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Results for “DERMATITIS HERPETIFORMIS”

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PubMed1997

T-cell receptor V beta expression is restricted in dermatitis herpetiformis skin.

An infiltrate of T-cells is found in lesional dermatitis herpetiformis skin, but the role of these cells in the pathogenesis of the skin lesions is unknown. The purpose of this study was to examine T-cell receptor V beta expression in skin biopsies taken from patients with dermatitis herpetiformis. Expression of eleven T-cell receptor V beta families in biopsies obtained from 10 patients was examined by immunoperoxidase staining and compared simultaneously with peripheral blood lymphocytes. Over-representation of V beta 2 (p < 0.02), V beta 5.2/5.3 (p < 0.01) and V beta 5.3 (p < 0.05) was found in lesional dermatitis herpetiformis skin compared with peripheral blood lymphocytes. These results suggest that recognition of an antigen(s) or superantigen is involved in the pathogenesis of dermatitis herpetiformis skin lesions.

Adult↗
PubMed1975

Scabies masquerading as dermatitis herpetiformis.

Scabies can be easily mistaken for dermatitis herpetiformis because the two conditions have features in common, namely, pruritic papules, vesicles, and crusted erosions in the sacral and gluteal regions. In five patients with scabies who were initially judged clinically to have dermatitis herpetiformis, histological examination was decisive in the eventual correct diagnosis.

Adult↗
PubMed1978

Dermatitis herpetiformis--a skin manifestation of a generalized disturbance in immunity.

Detailed investigations on 42 patients with dermatitis herpetiformis (DH) are presented, emphasis being placed on the presence of other disorders having a prominent immunopathogenic basis. These patients and 42 age and sex matched controls were submitted to an extensive clinical and investigative search for the presence of disorders with an immunological basis including the atopic disorders. The findings provided further evidence supporting the association of dermatitis herpetiformis with thyroid disease and pernicious anaemia. A statistically increased incidence of Raynaud's phenomenon and atopy was found in the patients with dermatitis herpetiformis compared to the control group. In addition, of the patients with dermatitis herpetiformis, two had rheumatoid arthritis, two had ulcerative colitis, one had systemic lupus erythematosus and four had splenomegaly. The possible basis for these associations is discussed and it is suggested that dermatitis herpetiformis may be part of a wider spectrum of disease. Genetic linkage and the formation of immune complexes following exposure to a dietary antigen may both be responsible for the disorders associated with DH.

Adult↗
PubMed1994

25 years' experience of a gluten-free diet in the treatment of dermatitis herpetiformis.

Gluten-free diets have been used in the treatment of patients with dermatitis herpetiformis in our department since 1967. Of the 212 patients with dermatitis herpetiformis attending between 1967 and 1992, 133 managed to take the diet, and 78 of these achieved complete control of their rash by diet alone. Of the remaining 55 patients taking a gluten-free diet, all but three were taking partial diets; over half of these patients managed to substantially reduce the dose of medication required. Of the 77 patients taking a normal diet, eight entered spontaneous remission, giving a remission rate of 10%; a further two patients who had been taking gluten-free diets were found to have remitted when they resumed normal diets. Loss of IgA from the skin was observed in 10 of 41 (24%) patients taking strict gluten-free diets. These patients had been taking their diets for an average of 13 years (range 5-24 years), and their rash had been controlled by diet alone for an average of 10 years (range 3-16 years). The advantages of a gluten-free diet in the management of patients with dermatitis herpetiformis are: (i) the need for medication is reduced or abolished; (ii) there is resolution of the enteropathy, and (iii) patients experience a feeling of well-being after commencing the diet. Thus, we propose that a gluten-free diet is the most appropriate treatment for patients with dermatitis herpetiformis.

Adolescent↗
PubMed1980

IgA-containing circulating immune complexes in dermatitis herpetiformis, Henoch-Schönlein purpura, systemic lupus erythematosus and other diseases.

