SEARCH · PubMed Health

Results for “DERMATITIS HERPETIFORMIS”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 145 records · Page 8Linked to original sources

PubMed2003

Long-term remission in patients with dermatitis herpetiformis on a normal diet.

BACKGROUND: A life-long gluten-free diet is the treatment of choice for dermatitis herpetiformis, which is considered to be coeliac disease of the skin. OBJECTIVES: To investigate the effects on long-term remission of dermatitis herpetiformis in patients who underwent a gluten challenge and subsequently reintroduced dietary gluten. PATIENTS AND METHODS: We studied 38 patients (14 male and 24 female) with biopsy-confirmed dermatitis herpetiformis. They had followed a gluten-free diet for a mean of 8 years, achieving clinical remission and intestinal normalization. The patients were asked to reintroduce gluten in their diet and agreed to undergo skin and intestinal biopsies during the follow-up. RESULTS: Of the 38 patients abandoning a gluten-free diet, 31 reported the onset of rash within an average of 2 months. Seven subjects (three males, mean age 15 years at challenge) experienced no clinical or histological relapses (median follow-up 12 years), and lost IgA immunoglobulin from the skin. The two series of patients differed in terms of age at diagnosis (mean age: 26.6 vs. 6 years), the use of dapsone (one of 31 vs. four of seven) and adherence to the gluten-free diet (strict compliance in 26 of 31 vs. none of seven). CONCLUSIONS: Our data suggest that the ingestion of small doses of gluten in childhood and/or the use of an anti-inflammatory drug may modify the immunological response inducing immune tolerance. We report long-term clinical and histological remissions in seven patients with dermatitis herpetiformis after the reintroduction of dietary gluten.

Adolescent↗

PubMed1977

Intestinal lymphoma complicating dermatitis herpetiformis.

A case is reported of a patient with dermatitis herpetiformis who has developed an intestinal lymphoma and a bladder carcinoma during the course of his illness. When considered in conjunction with three recently reported cases it is suggested that intestinal lymphoma may complicate the enteropathy of dermatitis herpetiformis.

Dermatitis Herpetiformis↗

PubMed2000

Concordance of dermatitis herpetiformis and celiac disease in monozygous twins.

Celiac disease can be defined as the classical manifestation of gluten sensitivity, which primarily affects the small intestine. Gluten sensitivity has also a skin manifestation, i.e., dermatitis herpetiformis. Both diseases have a strong genetic association with HLA DQ on chromosome 6. In this study we tried to estimate how much different clinical expressions of gluten sensitivity are determined by genetic factors, and hence how feasible they are for genetic mapping; therefore, we studied all six monozygous twin pairs found among 1292 prospectively collected patients of dermatitis herpetiformis in Finland. Three of the six twin pairs were concordant for dermatitis herpetiformis and for simultaneous enteropathy, celiac disease. Two other twin pairs were partially discordant, one of each pair had dermatitis herpetiformis and celiac disease, whereas the other had solely the gut manifestation of gluten sensitivity, i.e., celiac disease. Only one pair was found to be discordant for gluten sensitivity. All the pairs had typical risk alleles for gluten sensitivity, i.e., either HLA DQ2 or DQ8. These results demonstrate that the genetic component in gluten sensitivity as broadly defined is very strong (5/6 concordant). Genetically identical individuals can have clearly distinguished phenotypes, either dermatitis herpetiformis or celiac disease, suggesting that environmental factors determine the exact phenotype of this multifactorial disease. These findings are of importance in genetic linkage analyses, which focus to only certain phenotypic properties of a complex trait.

Adult↗

PubMed1983

Dermatitis herpetiformis and nephrotic syndrome.

A 6 year old girl is reported who suffered from dermatitis herpetiformis, nephrotic syndrome and celiac disease. HLA typing in our patient disclosed the HLA antigens B8 and DW3, which are known to be frequently associated with nephrotic syndrome, celiac disease and dermatitis herpetiformis. In the literature six cases have been reported of the association of glomerulonephritis and dermatitis herpetiformis. An explanation for the development of different immunological diseases in one patient is offered by the HLA type.

Celiac Disease↗

PubMed1980

Buccal mucosa immunofluorescence in coeliac disease and dermatitis herpetiformis.

The buccal mucosa in both coeliac disease and dermatitis herpetiformis behaves in the same manner as the skin with regard to immunofluorescence. The simple technique of buccal punch biopsy can be used to give further confirmation of the diagnosis of dermatitis herpetiformis and, especially in patients with an equivocal diagnosis, may prove easier than carrying out repeated skin biopsies.

Adolescent↗

PubMedDate not supplied

Dermatitis Herpetiformis: a review of fifty-four patients.

