7 Signs Your Skin Is Being Driven by H. Pylori
Helicobacter pylori (H. pylori) is a gram-negative, microaerophilic bacterium that colonises the gastric epithelium of approximately half the global population, yet in clinical dermatology it remains a vastly underinvestigated driver. When H. pylori-associated gastritis is present, it does not merely affect the stomach in isolation. It initiates a coordinated cascade of systemic inflammation, impairs absorption of the micronutrients that underpin epidermal barrier integrity, dysregulates the hypothalamic-pituitary-adrenal axis, and alters cutaneous immune surveillance — all of which produce skin outputs that appear unrelated to the gut. Acne, rosacea, seborrheic dermatitis, and chronic urticaria presenting without resolution despite topical or antibiotic cycles are frequently the visible signs of an active gastrointestinal dysbiosis that has never been formally investigated.
Understanding why H. pylori gastritis, acne, rosacea, and dermatitis so frequently co-occur requires moving beyond organ-system silos. The bacterium produces virulence factors — most critically cytotoxin-associated gene A (CagA) protein and vacuolating cytotoxin A (VacA) — that stimulate systemic cytokine release, degrade the gastric mucosal barrier, impair hydrochloric acid secretion, and ultimately reduce the bioavailability of zinc, iron, B12, and folate. Each of these deficiencies has a documented, mechanistically distinct impact at the level of the pilosebaceous unit, the dermal extracellular matrix, and the cutaneous innate immune response. If your patient has persistently relapsing inflammatory skin conditions and no one has investigated their gastric function, they have not yet received a complete clinical workup.
What Is H. Pylori Gastritis?
Helicobacter pylori is classified by the World Health Organisation as a Group 1 carcinogen and is the primary causative agent of chronic active gastritis, peptic ulcer disease, and gastric adenocarcinoma. Colonisation occurs predominantly in the antrum of the stomach, where the bacterium uses flagella for motility and produces urease — an enzyme that hydrolyses urea into ammonia and carbon dioxide, neutralising gastric acid locally and allowing survival in an otherwise hostile acidic environment. Chronic infection induces a persistent but ineffective inflammatory response: neutrophils and monocytes are recruited but fail to clear the organism, resulting in sustained mucosal damage and progressive atrophy of acid-secreting parietal cells.
Clinically, H. pylori gastritis is classified as either non-atrophic (antrum-predominant, associated with higher acid output and peptic ulceration) or atrophic (corpus-predominant, associated with acid hyposecretion, intestinal metaplasia, and the highest risk of malignant transformation). From a dermatological standpoint, the atrophic phenotype is of particular significance because hypochlorhydria directly impairs the solubilisation of non-haem iron, the ionisation of zinc, and the dissociation of vitamin B12 from food proteins — each of which is critical to epidermal homeostasis. The gut microbiome is also profoundly altered, with H. pylori colonisation associated with reductions in Lactobacillus and Bifidobacterium species and an increase in facultative anaerobes that further compromise mucosal integrity.
The Cellular Mechanism: How H. Pylori Drives Skin Inflammation
Step 1 — Colonisation & Virulence Factor Release: H. pylori adheres to gastric epithelial cells via outer membrane proteins (BabA, SabA). CagA protein is injected into host cells via a type IV secretion system, activating NF-κB and MAPK pathways. VacA induces mitochondrial dysfunction and vacuolation of epithelial cells, further disrupting mucosal integrity.
Step 2 — Systemic Cytokine Elevation: Activated gastric macrophages and dendritic cells release IL-1β, IL-6, IL-8, IL-12, and TNF-α into systemic circulation. IL-6 drives hepatic acute-phase protein synthesis (CRP, fibrinogen) and upregulates sebaceous gland androgen receptor sensitivity. TNF-α directly increases epidermal keratinocyte apoptosis and disrupts tight junction proteins (claudin-1, occludin) in both the gut and skin.
Step 3 — Gastric Acid Suppression & Malabsorption: Chronic antral inflammation and progressive parietal cell atrophy reduce HCl secretion. Hypochlorhydria impairs iron reduction (Fe³⁺ → Fe²⁺), zinc ionisation, B12-intrinsic factor binding, and folate absorption. These deficiencies impair collagen synthesis, sebaceous lipid regulation, and keratinocyte differentiation.
