1993 health care reforms at the state level: an update.

Health care system reform was one of the foremost political issues throughout 1993. While the Clinton Administration developed and proposed a national reform plan, many states enacted laws that call for altering the way in which health care is delivered to their residents. The following article examines health care reform legislation that was enacted at the state level in 1993. It focuses on managed competition plans, plans that seek to expand access to health insurance or to control health care expenditures, and plans that are aimed at reforming Medicaid and other state programs. Because so many states considered or enacted some type of health care reform legislation in 1993, this article provides an overview of the more significant reforms that became law, but it is not intended to serve as a comprehensive review of all state-level health care reforms.

Association of infection due to Helicobacter pylori with specific upper gastrointestinal pathology.

The association of infection with Helicobacter pylori and antral (type B) gastritis now is clear, and the development of sensitive and specific serologic assays for IgA and IgG allows for diagnosis of this infection by noninvasive means. With use of these assays, we studied the association of infection with H. pylori and four other upper gastrointestinal inflammatory conditions: Barrett's esophagus, pernicious anemia (which accompanies type A gastritis), and duodenal and gastric ulcers. H. pylori was present in only 39% of 41 patients with Barrett's esophagus whose gastric biopsy specimens were examined histologically. Each serologic assay correctly categorized 39 (95.1%) of the 41 patients. For both assays the frequency of seropositivity noted for 58 patients with Barrett's esophagus was not different from that noted for age- and sex-matched healthy controls. Among 40 patients with pernicious anemia, the results of assays for IgA and IgG were positive for 17.5% and 0%, respectively; these prevalences were significantly less than the 50% (IgA) and 40% (IgG) positivities noted for matched controls (P less than .01 for each; McNemar's test). Among 57 patients with documented duodenal or gastric ulcers, the results of assays for IgG and IgA were positive for 100% and 98.2%, respectively; these prevalences were significantly higher than the rate noted for matched controls (P less than .001 for duodenal ulcers and P = .02 for gastric ulcers for IgA assay). These data suggest that infection with H. pylori is strongly associated with duodenal and gastric ulcers, negatively associated with pernicious anemia, and independent of Barrett's esophagus.

A randomized study of maintenance therapy with ranitidine to prevent the recurrence of duodenal ulcer.

After an active duodenal ulcer has healed in response to medical therapy, the rate of recurrence during the subsequent year is relatively high. We therefore enrolled 140 patients with healed duodenal ulcers in a two-year randomized, double-blind trial comparing maintenance therapy (ranitidine, 150 mg nightly) with placebo for the prevention of recurrent duodenal ulceration. We performed endoscopy annually and when symptoms suggested the recurrence of ulcers. Verified recurrent ulcers in either group were treated for four or eight weeks with open-label ranitidine (150 mg twice a day). Patients whose ulcers healed within eight weeks resumed randomized treatment. Prophylactic therapy with ranitidine reduced the rate of ulcer relapses from 63 percent in the placebo group to 37 percent in the ranitidine group (P less than 0.05). Treatment with ranitidine extended the median ulcer-free interval from one to two years (P less than 0.05). The first recurrences of ulcer were asymptomatic in half the ranitidine group and in a quarter of the placebo group. Prophylactic therapy with ranitidine also reduced the frequency of recurrent ulcers that were unhealed by eight weeks, that were bleeding, that were in the stomach, or that were the second recurrent ulcer within six months, from 43 percent in the placebo group to 21 percent. Patients who drank alcohol, smoked, had a history of ulcer disease, or had duodenal scarring or erosion at the time of entry into the study were at the greatest risk for recurrence and benefited the most from prophylactic ranitidine. We conclude that prophylactic treatment with ranitidine is effective in preventing the recurrence of duodenal ulceration.

Sucralfate and cimetidine as single agents and in combination for treatment of active duodenal ulcers. A double-blind, placebo-controlled trial.

A randomized, double-blind, double-placebo study was conducted to compare the rates and predictors of healing in patients with endoscopically proved duodenal ulcers during treatment with sucralfate, cimetidine, or a combination of the two drugs. Standard therapeutic dosage regimens were used in each group. No antacids were allowed. Endoscopy was repeated at two weeks and, if needed, at four and eight weeks. Healing was defined as complete re-epithelialization of all ulcers. Cases in which there was a worsening of the ulcer or of symptoms were considered unhealed. Eight patients were dropped for protocol violations or unrelated medical illnesses; data from 61 patients were suitable for analysis. The healing rates achieved with sucralfate and cimetidine did not differ significantly at any time. However, the healing rate at two weeks for combination therapy (33 percent) was higher than for either sucralfate alone (15 percent) or cimetidine alone (10 percent). Cigarette smoking, a prior history of ulcer disease, and a low pepsinogen I to pepsinogen II ratio were significant predictors of delayed healing.