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Crohn’s disease is a chronic inflammatory bowel disease potentially involving any segment of the gastrointestinal tract. Extra-intestinal manifestations may occur in 6%–40% of patients, and disorders of the skin are among the most common. This manuscript will review skin manifestations associated to Crohn’s disease, with a particular focus on lesions associated to anti-tumour necrosis factor therapy.

Crohn’s disease is a chronic inflammatory bowel disease potentially involving any segment of the gastrointestinal tract. Extra-intestinal manifestations may occur in 6%–40% of patients, and disorders of the skin are among the most common. This manuscript will review skin manifestations associated to Crohn’s disease, with a particular focus on lesions associated to anti-tumour necrosis factor therapy.

Background and aims Recent studies suggest a potential relationship between rosacea and Helicobacter pylori(H. pylori) infection or small intestinal bacterial overgrowth (SIBO), but there is no firm evidence of an association between rosacea and H. pyloriinfection or SIBO. We performed a prospective study to assess the prevalence of H. pyloriinfection and/or SIBO in patients with rosacea and evaluated the effect of H. pylorior SIBO eradication on rosacea.Methods We enrolled 90 patients with rosacea from January 2012 to January 2013 and a control group consisting of 90 patients referred to us because of mapping of nevi during the same period. We used the 13C Urea Breath Test and H. pyloristool antigen (HpSA) test to assess H. pyloriinfection and the glucose breath test to assess SIBO. Patients infected by H. pyloriwere treated with clarithromycin-containing sequential therapy. Patients positive for SIBO were treated with rifaximin.Results We found that 44/90 (48.9%) patients with rosacea and 24/90 (26.7%) control subjects were infected with H. pylori(p= 0.003). Moreover, 9/90 (10%) patients with rosacea and 7/90 (7.8%) subjects in the control group had SIBO (p= 0.6). Within 10 weeks from the end of antibiotic therapy, the skin lesions of rosacea disappeared or decreased markedly in 35/36 (97.2%) patients after eradication of H. pyloriand in 3/8 (37.5%) patients who did not eradicate the infection (p< 0.0001). Rosacea skin lesions decreased markedly in 6/7 (85.7%) after eradication of SIBO whereas of the two patients who did not eradicate SIBO, one (50%) showed an improvement in rosacea (p= 0.284).Conclusions Prevalence of H. pyloriinfection was significantly higher in patients with rosacea than control group, whereas SIBO prevalence was comparable between the two groups. Eradication of H. pyloriinfection led to a significant improvement of skin symptoms in rosacea patients.

Recent studies suggest a potential relationship between rosacea and Helicobacter pylori(H. pylori) infection or small intestinal bacterial overgrowth (SIBO), but there is no firm evidence of an association between rosacea and H. pyloriinfection or SIBO. We performed a prospective study to assess the prevalence of H. pyloriinfection and/or SIBO in patients with rosacea and evaluated the effect of H. pylorior SIBO eradication on rosacea. We enrolled 90 patients with rosacea from January 2012 to January 2013 and a control group consisting of 90 patients referred to us because of mapping of nevi during the same period. We used the 13C Urea Breath Test and H. pyloristool antigen (HpSA) test to assess H. pyloriinfection and the glucose breath test to assess SIBO. Patients infected by H. pyloriwere treated with clarithromycin-containing sequential therapy. Patients positive for SIBO were treated with rifaximin. We found that 44/90 (48.9%) patients with rosacea and 24/90 (26.7%) control subjects were infected with H. pylori(p?=?0.003). Moreover, 9/90 (10%) patients with rosacea and 7/90 (7.8%) subjects in the control group had SIBO (p?=?0.6). Within 10 weeks from the end of antibiotic therapy, the skin lesions of rosacea disappeared or decreased markedly in 35/36 (97.2%) patients after eradication of H. pyloriand in 3/8 (37.5%) patients who did not eradicate the infection (p?