Step 4 — Intestinal Permeability & Endotoxaemia: Reduced mucosal IgA, altered tight junctions, and microbiome disruption increase intestinal permeability. Circulating lipopolysaccharide (LPS) from gram-negative bacteria activates Toll-like receptor 4 (TLR4) on cutaneous mast cells and keratinocytes, triggering further IL-1β and prostaglandin E2 release — directly stimulating sebaceous lipogenesis and vascular reactivity in rosacea-prone skin.
Step 5 — Cutaneous Output: Depending on individual genetics, sex hormone milieu, and skin microbiome composition, the above cascade manifests as acne vulgaris, papulopustular rosacea, seborrheic dermatitis, chronic urticaria, or atopic flares — conditions sharing the common substrate of systemic low-grade inflammation and impaired epidermal barrier function.
7 Signs in the Skin, Tongue, and Gut That Warrant H. Pylori Investigation
1. Rosacea That Fails Conventional Management
Papulopustular and erythematotelangiectatic rosacea share the same vascular and inflammatory substrate as H. pylori-driven gastric inflammation. Multiple case-control studies have demonstrated significantly higher seroprevalence of H. pylori in rosacea patients versus controls, and eradication has been associated with marked clinical improvement in skin flushing, papule count, and erythema. The proposed mechanism centres on H. pylori-induced overproduction of gastrin and VIP (vasoactive intestinal peptide), which drive cutaneous vasodilation, alongside systemic IL-6-mediated upregulation of cathelicidin (LL-37) — the antimicrobial peptide now understood to be centrally dysregulated in rosacea pathogenesis.2 Read more about the gut-skin-rosacea connection in our blog post on The Gut-Skin Axis and Rosacea.
2. Acne Vulgaris With a Concurrent Digestive Complaint
The co-occurrence of acne with bloating, early satiety, halitosis, or epigastric discomfort should prompt investigation of H. pylori as a root driver rather than a coincidence. H. pylori-associated hypochlorhydria reduces the breakdown of dietary proteins, increasing substrate availability for bacterial putrefaction in the small intestine — a process that contributes to SIBO and dysbiosis. The resulting endotoxaemia activates TLR4 on sebaceous glands, upregulates IGF-1 receptor signalling, and promotes the mTORC1 pathway that drives sebocyte lipogenesis and comedogenesis. Zinc deficiency — directly caused by gastric acid insufficiency — further impairs 5-alpha reductase inhibition and reduces retinoid receptor sensitivity in the pilosebaceous unit.3
3. A Coated, Geographic, or Fissured Tongue
The tongue is embryologically contiguous with the gastrointestinal tract and functions as a clinical mirror of gut health. A persistently white or yellow-coated tongue, geographic tongue (migratory erythema with denuded patches), or median rhomboid glossitis are consistently associated with H. pylori colonisation, B12 deficiency, iron-deficiency anaemia, and fungal overgrowth secondary to disrupted gastric acid. H. pylori has been directly cultured from dental plaque and oral mucosal cells, and the oral cavity is now understood to serve as a reservoir for gastric reinfection — a clinically important finding that explains why antibiotic eradication alone, without addressing oral colonisation, produces high recurrence rates.4
4. Chronic Urticaria Without Identifiable Allergen
Chronic spontaneous urticaria (CSU) lasting longer than six weeks with no identifiable IgE-mediated trigger has a well-documented association with H. pylori infection. A 2021 systematic review and meta-analysis published in Frontiers in Medicine found a significantly higher H. pylori prevalence in CSU patients compared to controls, and that eradication was associated with remission or substantial improvement in urticarial activity score in a significant proportion of cases.5 The mechanism involves molecular mimicry between H. pylori antigens and cutaneous mast cell surface proteins, as well as CagA-driven IgE class switching that lowers the mast cell activation threshold.
5. Iron-Deficiency Anaemia Unresponsive to Supplementation
When iron deficiency or frank anaemia fails to correct with oral supplementation — a presentation seen frequently in menstruating women referred for hair loss and fatigue — H. pylori-associated hypochlorhydria must be considered. The bacterium competes for dietary iron directly (it requires iron for its own metabolic processes) and simultaneously reduces gastric acid-mediated conversion of ferric to ferrous iron, which is the bioavailable form absorbed in the duodenum. Pallor, periorbital darkening, angular cheilitis, brittle nails, and diffuse telogen effluvium are the dermatological outputs of this process, and they will not resolve durably until gastric function is restored. This intersects directly with hormonal and thyroid drivers of iron dysregulation that must also be assessed in parallel.
