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At least 235 records · Page 13Linked to original sources
PubMed1997

Rapid progression of chronic myelomonocytic leukemia following diaminodiphenyl sulphone treatment for dermatitis herpetiformis.

A 41-year-old patient with dermatitis herpetiformis (DH) developed steroid-resistant blebs as a sign of exacerbating DH. The skin symptoms were resolved after 2 weeks of oral administration of diaminodiphenyl sulphone (DDS). However, 3 weeks after the start of DDS, he suffered from edematous eruption on the cheeks and neck, enlargement of the pharynx, systemic lymphoadenopathy and hepatomegaly. In addition, his leukocyte count increased rapidly from 10.1 x 10(9)/l with 13% monocytes just before the start of DDS, to 24.6 x 10(9)/l with 28% monocytes. Bone marrow aspirate showed trilineage dysplasia and chronic myelomonocytic leukemia (CMML) was diagnosed. The patient died from septic shock during neutropenia following cytotoxic chemotherapy. In this case, CMML was complicated with DH and the administration of DDS accelerated the progression of CMML with the manifestations of DDS syndrome. Although DDS is a well-established drug for DH, DDS should be used with great caution when a hematological malignancy coexists.

Adult↗
PubMed1982

IgA pseudo-linear deposits in glomerular basement membranes in dermatitis herpetiformis.

An 18-year-old-woman, with dermatitis herpetiformis, acute glomerulonephritis, malabsorption and villous atrophy due to massive infiltration of IgA producing plasma cells was studied. By light microscopy, her renal biopsy specimen showed heavy immunofluorescence for IgA, a mixed proliferative and membranous lesion with occasional crescents and focal sclerosis. Electron microscopic examination revealed three main lesions: (1) swelling and bleb formation in endothelial cells, (2) extensive fusion of foot processes of podocytes, and (3) a dense quasi-linear, continuous deposition of immune complexes, encompassing several loops; they were characteristically located within the basement membrane at the boundary between the lamina densa and the lamina rara interna. At occasional points where the immune complexes had reached the outer aspects of the basement membrane, there was damage to the podocyte cytoplasm. This electron microscopic aspect supports the interpretation that these immune complexes, although non-complement fixing, exhibit a high damaging potential, leading to relentless disease progression.

Adolescent↗
PubMed1977

Failure to detect specific gluten antigens associated with the immune aggregates in the skin in dermatitis herpetiformis.

The univolved skin of 10 patients with dermatitis herpetiformis (DH) was examined for the presence of gluten antigens with the immunofluorescence technique using a rabbit anti-gliadin antiserum, human antibodies to wheat and to reticulin conjugated to fluorescein-isothiocyanate (FITC) and class-specific anti-human IgA immunoglobulin. In all patients, IgA deposits were found in the tips of the dermal papillae of the uninvolved skin. With the anti-wheat and anti-reticulin conjugates, as well as with the rabbit anti-gliadin antiserum, no specific immunofluorescence was observed in any of the skin specimens. Skin biopsy sections of three DH patients were treated with an acid solution (pH 3.2) in an effort to dissociate antigen-antibody complexes that might be present. After the elution procedure the sections showed undiminished IgA fluorescence, and retesting with the anti-wheat- and anti-reticulin antisera again gave negative results. The skin eluates, two of which contained IgA, had no antibodies to wheat or reticulin. These findings do not give support to the hypothesis that the antigens in the suspected immune complexes in the DH skin consist of gluten.

Animals↗
PubMed1978

Rheumatoid factor in sera of dermatitis herpetiformis patients.

Serum specimens from 44 patients with dermatitis herpetiformis (DH) and 42 control patients were analyzed with solid-phase radioimmunoassay (RIA) developed to detect IgG and IgM class antibodies against herpes simplex virus (HSV) envelope antigen. They were also tested with different tests to detect rheumatoid factor (RF) as well as serum antibodies to gastric parietal cells, glomerular basement membrane, smooth muscle, mitochondria and nuclei. Total serum IgG, IgM and IgA quantification was performed concurrently. IgM class antibodies reacting in HSV envelope antigen RIA were found in 47.8% of the DH patients, but in none of the controls. The age distribution of the IgM positive patients was in accordance with the appearance of RF, representing elderly persons. The presence of RF in serum specimens was confirmed by removing the IgM reactivity with heat aggregated human gamma globulin adsorption and in 13 patients with positive serological tests for RF. No correlation was found with the appearance of RF and duration or severity of the disease or with the detection of RF and serum total IgM concentration. In DH patients antibodies to gastric parietal cells were found in 6 and to smooth muscle in 1 of 32 specimens tested.

