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PubMed1982

Endoscopic duodenal biopsy compared with biopsy with the Watson capsule from the upper jejunum in patients with dermatitis herpetiformis.

Forty-eight patients with dermatitis herpetiformis were investigated with duodenoscopy, endoscopic biopsy, and conventional upper jejunal biopsy. Three endoscopic biopsy specimens were obtained from the duodenal bulb, three to six specimens from the second part of the duodenum, and one suction biopsy from the upper jejunum. In 60%, 71%, and 65% of the patients subtotal or partial villous atrophy was found in biopsies from the three levels, respectively. In eight patients (17%) mucosal abnormalities were confined to the duodenal biopsies and in two patients to the jejunal biopsies. The technique of endoscopic biopsy is advocated because multiple visually selected duodenal specimens may be obtained and because this technique also enables a complete evaluation of the stomach.

Adult↗
PubMed1983

Skin biopsies in relatives of patients with dermatitis herpetiformis.

Out of 109 patients with dermatitis herpetiformis (DH) only one was known to have a first-degree relative with the disease. This is in keeping with previous reports that the familial incidence of DH is low. Study of the family in which two siblings were affected showed both to have HLA-B9 whereas a third, unaffected sibling did not have this antigen. This finding supports the view that both genetic and environmental factors are involved in the pathogenesis of DH, 20 first-degree relatives of 10 other patients with DH had skin biopsies examined by immunofluorescence for the presence of IgA, but none proved positive.

Adolescent↗
PubMed1975

Gastrointestinal investigations in dermatitis herpetiformis.

Thirty-seven patients with dermatitis herpetiformis (DH) have been investigated for gastric and small intestinal abnormalities. Evidence of an enteropathy was found in 86% of the patients who had IgA deposits in uninvolved skin. Villous atrophy of the small intestine was found in 29 patients. About one-half of the patients had reduced absorption of xylose and vitamin A. The Schilling test value was lowered in one-third. Serum B12 was too low in 5/28 patients whereas folic acid in serum and whole blood was too low in 14/29 and 5/19, respectively. Atrophic gastritis occurred in 14/28 patients and only about one-third of the whole patient material had normal gastric mucosal structure and secretion.

Adolescent↗
PubMed1976

Gastric lesion in dermatitis herpetiformis.

Five of 33 patients with dermatitis herpetiformis (DH) were found to have gastric parietal cell antibody in their sera, whereas it was not found in 30 healthy controls of comparable age distribution. Fifteen of the patients with DH underwent further studies to investigate the histological and functional state of their gastric mucosa. Atrophic gastritis was found in all five patients whose sera contained gastric parietal cell antibody and in three of 11 patients with no antibody in their sera. In addition, there was marked impairment of acid secretion in the DH group as a whole, but, apart from one patient with overt pernicious anaemia (PA), there was no evidence of malabsorption of B12.

Adolescent↗
PubMed1987

Striking elevation of serum IgA, IgA-containing immune complexes, and IgA rheumatoid factor in clinically silent dermatitis herpetiformis.

We describe a patient with dermatitis herpetiformis with immunoglobulin A (IgA)-containing circulating immune complexes and IgA rheumatoid factor who presented with acute renal insufficiency; a renal biopsy specimen showed IgA nephropathy. The renal function and proteinuria spontaneously returned to normal despite markedly elevated levels of IgA-containing circulating immune complexes, IgA rheumatoid factor, and IgA antibodies to some environmental antigens. IgA1 was the predominant subclass. IgA2-containing immune complexes and IgM rheumatoid factor were not detected. Cultures of peripheral blood mononuclear cells produced increased quantities of IgA and IgA rheumatoid factor spontaneously and after pokeweed mitogen stimulation. These data indicate that renal function can improve and remain normal despite the presence of increased levels of IgA-containing circulating immune complexes and IgA rheumatoid factor.

Acute Kidney Injury↗
PubMed1981

Polymorphonuclear leukocyte chemotaxis in dermatitis herpetiformis.