The sera of patients with dermatitis herpetiformis, Henoch-Schönlein purpura and systemic lupus erythematosus were examined for IgA-containing immune complexes using a newly described radioimmunoassay. The IgG Raji cell radioimmunoassay and the 125I-C1q binding assay were also used to detect IgG- and IgM- containing soluble immune complexes. IgA-containing immune complexes were found in the sera of twelve of forty-nine (24%) patients with dermatitis herpetiformis, four of six (67%) patients with Henoch-Schönlein purpura, and seven of ten (70%) patients with systemic lupus erythematosus. IgG- or IgM- containing immune complexes were also found in six of forty-seven patients with dermatitis herpetiformis, in one of six patients with Henoch-Schönlein purpura, and in nine of ten patients with systemic lupus erythematosus, by either the 125I-Clq binding assay or the IgG Raji cell assay. The finding of soluble IgA immune complexes in a high percentage of patients with systemic lupus erythematosus and Henoch-Schönlein purpura suggests that they may play an important role in the pathogenesis of these diseases. In contrast, their low prevalence in patients with dermatitis herpetiformis suggests that IgA-containing immune complexes may not play a major role in the pathogenesis of dermatitis herpetiformis.

Antigen-Antibody Complex↗
PubMed1975

Abnormal cutaneous reactions in dermatitis herpetiformis.

In 94% of the patients with dermatitis herpetiformis, a locally applied ointment with an ester of nicotinic acid (Trafuril) induced an abnormal reaction with erythema, edema, papules, and often vesicles. The appearance of the reaction to Trafuril is similar to DH lesions. It differs markedly from the reactions to iodide where, as a rule, only one large blister results. The reaction is most pronounced 12-24 hours after application of Trafuril. The reactivity is strongest in the predilection areas for dermatitis herpetiformis. Strongly increased reactivity to Trafuril in DH is induced by pretreatment with streptokinase, streptokinase-streptodornase, or urokinase. Diminished reactivity to Trafuril is seen after pretreatment with injections of Compound 48/80, tranexamic acid, cromoglycate, or application of fluocinolone-acetonide, as well as after stroking the skin.

Adult↗
PubMed1992

Helicobacter pylori serology in patients with coeliac disease and dermatitis herpetiformis.

AIMS: To investigate whether Helicobacter pylori infection or autoimmune gastritis is responsible for the reported increase in gastric pathology and abnormalities of gastric function in patients with coeliac disease and dermatitis herpetiformis (DH). METHODS: Serum H pylori IgG antibodies were assayed by enzyme linked immunosorbent assay and intrinsic factor antibodies by radioimmunoassay in 99 patients with coeliac disease and 58 patients with dermatitis herpetiformis from two geographic areas. RESULTS: H pylori positivity in patients with coeliac disease and dermatitis herpetiformis increased with age, reaching 50% and 70%, respectively, in patients over 50 years. The percentage H pylori seropositivity in coeliac disease did not differ from the percentage positivity observed in 250 similarly aged blood donors from the same geographic area (Leeds). Seropositivity in patients with dermatitis herpetiformis was not significantly different from the level of positivity observed in 98 age matched patients without dermatitis herpetiformis attending the same Edinburgh dermatology clinic. Only one patient with coeliac disease had positive intrinsic factor antibodies. H pylori seropositivity in Edinburgh control subjects under 30 years of age (41.9%) was significantly higher (p less than 0.03) than in Leeds controls (18%) of corresponding age. An increasing prevalence of H pylori seropositivity with age in coeliac disease and dermatitis herpetiformis paralleled that of the control groups. CONCLUSIONS: Gastritis in coeliac disease and dermatitis herpetiformis is largely caused by H pylori infection at a level that is no different from that of the general population. Any increase in the prevalence of gastritis in these two diseases might be caused by lymphocytic gastritis rather than pernicious anaemia.

Adolescent↗
PubMed1991

HLA association with dermatitis herpetiformis is accounted for by a cis or transassociated DQ heterodimer.

HLA-DR, DQ, and DP restriction fragment genotyping was undertaken in 23 dermatitis herpetiformis patients and 53 healthy control subjects. HLA-DQw2 was present in 100% of patients with dermatitis herpetiformis (23 of 23) versus 40% of control subjects (21 of 53). Significant secondary associations occurred with HLA-DR3 (91% of patients versus 28% of control subjects) and DPw1 (39% of patients versus 11% of control subjects). Dermatitis herpetiformis and coeliac disease thus share an identical HLA class II association. It is likely that HLA class II genes directly influence the immune responses leading to mucosal damage in both diseases. The strongest candidate for disease susceptibility to dermatitis herpetiformis is DQw2. The HLA molecule most likely to be involved in coeliac disease is a specific DQ alpha/DQ beta heterodimer, encoded in cis arrangement in DR3 haplotypes or in trans arrangement in a DR5, 7 genotype. Our data on dermatitis herpetiformis patients fits this model perfectly. All these patients are capable of expressing this molecule, which may be responsible for the gluten sensitive enteropathy seen in a subgroup of patients with dermatitis herpetiformis and coeliac disease.