Adult↗
PubMedDate not supplied

Antigliadin and antireticulin antibodies in children with dermatitis herpetiformis.

The serum samples of 27 children with dermatitis herpetiformis (DH) were examined for the presence of antigliadin (AGA) and antireticulin (ARA) antibodies. AGA were determined with an enzyme-linked immunosorbent assay (ELISA) and ARA with an immunofluorescence method. Increased IgA or IgG class AGA levels were found in four of ten children on a normal diet, in two of 25 on a gluten-free diet (GFD), and in two of four children on gluten challenge. The corresponding figures for ARA were nine of ten, two of 25, and four of four, respectively. All nine patients with ARA on a normal diet had either subtotal or partial villous atrophy, whereas the patient negative for ARA had a normal jejunal mucosa. ARA were mostly of IgA class, and after gluten withdrawal, increased levels fell to normal range. Four children were challenged with gluten, and they all developed subtotal villous atrophy and demonstrated IgA class ARA. These results suggest that in childhood DH, ARA is a more sensitive indicator of gluten-sensitive enteropathy than AGA, but both antibody determinations can be used in monitoring adherence to GFD treatment.

Adolescent↗
PubMed1981

Anti-gliadin antibodies and small intestinal mucosal damage in dermatitis herpetiformis.

Sera from forty-six patients with dermatitis herpetiformis (DH) were examined for anti-gliadin antibodies (AGA) by the enzyme linked immunosorbent assay (ELISA) test and by a simple new immunofluorescent (IF) test. AGA were present in fifteen out of thirty-two patients taking a normal diet, but in none of the fourteen taking a gluten-free diet (GFD). The presence of circulating AGA was related to the severity of the enteropathy. AGA were present in all ten patients with a flat mucosa and in four of six with a convoluted mucosa, but in only one out of thirty patients with normal morphology of the small intestine. However, in those patients taking a normal diet and with a normal morphology of the intestine there was evidence of gluten sensitivity compared to those taking a GFD, as the intraepithelial lymphocyte count (IELC) was significantly raised in the peri-nuclear and supra-nuclear positions. The study shows that the presence of AGA in the serum is a good indication of the degree of gluten sensitivity as expressed by severe mucosal damage in patients with DH.

Adolescent↗
PubMed1999

Circulating autoantibodies to tissue transglutaminase differentiate patients with dermatitis herpetiformis from those with linear IgA disease.

BACKGROUND: Dermatitis herpetiformis (DH) is highly associated with celiac disease. Recently, tissue transglutaminase (tTG) was identified as the autoantigen of IgA antibodies in celiac disease. The prevalence of antibodies to tTG in DH patients is not known. OBJECTIVE: The purpose of this study was to determine whether DH patients show circulating IgA autoantibodies to tTG, to compare their serum levels with those from patients with other subepidermal autoimmune bullous diseases, and to correlate levels of antibodies to tTG with the extent of small bowel disease. METHODS: Sera were obtained from consecutive patients with DH (n = 11), linear IgA disease (n = 15), bullous pemphigoid (n = 10), and epidermolysis bullosa acquisita (n = 6) and were studied by indirect immunofluorescence on monkey esophagus and NaCl-split human skin. IgA reactivity to tTG was measured by enzyme-linked immunosorbent assay. The extent of mucosal involvement in jejunal biopsy specimens was assessed according to the grading of Marsh. RESULTS: All untreated DH patients showed circulating IgA autoantibodies to tTG. One DH patient already undergoing therapy, the 15 patients with linear IgA disease, and all other controls revealed no autoantibodies to tTG. In addition, serum levels of IgA anti-tTG antibodies reflected the degree of histopathologic changes in jejunal mucosa from biopsy specimens in DH patients. CONCLUSION: Our results show that circulating IgA autoantibodies to tTG are detectable in DH but not in linear IgA disease or other subepidermal autoimmune bullous diseases. The levels of IgA anti-tTG antibodies reflect the extent of histopathologic changes of the jejunal mucosa in DH.

Adult↗
PubMed2000

Expression of eotaxin, interleukin 13 and tumour necrosis factor-alpha in dermatitis herpetiformis.