Polymorphonuclear leukocyte chemotaxis was investigated in 15 patients with dermatitis herpetiformis and was found not to be significantly increased when compared with the polymorphonuclear leukocyte chemotaxis of 15 normal healthy controls. These results indicate that accumulations of polymorphonuclear leukocytes found in the skin of patients with dermatitis herpetiformis are not due to an increased responsiveness of polymorphonuclear leukocytes to a chemotactic factor.

Adult↗
PubMed1986

IgA class antibody against human jejunum in sera of children with dermatitis herpetiformis.

Sera of 44 children with dermatitis herpetiformis with granular IgA deposits in the papillary dermis were investigated on cryostat sections of normal jejunum of three children aged 2 months, 1 year, and 10 years by indirect immunofluorescence. Eighteen of 25 patients on a normal diet had an IgA class antibody showing the following staining patterns on substrate jejunums: tubular positivity in the lamina propria--around the crypts, beneath the villous epithelial basement membrane, and in some instances in the middle of the villous also, following the capillary system of villi; coalescence of tubular positivity at the muscularis mucosae; and positive blood vessels and smooth muscle endomysium. Eleven of 18 children with positive sera were put on a gluten-free diet (GFD) and their sera became negative. One of these 11 patients was challenged with gluten and the antibody reappeared. Nineteen patients examined only on a GFD and 30 healthy blood donors did not have this antibody. There was no strict correlation between the titer of antibody and the severity of jejunal mucosal damage.

Antibodies, Anti-Idiotypic↗
PubMed1986

Dermatitis herpetiformis. Cutaneous deposition of polyclonal IgA1.

Dermatitis herpetiformis (DH) is a pruritic papulovesicular skin disorder of unknown cause, characterized by granular IgA deposits in the dermis along the dermoepidermal junction. It is associated with gluten-sensitive enteropathy and increased IgA production by gut lymphoid tissue. We report four cases of immunologically documented DH studied by immunofluorescence technique. Monoclonal antibodies against the IgA subclasses IgA1 and IgA2 were used. IgA1 without IgA2 was found in the cutaneous deposits in each case. The IgA1 had both kappa and lambda light chains in approximately equal quantities. Because normal gut-associated lymphoid tissue produces 70% IgA1 and 30% IgA2, while circulating IgA is primarily IgA1, it could be concluded that the IgA in the skin of DH patients is not produced in the gut. However, the subclass restriction of the IgA produced by pathologic gut-associated lymphoid tissue is unknown. Alternatively, both IgA1 and IgA2 may be produced by the gut, but only IgA1 is involved in the production of cutaneous lesions.

Animals↗
PubMedDate not supplied

Dermatitis herpetiformis presenting as chronic urticaria.

Childhood dermatitis herpetiformis (DH) is an immunobullous disease associated with gluten-sensitive enteropathy. This disease is rare in children and is typically characterized by intensely pruritic vesicles on the extensor surfaces. Definitive diagnosis of DH depends on the direct immunofluorescence finding of granular or fibrillar IgA deposits along the basement membrane zone of biopsied perilesional skin. We report an 11-year-old boy with an unusual presentation of DH characterized by a 7-month history of chronic urticaria-like skin lesions. He had evanescent, largely asymptomatic, urticarial wheals on his trunk, face, and extremities that were unresponsive to conventional therapy for urticaria. Skin biopsy specimen findings were consistent with DH and direct immunofluorescence of perilesional skin was diagnostic. The patient had no symptoms of gluten-sensitive enteropathy at the time of diagnosis, and his skin lesions rapidly cleared with dapsone therapy. This patient serves to highlight an unusual presentation of childhood DH and the need to consider this diagnosis when evaluating chronic urticarial lesions in children.

Anti-Inflammatory Agents, Non-Steroidal↗
PubMed1998

Dermatitis herpetiformis: coeliac disease of the skin.

