Sphincter of Oddi dysfunction: is there a role for medical therapy?

If the mechanism of pain in patients with sphincter of Oddi (SO) dysfunction is functional obstruction of the biliary tract, and at least in some patients it results from sphincter smooth muscle hypertrophy, then smooth muscle relaxants should have a theoretic role in the management of these patients. Calcium channel antagonists and other smooth muscle relaxants have been shown in "acute" manometric studies to alter SO motility. However, the effect of these agents on vascular smooth muscle remains a concern and often limits their use. At present the role of medical therapy is somewhat unclear because few well-conducted studies have used manometric criteria for the diagnosis of SO dysfunction and the selection of patients for therapy. The main drawback is that no drugs appear to be specific for the SO, long acting, and free of side effects.

Nifedipine for suspected type II sphincter of Oddi dyskinesia.

Endoscopic sphincterotomy may be the treatment of choice in type I sphincter of Oddi dyskinesia, but in type II dyskinesia the results are controversial, the complication rate may be high, and technically endoscopic sphincterotomy is not always possible. Nifedipine has been observed to relax the sphincter of Oddi and to enhance biliary drainage, especially in patients suffering from sphincter of Oddi dyskinesia. Therefore, nifedipine (10 mg, three times a day) was compared with placebo in treating suspected type II sphincter of Oddi dyskinesia in 13 cholecystectomized patients in a 16-wk study period in a double-blind "cross-over" manner. Daily, the patients completed a diary of the pains, need of pain medication, and headache. Clinical examinations and blood tests for liver chemistry were performed at 4-wk intervals. Nifedipine diminished the number of days on which the patients experienced biliary-type pains (10.5 +/- 8.6 vs. 5.8 +/- 4.1, p = 0.042), and the number of days when pain medication was needed was slightly reduced (5.2 +/- 3.9 vs. 3.6 +/- 3.2, p = 0.066). After the study, one patient preferred to undergo endoscopic sphincterotomy, eight patients preferred to continue with nifedipine, and four patients preferred analgesics only. Liver chemistry remained unchanged in this study. Also heart rate, blood pressure, and the number of days of headache were not different between the nifedipine and placebo periods. We conclude that nifedipine is well tolerated in patients with type II sphincter of Oddi dyskinesia, and nifedipine may be tried for reducing the number of painful days and need for analgesics in patients with this disorder.

Efficacy of nifedipine therapy in patients with sphincter of Oddi dysfunction: a prospective, double-blind, randomized, placebo-controlled, cross over trial.

1. Twenty-eight patients who fulfilled entry criteria for sphincter of Oddi dysfunction were randomly allocated to receive nifedipine and placebo in a cross over design with 12 week treatment periods separated by a 2 week wash-out. 2. All patients had episodic pain resembling biliary pain, had previously undergone cholecystectomy, had elevated alkaline phosphatase during episodes of pain and had elevated basal pressure on sphincter of Oddi manometry. 3. Compared with placebo, significant decreases in cumulative pain score, number of pain episodes, oral analgesic tablets consumed and emergency room visits were observed during nifedipine treatment. 4. Overall 21 patients improved during nifedipine therapy while seven patients did not. None of the following predicted response to nifedipine therapy: enzyme levels, morphine-Prostigmine test, fatty meal sonography, common duct diameter and pressure, sphincter of Oddi phasic pressure, frequency and duration of phasic waves and maximal fall in the basal pressure at sphincter of Oddi manometry after sublingual administration of nifedipine. However patients with predominant antegrade propagation of phasic contractions of sphincter of Oddi did significantly better on nifedipine than those with abnormal propagation of phasic contractions. 5. Nifedipine therapy orally in maximal tolerated doses relieves pain in patients with sphincter of Oddi dysfunction who have elevated basal pressure and sphincter of Oddi phasic contractions of predominantly antegrade nature.

[Laboratory and clinical studies on cefuroxime (author's transl)].

The authors have carried out the laboratory and clinical studies of cefuroxime (CXM). The results were as follows: The sensitivity was measured by plate dilution method on 26 strains of S. aureus, 22 strains of E. coli and 24 strains of K. pneumoniae isolated from patients. The distribution of sensitivity of S. aureus was 0.78 approximately 3.13 micrograms/ml and the peak of distribution was 1.56 micrograms/ml. The distribution of sensitivity of E. coli was 1.56 approximately 50 micrograms/ml and the peak was 6.25 micrograms/ml. The growth of 79.2% K. pneumoniae was inhibited in concentration of less than 3.13 micrograms/ml. CXM was given intravenously for 30 minutes at a single dose of 20 mg/kg to 3 children. The serum mean levels of CXM were 99.0 +/- 10.6 micrograms/ml at 30 minutes, 18.0 +/- 10.7 micrograms/ml at 1 hour, 7.0 +/- 2.0, 2.2 +/- 0.6, 0.79 +/- 0.2 microgram/ml at 2, 4 and 6 hours after drip infusion for 30 minutes, respectively. Mean half life was 48 minutes. The mean urinary recovery rate was 96.2% up to 8 hours after administration. CXM was effective in 9 of 10 cases of bacterial infections. No side effect was observed except for 1 case with elevation of serum transaminase.