Magnification endoscopy as a reliable tool for the early diagnosis of rejection in living related small bowel transplants: a case report.

The purpose was to determine whether magnification endoscopy (ME) accurately diagnosed rejection in living related small bowel transplants (LRSBTx) during initial morphological adaptation of segmental intestinal grafts. The small bowel recipient was a 44-year-old woman with short gut syndrome following multiple bowel surgeries for familial adenomatous polyposis. ME was enhanced by chromoendoscopy staining. Bowel mucosa was washed with acetic acid and stained with methylene blue for optimal visualization of mucosal villi and to improve the diagnostic yield of biopsies. The recipient underwent surveillance ME with biopsy 16 times through the ileostomy in the first 9 months following transplantation. The recipient developed diarrhea in the postoperative course, which led to the suspicion of rejection. ME findings of patchy villus blunting were consistent with biopsy samples that showed mild acute cellular rejection. Episodes of rejection were treated with high-dose immunosuppressants and steroids. Reversal of rejection was monitored by follow-up ME, which showed increased length of villi and normalization of morphology. Biopsy confirmed these findings. The first endoscopy, at 5 days posttransplant, showed no evidence of intestinal ischemia. LRSBTx involves early morphological adaptation of the recipient small bowel mucosa, characterized by an increased length of villi. ME is a reliable technique to follow adaptation and detect early rejection. The superior imaging of small bowel mucosa created by ME chromoendoscopy enables early diagnosis and delivery of more prompt antirejection therapy to prevent progression of rejection. ME also confirmed that segmental LRSBTx caused minimal ischemic injury to the recipient.

Interventional endoscopy.

Interventional endoscopy is a general label given to endoscopic procedures used to deal with a variety of gastrointestinal disorders. The interventional endoscopic procedures of interest in this review are those used specifically with gastric disorders. They include hemostasis, endoscopic ultrasound, endoscopic mucosal resection, stenting, percutaneous endoscopic gastrostomy tube placement and photodynamic laser therapy. Here, we review the latest data related to (a) a number of general issues having an impact on this diverse group of procedures (eg, such as proper patient selection criteria, consent in the era of open access endoscopy, protocol for anticoagulation, and sedation); (b) the methodology and outcomes of each of these unique procedures as they apply to the stomach; and (c) some of the latest technologic advances and developments that will potentially have an impact the future use of these procedures.

Nutrition in acute pancreatitis.

Pancreatitis is a common disorder. Numerous factors have been implicated in the pathogenesis of acute and chronic pancreatitis, but the exact mechanisms of these conditions are still poorly understood. Depending on the cause of the disorder, patients who have pancreatitis are usually not malnourished and are able to eat within 5 to 7 days of disease onset. In these patients, nutritional support is unnecessary. However, severe disease induces a catabolic state similar to that seen in trauma and sepsis, resulting in rapid weight loss and increased morbidity and mortality. Thus, vigorous nutritional support may be useful in the treatment of severe pancreatitis. Studies have shown that parenteral and enteral nutritional support are well tolerated and can maintain or improve nutritional status in patients with pancreatitis. This article reviews nutritional assessment and therapy in pancreatitis.

Dietary cow's milk protein does not alter the frequency of diabetes in the BB rat.

