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PubMed1988

Characterization of the mucosal immune response to dietary antigens in patients with dermatitis herpetiformis.

The association of dermatitis herpetiformis (DH) with granular IgA deposits at the dermal-epidermal junction and a gluten sensitive enteropathy (GSE) suggests that a mucosal immune response may play an important role in the pathogenesis of DH. The degree of antigenic restriction, the immunoglobulin class and subclass response to dietary antigens, and the relationship of antibodies against dietary antigens to IgA-containing circulating immune complexes (CIC) in patients with DH, however, are not known. We have examined the serum of 33 patients with DH for IgG and IgA antibodies against gliadin, and against 3 dietary proteins not thought to be related to GSE, beta-lactoglobulin (beta-lacto), bovine gamma globulin (BGG), and casein. Eleven of 33 (33%) patients with DH had IgA anti-gliadin antibodies, whereas IgA antibodies against beta-lacto were found in 11 of 33 patients (33%), against BGG in 15 of 32 (47%), and against casein in 6 of 33 (18%); 17 of 32 (53%) patients had IgA antibodies against one or more of these dietary antigens. Significantly higher levels of IgA antibodies were detected against beta-lacto (2,500 +/- 2,320 ng/ml, mean +/- SEM) and BGG (2,340 +/- 1,890 ng/ml) than gliadin (1,250 +/- 851 ng/ml) in this group of antibody positive patients (p less than 0.05, Wilcoxon signed ranks test). Eleven of 17 patients with IgA antibodies against dietary antigens were found to have IgA-containing CIC, whereas only one of the 15 antibody negative patients had IgA-containing CIC (p = 0.0008, Fisher's exact test). IgA anti-gliadin antibodies were found to contain both IgA1 and IgA2 with a significantly increased proportion of IgA2 when compared with the IgA2 composition of the total serum IgA (IgA2: anti-gliadin antibodies = 34 +/- 4.2%; total serum IgA = 19 +/- 4.8%, p = 0.02, Students paired t test). IgG antibodies against these antigens were found to occur slightly more frequently in amounts not significantly greater than IgA antibodies. This data demonstrates that a serum IgA and IgG antibody response to dietary antigens occurs in approximately 50% of DH patients with a higher proportion of IgA2 than total serum IgA and does not appear to be restricted to gliadin. This is significantly different from the pattern of cutaneous immunoreactants in patients with DH, and suggests that the deposition of IgA in DH skin may be the result of an atypical mucosal immune response, a non-immunologic interaction of IgA1 and DH skin, or arise from a non-mucosal source.

Antibodies, Anti-Idiotypic↗
PubMed1979

Dermatitis herpetiformis and Sjögren's syndrome.

Two patients are described with dermatitis herpetiformis and Sjögren's syndrome. The increased incidence of autoantibodies in dermatitis herpetiformis would suggest that this association is significant. Antinuclear antibodies commonly occur in dermatitis herpetiformis (Seah et al,, 1971) yet are rarely associated with autoimmune disease in these patients (Moncada, 1974). This report records two patients with dermatitis herpetiformis and Sjögren's syndrome.

Aged↗
PubMed2003

In patients with dermatitis herpetiformis distribution of transglutaminase in cutaneous tissue does not differ from controls.

BACKGROUND: Dermatitis herpetiformis may be regarded as the cutaneous counterpart of coeliac disease. These conditions are related to the ingestion of gluten and both are characterised by circulating antibodies against tissue transglutaminase. AIMS: To study the distribution of tissue transglutaminase in the skin of dermatitis herpetiformis patients and controls, and to investigate whether the dermal IgA deposits, diagnostic for dermatitis herpetiformis, are related to tissue transglutaminase expression in the skin. METHODS: A series of 11 patients with dermatitis herpetiformis had a 4 mm punch biopsy taken from the uninvolved perilesional skin. A group of 16 controls, undergoing surgical removal of benign nevi, gave perilesional skin. Biopsies were covered with OCT and frozen at -80 degrees C. After washing, skin biopsy sections were incubated with an IgG anti-tissue transglutaminase mouse monoclonal antibody. After washing, sections were incubated with anti-mouse IgG. RESULTS: The anti-tissue transglutaminase monoclonal antibody specifically recognised the basal epidermal cells. This staining was no different between patients and controls. CONCLUSION: Our results suggest that tissue transglutaminase can be recognised in the basal epidermal layer both of patients with dermatitis herpetiformis and controls. Since this distribution does not correspond to the distribution of dermal IgA deposits, it is concluded that dermatitis herpetiformis dermal IgA deposits are not due to antibodies directed against cutaneous tissue transglutaminase.