Celiac Disease↗
PubMed1992

The site of blister formation in dermatitis herpetiformis is within the lamina lucida.

BACKGROUND: Because the initial neutrophilic infiltrate in dermatitis herpetiformis is within the dermal papillae, most investigators have assumed the vesicles occur in this same area. This was supported by electron microscopy studies. In 1983 Klein et al. refuted this concept, suggesting that vesicle formation was within the lamina lucida above the lamina densa. Despite this study, current literature continues to state that blister formation is below the lamina densa. OBJECTIVE: Our purpose was to determine the ultrastructural site of blister formation in early and late vesicles of dermatitis herpetiformis. METHODS: We evaluated eight biopsy specimens from four patients by immunomapping with antibodies to bullous pemphigoid antigen, laminin, type IV collagen, and epidermolysis bullosa acquisita antigen. RESULTS: In both early and late vesicles blister formation was found to be above the lamina densa in the lamina lucida. CONCLUSION: These findings are contrary to the commonly held concept that the blister in dermatitis herpetiformis is below the lamina densa and confirm the findings of Klein et al. that the site of blister formation in dermatitis herpetiformis is above the lamina densa within the lamina lucida.

Basement Membrane↗
PubMed1991

[Polyneuropathy in Duhring dermatitis herpetiformis].

Polyneuropathies in patients with dermatitis herpetiformis (Duhring's disease) can be due to dapsone therapy as well as due to an associated enteropathy. Dapsone causes an axonal, purely motor neuropathy, whereas the neuropathy due to an enteropathy is mainly sensory in type. The characteristics of both neuropathies are described considering the clinical and electrophysiological findings in a patient with enteropathic neuropathy and improvement during continuous dapsone therapy.

Biopsy↗
PubMed1979

Immunologic and gastrointestinal abnormalities in dermatitis herpetiformis.

Eighty patients with untreated dermatitis herpetiformis (DH) were studied. The final diagnosis was made after completion of immunofluorescence (IF) studies of the skin, iodine provocation tests and gastrointestinal investigations. IgA deposits in the skin and the HLA-DRw3 B-cell alloantigen can be demonstrated in nearly all cases of DH. Positive iodine provocation test and gastrointestinal abnormalities are present in about 78% of the cases. For diagnostic purposes tissue typing and intestinal biopsy is of value in addition to IF studies of the skin.

Adolescent↗
PubMed1999

Childhood dermatitis herpetiformis: an unusual presentation.

Childhood dermatitis herpetiformis (DH) is rare. The true prevalence and incidence of this condition are unknown. We report a 7-year-old boy presenting with nonpruritic inflammatory papules on the buttocks and extensor surfaces, clinico-pathologically consistent with Sweet's neutrophilic dermatosis. Immunofluorescence studies showed IgA deposits in the dermal papillae consistent with DH. Remission was achieved with a gluten-free diet and dapsone. Childhood DH may present different clinical signs to the adult form and misdiagnosis can occur if immunofluorescence is not requested on skin biopsy.

Anti-Inflammatory Agents, Non-Steroidal↗
PubMed1992

Dietary treatment of dermatitis herpetiformis.

Essentially all patients with dermatitis herpetiformis (DH) and dermal granular IgA deposits have a gluten-sensitive enteropathy as seen in coeliac disease. A gluten-free diet would normally restore mucosal morphology within months. The dapsone medication required to suppress the skin lesions could be gradually reduced and/or finally discontinued in most patients if they constantly adhere to the diet. The immunological reactions may also be reduced. The gluten-free diet could thus be successful both concerning manifestations from the skin and the gut. Although well known in dermatological literature, diet therapy in DH has attracted little interest in journals of nutrition. A survey of this causal diet therapy for the disease therefore seems appropriate.

Dapsone↗
PubMed1994

Polymorphism of the tumor necrosis factor genes in patients with dermatitis herpetiformis.

