin. This is in agreement with the work of Villanova and others (2013) who stated that unspecific inflammatory markers such as platelet P-selectin, CRP, and haptoglobin increased in psoriatic patients.

Platelet P-selectin expressed as a biomarker for cutaneous inflammation was also monitored in a study done by Chandrashekar and others (2015), in which 62 psoriatic patients and 62 controls were enrolled for estimating levels of P-selectin and CRP. They documented that the levels of P-selectin were significantly elevated in patients with psoriasis compared with controls. Furthermore, Rocha-Pereira and others (2004) observed increased inflammatory marker levels such as haptoglobin and CRP, which increased with the severity of psoriasis. These authors suggested that haptoglobin and CRP can be utilized as markers of psoriasis. A possible explanation for the increase in haptoglobin levels in psoriatic patients may be attributed to the increase in its levels during the acute-phase response of inflammation (Maresca and others 2016).

Numerous studies have investigated a link between exposure to factors such as ultraviolet radiation, trauma, irritative topical therapy, and infections (H. pylori infection, Streptococcus pyogenes, Staphylococcus aureus, viruses, and fungi) and the initiation and exacerbation of psoriasis (Onsun and others 2012). The current data showed that pancreatic amylase levels were significantly elevated in G3, G4, and G5 compared with G1 and G2. Furthermore, psoriatic patients in the eliminated H. pylori infection group showed a significant attenuation in pancreatic amylase levels compared with patients with H. pylori infection and psoriatic patients with untreated H. pylori infection. These data are consistent with results of the study by Abd El-Maksoud and others (2016) who found an increase in pancreatic amylase levels in H. pylori patients compared with controls. These results could be attributed to a pathophysiological implication of H. pylori infection on pancreas through a decrease in pancreatic blood flow, activation of leukocytes, and systemic inflammation (Bulajic and others 2014).

The ¹³C-UBT depends on the ability of H. pylori infection to degrade the absorbed ¹³C-urea into ammonia and CO₂ so that the ¹³CO₂ can be detected in the exhaled air (Ferwana and others 2015). In the presented results, the ¹³C-UBT level in the group of psoriatic patients with untreated H. pylori infection (G4) was significantly elevated than in patients with H. pylori infection (G3). In addition, psoriatic patients in the eliminated H. pylori infection group (G5) showed a statistically significant decrease in its level compared with G3 and G4. The haptoglobin level was statistically significantly decreased in patients infected with H. pylori compared with the psoriatic patient group. On the other hand, the haptoglobin level was significantly elevated in psoriatic patients with untreated H. pylori infection compared with patients with H. pylori infection, but significantly diminished compared with psoriatic patients. This infection scavenges heme compounds from the host environment and thus this decrease could be triggered by the hemolytic activity of H. pylori infection as haptoglobin levels become depleted in the presence of large amounts of free hemoglobin (Abd El-Maksoud and others 2016). This was also confirmed by the significant negative correlation observed between haptoglobin and ¹³C-UBT.

In psoriatic patients, after H. pylori infection treatment, there was a statistically significant attenuation in levels of platelet P-selectin and CRP, CD4/CD8 ratios, and lymphocyte percentages compared with psoriatic patients with untreated H. pylori infection. On the other hand, the haptoglobin level was significantly diminished in psoriatic patients with treated H. pylori infection compared with psoriatic patients. This result was approved by the significant positive correlation between the PASI score and each of the ¹³C-UBT and pancreatic amylase levels, reflecting the crucial role of H. pylori infection in psoriasis pathogenesis and severity through immunomodulation and inflammation.

The H. pylori infection has been considered to trigger a bacterial agent that colonizes the gastric mucosa and, in turn, induces an immune response by macrophages, lymphocytes, and neutrophils, inducing local and systemic inflammatory responses, and this can lead to extragastrointestinal conditions such as skin disease (Testerman and Morris 2014). The current study revealed the significant positive correlation between ¹³C-UBT and CRP and platelet P-selectin and percentage of lymphocytes, confirming the crucial role of H. pylori infection in immune system modulation and inflammation. The present data are in line with the work of Onsun and others (2012). They revealed that the score of PASI was significantly elevated in patients with H. pylori infection.

Therefore, the current work suggests a probable relationship between H. pylori infection and psoriasis. Moreover, the observed significant decline in the score of PASI in psoriatic patients with treated H. pylori infection compared with G4 suggests that H. pylori treatment may ameliorate the severity of psoriasis and enhance the effectiveness of psoriasis treatment.

Interestingly, patients treated for psoriasis and H. pylori together presented further rapid improvement in the skin disease compared with those treated for psoriasis only. Obviously, psoriasis was also improved in patients receiving only H. pylori treatment (Ali and Whitehead 2008; Onsun and others 2012), confirming the current data, which revealed that the CD4⁺/CD8⁺ ratio and lymphocyte % were lower in G5 (psoriatic patients with treated H. pylori) compared with G2, psoriatic patients.

The current research concluded that H. pylori infection has a potential role in psoriasis pathogenesis. The treatment of H. pylori infection ameliorates psoriasis severity (PASI score attenuation). Haptoglobin can be utilized as a psoriatic biomarker with 1.95 g/L as the cutoff value. The most reliable predictor for psoriasis in patients with H. pylori infection is ¹³C-UBT. Therefore, routine testing for H. pylori infection in psoriatic patients is recommended.

Footnotes

Author Disclosure Statement

No competing financial interests exist.

Funding Information

No funding was received.

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Clinical Significance of Helicobacter pylori Infection on Psoriasis Severity

Abstract

Introduction

Subjects and Methods

Subjects

Inclusion criteria

Exclusion criteria

Data collection

Statistical analyses

Results

Demographic characteristics and PASI score in different groups

Biomarkers of H. pylori infection in different groups

Psoriatic and inflammatory biomarkers in different groups

Immunity-related biomarkers in different groups

Correlation of 13C-UBT and PASI score with other biomarkers

Correlation between different biomarkers

ROC analysis for haptoglobin, 13C-UBT, and pancreatic amylase

Discussion

Footnotes

Author Disclosure Statement

Funding Information

References

Correlation of ¹³C-UBT and PASI score with other biomarkers

ROC analysis for haptoglobin, ¹³C-UBT, and pancreatic amylase