One theory of the pathogenesis of IDDM proposes that exposure to cow's milk proteins triggers the disease in genetically susceptible individuals. We tested this hypothesis in the BB/Wor rat model of human IDDM. Diabetes-prone (DP) BB/Wor rats spontaneously develop IDDM. Coisogenic diabetes-resistant (DR) BB/Wor rats do not develop diabetes spontaneously, but IDDM can readily be induced by treatment with polyinosinic:polycytidylic acid and depletion of RT6+ T-cells. Pregnant BB/Wor rats were fed one of four experimental diets or a standard Purina commercial rat chow (5010) that was certified to be free of cow's milk protein. Offspring were maintained on the maternal diet after weaning. DP-BB/Wor rats, fed either of two experimental diets based on hydrolyzed casein and free of intact milk protein (Nutramigen or D11236), developed diabetes at only half the rate of animals fed Purina 5010 chow. Neither the addition of bovine serum albumin (BSA) to Nutramigen nor the substitution of total milk protein for the hydrolyzed casein in the D11236 diet increased the frequency of spontaneous diabetes. In contrast, there was no relationship between diet and susceptibility of DR-BB/Wor rats to IDDM induction. However, the methods used to induce IDDM in DR-BB/Wor animals were found to induce antibodies against BSA. We conclude the following: 1) Dietary modification can reduce spontaneous IDDM expression in DP-BB/Wor rats, but the agent of protection is not elimination of cow's milk protein. 2) The addition of BSA or intact milk protein does not abrogate the effectiveness of a protective diet. 3) The genetic susceptibility of the DR-BB/Wor rat to autoimmune diabetes is unaffected by any of the tested diets, but a role of anti-BSA-like autoreactivity in IDDM expression cannot be excluded.

Giant gastric ulceration associated with antiphospholipid antibody syndrome.

The anticardiolipin or antiphospholipid antibody syndrome is characterized by an increased incidence of venous and arterial thromboses. This syndrome may occur in association with systemic lupus erythematosus or independently. Gastroenterological manifestations have included Budd-Chiari syndrome, hepatic infarction, esophageal necrosis with perforation, intestinal ischemia and infarction, pancreatitis, and colonic ulceration. We report a 39-yr-old man with antiphospholipid antibody syndrome complicated by adrenal insufficiency secondary to bilateral adrenal infarction who presented with severe epigastric pain. Endoscopic evaluation disclosed progressive gastric ulceration with necrosis in the distal body. Angiography revealed no vasculitis. Because of intractable pain despite intravenous anticoagulation and narcotic analgesia, the patient was taken to surgery, and an antrectomy with Billroth II gastrojejunostomy was performed. Histological examination revealed widespread vascular occlusive disease involving veins, small arteries, and arterioles present in all layers of the stomach and the perigastric fat consistent with the vasculopathy of the antiphospholipid antibody syndrome. Treatment with high intensity oral anticoagulation and corticosteroids resulted in clinical and endoscopic improvement. This case report extends the gastroenterological manifestations of the antiphospholipid antibody syndrome to include giant gastric ulceration and emphasizes the importance of anticoagulation in treatment.

The effect of recombinant cytokines on [14C]-aminopyrine accumulation by isolated canine parietal cells.

Interleukin-1 (IL-1) and tumor necrosis factor-alpha (TNF-alpha) have been shown to inhibit basal and pentagastrin-stimulated gastric secretion in rats and histamine-stimulated secretion in dogs. IL-1 also reduces the severity of ethanol and stress-induced gastroduodenal damage. The aim of this study was to examine the effects of human recombinant IL-1 alpha and TNF-alpha on enzymatically dispersed and enriched (> 90%) parietal cells stimulated with histamine, histamine plus 3-isobutyl-1-methylxanthine (IMX) or carbachol (all 10(-5) M). Acid secretion was assessed indirectly by quantitating [14C]-aminopyrine (AP) accumulation. IL-1 alpha (500 and 1000 ng/ml) inhibited histamine-stimulated AP uptake by 53% and 60% respectively, and it inhibited IL-1 alpha (1500 ng/ml) by 69%. IL-1 alpha (500 and 1000 ng/ml) inhibited histamine plus IMX-stimulated AP uptake by 36% and 34%, respectively. IL-1 alpha (500 ng/ml) also inhibited carbachol-stimulated AP accumulation. TNF-alpha (100 and 250 ng/ml) inhibited histamine-stimulated AP accumulation by 38% and 36%, respectively. TNF-alpha also significantly inhibited histamine/IMX- and carbachol-stimulated AP uptake (P < or = .01). Indomethacin did not affect IL-1 alpha-induced inhibition. These results show that IL-1 alpha and TNF-alpha inhibit histamine- and carbachol-stimulated isolated parietal cell secretion and that, for IL-1 alpha, this effect does not depend on mucosal prostaglandin synthesis.

