Home About us Contact
|
Home About us Contact | ||
|
|
||
Psoriatic Skin Lesions (psoriatic + skin_lesion)
Selected AbstractsPrevention of psoriasis-like lesions development in fsn/fsn mice by helminth glycansEXPERIMENTAL DERMATOLOGY, Issue 6 2006Olga Atochina Abstract:, The helminth glycan LNFPIII is an immunomodulatory molecule, driving CD4+ Th2-type biasing as well as immune suppression. Psoriasis is an autoimmune disease where the immune mechanisms as well as the antigens responsible for development of immune autoreactivity are still not known. In the absence of defined immunological mechanisms, we asked whether LNFPIII would function as novel therapy for psoriasis. We tested the therapeutic efficacy of LNFPIII using the flaky skin (fsn)/fsn mutant mouse model of psoriasis-like lesion development. We found that treatment of mice with LNFPIII prevented the appearance of psoriatic skin lesions on fsn/fsn mice. Examination of the skin 2 weeks after treatment demonstrated that prevention of skin lesions was associated with maintenance of normal epidermis thickness in LNFPIII-treated mice as compared with a significantly thickened epidermis in control treated and diseased mice. In addition, cells from skin of LNFPIII-treated mice produced lower amounts of interferon-, as compared with cells from skin of control treated diseased mice. Examination of macrophages and T cells from peripheral lymph nodes of control and LNFPIII-treated fsn/fsn mice showed that glycan treatment reduced the numbers of Gr1+F4/80+ macrophages and the numbers of CD8+ T cells, restoring the numbers of these two cell populations as well as the CD4 : CD8 ratio to near normal levels. Overall, the results from this study suggest that the helminth immunomodulatory glycan LNFPIII functions to prevent development of psoriatic-like skin lesions in fsn/fsn mice. [source] Juvenile psoriatic arthritis with nail psoriasis in the absence of cutaneous lesionsINTERNATIONAL JOURNAL OF DERMATOLOGY, Issue 1 2000Carola Duran-McKinster MD A 4-year-old white boy without a significant family history had morning stiffness and painful swelling of his left knee and ankle, right elbow, and dorsolumbar region of 2 months' evolution. The following laboratory studies were within normal limits: complete blood cell count, C-reactive protein (CRP), latex, antistreptolysin, and antinuclear antibodies. Rheumatoid factor was negative and an increase in the erythrocyte sedimentation rate (ESR) was detected (56 mm/h). The pediatric department made an initial diagnosis of juvenile rheumatoid arthritis, and treatment with acetylsalicylic acid at 100 mg/kg/day and naproxen at 10 mg/kg/day was started. A thick, yellowish toenail was diagnosed as onychomycosis. No mycologic investigations were performed. Intermittent episodes of painful arthritis of different joints were present. The radiographic features of the peripheral joints included: narrow joint spaces, articular erosions, soft tissue swelling, and diffuse bony demineralization. Characteristic bilateral sacroiliitis and a swollen tendon sheath on the left ankle were detected. At 11 years of age the nail changes had extended to five other toenails and to four fingernails, were yellow,brown in color, and showed marked subungual hyperkeratosis ( Figs 1, 2). The rest of the nails showed significant nail pitting. Trials of griseofulvin alternated with itraconazole in an irregular form for five consecutive years resulted in no clinical improvement, which prompted a consultation to our dermatology department. On three different occasions, KOH nail specimens were negative for fungus, but the presence of parakeratotic cells aroused the suspicion of psoriasis. A complete physical examination was negative for psoriatic skin lesions. A nail bed biopsy specimen was characteristic of nail psoriasis ( Fig. 3). Figure 1. Thickened nails with severe subungual hyperkeratosis in five fingernails Figure 2. Secondary deformity of nail plate. No "sausage" fingers were observed Figure 3. Light microscopic appearance of a nail biopsy specimen showing parakeratotic hyperkeratosis, elongation of