A review of 54 patients with dermatitis herpetiformis presenting between 1984-1993 to The Regional Centre of Dermatology, Mater Misericordiae Hospital was undertaken. All patients had skin lesions clinically and histologically typical of dermatitis herpetiformis. Deposition of granular IgA at the dermoepidermal junction on direct immunofluorescence was present in each case. The average age of onset was 41.8 yr, patients having symptoms for an average of 1.6 yr before diagnosis. Six patients had a prior history of coeliac disease. Two patients had a family history of dermatitis herpetiformis, a father and son who were both propositi in this study. Small bowel biopsy was performed on 35 patients, 71.4 per cent of them showing evidence of villous atrophy. All patients were controlled on a gluten free diet or by dapsone or a combination of these. None of the patients experienced serious adverse effects of therapy, nor did any develop lymphoma of the small bowel with a mean follow up period of 4.2 yr (range 1-10 yr).

Adolescent↗

PubMed1988

Cellobiose/mannitol sugar absorption test in patients with dermatitis herpetiformis: a preliminary report.

An abnormal cellobiose/mannitol ratio is present in new patients presenting with dermatitis herpetiformis and in patients who have never adhered to a strict gluten-free diet. In patients with dermatitis herpetiformis in remission on a strict gluten-free diet, small bowel absorption as measured by the cellobiose/mannitol ratio is normal. It is suggested that cellobiose/mannitol ratio absorption is a useful screening test for the intestinal abnormality associated with dermatitis herpetiformis and failure of the test to return to normal could suggest poor dietary compliance.

Adult↗

PubMed1994

T lymphocytes bearing the gamma/delta T-cell receptor in cutaneous lesions of dermatitis herpetiformis.

T lymphocytes bearing the gamma/delta T-cell receptor are a rare component of normal human GI epithelium and skin. Recently, however, an unusually high percentage of T lymphocytes with gamma/delta receptors has been described in gastrointestinal biopsies from patients with dermatitis herpetiformis, implicating the gamma/delta T cell subset in the pathogenesis of this disease. We investigated a possible role for this subset of lymphocytes in the pathogenesis of the cutaneous lesions of dermatitis herpetiformis. Using a standard immunoperoxidase technique, we labelled perilesional skin biopsies from patients with dermatitis herpetiformis and other inflammatory dermatoses with monoclonal antibodies to CD3, CD4, CD8, alpha/beta T cell receptor, gamma/delta T cell receptor, and IL-2 receptor. We found no differences in the percentage of gamma/delta positive T lymphocytes in skin lesions of dermatitis herpetiformis as compared to other selected inflammatory conditions. These findings suggest that the pathogenesis of the cutaneous lesions of dermatitis herpetiformis is not mediated through gamma/delta T cells, and that the cutaneous lesions may develop through mechanisms different from those operative in the gastrointestinal tract.

Dermatitis Herpetiformis↗

PubMed1974

Amino acid and peptide absorption in patients with coeliac disease and dermatitis herpetiformis.

A double-lumen perfusion technique has been used to study amino acid and peptide absorption in eight normal control subjects, 13 patients with untreated adult coeliac disease, and 16 patients with dermatitis herpetiformis who had varying morphological abnormalities of the small bowel. All subjects were perfused with isotonic solutions containing 10 mM glycyl-L-alanine and 10 mM glycine + 10 mM L-alanine. Patients with adult coeliac disease had impaired absorption of glycine (p < 0.01) and L-alanine (p < 0.05) from the amino acid solution compared with the control subjects. Amino acid uptake from the dipeptide solution was not significantly impaired, although four individual patients had impaired uptake of both amino acids. In contrast to these findings, very few patients with dermatitis herpetiformis had impaired amino acid absorption from either solution. Sodium absorption was impaired from both solutions when the groups of patients with adult coeliac disease and dermatitis herpetiformis with subtotal villous atrophy and partial villous atrophy were studied, and there were patients in each group who secreted sodium and water. The results suggest that malabsorption of dietary protein is unlikely to occur in dermatitis herpetiformis but may occur and contribute to protein deficiency seen in some severe cases of adult coeliac disease. The impairment of sodium and water absorption provides evidence that there may be functional impairment of the jejunal mucosa in dermatitis herpetiformis as well as in adult coeliac disease.

Adult↗

PubMed1984

Dermatitis herpetiformis: jejunal findings and skin response to gluten free diet.

Fifty seven children with dermatitis herpetiformis, 18 from Finland and 39 from Hungary, were studied. Diagnostic criteria included the finding of granular IgA deposits in the skin of all patients. The mean age at onset of the rash was 7 X 2 years and favoured sites were the elbows, knees, and buttocks. Symptoms suggesting small intestinal disease were rare but in 35 (61%) of the children subtotal villous atrophy and in 16 (28%) partial villous atrophy were found on jejunal biopsy. Eighteen children underwent a second biopsy after a mean of 21 months on a gluten free diet; villous height was found to be increased and the intraepithelial lymphocyte count decreased in all these patients. Gluten challenge caused a reversal in the two children who underwent a third biopsy. The effect of the gluten free diet on the rash was examined in Finnish children by observing the daily requirements of dapsone, a drug used to control the rash at the beginning of the diet. Eight (67%) of the 12 children were able to stop taking dapsone after a mean of 11 months on the diet and all three patients treated with diet alone became asymptomatic after three to 6 months on the diet. These results confirm that most children with dermatitis herpetiformis have jejunal villous atrophy, though they rarely have gastrointestinal symptoms. The central role of gluten in childhood dermatitis herpetiformis is evidenced by the fact that a gluten free diet helps the damaged jejunal mucosa to recover and controls the rash even in those children who do not have an abnormal jejunal biopsy.

