Autoimmune pancreatitis is a recently defined nosological entity, which accounts for 4.6‐6% of all forms of chronic pancreatitis and is often associated with other autoimmune diseases, particularly Sjögren's syndrome. Possession of the HLA DRB1*0405‐DQB1*0401 genotype confers a risk for the development of autoimmune pancreatitis. Autoantibodies against carbonic anhydrase II and lactoferrin are frequently present in affected subjects and are suspected to have a pathogenic role. A link between gastric infection by Helicobacter pylori and autoimmune pancreatitis has been hypothesized. We used in silico protein analysis and search for HLA binding motifs to verify this hypothesis. We found a significant homology between human carbonic anhydrase II and α‐carbonic anhydrase of Helicobacter pylori, an enzyme which is fundamental for the survival and proliferation of the bacterium in the gastric environment. Moreover, the homologous segments contain the binding motif of the HLA molecule DRB1*0405. Our data strengthen the hypothesis that gastric Helicobacter pylori infection can trigger autoimmune pancreatitis in genetically predisposed subjects.
Management of psoriasis in elderly patients can be challenging, because of the impairment of immune system efficiency and the presence of comorbidities that contra-indicate systemic therapies. We studied the safety and efficacy of systemic traditional and biological treatments in 187 consecutive psoriatic patients aged > 65 years. At week 12 of therapy, Psoriasis Area and Severity Index 75 was achieved by 49%, 27%, 46% and 31% of patients who received methotrexate, acitretin, cyclosporine or PUVA, and 64.1%, 64.7%, 93.3%, 57.1% and 100% of patients who received etanercept, adalimumab, infliximab, efalizumab and ustekinumab. The rate of adverse events was 0.12, 0.32, 1.4 and 0.5 per patient-year in the methotrexate, acitretin, cyclosporine and PUVA groups and 0.11, 0.35, 0.19, 0.3 and 0.26 in the etanercept, adalimumab, infliximab, efalizumab and ustekinumab groups. Traditional drugs were less effective than biologics in our elderly population. Etanercept was associated with a lower rate of adverse events compared with other treatments.
A 9‐year‐old boy was brought by his mother to our department for a follow‐up visit and dermoscopy of melanocytic nevi. During the consultation, she complained of a gradually increasing, asymptomatic, cutaneous discoloration involving the trunk, arms, and lower limbs of her son which had appeared approximately at the end of the summer. The boy was healthy and was not taking any medication or nutritional supplements. Despite good hygiene, including showers and brushings with acid liquid soap at least three to four times per week, he showed no improvement of the condition. Physical examination revealed dirty‐appearing skin, composed of subtle, but clear‐cut, brown to blackish areas with a velvety texture, symmetrically involving the lateral sides of the trunk, umbilical, and periumbilical regions with light scaling, dorsal and volar surfaces of the arms, and posterior parts of the lower limbs (Figs 1 and 2). The neck, dorsum and anterior aspects of the lower limbs were uninvolved. 1 Diffuse brown–blackish hyperpigmentation of the lateral aspect of the trunk and of the dorsal surface of the arm 2 Subtle pigmentation of the abdomen Partial removal of these patches by isopropyl alcohol swabbing (Fig. 3) confirmed the clinical suspicion of terra firma‐forme dermatosis. The boy's mother refused our proposal of dermal scraping and 3‐mm punch biopsy when reassured about the benign nature of the condition and the ease of treatment. 3 Alcohol swabbing reveals a pink linear area of normal skin. The appearance of the alcohol pad after rubbing The patient was seen 24 h later for erythema and burning of lesional areas because of excessively vigorous and extensive rubbing, but with no residual signs of the disease (Fig. 4). 4 Absence of dermatosis after cleansing at home. Notice frictional erythema of the treated areas
NECL-5 is involved in regulating cell–cell junctions, in cooperation with cadherins, integrins and platelet-derived growth factor receptor, that are essential for intercellular communication. Its role in malignant transformation was previously described. It has been reported that transformation of melanocytes is associated with altered expression of adhesion molecules suggesting the potential involment of NECL-5 in melanoma development and prognosis. To shed light on this issue, the expression and the role of NECL-5 in melanoma tissues was investigated by bioinformatic and molecular approaches. NECL-5 was up-regulated both at the mRNA and the protein levels in WM35, M14 and A375 cell lines compared with normal melanocytes. A subsequent analysis in primary and metastatic melanoma specimens confirmed “in vitro” findings. NECL-5 overexpression was observed in 53 of 59 (89.8%) and 12 of 12 (100%), primary melanoma and melanoma metastasis, respectively; while, low expression of NECL-5 was detected in 12 of 20 (60%) benign nevi. A significant correlation of NECL-5 overexpression was observed with most of known negative melanoma prognostic factors, including lymph-node involvement (P = 0.009) and thickness (P = 0.004). Intriguingly, by analyzing the large series of melanoma samples in the Xu dataset, we identified the transcription factor YY1 among genes positively correlated with NECL-5 (r = 0.5). The concordant computational and experimental data of the present study indicate that the extent of NECL-5 expression correlates with melanoma progression.
The medical term onychomycosis should be understood as chronic infection of the nails caused by a fungus. The most common causative agents are the dermatophytes and Candida species. The less common are certain types of moulds (nondermatophyte moulds or NDMs). In approximately 60-80 % of the cases, onychomycosis is due to dermatophytes. Among dermatophytes, the most often isolated causative pathogen is Trichophyton (T.) rubrum. Other common species are T. interdigitale (formerly T. mentagrophytes), Epidermophyton floccosum, and T. tonsurans. The most significant yeasts causing onychomycosis are Candida albicans and Candida parapsilosis. Predisposing factors for onychomycosis include mainly diseases such as diabetes mellitus, peripheral vascular arterial disease, chronic venous insufficiency, polyneuropathies of diverse etiologies, and immunosuppression, e.g., myeloproliferative diseases (such as lymphoma and paraproteinemia), HIV/AIDS, etc. Other factors facilitating the fungal infection are frequent trauma in professional sportsmen, often accompanied by excessive perspiration. The diagnostic methods that are often applied in different dermatologic departments and ambulatory units are also different. This precludes the creation of a unified diagnostic algorithm that could be used everywhere as a possible standard. In most of the cases, the method of choice depends on the specialist's individual experience. The therapeutic approach depends mostly on the fungal organism identified by the dermatologist or mycologist. This review hereby includes the conventional as well as the newest and most reliable and modern methods used for the identification of the pathogens causing onychomycosis. Moreover, detailed information is suggested, about the choice of therapeutic scheme in case whether dermatophytes, moulds, or yeasts have been identified as causative agents. A thorough discussion of the schemes and duration of the antifungal therapy in certain groups of patients have been included.
Based on data available in the literature and the clinical experience of the authors, this article suggests the optimal approach to drug monitoring and antidrug antibody assay and the most effective use of biologic immunotherapies in this setting. Immunogenicity should be taken into account in the adoption of therapeutic choices in psoriatic patients, such as anti-TNFα agent intensification, or switching to another anti-TNFα agent or a drug with a different mechanism of action.
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