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Biomedical subjects

L Laine

Publications and source records attributed to L Laine.

At least 91 records · Page 5Linked to original sources
PubMed1993

Protein-losing enteropathy and hypoalbuminemia in AIDS.

OBJECTIVE: To assess the contribution of protein-losing enteropathy to AIDS-associated hypoalbuminemia. DESIGN: Prospective assessment of patients with AIDS. SETTING: An urban county hospital (Los Angeles & University of Southern California Medical Center. USA). PATIENTS: Four groups of patients with AIDS were studied: (1) patients with normal serum albumin (> or = 3.9 g/dl) and normal bowel habits; (2) patients with normal serum albumin and diarrhea (> or = four loose or watery stools per day for > or = 2 weeks); (3) patients with hypoalbuminemia (< or = 3.0 g/dl) and normal bowel habits; and (4) patients with hypoalbuminemia and diarrhea. MAIN OUTCOME MEASURE: Fecal alpha 1-antitrypsin concentration was used as a measure of protein loss in the gut. RESULTS: Patients with hypoalbuminemia had a significantly higher mean fecal alpha 1-antitrypsin concentration than those with normal albumin (10.8 +/- 3.0 mg/g dry stool versus 2.4 +/- 0.4 mg/g dry stool; P < or = 0.001). Although mean fecal alpha 1-antitrypsin concentrations were similar in patients with and without diarrhea in the normal albumin group, patients with hypoalbuminemia and diarrhea had significantly higher levels of fecal alpha 1-antitrypsin than those with hypoalbuminemia and normal bowel habits (17.3 +/- 5.8 mg/g dry stool versus 4.6 +/- 1.0 mg/g dry stool; P = 0.009). Twelve out of 36 (33%) patients with normal albumin had elevation of fecal alpha 1-antitrypsin compared with 33 (70%) of 47 patients with hypoalbuminemia (P < or = 0.001). Linear regression analysis showed a significant negative correlation between serum albumin and fecal alpha 1-antitrypsin concentration (r = -0.38; P < or = 0.001). Fecal alpha 1-antitrypsin was significantly higher in patients with mucosal disease visualized at upper endoscopy or flexible sigmoidoscopy than in those without gross abnormalities (13.5 +/- 5.8 mg/g dry stool versus 2.4 +/- 0.7 mg/g dry stool; P = 0.005). CONCLUSION: Protein-losing enteropathy is common in patients with AIDS and may contribute to the development of hypoalbuminemia in these patients.

AIDS-Related Opportunistic Infections↗
PubMed1993

Histopathology of human immunodeficiency virus-associated esophageal disease.

We evaluated the histopathologic features of the esophageal mucosa in 88 patients seropositive for human immunodeficiency virus (HIV). All patients had an upper endoscopy because of esophageal symptoms. Forceps biopsies and brushings of the esophagus were examined histologically and cytologically for evidence of viral, fungal, and mycobacterial infections: in addition, biopsies and brushings were cultured for cytomegalovirus and herpes simplex. Esophageal inflammation (acute or chronic) was graded 0 through 3. Twenty-one patients (24%) had a normal endoscopy; none displayed high grade (grade 2 and 3) acute inflammation and only two (9.5%) had high grade chronic inflammation in the esophagus. Moreover, no fungi or viral inclusions were seen in samples from these patients. Eleven patients (12%) had an abnormal esophageal mucosa but no pathogen detected and were categorized as "idiopathic esophagitis." The percent with high-grade inflammation (27%) was not significantly different from the normal group. Fifty-six patients (64%) had an infectious diagnosis. Forty-six percent had Candida, 16% had viral esophagitis alone, and one patient had Kaposi's sarcoma. Infections were associated with high-grade acute and chronic inflammation in 53% and 47% of patients, respectively. The location of the infiltrate did not predict the type of infection. In conclusion, if esophagoscopy is normal in patients with HIV infection and esophageal symptoms, a biopsy is not necessary.