Adolescent↗

PubMed1986

Dermatitis herpetiformis and vitiligo.

We report the fourth case of coexisting dermatitis herpetiformis and vitiligo. This patient's HLA haplotype is HLA-B8 DR3, which is characteristic of dermatitis herpetiformis. The autoimmune features of both disorders suggest that their coexistence is not coincidental.

Dermatitis Herpetiformis↗

PubMed2002

Epidermal transglutaminase (TGase 3) is the autoantigen of dermatitis herpetiformis.

Gluten sensitivity typically presents as celiac disease, a common chronic small intestinal disorder. However, in certain individuals it is associated with dermatitis herpetiformis, a blistering skin disease characterized by granular IgA deposits in the papillary dermis. While tissue transglutaminase has been implicated as the major autoantigen of gluten sensitive disease, there has been no explanation as to why this condition appears in two distinct forms. Here we show that while sera from patients with either form of gluten sensitive disease react both with tissue transglutaminase and the related enzyme epidermal (type 3) transglutaminase, antibodies in patients having dermatitis herpetiformis show a markedly higher avidity for epidermal transglutaminase. Further, these patients have an antibody population specific for this enzyme. We also show that the IgA precipitates in the papillary dermis of patients with dermatitis herpetiformis, the defining signs of the disease, contain epidermal transglutaminase, but not tissue transglutaminase or keratinocyte transglutaminase. These findings demonstrate that epidermal transglutaminase, rather than tissue transglutaminase, is the dominant autoantigen in dermatitis herpetiformis and explain why skin symptoms appear in a proportion of patients having gluten sensitive disease.

Autoantibodies↗

PubMed1978

[Localized dermatitis herpetiformis Duhring of the Cottini type].

Dermatitis herpetiformis Duhring restricted to knees and ellbows is relatively unknown and is called Cottini type. We observed a 23 year old female patient, in whom the resolution of the lesions occured after topical steroids. The dermatitis flared possibly following treatment with an iodine-containing coughing sirup.

Adult↗

PubMed1980

Treatment of dermatitis herpetiformis with cholestyramine.

Two patients with clinically and histologically typical dermatitis herpetiformis showed a dramatic clearing of their skin lesions in association with an oral dose of 4 g of cholestyramine three times a day. Reappearance of the lesions occurred on the discontinuance of the therapy, followed by remission on resumption of cholestyramine. It is postulated that the non-absorbable anion exchange resin, cholestyramine, may have bound and hence blocked absorption of an unidentified compound (possibly gluten, iodine, or endotoxin) critical to the pathogenesis of dermatitis herpetiformis.

Aged↗

PubMed1987

Dermatitis herpetiformis and hemodialysis.

A case of dermatitis herpetiformis in a 60-year-old woman with polycystic kidney disease on hemodialysis is reported. Bullous dermatoses associated with hemodialysis are analyzed.

Dermatitis Herpetiformis↗

PubMed1986

Dermatitis herpetiformis and growth retardation.

We report a juvenile patient with dermatitis herpetiformis, growth retardation and delayed onset of puberty. All symptoms reversed on gluten withdrawal and drug therapy was not required. It is suggested that dermatitis herpetiformis in this patient is the result of long-standing coeliac disease.

Adolescent↗

PubMed1994

Malignant lymphoma and dermatitis herpetiformis.

We report 2 cases of dermatitis herpetiformis (DH) with lymphoma: a non-Hodgkin's malignant histiocytic lymphoma and a rare phenotype of Hodgkin's disease. With these 2 cases, 32 cases of DH complicated by lymphoma have now been documented. Reviewing the literature we show that the majority of lymphomas (78.1%) arises from the gastro-intestinal tract and that almost all cases of DH with lymphoma are associated with coeliac disease. The possible preventive role of a gluten-free diet is discussed.

Adult↗

PubMed1972

Splenic atrophy in dermatitis herpetiformis.

Twenty-four patients with dermatitis herpetiformis were investigated for splenic atrophy by splenic scan and clearance of (51)Cr-labelled heat-damaged red blood cells. Eight of them had definite splenic atrophy. The average splenic cross-sectional area of the remaining 16 with normal clearance times was substantially smaller than normal, suggesting some degree of splenic atrophy. No relationship of splenic hypofunction to intestinal biopsy findings, folate status, reticulin antibody, or treatment with a gluten-free diet or dapsone was evident.

Adult↗