In 18 patients with dermatitis herpetiformis (DH) of whom 16 were HLA-DR3 positive and 14 had the HLA-B8, -DR3 haplotype, the frequencies of known mutations of the tumor necrosis factor alpha (TNF-alpha) and TNF-beta genes were investigated using restriction fragment length polymorphism analysis and the single-strand conformational polymorphism technique. In DH, the phenotype frequency (28%) and allele frequency (0.58) of the rare TNF-beta allele TNFB*1 were significantly increased (normal control 12.4% and 0.37). For the TNF-alpha promoter/enhancer polymorphism, the rare allele TNF2 was more frequent in DH patients (11%, 0.47) compared to controls (2%, 0.16). Since functional studies have associated the rare TNFB*1 and TNF2 alleles with a higher secretion of TNF upon activation in vitro, the predominance of these two 'high-response' TNF alleles in DH patients may represent a genetic basis for the chronic inflammatory response in the skin and mucosal tissues of patients with DH.

Alleles↗
PubMed1998

Similar IL-5, IL-3, and GM-CSF syntheses by eosinophils in the jejunal mucosa of patients with celiac disease and dermatitis herpetiformis.

Celiac disease (CD) and dermatitis herpetiformis (DH) are gluten-sensitive diseases with different clinical features that can initiate similar intestinal changes. The flat-destructive stage corresponds to severe lesions involving activated T-cells. However, other inflammatory cells such as eosinophils are also abundant. The mechanisms for the intestinal recruitment of eosinophils in patients with CD and DH remain unknown. Eosinophil recruitment and activation are induced in vitro by three main cytokines: interleukin-3 (IL-3), interleukin-5 (IL-5), and granulocyte-macrophage colony-stimulating factor (GM-CSF). In this study, IL-3, IL-5, and GM-CSF were detected by immunohistochemistry in all patients with CD and DH but not in the control group. By ultrastructural immunogold staining, these three cytokines had the same subcellular localization in the granule matrix of eosinophils. This result suggests that eosinophils may be involved in the immune response at the flat-destructive stage of both CD and DH.

Adolescent↗
PubMedDate not supplied

Dermatitis herpetiformis: problems, progress and prospects.

Dermatitis herpetiformis (DH) is an IgA mediated blistering skin disease characterized by the presence of granular deposits of IgA in papillary dermis. The major significant advances in our understanding of DH have been the demonstration that DH patients also have coeliac diseases (CD) and that the rash is also gluten dependent. As a result, it is now possible to cure patients by gluten withdrawal from the diet. The other major significant finding has been the presence of IgA in the uninvolved, now used as the diagnostic criterion for the disease. Despite the fact that it has been known for over fifty years that gluten causes the enteropathy of CD, and for over thirty years the rash of DH, it is still not known how gluten produces these effects. Future immunological studies may look at ways of inducing tolerance to gluten peptides once the toxic ones have been identified. Vaccination against gluten peptides may also be possible in those affected with gluten sensitive disorders.

Adolescent↗
PubMed2002

Characterization of a subgroup of patients with dermatitis herpetiformis with nonclassical histologic features.

Dermatitis herpetiformis (DH) is an autoimmune disease mediated by IgA antibodies. The diagnosis of DH is based on clinical presentation, biopsy for hematoxylin and eosin, and direct immunofluorescence. The chief hematoxylin and eosin finding is a subepithelial blister with neutrophils in dermal papillae. The direct immunofluorescence findings are deposition of IgA and sometimes C3 at the basement membrane with accentuation in dermal papillae. Immunofluorescence is thought to be a sensitive and specific assay in DH, and there are no other known diseases with this pattern of immunofluorescence. The aim of this project was to determine the prevalence of nonclassical histologic findings in DH. We studied 24 cases of DH received at our institution. All cases had clinical findings of DH as well as positive direct immunofluorescence with IgA. We found that 9 of 24 cases (37.5%) had nonspecific H&E findings of a lymphocytic infiltrate only with fibrosis in the dermal papillae and ectatic capillaries. The remaining 15 cases had classic findings of multilocular neutrophilic microabscesses in the dermal papillae. These findings were reproduced on step sectioning. These findings suggest that routine histology may be quite nonspecific in DH and direct immunofluorescence or other more specific immunologic assay is an essential adjunct to diagnosis.

Basement Membrane↗