Esophageal Diseases↗
PubMed1993

Helicobacter pylori, gastric ulcer, and agents noxious to the gastric mucosa.

Conclusions regarding the interaction of H. pylori infection with noxious agents such as NSAIDs, alcohol, and smoking in the development of histologic gastritis and gross gastric injury are limited by the paucity of well-performed studies specifically addressing this problem. At present, we can conclude that H. pylori prevalence is not affected by NSAIDs, alcohol, or smoking. On the other hand, reflux of duodenal contents may play a role in eradication of H. pylori after gastroenterostomy. Although NSAIDs and alcohol do cause gross gastric injury they do not appear to induce changes in the inflammatory cell infiltrate of the gastric mucosa. Rather, the histologic gastritis sometimes attributed to NSAIDs or alcohol seems to be related to the underlying presence of H. pylori. Furthermore, HP does not clearly influence the development of gross injury by NSAIDs or alcohol, and these noxious agents do not influence the H. pylori-associated histologic gastritis. Patients with NSAID-associated gastric ulcers have an H. pylori prevalence similar to that of NSAID users without gastric ulcers and lower than that of patients with gastric ulcers who do not take NSAIDs. These findings suggest that NSAIDs induce ulcers through a mechanism that does not require H. pylori and histologic gastritis. Because NSAIDs are much more likely to cause gastric than duodenal ulcers, this information may explain why patients with gastric ulcers are more commonly H. pylori negative than are patients with duodenal ulcers.

Alcohol Drinking↗
PubMed1992

Fluconazole compared with ketoconazole for the treatment of Candida esophagitis in AIDS. A randomized trial.

OBJECTIVE: To determine the clinical and endoscopic response of candida esophagitis to antifungal therapy and to compare the two oral antifungal agents, fluconazole and ketoconazole. DESIGN: Multicenter, randomized, double-blind trial. SETTING: Fifteen U.S. centers including university, private practice, and county hospital settings. PATIENTS: A total of 169 patients with the acquired immunodeficiency syndrome (AIDS); odynophagia, dysphagia, or retrosternal pain; white esophageal plaques at endoscopy; and pseudohyphae on esophageal brushings or biopsies. INTERVENTION: Patients were randomly assigned to fluconazole (100 mg/d) or ketoconazole (200 mg/d). Doses were doubled at week 1 or 2 if no symptomatic improvement had occurred during the preceding week. Therapy was continued for 2 weeks after resolution of symptoms or for a maximum of 8 weeks. MEASUREMENTS: Patients were clinically evaluated weekly, and laboratory tests were done every 2 weeks. Endoscopy was repeated within 5 days after the end of therapy. RESULTS: A total of 143 patients were clinically evaluable (assessed within 7 days after therapy), and 129 patients were endoscopically evaluable (endoscopy repeated after therapy). Endoscopic cure occurred in 91% of patients treated with fluconazole and in 52% of those given ketoconazole for a difference of 39% (95% Cl, 24% to 52%; P less than 0.001). Esophageal symptoms resolved in 85% of fluconazole-treated patients and in 65% of ketoconazole-treated patients for a difference of 20% (Cl, 6% to 34%; P = 0.006). Intention-to-treat analyses also yielded statistically significant differences for the comparisons listed above. Side effects were minimal and comparable in the two groups; only one patient in each group had therapy discontinued for adverse effects that were possibly related to the study medications. CONCLUSIONS: Fluconazole is associated with significantly greater rates of endoscopic and clinical cure than ketoconazole in patients with AIDS and candida esophagitis. Both drugs appear to be safe and well tolerated.

Acquired Immunodeficiency Syndrome↗
PubMed1992

Prospective evaluation of immediate versus delayed refeeding and prognostic value of endoscopy in patients with upper gastrointestinal hemorrhage.