Adult↗
PubMed1984

Dermatitis herpetiformis: diagnosis, diet and demography.

We describe a long term study of 76 patients with dermatitis herpetiformis. Unlike patients with coeliac disease, where the peak incidence was during the first and fourth decades, no dermatitis herpetiformis patients presented in the first decade; also, there was a male preponderance in dermatitis herpetiformis which contrasts with the excess of females in coeliac disease. The apparent prevalence of dermatitis herpetiformis was 11 per 100 000 in our population; approximately one fifth of that of coeliac disease. Jejunal villous atrophy was present in 78% of our dermatitis herpetiformis patients, and a single jejunal biopsy was as effective at detecting this as the multiple biopsy technique. A majority of patients were able to stop, or radically reduce their dapsone or sulphapyridine treatment after the institution of a gluten free diet. Spontaneous remission of the skin lesion occurred in only two patients not receiving a gluten free diet. Gastric parietal or thyroid antibodies were detected in 38% of patients, and three cases of thyroid disease and two cases of pernicious anaemia were detected. Lymphoma developed in two patients, one being intestinal in origin. We conclude that a gluten free diet is of therapeutic benefit in dermatitis herpetiformis and that spontaneous remission is uncommon in those not on a diet. Despite patchiness of the enteropathy, a single jejunal biopsy is quite adequate to diagnose the presence of upper intestinal villous atrophy.

Adolescent↗
PubMed1989

Polymyositis/dermatomyositis associated with dermatitis herpetiformis.

We describe 2 patients with dermatitis herpetiformis who developed polymyositis/dermatomyositis. On HLA typing, both patients were found to be HLA-B8, DR3 positive. The concurrence of these two relatively rare diseases, both associated with immunologic abnormalities, further supports the role of autoimmunity in their pathogenesis and indicates a possible common genetic basis. It also suggests that myositis may be more common in patients with dermatitis herpetiformis than in the general population.

Adult↗
PubMed1996

Protective effect of gluten-free diet against development of lymphoma in dermatitis herpetiformis.

A retrospective study of 487 patients with dermatitis herpetiformis showed that lymphoma developed in eight patients, the expected incidence being 0.21 (standardized registration ratio 3810). All lymphomas occurred in patients whose dermatitis herpetiformis had been controlled without a gluten-free diet (GFD) or in those who had been treated with a GFD for less than 5 years. The results are suggestive of a protective role for a GFD against lymphoma in dermatitis herpetiformis and give further support for advising patients to adhere to a strict GFD for life.

Adult↗
PubMed1992

Coeliac-type dental enamel defects in patients with dermatitis herpetiformis.

The teeth of 30 adult patients with dermatitis herpetiformis and 66 sex- and age-matched healthy controls were examined for dental enamel defects. Sixteen of the patients (53%) with dermatitis herpetiformis, opposed to only one (2%) of the healthy controls (p less than 0.001), were found to have coeliactype permanent-tooth enamel defects. The grades of these defects were milder than those described for severe coeliac disease. There was no correlation between the degree of enamel defects and jejunal villous atrophy. The present finding of frequent coeliactype dental enamel defects in adults with dermatitis herpetiformis suggests that these patients were already suffering from subclinical gluteninduced enteropathy in early childhood, at the time when the crowns of permanent teeth develop.

Adult↗
PubMed1991

The effect of an elemental diet with and without gluten on disease activity in dermatitis herpetiformis.