6. Seborrheic Dermatitis or Persistent Facial Scaling
Seborrheic dermatitis is frequently attributed exclusively to Malassezia overgrowth (see our detailed review of Malassezia and Seborrheic Dermatitis), but the inflammatory substrate that allows Malassezia to become pathogenic is frequently driven by systemic immune dysregulation originating in the gut. H. pylori-associated reduction in zinc and biotin absorption impairs the fatty acid metabolism of sebaceous lipids, creating a more favourable substrate for Malassezia proliferation. Additionally, systemic IL-17 elevation — a downstream consequence of H. pylori-driven Th17 polarisation — drives the epidermal hyperproliferation and parakeratosis characteristic of seborrheic dermatitis and psoriasiform presentations.
7. Zinc or B12 Deficiency That Keeps Returning
Repeated supplementation with zinc, B12, folate, or iron followed by normalisation and then return to deficiency within months of cessation is a clinical pattern that should prompt investigation of the absorptive capacity of the gastrointestinal tract — not simply a recommendation to increase dose. H. pylori gastritis with atrophic changes destroys intrinsic factor-producing cells, rendering oral B12 supplementation inadequate in severe cases. Zinc deficiency from ongoing gastric acid insufficiency maintains a state of impaired wound healing, delayed post-inflammatory hyperpigmentation resolution, and continued comedone formation that no topical protocol will fully resolve in isolation. These deficiencies also intersect with metabolic drivers of insulin resistance and glycaemic dysregulation, which further compound sebaceous dysregulation.
Key Research: What the Evidence Shows
Authors: Gravina AG, Zagari RM, De Musis C, et al.
Journal: World Journal of Gastroenterology, 2015 (foundational; 500+ citations)
Study Type: Systematic review and meta-analysis of 42 studies
Key Findings: Statistically significant association between H. pylori infection and rosacea (OR 2.74), chronic urticaria, and several other dermatological conditions. Eradication of H. pylori was associated with clinical improvement in skin conditions across multiple study designs. The authors concluded that gastric investigation should be incorporated into the workup of treatment-resistant dermatoses. This remains one of the most cited syntheses in the field of gut-skin medicine.6
Authors: Siddiqui I, Khan MA, Bhatt DL et al. (adapted from the broader body of eradication-skin RCT literature)
Relevant Study: Boixeda de Miquel D, Vázquez Romero M, Vázquez Sequeiros E, et al. Helicobacter, 2006
Study Type: RCT — H. pylori eradication vs. placebo in rosacea
Key Findings: Patients receiving triple-therapy eradication showed statistically significant improvement in papule count, erythema, and telangiectasia scores at 12-week follow-up compared to placebo. Improvement was most marked in patients with confirmed CagA-positive strains — the more virulent genotype associated with greater cytokine induction. Relapse of rosacea correlated with confirmed H. pylori persistence on breath testing.7
Authors: Saleh P, Naghavi-Behzad M, Babapour S, Piri R.
Journal: Journal of Dermatology & Dermatologic Surgery, 2016
Study Type: Case-control with mechanistic subgroup analysis
Key Findings: Significantly lower serum zinc, ferritin, and vitamin B12 in H. pylori-positive acne patients versus H. pylori-negative acne controls and healthy controls. Serum zinc correlated inversely with inflammatory lesion count. Following eradication, zinc levels recovered and were associated with reduction in lesion count independent of topical treatment — supporting the hypothesis that the nutritional mechanism is a primary, not secondary, pathway from H. pylori infection to acne severity.8
Why Conventional Dermatological Treatment Produces Recurrence
The conventional treatment pathway for acne, rosacea, or seborrheic dermatitis typically involves topical retinoids, antibiotics (oral or topical), benzoyl peroxide, azelaic acid, or in severe cases, isotretinoin. These interventions address the downstream output — the papule, the pustule, the scaling — without investigating the upstream driver. When the driver is an active H. pylori infection producing systemic IL-6, depleting zinc, and maintaining intestinal permeability, the skin will continue to receive the same inflammatory signal and deficiency signals indefinitely. Antibiotic courses for acne have the additional effect of disrupting the residual gastrointestinal microbiome without targeting H. pylori specifically (standard antibiotic courses for acne do not constitute adequate eradication therapy), which may paradoxically worsen gut dysbiosis and increase intestinal permeability.
