[Multiple colonic ulcers in a patient with Sjögren's syndrome].

A 25-year-old female with Sjögren's syndrome was admitted to our hospital because of fever and abdominal pain. Multiple colonic ulcers were demonstrated by gastrographin enema and colonoscopy. Histological examination revealed the presence of necrotizing vasculitis in the submucosal region. Large dose of prednisolone (60 mg/day) brought a prompt relief of her symptoms and an improvement of positive inflammatory signs. Pseudoaneurysm in the arteria colica media, which had been demonstrated by abdominal selective angiography at the time of diagnosis, became extinct after the steroid treatment. Healing of ulcers were also noted by colonoscopy. A variety of extraglandular symptoms has been reported in Sjögren's syndrome. Multiple colonic ulcers due to vasculitis are rarely complicated but may have a great impact on the prognosis of the disease.

Inhibition of the metabolism of ethyl carbamate by acetaldehyde.

Ethyl carbamate is an animal carcinogen when administered in large doses; it is naturally present in minute concentrations in fermented foods and beverages. Previous studies from this laboratory have demonstrated that ethanol, in vivo, inhibits the metabolism of ethyl carbamate in mice, but the enzyme system has not been identified. In an effort to further characterize the enzyme system responsible, the metabolic products of ethanol metabolism were studied to determine whether ethanol or either of its metabolites is inhibitory. Acetaldehyde (400 mg/kg) is a potent inhibitor of ethyl carbamate metabolism for about 2 hr in vitro, but sodium acetate is not. Paraldehyde (250 mg/kg) has a slower onset and longer duration of inhibition, suggesting that its conversion to acetaldehyde produces the inhibitory molecule. Disulfiram (200 mg/kg) has a prolonged inhibitory effect; this effect is enhanced and extended when the disulfiram is combined with acetaldehyde (400 mg/kg). D-Penicillamine, given in a regimen of 1.2 g/kg 0.5 hr before and 0.6 g/kg 1.5 and 3.5 hr after ethyl carbamate, is not inhibitory; however, it abolishes the inhibitory effect of acetaldehyde, presumably from sequestration of acetaldehyde. These studies demonstrate that acetaldehyde is an inhibitor of the metabolism of ethyl carbamate and suggest that acetaldehyde is one, and perhaps the only, molecule responsible for the inhibition seen when ethanol is administered to mice. In vitro incubation studies determined that ethyl carbamate was not metabolized by human plasma.

Treatment of angina pectoris patients with niludipine a new calcium antagonistic drug.

The antianginal effectivity of niludipine (Bay a 7168), a new calcium antagonistic drug, was investigated in angina pectoris patients, selected for admission to the trials by pre-determined strict criteria. Oral administration of from 60--120 mg niludipine daily for 4--8 weeks, resulted in the following: 1. Number of anginal attacks significantly reduced. 2. Nitrate consumption markedly lowered. 3. Investigating physicians assessed globally the clinical results of niludipine treatment on the basis of the reduction of the number of anginal attacks, nitrate consumption, improved physical ability and reports by the patients as to their subjective evaluation of the test drug. Niludipine was judged clinically effective in 21 out of 27 patients (77.8%). 4. Full records of ECGs, a necessary item for assessment, were obtained from 24 out of 27 patients. Ischemic ECGs were improved or normalized in 6 out of 24 patients (25%). 5. In the investigators' final overall assessment, including the evaluation of ECG changes, niludipine was rated effective for 20 out of 27 patients (74.1%). 6. Tolerance to the test drug was excellent. Only one patient complained of transient, mild nausea. After reduction of the daily dose, the patient completed the trial without any further appearance or complaints of side effects. Results suggest that niludipine is a useful antianginal drug in the management of coronary artery disease patients. Further clinical investigations with a larger number of patients should be conducted.

Effects of dietary trans acids on the biosynthesis of arachidonic acid in rat liver microsomes.

Effects of dietary trans acids on the interconversion of linoleic acid was studied using the liver microsomal fraction of rats fed a semipurified diet containing fat supplements of safflower oil (SAFF), hydrogenated coconut oil (HCO) at 5 and 20 at and 20% levels or a 5% level of a supplement containing 50.3% linolelaidic and 24.3% elaidic acids devoid of cis,cis-linoleic acid (TRANS). Growth rate was suppressed to greater extent with the animals fed the 20% than the 5% level of the HCO-supplemented diets and still further by the TRANS diet compared to the groups fed the SAFF diets. Food intake was greater in the groups fed the HCO than the SAFF-supplemented diets, demonstrating the marked effect of an essential fatty acid (EFA) deficiency on feed efficiency. In contrast to an EFA deficiency produced by the HCO supplement, which stimulated the in vitro liver microsomal biosynthesis of arachidonic acid, diets containing the TRANS supplement exacerabated the EFA deficiency and depressed 6-desaturase activity of the liver microsomal fraction. The liver microsomal fraction of the animals receiving this supplement also was more sensitive to fatty acid inhibition of the desaturation of linoleic acid than those obtained from animals fed either the SAFF or HCO diets. It is suggested that dietary trans acids alter the physical properties of the 6-desaturase enzyme system, suppressing its activity, which increases the saturation of the tissue lipids and, in turn, the requirement for EFA or polyunsaturated fatty acids.