Hepatic schistosomiasis: report of two cases and literature review.

Two Filipino patients were referred for evaluation of abnormal liver enzymes. Both patients were known to come from regions endemic for Schistosoma japonicum. The clinical laboratory and radiological features of these patients are presented. We highlight the findings of radiologic evaluation, including magnetic resonance imaging (MRI). The epidemiology, clinical manifestations, diagnostic strategies including a comparison of the utility of ultrasound, computed tomography, and MRI are reviewed. The pathophysiology responsible for hepatic manifestations of schistosomiasis is reviewed. An increased influx to the United States of persons from regions endemic for schistosomiasis, such as South America, Southeast Asia, and the Philippines, will result in an increase in the prevalence of the disease in this country. The diagnosis of hepatic schistosomiasis will need to be considered in populations at risk for contracting this common worldwide problem.

The role of albumin in human physiology and pathophysiology, Part III: Albumin and disease states.

The serum albumin level is one of several clinical parameters of the status of general health. There is a marked correlation between low albumin levels and the incidence of morbidity and mortality in hospitalized patients. Therefore, it is not surprising to find that hypoalbuminemia is a common finding among hospitalized patients. This results from alterations in the catabolic or anabolic rates, losses of albumin, or redistribution between the various fluid compartments of the body. Somewhat less well defined than the role of albumin as a prognostic indicator is its role in compounding pathophysiology. Hypoalbuminemia is known to be associated with delayed wound healing. The hypoalbuminemic state interferes with the normal functioning of the gastrointestinal tract. Qualitative changes in the albumin molecule which occur in renal disease may damage the nephron. Low serum albumin levels may adversely affect the coagulation system. Further investigation into the role of albumin in pathophysiology is warranted.

Use of albumin as a volume expander.

In some hospitals, albumin products account for 10% of the pharmaceutical budget. As much as 60% of these prescriptions are empiric, and from 40 to 70% of albumin that is administered is given for inappropriate reasons. Although the reasons for albumin administration vary, prevention or reversal of hypovolemia is part of the reason in the majority of cases.

Role of albumin in human physiology and pathophysiology.

Albumin is one of the major products of hepatic protein synthesis. Although it is a small molecule, it is an important diagnostic and prognostic determinant, as well as a useful therapeutic agent. A review of the evolution and structure of albumin as well as a description of its colloidal and buffering properties is presented. Synthesis, distribution, and catabolism, the major determinants of serum albumin level, are discussed. Emphasis is given to those mechanisms responsible for the regulation of these processes, including the importance of nutritional status on substrate availability, energy supply, and hormonal modulation.

Continuous v intermittent cimetidine infusion in critically ill hospitalized patients: role of TPN admixture as drug vehicle.

Previous studies suggest that continuous or intermittent cimetidine infusion provides a stable and sustained therapeutic blood concentration that maintains a gastric pH greater than 4.0. Twenty-seven patients receiving cimetidine were randomized to one of five treatments. Groups 1 and 2 were given cimetidine intermittently, whereas Groups 3, 4, and 5 received the drug continuously via a total parenteral nutrient (TPN) admixture. Group 1 was given 300 mg every 8 hours, and Group 2 received 300 mg every six hours. Groups 3, 4, and 5 received 600, 900, and 1200 mg per day, respectively, as a continuous infusion in the TPN admixture. Forty-eight individually prescribed TPN admixtures were used to deliver cimetidine continuously; 23 were composed of amino acids and glucose as base nutrients, whereas 25 contained amino acids, glucose, and lipids (3-in-1 or total nutrient admixtures). Serum levels of cimetidine were measured six times in 40 h (Group 1) or 42 h (Group 2-5). A two-way analysis of variance (ANOVA) revealed statistically significant differences in the serum cimetidine concentrations between groups (p less than 0.0001), but not with respect to time interval (p = 0.8687). No significant differences were noted in mean serum cimetidine concentrations between Groups 2 and 3, despite employing half the total dose in Group 3. Equivalent daily dosages were then stratified as the percentage of subtherapeutic (less than 500 ng/ml), therapeutic (500-1250 ng/ml), and supratherapeutic (greater than 1250 ng/ml) values.(ABSTRACT TRUNCATED AT 250 WORDS)

Overview of gastrointestinal disorders due to diabetes mellitus: emphasis on nutritional support.