Elemental diets are reported to decrease activity of patients with dermatitis herpetiformis. We tested the hypothesis that gluten, given in addition to an elemental diet, is responsible for the intestinal abnormalities, cutaneous immunoreactant deposition, and skin disease activity in dermatitis herpetiformis. At entry eight patients with dermatitis herpetiformis, who were consuming unrestricted diets, were stabilized on their suppressive medications at dosage levels that allowed individual lesions to erupt. Six patients were then given an elemental diet plus 30 of gluten for 2 weeks, followed by the elemental diet alone for 2 weeks. Conversely, two patients received an elemental diet alone for 2 weeks followed by an elemental diet plus gluten during the final 2 weeks. Small bowel biopsies, skin biopsies, and clinical assessments were done at 0, 2, and 4 weeks. Suppressive medication dose requirement decreased over the 4 weeks by a mean of 66%. Six of eight subjects significantly improved clinically during the gluten-challenge phase of the elemental diet and all were improved at the end of the study. The amount of IgA in perilesional skin did not change significantly, but the amount of C3 increased in five of seven evaluable subjects after gluten challenge. Circulating anti-gluten and anti-endomysial antibodies were not significantly affected by the diets. All subjects completing evaluable small bowel biopsies (seven of seven) demonstrated worsening of their villus architecture (by scanning electron microscopy and intraepithelial lymphocyte counts) during gluten challenge and improvement (six of six subjects) after 2 weeks of elemental dietary intake. We conclude that 1) there is a significant improvement in clinical disease activity on an elemental diet, independent of gluten administration, 2) small bowel morphology improves rapidly on an elemental diet, and 3) complement deposition but neither IgA deposition nor circulating antibody levels correlate with gluten intake. It seems likely that dietary factors other than gluten are important in the pathogenesis of the skin lesions in dermatitis herpetiformis.

Adult↗
PubMed1980

Dermatitis herpetiformis: the skin and the gut.

Dermatitis herpetiformis is an intensely itchy, chronic, papulovesicular eruption that is usually symmetrically distributed on extensor surfaces. Histologically, it is characterized by dermal papillary collections of neutrophils and subepidermal vesicle formation. The skin has IgA deposits in areas corresponding to the earliest histopathologic change; that is, at the epidermal-dermal junction. Most patients have an associated asymptomatic gluten-sensitive enteropathy that mimics ordinary gluten-sensitive enteropathy (celiac disease) both morphologically and in its response to gluten protein. There is a marked increase in the prevalence of the major histocompatibility antigens, HLA-B8 and HLA-Dw3, and in certain B cell antigens in these patients. Although the sulfones or sulfapyridine have been the mainstay of treatment, it is now clear that the skin disease responds to strict adherence to a gluten-free diet. These findings are reviewed and from them are drawn certain conclusions as to possible pathophysiologic mechanisms involved in dermatitis herpetiformis.

Antigen-Antibody Complex↗
PubMed1995

Lack of proliferative response by gluten-specific T cells in the blood and gut of patients with dermatitis herpetiformis.

The majority of patients with Dermatitis Herpetiformis (DH) have a gluten-sensitive enteropathy which may be triggered by a T cell-mediated immune response to gluten. Using a proliferative assay, the responses to gluten fraction III, recall antigens and mitogens of peripheral blood mononuclear cells (PBMC) and gut T cell lines (TCL) isolated from patients with Dermatitis Herpetiformis (DH) and normal controls were studied. In most cases, neither PBMC nor gut T cell lines (which were predominantly CD3+, CD4+, TCR alpha beta +) from either controls or patients proliferated in response to gluten fraction III alone. However, the addition of 10 U/ml IL-2 to PBMC cultures containing gluten fraction III resulted in a marked increase in proliferation in 9/19 DH patients and 7/11 controls compared to IL-2 alone. Furthermore, gluten-induced upregulation of IL-2 receptor (CD25) expression was demonstrated on PBMC from 4/4 patients with DH and 2/3 controls after 7 days' culture with antigen. A similar effect by exogenous IL-2, or the same concentration of IL-4, was observed in 8/11 (P = 0.02) and 5/6 respectively DH, and 3/4 normal gut T cell lines. No difference was observed in the response of DH and control PBMC to Tetanus toxin, Candida albicans and PPD; both normal and DH gut T cell lines were unresponsive to these antigens. However, the addition of IL-2 increased the response to Candida albicans by DH gut T cell lines. Moreover, the response of DH gut T cell lines to PHA (P < 0.001), Concanavalin A and anti-CD3 were markedly reduced compared to PBMC from the same patients. These findings suggest that gluten-specific T cells present in the blood and gut of normal and DH individuals are activated by but do not proliferate in response to specific antigen.

