Background: The question of whether solid malignancies (SMs) are associated with pyoderma gangrenosum (PG) remains to be conclusively answered.Objective: To evaluate the risk of SM among patients with PG and the odds of PG after a diagnosis of SM.Methods: A population-based retrospective cohort study was conducted to study the risk for SM in patients with PG (n = 302) as compared with age-, sex-and ethnicity-matched control subjects (n = 1799). A case-control design was used to estimate the odds of PG in those with a preexisting history of SM. Results:The prevalence of a preexisting SM was comparable in patients with PG and controls (7.5% vs. 8.8%, respectively; P = 0.490). The odds of having PG following a diagnosis of a SM was not statistically increased (OR, 0.85; 95% CI, 0.53-1.36). The incidence of SM was 6.8 (95% CI, 3.5-12.2) and 7.9 (95% CI, 6.1-10.1) per 1000 person-years among patients with PG and controls, respectively. Patients with PG were not more likely to develop SM as compared to controls (HR, 0.86; 95% CI, 0.44-1.69). Patients with a dual diagnosis of PG and SM were older and had more frequent comorbid conditions and increased mortality.Conclusions: SM is not associated with provoking PG, and patients with PG are not at an increased risk of developing SM. A thorough routine screening for SM in patients with new-onset PG is an unnecessary approach based on the study findings.
Background Current treatment paradigms in anti‐p200 pemphigoid rely on low levels of evidence, primarily originating from case reports and case series. Objective To systematically review the utilized treatment modalities for anti‐p200 pemphigoid and to synthesize the available clinical outcomes of treated patients. Methods We conducted a systematic review of the literature using Ovid‐Medline (1946–2018), Embase (1947–2018) and Web of Science (1900–2018) databases with a broad and inclusive search strategy along with a subsequent search of retrieved articles. All case reports and case series of patients with anti‐p200 pemphigoid were included. Results Sixty‐eight eligible studies comprising 113 anti‐p200 pemphigoid patients with a mean age of 65.5 years were included in the qualitative synthesis. The clinical outcome of patients following treatment was reported for 91 (80.5%) patients, of whom 83 (91.2%) had achieved complete remission at least once. Complete remission on‐therapy was observed in 51 (56.0%) and complete remission off‐therapy in 12 (13.2%) patients. Thirty‐six (39.6%) patients had experienced at least one flare during the duration of follow‐up. A combination of systemic corticosteroids and adjuvant immunomodulatory agents was the leading therapeutic approach (63.0%) required for disease control. Systemic and topical corticosteroids as monotherapy were sufficient to control the disease in 19.6% and 13.0% of cases, respectively. Dapsone was the most commonly used (41.3%) adjuvant agent. The highest rates of complete remission were achieved in patients managed by systemic corticosteroids as monotherapy (100%) and in those managed by systemic corticosteroids with adjuvant agents (90.7%). Conversely, 45.5% of patients treated only by topical corticosteroids experienced at least one relapse during follow‐up. Conclusion The vast majority of patients had reached a complete remission during the course of the disease, whereas a considerable proportion of patients experienced at least one relapse. A combination of systemic corticosteroids and adjuvant immunomodulatory agents was the most frequently utilized therapeutic approach.
skin diseases reflected in the Cochrane Database of Systematic Reviews, 5 where psoriasis and decubitus ulcer were overrepresented diseases in terms of research, whereas urticaria and bacterial skin infections were underrepresented. A strength of this study is the interrelationship made between two large national datasets, from studies designed to be representative both of outpatient consultations and research activity in Spain, 3,4 and data from the GBDS. Among the limitations are that this study is restricted to 14 groups of diseases and only outpatient consultations, which may not be representative of all skin conditions, and that the unweighted number of publications might not be a good measure of research activity. Another limitation is that the periods of the three studies did not match exactly, which could affect the comparability of the data. However, burden of skin diseases and frequency of consultations are unlikely to differ from those in the period of the MaIND study. Our data suggest that melanoma might be overrepresented in research, whereas acne and viral infections could be underrepresented according to the demand for consultations and the disease burden. Research in psoriasis and dermatitis is proportional to the disease burden and demand for consultations whereas research in NMSC is scarce according to demand for consultations but disproportionate according to disease burden. Research priorities, should be conscious decisions that take into account quantitative data, such as the burden of skin conditions and the demand for clinical assistance in order to sort the need for resources, and qualitative research, such as James Lind Alliance Prioritization exercises, could be useful to select the main research questions within each topic.