interpapillary processes, and Munroe abscess (arrow) (hematoxylin and eosin stain, ×40) The following human leukocyte antigens (HLAs) were positive: A9, A10, B12, B27, Cw1, Bw4, DR6, DR7, DQ1, DQ2, and DR53. A diagnosis of juvenile psoriatic arthritis associated with nail psoriasis was made. Toenail involvement became so painful that walking became very difficult. Occlusive 40% urea in vaseline applied to the affected toenails for 48 h resulted in significant improvement. Currently, the patient is 20 years old with nail involvement, but no psoriatic skin lesions have ever been observed. [source] Juvenile psoriatic arthritis carrying familial Mediterranean fever gene mutations in a 14-year-old Turkish girlTHE JOURNAL OF DERMATOLOGY, Issue 5 2007Betul Sozeri YENIAY ABSTRACT Juvenile psoriatic arthritis (JPsA) is characterized by asymmetric arthritis of big and small joints, enthesitis, dactylitis, psoriatic skin lesions and nail pitting. Investigators agree that JPsA is a relatively common chronic arthropathy of childhood that differs clinically, serologically, and genetically from both juvenile idiopathic arthritis and juvenile ankylosing spondylitis. Familial Mediterranean fever (FMF) is a multisystemic autosomal recessive disease occasionally accompanied by sacroiliitis. This is characterized by recurrent self-limited attacks of fever and accompanying abdominal, chest and arthricular pain. We present a 14-year-old Turkish girl with JPsA and carrying FMF gene mutations. In this patient, JPsA was diagnosed according to her physical, laboratory and skin biopsy findings and a treatment with methotrexate and sulfasalazine was started. As an inadequate clinical and laboratory response was obtained after the first month of therapy, the patient was investigated for FMF, and was diagnosed by molecular analyses of related gene (E148Q heterozygous/V726A homozygous mutation) besides clinical findings. After 2 weeks of the colchicine treatment, symptoms of the patient regressed and acute phase reactants decreased. To our knowledge, this is the first case presenting with psoriatic arthritis and FMF gene mutations together and responds to colchicine, methotrexate and sulfasalazine dramatically in clinical and laboratory findings. This case has been presented to remind that cases with psoriatic arthritis may also carry mutations in the MEFV gene. [source] Psoriatic skin expresses the transcription factor Gli1: possible contribution of decreased neurofibromin expressionBRITISH JOURNAL OF DERMATOLOGY, Issue 4 2006H. Endo Summary Background, Psoriasis is a chronic inflammatory disorder of skin characterized by hyperproliferation of keratinocytes. Intracellular signalling pathways inducing the hyperproliferation of keratinocytes remain to be elucidated. An inhibitor of Hedgehog (Hh) signalling, cyclopamine, was recently reported to clear psoriatic skin lesions, suggesting involvement of the Hh signalling pathway in the hyperproliferation of lesional keratinocytes. We have previously observed activation of the Hh signalling pathway in Schwann cells of plexiform neurofibroma in neurofibromatosis type 1 (NF1), which results from functional loss of the NF1 encoding protein, neurofibromin. In psoriasis, deficiency of neurofibromin expression has been observed in lesional keratinocytes. Objectives, To investigate whether the Hh signalling pathway would be activated in psoriasis and whether inhibition of neurofibromin expression would enhance the activation of the Hh signalling pathway. Methods, Activation of the Hh signalling pathway was examined by protein expression of one of the target genes, GLI1, coding for the transcription factor Gli1. Immunohistochemical studies were performed on seven psoriatic skin samples and seven control normal skin samples with a standard immunoperoxidase technique. mRNA expression of GLI1 was analysed by reverse transcriptase,polymerase chain reaction in HaCaT cells transfected with double-strand small interfering RNA for NF1. Results, Our results showed Gli1 expression in psoriatic skin but not in control normal skin. Inhibition of neurofibromin expression