Candida albicans↗
PubMed1985

Immunoelectron microscopic findings in oral mucosa of patients with dermatitis herpetiformis and linear IgA disease.

Two patients with dermatitis herpetiformis and one with linear IgA disease were examined. Two of the patients had oral lesions and all three showed IgA deposits detected by direct immunofluorescence in apparently normal buccal mucosa. To localize the target structures for IgA deposition, biopsy specimens were taken from normal appearing buccal mucosa for immunoelectron microscopy. The patients with dermatitis herpetiformis had distinct IgA deposits in the upper connective tissue. These were often associated with elastic fibers and occasionally also with capillary walls. In contrast, the patient with linear IgA disease had IgA deposition at the subbasal lamina. Though the clinical expressions may be similar the present immunoelectron microscopic findings in oral mucosa clearly differentiate dermatitis herpetiformis from liner IgA disease.

Adult↗
PubMed1983

Class-specific antibodies to gluten in dermatitis herpetiformis.

An immune reaction to wheat protein has been previously proposed to explain the pathogenesis of dermatitis herpetiformis. In order to detect and characterize antibodies to gluten in human sera, we developed an enzyme immunoassay for class-specific antibodies. Results of this assay in 49 patients with dermatitis herpetiformis were compared with those of 38 normal control subjects, 11 patients with celiac disease, and 6 small-bowel bypass patients. IgA antibodies to gluten were significantly more frequent in dermatitis herpetiformis sera (28/49) than in normal control sera (4/38). IgG antibodies to gluten were significantly more frequent in both celiac disease (10/11) and dermatitis herpetiformis (16/49) sera than in control (5/38) sera. Dermatitis herpetiformis sera also had an increased prevalence of IgM antibodies to gluten (19/49). Small-bowel bypass patients demonstrated no antibody to gluten. Antibodies to gluten in dermatitis herpetiformis objectively mark a state of immune reactivity to wheat protein and may be involved in the genesis of the cutaneous IgA immune deposits and the skin disease.

Adult↗
PubMed1979

Failure to detect gliadin or gliadin binding sites in the skin of patients with dermatitis herpetiformis: immunofluorescence, organ culture and autoradiographic studies.

Recent investigations indicate an abnormal binding of gluten or gliadin to lymphocytes or intestinal mucosa cells in gluten sensitive enteropathy. Since dermatitis herpetiformis is closely associated to gluten sensitive enteropathy, similar receptors could also exist in the skin of patients with dermatitis herpetiformis. To prove this hypothesis, skin of normal volunteers and uninvolved skin of 3 patients with dermatitis herpetiformis was investigated for the presence of gliadin and gliadin binding sites. In vivo bound gliadin was not found by direct immunofluorescence using 3 different rabbit antigliadin antisera. In order to test skin for gliadin binding sites, normal sera and autologous dermatitis herpetiformis sera containing 25 mg% gliadin and tritium labeled gliadin, respectively, were used for incubation of normal and dermatitis herpetiformis skin cryocut sections and of normal and dermatitis herpetiformis skin specimens, grown under organ culture conditions. As checked by direct immunofluorescence and autoradiography, there was no specific in vitro binding of gliadin, indicating that gliadin does not fix to normal human or dermatitis herpetiformis skin. Thus, the role of gliadin in the fixation in vivo, of antibodies or immune complexes to skin in dermatitis herpetiformis, remains obscure.

Antibodies↗
PubMed1988

The prevalence of thyroid autoantibodies in dermatitis herpetiformis.

The prevalence of IgG class thyroglobulin and microsomal antibodies, estimated using a sensitive ELISA, was 48% in 115 patients with dermatitis herpetiformis, which was significantly greater than the prevalence of 16% in 107 unselected controls without dermatitis herpetiformis. IgA class thyroid antibodies were found in 29% of dermatitis herpetiformis patients. Overt thyroid disease had been diagnosed in six (5%) of the dermatitis herpetiformis group and a further six patients had elevated TSH levels. The presence of thyroid antibodies was not associated with particular HLA-DR antigens. These results demonstrate the frequent occurrence of thyroid antibodies in dermatitis herpetiformis, although thyroid failure is less commonly associated with this condition. Immune response genes outside the HLA-DR region may be involved in the immune hyper-responsiveness seen in dermatitis herpetiformis which is reflected in the high prevalence of thyroid autoimmunity.

