Small-intestinal bacterial flora in dermatitis herpetiformis

Rc, Heading; Dm, Parkin; Rs, Barnetson; Db, McClelland; Dj, Shearman

doi:10.1007/bf01844939

Cited by 17 publications

(6 citation statements)

References 14 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The finding of low gastric acid secretion in nine patients (seven achlorhydria, two hypochlorhydria) is in agreement with the high prevalence of impaired acid secretion in DH reported by other authors (Heading et al, 1974). Only one patient with reduced acid secretion had normal gastric morphology, thus demonstrating a good correlation between gastric acid production and an atrophic stomach mucosa.…”

Section: Discussionsupporting

confidence: 91%

See 1 more Smart Citation

Gastric lesion in dermatitis herpetiformis.

O’Donoghue¹,

Lancaster-Smith²,

Johnson³

et al. 1976

Gut

View full text Add to dashboard Cite

SUMMARY 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 B,2.Recent studies of patients with DH have shown marked impairment of gastric acid production in response to pentagastrin (Heading et al., 1974). The presence of gastric parietal cell antibody (Fraser, 1970) and an increased prevalence of PA in DH has been noted (Cream and Scott, 1970). These reports, together with the findings of gastric parietal cell antibody in five of our 33 patients with DH, stimulated us to investigate further these patients with regard to gastric morphology and pentagastrin stimulated acid secretion. Methods PATIENTSThe sera of 33 patients with DH (24 male and nine female; age range 17-73 years) and 30 healthy controls (14 male and 16 female; age range 20-71 years) were screened for gastric parietal cell antibody. Sixteen of the DH patients (13 male and three female; age range 21-77 years) consented to further investigation including a gastric biopsy, a pentagastrin test meal, and tests of B12 absorption.GASTRIC PARIETAL CELL ANTIBODY A 1 in 10 dilution of serum was examined by standard indirect immunofluorescencemethods (Seah et al., 1971) for the presence of antibodies against gastric parietal cell using cryostat sections of rat 'Requests for reprints: Dr.

show abstract

Section: Discussionsupporting

confidence: 91%

“…Recent studies of patients with DH have shown marked impairment of gastric acid production in response to pentagastrin (Heading et al, 1974). The presence of gastric parietal cell antibody (Fraser, 1970) and an increased prevalence of PA in DH has been noted (Cream and Scott, 1970).…”

mentioning

confidence: 99%

Gastric lesion in dermatitis herpetiformis.

O’Donoghue¹,

Lancaster-Smith²,

Johnson³

et al. 1976

Gut

View full text Add to dashboard Cite

show abstract

“…It is possible that cholestyramine may act by reducing the absorption of iodine to below critical levels. Its role in reducing endotoxin absorption is also intriguing because in dermatitis herpetiformis there is an overgrowth of bacteria in the small bowel (Heading et al, 1974), possibly due to the atrophic gastritis which may develop. Cholestyramine may also be binding critical acidic fractions of gluten and its component gliadins and glutenins.…”

Section: Discussionmentioning

confidence: 99%

Treatment of dermatitis herpetiformis with cholestyramine

Shelley

1980

Br J Dermatol

View full text Add to dashboard Cite

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.

show abstract

“… 51 Other investigators reported even higher rates of gastric atrophy, in 50-70% of patients with DH, and gastric hypochlorhydria in up to 90%. 52 - 56 …”

Section: Correlated Diseasesmentioning

confidence: 99%

Dermatitis herpetiformis: pathophysiology, clinical presentation, diagnosis and treatment

Clarindo

Possebon

Soligo

et al. 2014

An. Bras. Dermatol.

View full text Add to dashboard Cite

Researches on DH have shown that it is not just a bullous skin disease, but a cutaneous-intestinal disorder caused by hypersensitivity to gluten. Exposure to gluten is the starting point of an inflammatory cascade capable of forming autoantibodies that are brought to the skin, where they are deposited, culminating in the formation of skin lesions. These lesions are vesico-bullous, pruritic, and localized especially on elbows, knees and buttocks, although atypical presentations can occur. Immunofluorescence of perilesional area is considered the gold standard for diagnosis, but serological tests help in cases where it is negative. Patients who follow glutenfree diets have better control of symptoms on the skin and intestine, as well as lower risks of progression to lymphoma. Dapsone remains the main drug for treatment, but it requires monitoring of possible side effects, some potentially lethal.

show abstract

Small-intestinal bacterial flora in dermatitis herpetiformis

Cited by 17 publications

References 14 publications

Gastric lesion in dermatitis herpetiformis.

Gastric lesion in dermatitis herpetiformis.

Treatment of dermatitis herpetiformis with cholestyramine

Dermatitis herpetiformis: pathophysiology, clinical presentation, diagnosis and treatment

Contact Info

Product

Resources

About