Gastrointestinal disorders associated with diabetes mellitus have a prevalence rate of 30 to 75%. The most prominent disorders are gastroparesis, diarrhea, and constipation. Severity of symptoms range from mild to severe with the most affected patients being at risk for the development of protein calorie malnutrition. An historical review of the major studies which defined the diagnosis, pathophysiology, and prevalence of these disorders is presented. Guidelines for accurate nutritional assessment, which is essential to the decision to initiate nutritional therapy in this difficult to assess population, are also included. Current methods devised for treatment of diabetic gastroparesis and related disorders are presented. Emphasis is placed on recent developments in nutritional support techniques which make it possible to meet the energy requirements of all such patients. Practical outlines for glucose control in patients receiving TPN or enteral feeding and guidelines for transitioning from parenteral feeding to an oral diet are also presented.

Histamine H2 receptor stimulation increases gastric emptying in monkeys.

We studied the effect of the specific H2 receptor agonist dimaprit on gastric emptying using a dye dilution technique in five chair-adapted rhesus monkeys to determine simultaneously gastric emptying and H+ secretion. Continuous subcutaneous injections of either saline alone or dimaprit (15, 30, 60, 120, and 240 nmol.kg-1.min-1) were given in random order on separate days. Both fractional emptying rate and H+ output were significantly increased by higher doses of dimaprit, with resulting twofold concurrent increase of intragastric H+ concentration. Because intragastric administration of H+ decreases gastric emptying and secretion, we evaluated the possibility that the stimulatory action of a histamine H2 agonist was underestimated when gastric pH was greater during control than after dimaprit. When exogenous HCl was added to the stomach to achieve H+ concentrations similar to those measured after dimaprit, both fractional emptying and H+ secretion were decreased twofold. When these "acidified control values" were used as a point of comparison, the stimulatory effect of dimaprit on both fractional emptying and gastric secretion was greater, suggesting that the stimulatory actions of dimaprit are underestimated if one does not take into account the differences in intragastric H+ concentrations.

A prostaglandin endoperoxide analog increases gastric emptying and suppresses gastric secretion in rhesus monkeys.

The effects of a stable endoperoxide analog, U-46619, were studied in five conscious chair-adapted rhesus monkeys. A dye dilution technique was used to determine simultaneously gastric fractional emptying, fluid output and ion output. A continuous infusion of either saline or U-46619 (0.2 micrograms/kg/min i.v.; 1 or 2 micrograms/kg/min s.c.) was given during a basal period and after distension of the stomach with an 80-ml water load. These studies demonstrate that U-46619 increases basal, but not postload fractinal emptying, and inhibits parietal secretion. These actions are similar to some of the effects of prostacyclin, prostaglandin E2 and prostaglandin F2 alpha on gastric emptying and secretion.

Effect of a prostaglandin F2 alpha analog on gastric emptying and secretion in rhesus monkeys.

The effects of 15(S)-15 methyl prostaglandin (PG) F2 alpha (mePGF2 alpha) on gastric emptying and secretion were studied in five conscious chair-adapted rhesus monkeys. A dye dilution technique was used to determine simultaneously fractional emptying rate, hydrogen ion (H+) output, fluid output and H+ concentration of the gastric juice. A continuous s.c. infusion of either saline or mePGF2 alpha (1 or 2 micrograms/kg/min) was given during a 40-min basal period and after intragastric administration of an 80-ml water load. The PGF2 alpha analog significantly inhibited both basal and postload H+ output but did not alter fluid output. As a result, the basal and postload H+ concentration of the gastric juice was significantly decreased. In addition to its antisecretory effect, mePGF2 alpha significantly enhanced postload gastric fractional emptying.