دانلود ترجمه مقاله تشخیص مدیریت و پیش آگهی از بیماری درماتیت هرپتی فرم – نشریه NCBI

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 تشخیص
نکات کلیدی
مدیریت
نکات کلیدی
پیش بینی
نکات کلیدی

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پیش بینی
نکات کلیدی :
 بیماران مبتلا به Dermatitis herpetiformis نیازمند یک طرح درمانی multidisciplinary هستند.
 غربالگری اعضای خانواده باید در درمان تشخیص بحث و بررسی شود.
 Dermatitis herpetiformis یک وضعیت درمان پذیر با پیش شناخت مساعد می باشد.
درمان بیماران با DH باید با تیمی متشکل از درماتولوژیست، گاستروآنترولوژیست و متخصص تغذیه انجام گیرد. بیماران به خاطر استعمال بلند مدت دارو و مدیریت flareها باید مرتباً تحت نظر باشند. ویزیت های منظم امکان غربالگری (اسکرینگ) و آشکارسازی به هنگام وضعیت نئوپلاستیک یا اتوایمون که با DH ارتباط دارد را فراهم می کند. آزمایشات لابراتواری منظم (مثل شمارش کامل گویچه های سفید خون جهت غربال تهی سازی تغذیه ائی) در صورتی که بیمار سیمپتوماتیک (دارای علامت) باشد ضروری است و برای کسانی که تحت تراپی سیستمیک قرار می گیرند، الزامی است (جدول ۲). مشاوره درخصوص غربالگری خانوادگی باید در زمان پیش شناخت رخ دهد. منابع متعددی مثل کارگاه های آموزشی و غربالگری رایگان CD در اختیار بیماران قرار داده شده است. یکی از برنامه های آموزشی مفید در این خصوص هر ساله ماه دسامبر در مرکز بیماری های سلیاک شیکاگو برگزار می شود. اطلاعات بیشتر را می توانید در پایگاه اینترنتی WWW.Celiacdisease.net جستجو کنید، یا این که با شماره (۰۷۷۳) ۷۰۲۷۳۹۵ تماس بگیرید. با توجه به افزایش شمار موارد خانوادگی DH، مانیتورینگ دقیق بستگان درجه یک بیماران DH باید در اولویت کار قرار گیرد.

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DIAGNOSIS Key points d Physical examination and routine histopathology are often suggestive of dermatitis herpetiformis, while direct immunofluorescence findings in perilesional skin are pathognomonic d Serologic testing is a useful adjunct for diagnosis and may be used to monitor dietary adherence d Genetic testing for human leukocyte antigens DQ2 and DQ8 is useful in ruling out dermatitis herpetiformis The diagnosis of dermatitis herpetiformis (DH) is based on a constellation of findings on physical examination, routine histopathology, immunofluorescence studies, and serologic testing (Fig 1). Physical examination alone may be suggestive; however, given the varied morphologic presentation of DH, additional testing is usually required.1 Biopsy specimens for routine histopathology should ideally contain an intact vesicle.2 The classic histopathologic features of DH seen on light microscopy include a subepidermal cleft with neutrophils and a few eosinophils at the tips of dermal papillae (Fig 2, A).1,2 These findings are often accompanied by a perivascular mixed inflammatory infiltrate (Fig 2, A).1,2 While routine histopathology may be highly suggestive of DH, other conditions, such as linear immunoglobulin A bullous dermatosis (LABD) and bullous lupus erythematosus, can present nearly identical histologic findings. Therefore, immunofluorescence studies are critical for definitive diagnosis. Granular deposits of IgA at the tips of dermal papillae are pathognomonic for DH (in contrast to the linear pattern of IgA deposition seen in LABD; Fig 2, B).1-4 The IgA deposits in DH are thought to be polyclonal but are mainly composed of IgA1.5 Occasionally, granular deposits along the basement membrane zone occur in DH, which can lead to misdiagnosis as LABD.1 Interestingly, these deposits are not altered by pharmacologic therapy for DH, but do slowly resolve on a gluten-free diet (GFD).2,3 The site of biopsy for direct immunofluorescence is of vital importance. Although IgA deposition occurs in both lesional and nonlesional areas, a study comparing lesional, perilesional, and nonlesional skin in DH showed significantly greater IgA deposition in normal appearing perilesional skin.3 In fact, biopsy specimens of lesional skin often yield false-negative results on direct immunofluorescence.3,6 Serologic testing is a useful adjunct to tissue-based studies. A number of serologic markers are shared between DH and CD, as might be expected given their close relationship. Circulating IgA antibodies to endomysium, the fine connective tissue sheath surrounding a muscle fiber, are detected in both conditions.5 Testing for antiendomysial antibody is based on indirect immunofluorescence using monkey esophagus as substrate; despite some operator-dependent variability, it is a highly specific and moderately sensitive test for the diagnosis of DH.1,5 IgA antitissue transglutaminase (tTG) testing is performed by a widely available enzyme-linked immunosorbent assay (ELISA)ebased test and has a specificity range of 97.6% to 100% and sensitivity of 48.8% to 89.1%.5,7,8 This test may be useful in differentiating DH from LABD and reflects the degree of mucosal changes on small bowel biopsy specimens in these patients.7 With the discovery that epidermal transglutaminase (eTG) is the key autoantigen in DH, serologic testing for autoantibodies against this protein has attracted increasing interest. Recent studies report a high sensitivity (60-80.8%) and specificity (92.8- 100%) of serologic testing for DH with a commercially available ELISA-based assay to detect IgA anti-eTG antibodies.8,9 Serologic testing offers the advantages of entailing a generally lower cost and being less invasive than a skin biopsy; pending more validation, it may become a useful initial screening method in patients in whom DH is suspected clinically. Levels of anti-tTG and anti-eTG IgA correlate with the extent of small bowel pathology.10 Finally, levels of antiendomysial, anti-tTG, and anti-eTG antibodies are low or undetectable in patients following strict GFD and, therefore, these may be useful quantitative markers of adherence to this dietary regimen. Although promising, the anti-eTG assay has not yet been approved in the United States for in vitro use to diagnose DH.8 Selective IgA deficiency is about 10 to 15 times more prevalent in patients with celiac disease (CD) compared with the general population.11,12 The presence of selective IgA deficiency often leads to a delay in diagnosis of CD because of the lower detection rates of IgA autoantibodies through serologic testing. No cases of selective IgA deficiency in DH have been reported, emphasizing the critical role of IgA autoantibodies in the pathogenesis of skin lesions in DH. However, partial IgA deficiency has been reported in DH and needs to be considered during the serologic work-up.12 In patients with IgA deficiency, IgG antibodies to endomysium and transglutaminases may be useful to monitor disease. Genetic testing to determine a patient’s HLA haplotype is useful in cases where DH cannot be excluded. The absence of human leukocyte antigens (HLAs)-DQ2 or -DQ8 has a high negative predictive value, such that patients lacking these alleles are very unlikely to have DH.

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