The effects of immediate vs. delayed refeeding and the prognostic value of endoscopic findings in patients with major upper gastrointestinal hemorrhage were assessed in a prospective randomized study. Entry criteria were clinical evidence of major hemorrhage and endoscopic evidence of a Mallory-Weiss tear or an ulcer with a clean base, flat spot, or clot. Two hundred fifty-eight patients were randomly assigned to groups receiving a regular diet immediately or nothing by mouth for 36 hours, then clear liquids for 12 hours, and a regular diet thereafter. Outcomes in the immediate and delayed refeeding groups were comparable: rebleeding occurred in 4% vs. 5%; urgent intervention, 2% vs. 2%; and deaths, 1% vs. 1%, respectively. Rebleeding occurred in 2 (2%) of 96 patients with cleanbased ulcers, 5 (8%) of 65 with ulcers with spots, 3 (14%) of 21 with ulcers with clots (P = 0.05, 3 x 2 chi2 test), and 1 (2%) of 66 with Mallory-Weiss tears. It is concluded that the time of refeeding does not influence the hospital course of patients with a low risk of recurrent bleeding. Patients with clean-based ulcers or nonbleeding Mallory-Weiss tears may be refed and discharged home immediately after stabilization.

Endoscopy↗
PubMed1992

Cholecystokinin and satiety: effect of hypothalamic obesity and gastric bubble insertion.

Cholecystokinin (CCK) is a gut peptide whose proposed effect on satiety is thought to be related to gastric volume and to be signaled through vagal afferent fibers to the medial hypothalamus. To test these hypotheses we infused CCK C-terminal octapeptide (CCK-8) or saline in a random double-blind fashion in three groups of subjects: 17 obese subjects, 6 of whom subsequently received a gastric bubble, and 5 obese subjects whose obesity was due to hypothalamic injury. The number of sandwich canapes eaten after saline or CCK-8 infusion was recorded during three consecutive 10-min eating periods. Each subject served as his/her own control. The prior infusion of CCK-8 significantly decreased the consumption of sandwich canapes in the first eating period in both the control obese subjects and the subjects with obesity due to hypothalamic injury. Insertion of a gastric bubble did not enhance the satiety effect of CCK-8. These studies support the hypothesis that CCK produces satiety in a time-dependent manner that is not enhanced after the insertion of a gastric bubble but is operative in obese subjects with hypothalamic injury.

Cholecystokinin↗
PubMed1992

Preoperative systemic chemotherapy followed by adjuvant postoperative intraperitoneal therapy for gastric cancer: a University of Southern California pilot program.

PURPOSE: A clinical trial for patients with gastric cancer amenable to curative resection was undertaken to determine feasibility and response to preoperative systemic chemotherapy followed by postoperative intraperitoneal (IP) chemotherapy. METHODS AND MATERIALS: Thirty-eight patients with resectable gastric tumor received two cycles of protracted intravenous (IV)-infusion fluorouracil (5FU), 200 mg/m2/d, for 3 weeks with weekly IV leucovorin 20 mg/m2 and IV cisplatin 100 mg/m2 days 1 and 29. Resection of the gastric tumor followed within 3 weeks of completion of systemic chemotherapy. Those who had all visible tumor removed with clear margins received two cycles of IP floxuridine 3,000 mg (total dose) per day for 3 days and IP cisplatin 200 mg/m2 with IV sodium thiosulfate on the fourth day of IP therapy. RESULTS: Thirty-seven of 38 patients (97%) received two cycles of systemic chemotherapy. Thirty-five of 38 patients (92%) underwent laparotomy for gastric tumor resection. Thirty-three patients (87%) had gastric resections performed; 29 (76%) had all visible tumor removed with microscopically negative margins. No operative mortality was encountered. Twenty-six patients (68%) received IP treatment. IV neoadjuvant treatment was well tolerated and resulted in 68% of the patients reporting improvement in abdominal pain, 45% objective remissions by computed tomography (CT), 38% objective remissions by gastroscopy and biopsy, and 8% had complete surgical pathologic response. Neutropenic sepsis during the IP treatment phase contributed to the only treatment-related death. Four of 29 completely resected patients (14%) have had tumor recurrence. The median follow-up time of patients remaining alive is now 19 months. The median survival for 38 patients entered onto this protocol has not been reached at 17+ months. CONCLUSION: This novel approach to the treatment of adenocarcinoma of the stomach is feasible. The neoadjuvant systemic therapy results in significant primary tumor regression. The determination of whether systemic or IP components of the program contribute to decreased recurrence or increased survival awaits a prospectively randomized clinical trial.

