Riesgo de reactivación de hepatitis B pasada en pacientes con psoriasis tratados con biológicos. Análisis retrospectivo de 20 casos. Registro de BIOBADADERM
J. Sanz‐BuenoF. VanaclochaI. García‐DovalR. TorradoG. CarreteroE. DaudénDiana Ruíz‐GenaoM. Alsina‐GibertBeatriz Pérez-ZafrillaG. Pérez-RialR. Rivera
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Hepatitis B
OBJECTIVE To know more clearly about the situation of Hepatitis B virus markers in clinical medical workers and take further interventional strategies to protect high risk medical workers.METHODS Hepatitis B virus markers in doctors,nurses and medical checkers who have contacted with patients′ blood,body fluid,or other occupational hazard situation,were detected by of ELISA.RESULTS Among the 587 medical workers detected,311 were with deficiency of active immunity(52.98%),196 were HBV infectors(33.39%).CONCLUSIONS Medical workers are in high risk groups of HBV infection.Medical institutions should attend to their self-protection and encourage them to take HBV vaccine to prevent iatrogenic transmission.
Hepatitis B
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Drug ingestion may play an important role in the induction and exacerbation of psoriasis. Drugs may directly induce the occurrence of psoriasis in susceptible individuals, or cause the recurrence or exacerbation of preexisting psoriasis. In view of their relationship with psoriasis, drugs can be classified as follows: drugs that are definitely able to induce or exacerbate psoriasis (e.g., lithium), and drugs that are possible to induce or exacerbate psoriasis (e.g., interferon). Clinical and histological studies on drug-induced or-exacerbated psoriasis are helpful to investigate into the pathogenesis of psoriasis. Further studies are still needed for drugs that are possible to induce or exacerbate psoriasis, which may be of great importance for the prevention of psoriasis in susceptible individuals.
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Psoriasis; Pharmaceutical preparations; Lithium compounds; Antimalarials; Biological agents; Provoke; Exacerbate
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Objective To Investigate whether the PDEs activities is abnormal or not in psoriasis patients by detecting the PDEs activities of both psoriasis patients and healthy controls, and explore the potential role of PDEs activities changes in the pathogenesis of psoriasis. Methods PDEs activities were detected by using high performance liquid chromatography(HPLC) in 50 patients with psoriasis and 60 healthy controls. Results The PDEs activities is 10.40%±3.54% in psoriasis patients,and 8.60%±2.25% in the healthy controls. The PDEs activities in patients with psoriasis is significant higher than that in the controls (P0.05). Conclusions The PDEs activities may be a risk factor for psoriasis.
Pathogenesis
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Psoriasis is a chronic, immune-mediated, inflammatory disorder characterized by erythema, redness, thickening, and scaling of the skin. Psoriasis is caused by the accelerated keratinocyte cell proliferation and dysregulation of the immune system. The cause of psoriasis is unknown, but it can be a genetic component. Several factors are thought to aggravate psoriasis. These include stress, excessive alcohol consumption, and smoking. The concept of the pathogenesis of psoriasis is based on the proliferation and differentiation of keratinocytes, recent studies have proved that the dysregulation of the immune system plays a critical role in the development of psoriasis. Immune cells release T cells, keratinocytes, neutrophils, and the cytokines, have a specific interaction with each other that is the core mechanism of the development of psoriasis. Trigger factors of psoriasis is also genetic, environmental and behavioral factors. The prevalence of psoriasis is estimated to range from 0.91% to 8.5% worldwide in adults. Clinically, psoriasis vulgaris is the most common subtype of psoriasis and affects approximately 90% of patients.
Immune Dysregulation
Pathogenesis
Erythema
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Sun Exposure
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【Objectives】 To test the expression levels of soluble CD147(sCD147) in plasma of psoriasis vulgaris(PV) patients and normal controls. Describe disease severity of PV with psoriasis lesion degree score(PASI) and analyze the correlation between the expression levels of sCD147 in psoriasis patients and disease severity. To test the expression levels of sCD147 in plasma of different subtypes of psoriasis patients, and study the roles of sCD147 play in the psoriasis classification. 【Methods】 Detect the expression levels of sCD147 in 74 PV patients and 41 normal controls by enzyme-linked immunosorbent assay(ELISA). Analyze the correlation between sCD147 expression levels and PASI score. Detect the expression levels of sCD147 of plasma in 10 patients with psoriasis pustulose(PP), 12 patients with arthritis psoriasis(PsA) and 7 patients with psoriasis erythrodermic(PE). Statistical analyze the difference of sCD147 expression levels in patients with different subtypes of psoriasis. 【Results】 The sCD147 expression levels in plasma of PV patients were significantly higher than those in normal controls(Ctrl)(P 0.01). Statistical analysis showed that there was no correlation between sCD147 expression level and PASI score(r =0.123, P =0.298). There was significant difference of sCD147 expression levels in different subtypes of psoriasis patients(PV PP PsA PE)(P 0.001). 【Conclusion】The expression levels of sCD147 is significantly increased in psoriasis patients. There is statistical significance of sCD147 expression levels in four subtypes of psoriasis. Thus, sCD147 may become a new target for psoriasis drug treatment.
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This chapter contains sections titled: Introduction History of psoriasis Who gets psoriasis? Biology of psoriasis Comorbidities associated with psoriasis Clinical variants of psoriasis Physical symptoms that accompany psoriasis Trigger factors in psoriasis Treatments for psoriasis Measuring quality of life Conclusion References
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Interleukin-20 (IL-20) is suggested as a new target in psoriasis treatment. It was first described in 2001, and the potential role of this cytokine in psoriasis was suggested because mice which were over-expressing IL-20 developed a psoriasis-like phenotype of the skin. Subsequently, IL-20 expression levels were found to be increased in psoriasis skin, and it was observed that these levels normalized upon psoriasis treatment. In the psoriasis xenograft transplantation model, administration of IL-20 to non-lesional psoriasis skin transplanted onto immune-deficient mice demonstrated that IL-20 was involved in the psoriasis induction. More interestingly, improvement of psoriasis was induced by blocking IL-20 signaling.
Interleukin 22
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Psoriasis treatment using psorinum autonosode is discussed. 50 years old male has been suffering from psoriasis for over three years with multiple psoriasis patches on his hands and feet. Psorinum autonosode was prepared from psoriasis scales using Korsakov’s method and taken twice a day. In about a month of taking the autonosode, the psoriasis patches disappeared completely and have not come back for over two years.
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Examining HIV Viral Load in a Matched Cohort of HIV Positive Individuals With and Without Psoriasis.
BACKGROUND: HIV-associated psoriasis is well-documented. Genetic, cellular, and cytokine profiles have been used as evidence to suggest psoriasis activates antiviral pathways. There has been a lack of epidemiologic evidence investigating whether psoriasis patients have lower HIV viral counts compared to non-psoriasis patients. OBJECTIVE: Compare the viral load set point of HIV positive patients with and without psoriasis. METHODS: A retrospective matched cohort study of HIV positive patients with and without psoriasis using the Kaiser Permanente Southern California Health Plan database. RESULTS: We identified 101 HIV-positive psoriasis cases; 19 met inclusion criteria and were matched with 3-5 control patients; 94 total patients were analyzed. The mean age was 41.4 (12.07) years and 83% were male. Overall, the median log of the viral load of cases was slightly higher than controls (4.3 vs 4.2; P less than 0.01). CONCLUSIONS: The serum viral load set point of patients with HIV and psoriasis was slightly higher than the viral load set point of HIV patients without psoriasis. J Drugs Dermatol. 2017;16(4):372-377. .
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