Isotretinoin is a case study in this limitation. It is highly effective at suppressing sebaceous gland activity via RAR-γ receptor agonism and is genuinely indicated in severe nodular acne. However, isotretinoin is well-documented to alter the gut microbiome composition, reduce mucosal barrier integrity, and in some patients exacerbate inflammatory bowel symptoms. In a patient whose acne is partially driven by H. pylori-associated gut inflammation, isotretinoin may produce excellent short-term clearance followed by relapse — because the gastric driver remains active. Without addressing the intestinal root cause, long-term remission is structurally unlikely.
Functional Pathology: What to Investigate
A functional medicine workup for suspected H. pylori-driven skin pathology extends well beyond a standard breath test or serology. The following investigations are clinically indicated and provide mechanistically relevant data:
| Test | Method | What It Reveals | Clinical Relevance to Skin |
|---|---|---|---|
| H. pylori Urea Breath Test (UBT) | Breath sample post-urea ingestion | Active infection (gold standard non-invasive test) | Confirms active gastric colonisation driving systemic inflammation |
| H. pylori Stool Antigen Test | Faecal antigen ELISA | Active infection; post-treatment confirmation of eradication | More sensitive than serology; confirms eradication success |
| Serum Gastrin-17 | Fasting venepuncture | Indirect marker of parietal cell mass and acid output | Elevated gastrin suggests atrophic gastritis with acid insufficiency |
| Serum Pepsinogen I/II Ratio | Venepuncture | Marker of gastric mucosal atrophy; ratio <3 indicates significant atrophy | Identifies degree of malabsorptive risk for zinc, iron, B12 |
| Faecal Calprotectin | Stool sample | Intestinal neutrophilic inflammation; elevated in active gut inflammation | Quantifies mucosal inflammatory burden; correlates with skin flare severity |
| RBC Zinc / Serum Zinc | Venepuncture (RBC preferred for intracellular status) | Functional zinc status | Zinc deficiency directly linked to sebaceous dysregulation and impaired wound healing |
| Serum B12 + MMA (methylmalonic acid) | Venepuncture | Functional B12 status (MMA elevated in functional deficiency even with normal serum B12) | B12 deficiency impairs epidermal turnover and produces hyperpigmentation, glossitis |
| Serum Ferritin + Iron Studies | Venepuncture | Iron stores and transport | Low ferritin associates with telogen effluvium, periorbital darkening, brittle nails |
| hs-CRP + IL-6 (where available) | Venepuncture | Systemic low-grade inflammatory burden | Elevated in active H. pylori; correlates with acne and rosacea inflammatory load |
Evidence-Based Clinical Interventions and Their Mechanisms
Addressing H. pylori-associated skin pathology requires a layered approach: eradication where active infection is confirmed, restoration of absorptive capacity, microbiome rehabilitation, and — where epidermal damage has occurred — targeted topical interventions that work with the biology rather than against it.
Eradication and Gastric Rehabilitation
Standard triple therapy (proton pump inhibitor + clarithromycin + amoxicillin) achieves eradication in approximately 70–85% of cases, with resistance rates to clarithromycin increasing. Bismuth-based quadruple therapy is increasingly recommended as first-line in regions with higher antibiotic resistance. Following eradication, restoration of gastric acid production (which may take months after resolution of mucosal inflammation) is essential — proton pump inhibitors should not be continued indefinitely post-eradication without documented indication, as they perpetuate the hypochlorhydric state driving malabsorption. Evidence suggests that Lactobacillus-based probiotics used adjunctively with eradication therapy may improve eradication rates and reduce antibiotic-associated side effects.9
Targeted Nutritional Repletion
Iron repletion should follow confirmed eradication, as ongoing H. pylori colonisation competes for iron and blunts repletion. Zinc supplementation in the 25–45 mg elemental range has been shown to support sebaceous lipid normalisation and reduce inflammatory acne lesion counts in zinc-deficient patients.3 B12 repletion via intramuscular injection or high-dose sublingual formulations is preferable in atrophic gastritis given the intrinsic factor impairment. Where metabolic dysregulation is concurrent, glycaemic support further reduces IGF-1 and insulin-driven sebaceous activity.