in HaCaT cells upregulated mRNA expression of GLI1. Conclusions, Our findings indicate that the Hh signalling pathway is activated in psoriasis and that neurofibromin deficiency may upregulate the pathway. [source] Inefficacy of topical thyroid hormone analogue TriAc in plaque psoriasis: results of a double-blind placebo-controlled trialBRITISH JOURNAL OF DERMATOLOGY, Issue 2 2004A. Vahlquist Summary Background, Thyroid hormone receptors are expressed in human skin and are believed to be involved in the regulation of epidermal proliferation and differentiation, i.e. processes which are disturbed in psoriatic skin lesions. Ligands of the thyroid hormone receptors have so far not been tested as antipsoriatic agents. TriAc (3,3,,5-triiodo-thyroacetic acid) is a well-known thyroid hormone analogue with much reduced cardiac thyrotoxic activity compared with the classical thyroid hormones. Objectives, To determine the effectivness and side-effects of topical TriAc in patients with chronic plaque psoriasis. Methods, Twelve patients with mild to moderate psoriasis were treated with TriAc (0·1% in hydrophilic ointment) and placebo applied twice daily to either of two (or several) bilaterally symmetrical plaques for 8 weeks. The patients and investigator were blinded as to the content of the tubes. Every 2 weeks the treated plaques were evaluated by the patient (using a balanced visual analogue scale for a right,left comparison) and by the investigator (using a psoriasis severity index and a global assessment of each plaque). Results, After 8 weeks of treatment, more than 33% improvement of the psoriasis index occurred in 10 of 12 TriAc-treated and nine of 12 placebo-treated plaques. There were no statistically significant differences between the treatments in terms of reduction of the scores for erythema, scaling, induration or pruritus during the study. Half of the patients considered TriAc superior to placebo, whereas three of 12 were of the opposite opinion (P > 0·05). The global assessment showed marked improvement or remission in six TriAc-treated and five placebo-treated cases (P > 0·05 for difference). No adverse effects were noted. Conclusions, TriAc in the dosage and formulation studied was safe but no more effective than placebo in treating plaque psoriasis. However, newer thyroid hormone analogues (agonists or antagonists) might be more active and should be further explored in this context. [source] A role for T cell-derived interleukin 22 in psoriatic skin inflammationCLINICAL & EXPERIMENTAL IMMUNOLOGY, Issue 3 2007K. Boniface Summary Interleukin (IL)-22 is a T cell-derived cytokine that has been reported recently to induce cutaneous inflammation in an experimental murine model of psoriasis, and to induce in vitro an inflammatory-like phenotype. In the present study, we assessed the presence of IL-22 and the IL-22 receptor 1 (IL-22R1) in skin lesions, skin-derived T cells, as well as IL-22 levels in sera from patients with psoriasis. IL-22R1 and IL-10R2 transcripts are expressed at a similar level in psoriatic and healthy skin. In contrast, IL-22 mRNA expression was up-regulated in psoriatic skin lesions compared to normal skin, whereas IL-22 mRNA levels in peripheral blood mononuclear cells from psoriatic patients and normal subjects were similar. Circulating IL-22 levels were significantly higher in psoriatic patients than in normal subjects. T cells isolated from psoriatic skin produced higher levels of IL-22 in comparison to peripheral T cells isolated from the same patients. IL-10 was expressed at similar levels in skin biopsies and peripheral blood mononuclear cells of psoriatic patients and normal subjects. Finally, we show here that supernatants of lesional psoriatic skin-infiltrating T cells induce an inflammatory response by normal human epidermal keratinocytes, resembling that observed in psoriatic lesions. Taken together, the results reported in this study indicate that IL-22 is a cytokine produced by skin-infiltrating lymphocytes that is potentially involved in initiation and/or maintenance of the pathogenesis of psoriasis. [source] | ||||||||||