Dermatitis herpetiformis (DH) is a lifelong, gluten-sensitive, blistering skin disease with pathognomonic immunoglobulin (Ig)A deposits in the papillary dermis. Less than 10% of patients with DH have gastrointestinal symptoms suggestive of coeliac disease, yet they all have gluten-sensitive enteropathy. The rash, too, responds to gluten withdrawal. Therefore, DH provides a unique example of the frequent existence of gastroenterologically 'silent' but dermatologically active coeliac disease. DH and coeliac disease are strictly associated with class II HLA alleles A1*0501 and B1*02 encoding the HLA-DQ2 heterodimer. Coeliac disease segregates in the families of patients with DH, also supporting a shared genetic background. Monozygotic twins, one with DH and the other with coeliac disease, show that environmental, not genetic, factors seem to be responsible for the development of the rash in DH. A clinically silent but immunologically active coeliac disease in the gut could well produce IgA autoantibodies which react also with the connective tissue in the skin. The antigen for deposited IgA and its role, if any, in the blister formation in DH remains, however, to be elucidated.

Adult↗
PubMed1999

Hemidesmosomal molecular changes in dermatitis herpetiformis; decreased expression of BP230 and plectin/HD1 in uninvolved skin.

Recent BP230-knockout experiments with subsequent blistering and recently identified plectin/HD1 mutations in epidermolysis bullosa simplex patients suggest that defective expression of BP230 and plectin/HD1 may predispose to blister formation in human skin. We have studied the expression of the epithelial adhesion complex as well as the basement membrane and anchoring fibril antigens in uninvolved dermatitis herpetiformis skin to find out if alterations can be detected in these structures predisposing to the blister formation typical of the disease. Ten uninvolved dermatitis herpetiformis skin specimens, which all showed clear granular deposits of IgA under the basement membrane in direct immunofluorescence and five normal skin specimens, were studied by indirect immunofluorescence technique. Six uninvolved dermatitis herpetiformis skin specimens showed distinctly decreased immunoreaction for BP230 and four uninvolved dermatitis herpetiformis skin specimens showed distinctly decreased immunoreaction for plectin/HD1. All five skin controls showed strong immunoreactions for BP230 and plectin/HD1. Other hemidesmosomal proteins including BP180 and integrin alpha6beta4, as well as basement membrane proteins laminin-5, laminin-1, nidogen and type IV collagen, and the anchoring fibril protein type VII collagen showed a normal strong expression. Our results suggest that alterations in BP230 and plectin/HD1 may contribute or predispose to blister formation in dermatitis herpetiformis skin.

Autoantigens↗
PubMed1992

The protective effect of vitamin E on the hemolysis associated with dapsone treatment in patients with dermatitis herpetiformis.

OBJECTIVE: This study looked at whether oral vitamin C and vitamin E would protect the erythrocyte from oxidant damage caused by dapsone in patients with dermatitis herpetiformis. DESIGN: Fifteen consecutive patients with dermatitis herpetiformis taking dapsone therapy received, in addition, 800 U/d of vitamin E for 4 weeks; then 1000 mg of vitamin C per day for 4 weeks, and, finally, combined vitamin E and vitamin C therapy for 4 weeks. Hemolysis indexes were assessed at baseline and after each 4-week period. RESULTS: Statistical analysis of the results suggests that oral administration of 800 units of vitamin E daily for 4 weeks confers partial protective effect against dapsone-induced hemolysis in patients with dermatitis herpetiformis. CONCLUSION: Partial protection against dapsone-induced hemolysis by orally administered vitamin E, if confirmed as being clinically relevant by further trials, may allow clinicians to continue dapsone therapy orally in patients who develop significant hemolysis. Prophylactic vitamin E to minimize potential hemolysis at the initiation of dapsone therapy may also be appropriate.

Adult↗
PubMed1986

Avidity of antigliadin IgA and IgG antibodies in gluten-sensitive enteropathy and dermatitis herpetiformis.