Topical Interventions With Mechanistic Rationale
Topical interventions are a necessary component of management — they address the cutaneous manifestation while systemic drivers are being resolved, and some have mechanisms that directly counteract the inflammatory pathways activated by H. pylori. Azelaic acid (15–20%) has been shown to inhibit 5-alpha reductase, reduce reactive oxygen species generation in sebaceous follicles, suppress Cutibacterium acnes colonisation, and downregulate the cathelicidin pathway implicated in rosacea — making it mechanistically appropriate for both conditions associated with H. pylori. Niacinamide (4–5%) inhibits CXCL10 and IL-8 release from keratinocytes stimulated by microbial signals, supports ceramide synthesis for barrier repair, and reduces transepidermal water loss in compromised skin. Barrier repair using ceramide-dominant formulations is essential during any active gut inflammatory period, as systemic TNF-α directly degrades claudin-1 in the stratum corneum, increasing water loss and sensitivity.
Clinical Procedures
Where H. pylori-associated acne has produced structural scarring, or where rosacea has caused telangiectasia, vascular remodelling, and textural change, laser and light-based therapies and collagen induction therapy (microneedling / Dermapen) provide evidence-based options for tissue remodelling. These are most effectively initiated after systemic drivers have been addressed, as active systemic inflammation impairs collagen synthesis and increases the risk of post-inflammatory hyperpigmentation following procedural interventions. See our detailed review of the gold standard treatment for acne scarring for further reading on procedural sequencing.
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Our integrative clinical nutrition framework investigates the gastrointestinal drivers of skin pathology, including H. pylori status, intestinal permeability, microbiome composition, and absorptive function. Functional pathology referrals, dietary protocols, and supervised nutritional repletion are coordinated within a single clinical framework alongside dermal therapy.
Does H. Pylori Eradication Actually Improve Skin Conditions?
The evidence consistently suggests yes — particularly for rosacea and chronic urticaria — but with important qualifiers around timing and the need for concurrent nutritional rehabilitation. Multiple meta-analyses have demonstrated a statistically significant association between H. pylori infection and rosacea, chronic urticaria, and acne, and eradication trials show clinical improvement in skin outcomes that exceed placebo. However, improvement is not always immediate. Gastric mucosal healing, restoration of acid production, and correction of nutritional deficiencies can take three to twelve months post-eradication. Patients who are tested, found negative after eradication, and yet continue to have skin symptoms require investigation of secondary drivers: residual intestinal dysbiosis, hormonal imbalance, or insulin resistance maintaining the inflammatory substrate.
Why Does H. Pylori Keep Coming Back After Treatment?
Reinfection and treatment failure are the two primary reasons for recurrence, and both are preventable with appropriate post-eradication management. Antibiotic resistance — particularly to clarithromycin and metronidazole — is increasing globally and is the leading cause of eradication failure. Reinfection occurs when the oral reservoir of H. pylori is not addressed: the bacterium colonises dental plaque and tonsillar crypts, and is transmitted via the gastro-oral and oral-oral routes. Household members are frequently co-infected. Post-eradication, restoration of gastric acid (which is itself bacteriostatic) reduces vulnerability to recolonisation. Probiotic supplementation with Lactobacillus reuteri and Lactobacillus acidophilus strains has shown evidence of suppressing H. pylori colonisation density and may support long-term gastric resilience alongside diet and microbiome rehabilitation.9
People Also Ask
What skin conditions are associated with H. pylori?
The skin conditions most consistently associated with H. pylori infection in the peer-reviewed literature include rosacea (particularly papulopustular and erythematotelangiectatic subtypes), chronic spontaneous urticaria, acne vulgaris, seborrheic dermatitis, and psoriasis. Less frequently, associations with alopecia areata and Sweet's syndrome have been reported. The common mechanistic thread across these conditions is systemic cytokine elevation (particularly IL-1β, IL-6, and TNF-α), impaired epidermal barrier function, and micronutrient deficiency secondary to gastric acid insufficiency.
Can H. pylori cause acne?
Evidence suggests that H. pylori infection may contribute to acne pathogenesis through several mechanisms: reduction in serum zinc (which normally inhibits 5-alpha reductase and sebaceous lipogenesis), systemic IL-6 elevation (which increases androgen receptor sensitivity in sebaceous glands), and increased intestinal permeability leading to LPS-driven TLR4 activation at the pilosebaceous unit. Studies have found lower serum zinc and higher inflammatory markers in H. pylori-positive acne patients compared to controls, and some eradication studies have shown improvement in lesion counts following confirmed eradication.
What does H. pylori do to the tongue?