Adolescent↗
PubMed1985

Intestinal permeability in patients with coeliac disease and dermatitis herpetiformis.

Intestinal permeability was investigated in patients with coeliac disease and dermatitis herpetiformis by a 51Chromium-labelled ethylenediaminetetraacetate (51Cr-EDTA) absorption test and the results correlated with histomorphometric analysis and intraepithelial lymphocyte counts of jejunal biopsies. The mean (+/- SD) 24 hour urine excretion of 51Cr-EDTA in 34 healthy volunteers was 1.9 +/- 0.5% of the orally administered test dose. Patients with untreated coeliac disease (19) or untreated dermatitis herpetiformis (five) excreted significantly more 51Cr-EDTA than controls (5.9 +/- 2.7% and 4.6 +/- 2.1%, respectively, p less than 0.001) and all were outside the normal range of 1.0-2.6%. Patients with coeliac disease (42) treated for 6 months-23 years (mean 5 years) and patients with dermatitis herpetiformis (11) treated for 6 months-8 years (mean 3 years) excreted significantly more 51Cr-EDTA than controls, 4.2 +/- 2.4% p less than 0.0001 and 3.0 +/- 0.9% p less than 0.003 respectively. Eleven of 14 (79%) treated patients with coeliac disease with an entirely normal jejunal mucosae demonstrated abnormal intestinal permeability. Intestinal permeability did not correlate significantly with either the mucosal height/crypt depth ratio or intraepithelial lymphocyte counts in jejunal biopsies from patients with untreated or treated coeliac disease. The demonstration of a persistent increase in intestinal permeability in patients with both coeliac disease and dermatitis herpetiformis may suggest a common pathogenetic mechanism in both disorders. It is postulated that altered permeability may facilitate the entry of gluten or a fraction thereof into the lamina propria where it causes a cascade of immunological events.

Adolescent↗
PubMed1986

Dermatitis herpetiformis: oral lesions as an early manifestation.

Dermatitis herpetiformis is an uncommon chronic skin disease that rarely affects the oral cavity. An unusual case of dermatitis herpetiformis, starting with oral lesions 6 months prior to the onset of skin lesions, is reported. The diagnosis was based on the typical histopathologic features and on positive direct immunofluorescence. The literature is briefly reviewed. Evaluation of laboratory findings, clinical picture, and response to sulfones is essential to the final diagnosis and is emphasized.

Dermatitis Herpetiformis↗
PubMed1992

Increase of lymphocytes bearing the gamma/delta T cell receptor in the jejunum of patients with dermatitis herpetiformis.

The densities of T cells and of cells bearing the T cell receptors gamma/delta and alpha/delta and the surface antigens CD4 and CD8 in jejunal specimens from 21 patients with dermatitis herpetiformis were compared with those in specimens from 13 untreated adults with coeliac disease and 13 control subjects. In the lamina propria of the jejunum the median density of gamma/delta+ cells was significantly (p less than 0.001) greater in untreated patients with dermatitis herpetiformis than in control subjects (114 v 36 cells/mm2) and similar to that found in the patients with coeliac disease (115 cells/mm2). The difference in gamma/delta+ cell density between patients with dermatitis herpetiformis and control subjects was much greater in the surface epithelium of the jejunum: the median density for 14 untreated patients with dermatitis herpetiformis was 39 cells/mm, for seven patients with dermatitis herpetiformis on a gluten free diet 34 cells/mm, and for control subjects 2 cells/mm; the coeliac patients had the same density as the patients with dermatitis herpetiformis (45 cells/mm). The higher density of cells bearing the alpha/delta T cell receptor in the epithelium (median 77 cells/mm) of untreated patients with dermatitis herpetiformis was associated with a gluten containing diet; in specimens taken from patients with dermatitis herpetiformis on a gluten free diet the median density was similar to that in the control subjects (44 v 39 cells/mm). The increase in the number of lymphocytes bearing the T cell receptor gamma/delta, particularly in the epithelium of the jejunum, seems to be a constant marker for these closely related diseases, whereas the density of alpha/delta+ T cells is dependent on the diet.

Adolescent↗