BACKGROUND: The dermal and perivascular infiltrate in dermatitis herpetiformis (DH), which is mainly composed of CD4+ lymphocytes, neutrophils and eosinophils, is believed to play an important part in the pathogenesis of the disease. Previous studies suggest that cytokines such as interleukin (IL) -8, granulocyte-macrophage colony-stimulating factor, IL-4 and IL-5 could be involved in the pathogenesis of DH. These cytokines appear to drive tissue infiltration and maturation of eosinophils. Part of the effect of T-helper (Th) 2-type cytokines (IL-4, IL-5) on eosinophils could be mediated by eotaxin, which is a highly specific chemotactic protein induced by various cytokines [IL-4, IL-13, tumour necrosis factor (TNF) -alpha and interferon-gamma]. OBJECTIVES: To evaluate the expression of eotaxin and its inducers, IL-13 and TNF-alpha, in DH. METHODS We examined lesions collected from 10 DH patients with active disease. Sections from each specimen were incubated with anti-IL-13, anti-TNF-alpha and anti-eotaxin antibodies. Chloroacetyl esterase reaction was performed to show mast cell infiltration. RESULTS: Eotaxin was mainly expressed at the tips of the dermal papillae, within the microabscesses. Positivity was also found in the lymphomonocytic infiltrate in the dermis. IL-13 was expressed in the dermal infiltrate and TNF-alpha was found in the inflammatory infiltrate and in dermal vascular cells. CONCLUSIONS: These findings confirm the importance of the lymphomonocytic infiltrate and of Th2 cytokines in the pathogenesis of this disease, suggesting that tissue infiltration in DH is mediated by cell-specific chemokines such as eotaxin and not only by non-specific chemokines such as IL-8.

Adult↗
PubMed1990

Recurrent pericarditis and dermatitis herpetiformis. Evidence for immune complex deposition in the pericardium.

Recurrent pericarditis can be associated with many chronic illnesses. Dermatitis herpetiformis is a chronic papulovesicular eruption which is characterized by granular IgA deposits in the dermal papillary tips and associated with a gluten-sensitive enteropathy. We describe the first case of recurrent pericarditis in association with dermatitis herpetiformis. This supposition is supported by exclusion of other possible etiologies and pericardial biopsy which revealed the deposition of IgG, IgA and complement.

Complement System Proteins↗
PubMed1986

Dermatitis herpetiformis and glomerulonephritis. Case report and review of the literature.

A patient who had a history of successfully treated dermatitis herpetiformis and in whom membranous glomerulopathy later developed is described. The predominant immunoglobulin present in the renal biopsy specimen was IgA. It is suggested that the dermatologic and renal diseases had a common immunologic origin. A review of the literature dealing with dermatitis herpetiformis and glomerulonephritis is included.

Adult↗
PubMed1977

Dermatitis herpetiformis: a comparative assessment of skin and bowel abnormality.

We reviewed 18 patients with a clinical diagnosis of dermatitis herpetiformis who were being treated with dapsone and were on an unrestricted diet. Diagnosis was confirmed by finding IgA deposits in the dermal papillae of unaffected skin. Dapsone was discontinued and biopsy of affected skin was carried out when the typical rash reappeared. The biopsy findings were graded according to the severity of the histological changes. Small bowel tissue from each patient was examined and graded by stereo- and routine microscopy. Thirteen specimens (72%) were stereomicroscopically abnormal; all 18 showed villous atrophy, either partial or subtotal; and in 13 (72%) the interepithelial lymphocyte count was increased. No correlation was found between the histological severity of the skin and the small bowel lesions. Seemingly the severity of the skin rash in dermatitis herpetiformis is no guide to the degree of small bowel abnormality.

Adolescent↗
PubMedDate not supplied

Dermatitis herpetiformis: should direct immunofluorescence be the only diagnostic criterion?

We describe a 7-year-old boy with dermatitis herpetiformis (DH) diagnosed on clinical and histologic evidence, negative direct immunofluorescence (DIF) findings for junctional IgA deposits in uninvolved skin, positive IgA endomysial and gliadin antibodies, and jejunal biopsy revealing a gluten-sensitive enteropathy. Treatment with dapsone led to the disappearance of cutaneous lesions and pruritus within 48 hours. Demonstration of IgA immune deposits in the dermal papillae has been the only acceptable criterion for the diagnosis of dermatitis herpetiformis. However, considering several reports in the literature of DH with a negative DIF and our own case, we believe that in the absence of the characteristic DIF pattern, one needs the combination of clinical, histologic, and immunologic data to support the diagnosis of DH. We also discuss recent developments in the diagnosis of DH.