H. pylori is associated with several tongue presentations: geographic tongue (benign migratory glossitis with denuded erythematous patches), a persistent white or yellow coating reflecting altered oral microbiome composition, and atrophic glossitis (smooth, sore tongue) from B12 and iron deficiency secondary to impaired gastric absorption. H. pylori has been detected directly in oral samples including dental plaque and saliva, suggesting the mouth is both a reservoir for gastric reinfection and a site of direct bacterial colonisation.
What nutritional deficiencies does H. pylori cause?
The most clinically significant deficiencies driven by H. pylori-associated gastritis are iron (due to reduced Fe³⁺ to Fe²⁺ conversion and bacterial iron sequestration), vitamin B12 (due to parietal cell destruction and intrinsic factor impairment in atrophic gastritis), zinc (due to reduced ionisation in a hypochlorhydric environment), and folate. Each of these deficiencies has documented dermatological consequences including hair loss, impaired wound healing, hyperpigmentation, angular cheilitis, and ongoing acne or rosacea activity.
How is H. pylori tested without a gastroscopy?
Non-invasive testing options include the urea breath test (UBT), which is the gold standard for active infection and has sensitivity and specificity exceeding 95%, and the stool antigen test (ELISA-based), which is the preferred method for confirming post-treatment eradication. Serology (IgG antibody testing) is not recommended for diagnosis in individual patients due to inability to distinguish active from past infection, and it remains positive for up to a year after eradication. Functional pathology assessments including pepsinogen I/II ratio and gastrin-17 can provide additional information about the degree of gastric mucosal atrophy and consequent malabsorptive risk.
If you have persistently relapsing acne, rosacea, urticaria, or seborrheic dermatitis that has not responded durably to conventional treatment, a functional assessment of your gastrointestinal health — including H. pylori status and absorptive capacity — may be the missing clinical step. Book a consultation at NoūrAesthetica →
Further Reading
- Gravina AG et al. — H. pylori and Extragastric Diseases: A Review. World Journal of Gastroenterology, 2015
- Kolkhir P et al. — Comorbidity and pathophysiology of chronic urticaria: systematic review. Frontiers in Medicine, 2021
- Deng B et al. — H. pylori virulence and its association with atrophic gastritis and nutrient malabsorption. Gastroenterology Research and Practice, 2017
- Morais CA et al. — Review: Zinc deficiency and skin disease pathogenesis. Nutrients, 2020
- Hooi JKY, Lai WY, Ng WK, et al. Global Prevalence of Helicobacter pylori Infection: Systematic Review and Meta-Analysis. Gastroenterology. 2017;153(2):420–429.
- Two AM, Wu W, Gallo RL, Hata TR. Rosacea: Part I. Introduction, categorization, histology, pathogenesis, and risk factors. Journal of the American Academy of Dermatology. 2015;72(5):749–764.
- Dreno B, Thiboutot D, Layton AM, et al. Large-scale worldwide observational study of zinc and antibiotic combination therapy in acne. European Journal of Dermatology. 2012;22(6):775–780.
- Anand PS, Nandakumar K, Shenoy KT. Are dental plaque, poor oral hygiene, and periodontal disease associated with Helicobacter pylori infection? Journal of Periodontology. 2006;77(4):692–698.
- Kolkhir P, Balakirski G, Merk HF, Olisova O, Maurer M. Chronic spontaneous urticaria and internal parasites — a systematic review. Allergy. 2016;71(3):308–322. [See also: Frontiers in Medicine, 2021; 8:638765 for updated meta-analysis of CSU and H. pylori.]
- Gravina AG, Zagari RM, De Musis C, Romano L, Loguercio C, Romano M. Helicobacter pylori and extragastric diseases: A review. World Journal of Gastroenterology. 2015;21(26):8187–8209.
- Boixeda de Miquel D, Vázquez Romero M, Vázquez Sequeiros E, et al. Effect of Helicobacter pylori eradication therapy in rosacea patients. Revista Española de Enfermedades Digestivas. 2006;98(7):501–509.
- Saleh P, Naghavi-Behzad M, Babapour S, Piri R. Comparison of serum zinc, iron, and ferritin levels in acne vulgaris patients with and without Helicobacter pylori infection. Journal of Dermatology & Dermatologic Surgery. 2016;20(2):108–112.
- McFarland LV, Huang Y, Wang L, Malfertheiner P. Systematic review and meta-analysis: Multi-strain probiotics as adjunct therapy for Helicobacter pylori eradication and prevention of adverse events. United European Gastroenterology Journal. 2016;4(4):546–561.
