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Iron absorption has been studied in patients with dermatitis herpetiformis (DH). Four patients out of 20 had iron deficiency, defined as absence of or only traces of haemosiderin in bone marrow smears. These four had adequate absorption of ferrous iron. The iron deficiency in at least 3 of them was ascribed to increased iron loss. The results indicate that, although having a mild to moderate malabsorption syndrome, DH patients can be expected to exhibit adequate absorption of orally administered iron. Explanations of a negative iron balance other than defective absorption should therefore be sought.

In order to study the development of atrophic gastritis, gastric secretory function was examined by a standard pentagastrin test 24 to 78 months after a previous examination (Ex I). The study included 12 patients with dermatitis herpetiformis (DH), 6 patients with functional signs of atrophic gastritis previously, and 8 healthy controls. The surrent examination (Ex II) also included microbiological culture of gastric juice and estimation of gastrin(s), parietal cell and thyroidal antibodies. Most of the controls had increased their maximum acidity and maximum acid output (MAO) between the examinations. This may indicate an altered potency of pentagastrin in recent years. Conversely, 5 of the 6 patients with atrophic gastritis showed a further reduction of maximum acidity and MAO, indicating progressive parietal cell atrophy. In the DH-group, two tendencies were observed: 6/12 patients had an increased MAO at Ex II. They had had lower mean age and higher mean MAO at Ex I, as compared with the remaining 6 patients who had a decreased MAO at Ex II. The latter group more often had parietal cell antibodies.

The gluten intake was quantitated utilizing a dietary history method in 43 patients with dermatitis herpetiformis on non-restricted diet. The mean daily gluten intake was 15 g. The individual intake of gluten was related to the maintenance dose of dapsone. It was significantly higher in patients on 100-150 mg dapsone daily than in those taking 0-25 mg daily. There was a significant correlation between amount of gluten in the diet and the dapsone dose (p less than 0.01, rs = 0.43). Villous atrophy was not related to the dapsone dose. It is suggested that the gluten-sensitive enteropathy changes the intestinal permeability and thus contributes to the development of blisters.

Dietary intakes of energy and nutrients were calculated from diet history interviews in 30 patients with dermatitis herpetiformis, before and after 18 months on a gluten-free diet. In spite of great changes in the intake of different foods, the mean intake of dietary fibre did not decrease. There was only a small decrease in the intake of iron in women, while the intake in men did not change. Patients with a previous high intake of gluten had indirect evidence of malabsorption.

The individual daily intake of gluten was calculated in 45 patients with dermatitis herpetiformis (DH) on the basis of a depth interview about food habits. Gastric and small intestinal morphology and function were studied concurrently. Mean daily gluten intake was estimated to be 15 g, a figure which corresponds well to the average gluten intake in Sweden. There was a significant correlation between the degree of morphological mucosal changes of the small intestine and the quantity of gluten ingested. All patients with jejunal villous atrophy consumed more than 10 g gluten daily and all but one patient with normal jejunal villous structure had a gluten intake of less than 10 g/d. The findings suggest a dose-dependent effect of gluten on the intestinal mucosa. Conversely, the daily gluten intake was not correlated to gastric morphology, gastric acid secretion, serum gastrin levels or serum parietal cell antibodies. Patients with reduced ability to secrete gastric acid did not differ from the remaining patients in this respect. Whereas the coeliac-like enteropathy in DH seems to be caused by ingested gluten, the frequently occurring achlorhydric atrophic gastritis must be assumed to be of different immunopathogenesis.

Single application of 600-750 mug phalloidine/kg body weight produces within 4-6 h a decrease of serum cholesterol esters and a rising concentration of free fatty acids and lysophosphatidyl choline in liver homogenate. Analysis of fatty acids compounds in liver lipid fractions indicates an increase of shorter-chain fatty acids and a percentage diminution of highly unsaturated longer-chain fatty acids. In the prophylactic test, and also when giving silymarine-N-methylglucamine-salt simultaneously with the toxic agent, most analysed parameters show a variance according to those of the nonintoxicated control group. Correlation analysis of paramenters points out typical variations between normal, control and experimental animals.

For two patients with psoriasis arthropathica therapy with gold salts was started. In both cases a serious psoriasis pustulosa occurred after the first injection together with a leucemic reaction. The mechanism of gold side effects is discussed on the basis of the literature and these cases. The value of the therapy of the psoriatic arthropathie with gold is questioned.

Seventeen patients with dermatitis herpetiformis were tested for gastric hydrochloric acid secretion. Seven were found to be achlorhydric. Atrophic gastritis in these patients probably had an auto-immune pathogenesis, as judged by elevated serum gastrin level, high prevalence of antibodies against gastric parietal cells and antrum sparing of the gastric atrophy. This type of atrophic gastritis is considered to indicate a precursor state to pernicious anemia.

Approximately 38 cases of the yellow nail syndrome have been described in the literature and one further case of this rare condition is added. The symptoms and various associated conditions are discussed. The lymphographic findings in one case are described in detail.