Biopsy, Needle↗
PubMed1976

Pemphigus foliaceus. Early clinical appearance as dermatitis herpetiformis with eosinophilic spongiosis.

We encountered an unusual case of pemphigus foliaceus in which there were early clinical signs of dermatitis herpetiformis with eosinophilic spongiosis histologically. Numerous authors have appreciated that eosinophilic spongiosis occurs in early pemphigus foliaceus, usually in the preacantholytic stage when the lesions may clinically simulate dermatitis herpetiformis. Recognition of eosinophilic spongiosis may help differentiate early pemphigus from other vesiculobullous disorders.

Acantholysis↗
PubMed1979

Wheat protein antibodies in dermatitis herpetiformis.

An enzyme-linked immunosorbent assay was used to detect class-specific antibodies to wheat protein antigens. Antibodies which we detected by this technique reacted indistinguishably with antigens prepared from crude gluten, crude gliadin, alpha-gliadin, Frazer fraction III, and subfraction B and B3 of Frazer fraction III. No sera reacted with a human serum albumin control antigen. The prevalence of IgG antibodies to wheat protein antigens was significantly greater in patients with gluten sensitive enteropathy, 12 of 17, (p = .00011) and in patients with dermatitis herpetiformis, 5 of 14, (p = .046) than in normal control subjects. Strongly positive reactions for IgG antibodies were present only in patients with gluten sensitive enteropathy or dermatitis herpetiformis. IgA antibodies to wheat protein antigens were found only in gluten-sensitive enteropathy patients. We have found this to be a sensitive, precise technique for measurement of antibodies to wheat protein antigens and feel that it will prove useful in evaluation of the role of immune complexes involving wheat protein antigens and their antibodies in the pathogenesis of dermatitis herpetiformis.

Adult↗
PubMed1981

Dermatitis herpetiformis: immune complex detection with C1q and monoclonal rheumatoid factor.

To determine the significance of circulating immune complexes in dermatitis herpetiformis, serum samples from thirty patients with active disease were tested by a C1q binding radioassay, while serum samples from twenty-one of these patients were tested by a monoclonal rheumatoid factor (mRF) inhibition radioassay. By direct immunofluorescence, all patients demonstrated typical IgA deposition in dermal papillae. Using the C1q binding assay, only seven of forty-two serum samples had elevated C1q binding activity, while by the mRF inhibition assay, thirteen of twenty-five samples had elevated immune complex levels. Nine of these latter thirteen positive serum samples, however, were minimally elevated. Thus, IgG and/or IgM containing immune complexes are infrequently present, or at very low levels, in sera of patients with active dermatitis herpetiformis.

Antigen-Antibody Complex↗
PubMed1989

Comparison of IgA-class reticulin and endomysium antibodies in coeliac disease and dermatitis herpetiformis.

The occurrence of IgA class reticulin and endomysium antibodies was examined with the standard immunofluorescence method in coeliac disease and dermatitis herpetiformis. Similar high antibody frequencies were detected in 32 untreated adults (91%) and 18 children (100%) with coeliac disease and in 14 dermatitis herpetiformis patients with subtotal villous atrophy (reticulin antibodies 93% and endomysium antibodies 100%). The specificity of IgA class reticulin antibodies and endomysium antibodies was high because all 45 adult patients with ulcerative colitis or Crohn's disease, 24 non-coeliac children with abdominal symptoms and 99/100 healthy blood donors were negative for these antibodies. The only positive blood donor had both IgA class reticulin antibodies and endomysium antibodies but also she was found to have coeliac disease. IgA class reticulin antibodies and endomysium antibodies declined in parallel during treatment with a gluten free diet and increased on gluten challenge. This suggests that these antibodies can be used to screen for gluten sensitive enteropathy and to monitor dietary treatment. To characterise the tissue specificity of reticulin antibodies and endomysium antibodies four positive sera were absorbed with human and several rodent liver homogenates. Absorption with rat or other rodent livers removed the rodent-specific reticulin antibodies but not the reticulin antibodies detectable with human tissues or the endomysium antibodies detectable with monkey oesophagus. These results show that reticulin antibodies can be divided into the rat and human subtypes. The human subtype could not be separated from endomysium antibodies in the present absorption experiments.

Adolescent↗