For the last several decades, there are numbers of research done to reveal the importance of gut microbiome regarding human health and disease. One of the typical inflammatory skin disease is atopic dermatitis. The role of gut microbiome is becoming known in atopic dermatitis and the bacteria to cause the disease and probiotics to prevent the disease is being researched. We analyzed the gut microbiota of the inflammatory skin model mouse named ICE (keratin 14-specific Interleukin-1 converting enzyme overexpressing transgenic mouse). ICE had an elevatedcolonization of Staphylococcus genus and Streptococcus genus compare to those of wild type. When the ICE was treated with anti TNF-a antibody, the percentage of these bacteria had significantly decreased (p ¼ 0.018, p ¼ 0.031, respectively). We are going to present in this poster about the differences of skin reaction and cytokine production by orally administrating of isolated bacteria into sterilized wild type mice and causing skin inflammation. Our skin is daily aggressed by environmental factors and by certain personal care products (cleansers, deodorants, etc).Our obsession with cleanliness may do more harm than good for the balance of our skin's microbiota and skin health. It has been observed that overcleanliness leads to an impairment of the skin barrier function and of skin microbiome balance leading to increased sensitivity, irritation and dryness. We explored the effect of a common surfactant found in hygiene products, on the physical skin and microbiotic barrier in vivo. At first, we applied SLS (Sodium Lauryl Sulfate, 0.5% occlusive patch for 24h) and we explored its effect on the skin microbiota using metagenomic sequencing (16S rDNA) before and 1 day after SLS application. Secondly, we explored skin microbiota and skin barrier function evolution over 7 days after a 1% SLS challenge in the presence of a formula containing purified rapeseed phytosterols and one containing its vehicle. Skin barrier function was assessed before, after SLS and 7 days after applying phytosterols and vehicle by measuring TEWL. Finally, skin microbiota recovery after a 0.5% SLS patch in presence of the same formula containing phytosterols was assessed at the same timepoint; (16S metasequencing). We confirmed that the surfactant impaired skin barrier function and evidenced that it decreased the commensal bacteria while increasing the opportunistic pathogenic bacteria. At the phylum level actinobacteria were decreased by 14% and at the family level, corynebacteriaceae, micrococcaceae and propionibacteriacea were decreased (-42%, -34%, -11%). At the genus level corynebacterium, micrococcus, paracoccus and propionibacterium were decreased (-42%, -39%, -36%, -11%), whereas pseudomonas and pantoea were increased (x2, x117). Interesting results were also obtained on staphylococcus (+38%), but a more resolutive technic is necessary to discriminate between strains. To counterbalance these SLS induced-modifications, we evidenced that purified phytosterols provide benefits to restore sk...
Here, we have explored the involvement of innate lymphoid cells-type 1 (ILC1) in the pathogenesis of alopecia areata (AA), because we found them to be significantly increased around lesional and non-lesional HFs of AA patients. To further explore these unexpected findings, we first co-cultured autologous circulating ILC1-like cells (ILC1lc) with healthy, but stressed, organ-cultured human scalp hair follicles (HFs). ILClc induced all hallmarks of AA ex vivo: they significantly promoted premature, apoptosis-driven HF regression (catagen), HF cytotoxicity/dystrophy, and most important for AA pathogenesis, the collapse of the HFs physiological immune privilege. NKG2D-blocking or IFNγ-neutralizing antibodies antagonized this. In vivo, intradermal injection of autologous activated, NKG2D+/IFNγ-secreting ILC1lc into healthy human scalp skin xenotransplanted onto SCID/beige mice sufficed to rapidly induce characteristic AA lesions. This provides the first evidence that ILC1lc, which are positive for the ILC1 phenotype and negative for the classical NK markers, suffice to induce AA in previously healthy human HFs ex vivo and in vivo, and further questions the conventional wisdom that AA is always an autoantigen-dependent, CD8 +T cell-driven autoimmune disease.
The coexistence of pyoderma gangrenosum (PG) and chronic renal comorbidities has been reported anecdotally. We aimed to assess the bidirectional association between PG and the following chronic renal comorbidities: chronic renal failure (CRF), dialysis, kidney transplantation (KT), and other kidney diseases (OKD). That is to evaluate (i) the risk of the aforementioned diseases among patients with PG (ii) and the odds of PG after a diagnosis of renal comorbidities. A population-based retrospective cohort study was conducted comparing PG patients (n=302) with age-, sex-, and ethnicity-matched control subjects (n=1497) with regard to incident cases of renal comorbidities. A case-control design was additionally adopted to estimate the odds of PG in those with a preexisting history of renal comorbidities. Adjusted hazard ratios (HRs) and adjusted odds ratios (ORs) were estimated by Cox regression and logistic regression, respectively. Patients with PG demonstrated an increased risk of CRF (adjusted HR, 3.68; 95% CI, 2.72–5.97), dialysis (adjusted HR, 27.79; 95% CI, 3.24–238.14), and OKD (adjusted HR, 2.71; 95% CI, 1.55–4.74). In addition, the odds of PG were increased after the diagnosis of CRF (adjusted OR, 2.34; 95% CI, 1.33–4.11), KT (adjusted OR, 5.03; 95% CI, 1.01–25.12), and OKD (adjusted OR, 1.69; 95% CI, 1.04–2.74). Patients with a dual diagnosis of PG and renal diseases presented with PG at an older age and had a higher prevalence of comorbid conditions. In conclusion, a bidirectional association exists between PG and chronic renal conditions. Awareness of this comorbidity may be of benefit for physicians managing patients with PG.
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