One-Year Follow-up of Duodenal Ulcers after 1-Wk Triple Therapy for Helicobacter pylori

Objective : to study the ulcer recurrence rate of Helicobacter pylori-positive duodenal ulcers at 1 yr after eradication of the bacteria by triple therapy. Method : Patients with H. pylori-positive duodenal ulcers were randomized to receive either triple therapy for 1 wk plus omeprazole for 4 wk (THple+OMP) (n = 78), or omeprazole alone (OMP) for 4 wk (N = 77). Patients were followed up every 3 months for symptom enquiry. At 1 yr, all asymptomatic patients were invited to attend for gastroscopy. Results : At 8 wk, 16 patients in the OMP group and four in the Triple+OMP group had an ulcer. During the 1-yr period, 12 patients in the OMP group and no patient in the Triple+OMP group developed symptomatic ulcers. At follow-up endoscopy at 1 yr, another 10 ulcers were detected in the OMP group and two in the Triple+OMP group. Fifteen patients in the OMP group and 13 in the Triple+OMP group were lost to follow-up. In total, ulcers were de-tected in 39 of 61 (64%) assessahle patients in the OMP group, and in six of 65 (97o) assessahle patients in the Triple+OMP group after I yr (χ² test: p < 0.001). Of the patients whose H, pytori were successfully eradicated hy Triple+OMP at 8 wk, 90% remained H. pylori negative at 1 yr. Conclusion : Triple therapy for 1 wk eradicates H, pylori infection and significantly reduces duodenal ulcer relapses.     

Efficacy of nimodipine in the prophylaxis of migraine

The efficacy of nimodipine in the prophylaxis of migraine was assessed in a double-blind, placebo-controlled, cross-over study carried out on 33 patients, 20 of whom suffered from classic and 13 from common migraine. Four patients dropped out, but not as a result of the side effects of the drug. The duration of drug treatment was 8 weeks. The dosage used was 30 mg four times daily. Nimodipine proved to be better than placebo, the number of migraine attacks and severity of headache showing a significant reduction. The drug was well tolerated and no marked side effects were noted. The results suggest that nimodipine is a useful new prophylactic drug for migraine, but further studies are needed before its final value can be evaluated.     

Hypothesis for the initiation of vasomotion

Vasomotion is the regular variation in tone of arteries. In our study, we suggest a model for the initiation of vasomotion. We suggest that intermittent release of Ca(2+) from the sarcoplasmic reticulum (SR, cytosolic oscillator), which is initially unsynchronized between the vascular smooth muscle cells, becomes synchronized to initiate vasomotion. The synchronization is achieved by an ion current over the cell membrane, which is activated by the oscillating Ca(2+) release. This current results in an oscillating membrane potential, which synchronizes the SR in the vessel wall and starts vasomotion. Therefore, the pacemaker of the vascular wall can be envisaged as a diffuse array of individual cytosolic oscillators that become entrained by a reciprocal interaction with the cell membrane. The model is supported by experimental data. Confocal [Ca(2+)](i) imaging and isometric force development in isolated rat resistance arteries showed that low norepinephrine concentrations induced SR-dependent unsynchronized waves of Ca(2+) in the vascular smooth muscle. In the presence of the endothelium, the waves converted to global synchronized oscillations of [Ca(2+)](i) after some time, and vasomotion appeared. Synchronization was also seen in the absence of endothelium if 8-bromo-cGMP was added to the bath. Using the patch-clamp technique and microelectrodes, we showed that Ca(2+) release can activate an inward current in isolated smooth muscle cells from the arteries and cause depolarization. These electrophysiological effects of Ca(2+) release were cGMP dependent, which is consistent with the possibility that they are important for the cGMP-dependent synchronization. Further support for the model is the observation that a short-lasting current pulse can initiate vasomotion in an unsynchronized artery as expected from the model.     

Dural fistulas involving the cavernous sinus: results of treatment in 30 patients

Thirty symptomatic indirect carotid cavernous fistulas were treated between 1978 and 1986 with a variety of treatment modalities. Combined carotid artery and jugular vein compression resulted in a complete cure in seven of 23 patients (30%) and improvement in one additional patient. There were no complications from this treatment, which is performed by the patient on an outpatient basis. Patients in whom carotid jugular compression therapy failed or who demonstrated cortical venous drainage or visual decline were treated with intravascular embolization. Embolization resulted in complete cure in 17 of 22 (77%) and improvement in four of 22 (18%). One patient required surgical excision of the involved dura after embolization to achieve complete cure. There was one permanent complication (stroke), which resulted in mild weakness caused by clot formation on a catheter.