Antigliadin antibodies (AGA) of IgG and IgA class were assayed with a modified enzymeimmunoassay in serum samples of 18 patients with gluten-sensitive enteropathy and 30 patients with dermatitis herpetiformis. No difference between antibody amount or avidity of the two groups of patients was observed. Avidity and total amount of AGA were also compared in 15 patients with a recent diagnosis of dermatitis herpetiformis and in 15 patients with a disease history of several years without a proper gluten-free diet. No difference in IgG antibodies was found but the amount of high avidity IgA antibodies was significantly higher in patients with several years' experience of dermatitis herpetiformis than in those with a recent diagnosis. The results indicate that in dermatitis herpetiformis, maturation of IgA response occurs. Further, clinically, maturation of anti-gliadin IgA response during the disease can increase the sensitivity of the patient against diet-derived gliadin.

Antibody Affinity↗
PubMed1990

Similarities in intestinal humoral immunity in dermatitis herpetiformis without enteropathy and in coeliac disease.

Intestinal humoral immunity was examined in eight patients with dermatitis herpetiformis and normal jejunal histology (as determined by quantitative morphometry) on a gluten-containing diet. Jejunal aspirate was taken at the time of jejunal biopsy, and levels of total immunoglobulins (IgA, IgM, IgG) and specific antibody to gliadin and two other dietary proteins, betalactoglobulin and ovalbumin, were measured. The pattern of secretory immune responses in the dermatitis herpetiformis patients was similar to that in twenty-six patients with untreated coeliac disease--ie, higher than normal concentrations of IgA, IgM, and IgG and high levels of specific antibodies (IgA and IgM) to the three dietary proteins. Serum levels of IgA antigliadin were similar in the dermatitis herpetiformis and control (twenty-eight patients who underwent jejunal biopsy to exclude coeliac disease) groups, and serum levels of IgG antigliadin were intermediate between those of the control and coeliac disease groups. These findings suggest that investigation of gut humoral immunity may provide a diagnostic index of latent coeliac disease. The definition of coeliac disease as a permanent gluten-sensitive enteropathy may have to be revised if the proposed two-stage model is confirmed.

Adolescent↗
PubMed1985

Thyroid abnormalities in dermatitis herpetiformis. Prevalence of clinical thyroid disease and thyroid autoantibodies.

We studied thyroid abnormalities in 50 patients with dermatitis herpetiformis. Two patients had a history of hyperthyroidism, and 5 had hypothyroidism and were on thyroid replacement therapy. Three patients had had thyroidectomies for nodules, and 5 had asymptomatic goiter. Two patients were clinically euthyroid with elevated thyrotrophin and low normal thyroxine levels, indicating early thyroid insufficiency. Thyroid microsomal antibodies were seen in 38% of patients with dermatitis herpetiformis compared to 12% of controls. The presence of clinical or serologic thyroid abnormalities in 26 of 50 patients shows a significant but unexplained association between dermatitis herpetiformis and thyroid disease.

Adolescent↗
PubMed1984

Demonstration of tissue 90 kD glycoprotein as antigen in circulating IgG immune complexes in dermatitis herpetiformis and coeliac disease.

Mannose-rich 90 kD glycoprotein, a constituent of skin and small-bowel mucosa, was identified as antigen in circulating IgG-type immune complexes in dermatitis herpetiformis and coeliac disease by means of an enzyme-linked immunosorbent assay. High levels of 90 kD glycoprotein-IgG complexes were found in 7 out of 12 patients with dermatitis herpetiformis and in 10 out of 20 patients with coeliac disease but in only 2 out of 20 patients with systemic lupus erythematosus. The highest levels of 90 kD antigen-IgG complexes were found in patients with dermatitis herpetiformis. The amount of these complexes did not correlate with the degree of jejunal villous atrophy. The 90 kD glycoprotein-containing immune complexes with targets in skin and gut may be involved in the pathogenesis of dermatitis herpetiformis and coeliac disease.

Adult↗