Adenocarcinoma↗
PubMed1992

Cytomegalovirus and Candida esophagitis in patients with AIDS.

We define the clinical importance of cytomegalovirus (CMV) in the natural history of patients with concomitant candida and CMV infection of the esophagus. Prospective evaluation was made of patients with Candida and CMV esophagitis enrolled in a trial of antifungal therapy for Candida esophagitis. Retrospective review was also made of the course of patients who had been found to have both Candida and CMV infection during a previous prospective endoscopic study investigating the etiology of esophageal symptoms in HIV infection. Ten (21%) of 48 patients with Candida esophagitis in the prospective study had evidence of esophageal CMV (nine by culture, one by histology). One died after 4 weeks of therapy, with minimal retrosternal pain. None of the remaining nine had any symptoms or gross CMV esophagitis after antifungal therapy. Thirteen other patients with CMV and Candida were included in the retrospective review (mean follow-up of 8 months). Eight patients received antifungal therapy alone: six (CMV determined by histology in three and by culture in three) had symptomatic resolution; one (CMV by culture) had ongoing symptoms, and a second endoscopy showed an esophageal ulcer due to CMV (histology and culture); and one had ongoing symptoms but a negative repeat endoscopy. Two died without receiving treatment, and three were treated with antifungal and anti-CMV therapy together because of concurrent CMV retinitis (esophageal symptoms resolved in all three). Thus, CMV was of clinical importance in the esophagus in only one of 18 patients with CMV and Candida who received antifungal therapy alone.(ABSTRACT TRUNCATED AT 250 WORDS)

Acquired Immunodeficiency Syndrome↗
PubMed1992

Nonsteroidal antiinflammatory drug-associated gastric ulcers do not require Helicobacter pylori for their development.

Nonsteroidal antiinflammatory drugs (NSAIDs) have been linked with a high incidence of ulcer complications. Histologic gastritis is present in most patients with standard peptic ulcers, and this gastritis is generally related to Helicobacter pylori (HP). We questioned whether gastric ulcers associated with nonsteroidal antiinflammatory drugs (NSAIDs) develop via a novel mechanism, distinct from the usual HP-gastritis-ulcer diathesis. Two groups of patients with newly discovered gastric ulcers were assessed: 1) daily NSAID use > 1 month (n = 19), 2) no NSAID use (n = 36). Biopsy specimens from the rim of the ulcer and adjacent normal mucosa were coded, randomized, and evaluated for histologic features and HP. HP prevalence was significantly lower in the NSAID group (10/19 (53%) vs. 30/36 (83%), p = 0.01). In biopsies from the ulcer rim, inflammatory cell density and epithelial abnormalities were significantly less in the NSAID group than in the no-NSAID group. Biopsies from adjacent mucosa exhibited the same trends, but the differences did not reach statistical significance (inflammation, p = 0.06; epithelium, p = 0.05). HP-positive patients had similar inflammation and epithelium scores, whether or not they took NSAIDs. However, HP-negative NSAID patients had significantly lower scores than HP-positive NSAID users (inflammation, 0.6 +/- 0.2 vs. 2.4 +/- 0.4; epithelium, 1.1 +/- 0.6 vs. 3.5 +/- 0.7). Patients with NSAID-associated gastric ulcers have a lower prevalence of HP and less histologic gastritis than patients with non-NSAID gastric ulcers. The gastritis is related to the underlying HP and not to NSAID ingestion. NSAID-associated gastric ulcers may represent a major subset of peptic ulcers that do not require HP for their development.

Anti-Inflammatory Agents, Non-Steroidal↗