The mechanism of acantholysis in pemphigus vulgaris (PV) is an intriguing argument since several chemical mediators are implicated. We previously reported a central role for IL-1α and TNF-α, both able to regulate complement activation and plasminogen activators. Very little is known about what triggers the disease (drugs, viruses or food). In this study, we evaluate the molecular role of tannins in acantholysis. By HPLC chromatography we measured tannic acid (TA) and gallic acid (GA) in blister fluid of 4 groups of patients divided according to their dietary habits, including a regular diet, a diet rich in tannins, a diet free of tannins, and a group of pemphigus patients. Blister fluid was obtained from patients using a suction blister apparatus. We show that people with a diet rich in tannins have increased tannin metabolites (TA and GA) in the skin in respect to controls (tannin-rich diet: GA = 194.52±2.39 nmol/ml; TA = 348.28±1.4 nmol/ml versus tannin-Mediterranean diet: GA = 15.28±1.63 nmol/ml; TA = 22.81±1.68 nmol/ml). PV patients showed similar values to the Mediterranean diet population (PV patients: GA = 95.8±1.97 nmol/ml; TA = 199.09±4.15 nmol/ml versus Mediterranean diet: GA = 83.53±2.35 nmol/ml; TA = 195.1±2.50 nmol/ml). In an in vitroacantholysis system using TA and PV-IgG we show that TA 0.1 mM in NHEK culture is able to induce acantholysis. This effect was able to amplify the acantholytic action of PV-IgG in vitro. A blocking study using anti IL-1α and anti TNF-α antibodies showed a reduction in TA-induced acantholysis. Taken together, these results suggest that a diet rich in tannins could be a trigger in genetically predisposed patients. If these data are confirmed, a complementary diet poor in tannins may be useful in patients affected by PV.

The reports on induced pemphigus have multiplied over the last 10 years. Several heterogeneous factors, such as drugs (penicillamine, pyritinol, captopril, rifampicin, etc.), physical agents (burns, UV, and ionizing radiation) and viruses, can play an inducing role. Usually, the disease in preceded by prodromal, non-specific lesions. The full-blown stage shows features of pemphigus foliaceus, erythematosus or herpetiformis. Histologically, acantholytic splits mostly occur at the highest malpighian layers. Intercellular antibodies and frequently concomitant other auto-antibodies are found in the serum, the titre of the former usually being low and unrelated to the severity or course of the disease.

3H-labeled d-penicillamine has been injected in mice in order to study by autoradiography its distribution in the kidney. The results show heavy accumulation of the drug in the epithelial cells of the proximal tubules of the kidney, whereas glomeruli and distal tubules do not show any significant accumulation. This peculiar tropism of penicillamine to proximal tubules is entirely consistent with the Heymann's nephritis model suggested by Bacon as a pathogenetic model for penicillamine-induced nephropathy.

A typical case of Cowden disease is presented. This is a rare mucocutaneous disease, genetically determined, with multiple organ system involvement in which a malignancy, particularly of breast and thyroid gland, may develop. The disease can be diagnosed in its early stages by gingival and cutaneous manifestations. We emphasize that the dentist may be the first health care professional who recognizes the syndrome, which is a crucial step to prevent and cure the predictable malignancy.

The stability of polymer-to-polymer joints was assessed using a thermodynamic method based on surface tension components, similar to that developed by Kinloch et al.,1 showing that joint stability is improved in air by plasma treatments, while it is depressed in water. Shear strength tests showed qualitative agreements with these suggestions.Surface analysis by contact angle measurements, SSIMS and XPS allowed the clarification of contributions which originated from phenomena unaccounted for by thermodynamic analysis. Plasma treatment was shown to form a weak boundary layer on polypropylene surfaces, possibly due to depolymerization. In the case of polycarbonate a water sensitive, possibly water soluble, layer is formed, therefore inducing a remarkable decrease in shear strength upon immersion in water.