Gastrin and gastrointestinal disease.
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Diseases of the skin and the gastrointestinal tract may occur together. It is important to examine the skin of everyone showing a gastrointestinal problem. Gastrointestinal signs and symptoms in dermatologic diseases may occur with dysphagia, abdominal pain, gastrointestinal bleeding and diarrhea with or without malabsorption. In general the cause is found in a genetic disorder, or it is infectious, drug-induced, inflammatory or related to a malignant disorder. Polyposis are hamartomatous tumors or result as an inflammatory reaction. All these syndromes may present with cutaneous lesions. As malignant degeneration of polyps often develops, the early diagnosis and preventive treatment is crucial. Inflammatory bowel disease is often associated with skin complications such as pyoderma gangrenosum and erythema nodosum. Malignant disorders in the gut may metastasize into the skin or may produce rather typical paraneoplastic changes.
OBJECTIVE: To describe all the clinical settings, endoscopic findings and response to therapy in a series of HIV-positive patients with biopsy proven gastrointestinal CMV disease. PATIENTS: We retrospectively reviewed the medical records of all HIV-infected patients who underwent digestive endoscopies at our Hospital from June 1990 to October 1993. RESULTS: Twelve (7.5%) of 158 HIV-positive patients had gastrointestinal CMV disease. Sites of prove infection included the esophagus (n = 6, 50%), stomach (n = 2, 17%), duodenum (n = 4, 33.3%), ileum (n = 1, 8.5%) and colon (n = 2, 17%). The most common endoscopic findings were focal or diffuse mucosal ulcers. Three patients had pseudotumoral mucosal lesions. Cytomegalic cells were observed in 11 patients (91.6%) and immunohistochemical staining was positive in 9 (81.8%) of 11 patients tested. Eight patients completed a course of treatment with ganciclovir or foscarnet and all of them showed clinical improvement. The median survival time of our AIDS patients with CMV gastrointestinal disease was 7 weeks (range 1-39 weeks). CONCLUSIONS: Gastrointestinal CMV disease may damage any site of the digestive tract in AIDS patients. Routine histopathologic examination was better than immunohistochemical staining for the diagnosis. Treatment improves the clinical situation in most of them. The mean survival is low and it is related to the degree of immunosuppression.
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Molecular analyses have become an integral part of biomedical research as well as clinical medicine. The definition of the molecular and genetic basis of many human diseases has led not only to a better understanding of their pathogenesis, but has in addition offered new perspectives for their diagnosis, therapy, and prevention. Genetically, human diseases can be classified as monogenetic, complex genetic, and acquired genetic diseases. Based on this genetic classification, gene therapy involves four concepts: gene substitution, gene augmentation, block of gene expression or function as well as somatic transgene vaccination. Despite exciting recent developments, various delivery, targeting, and safety aspects need to be addressed before gene therapy will enter clinical practice. Clearly, molecular diagnosis and gene therapy of gastrointestinal diseases will be increasingly part of our patient management, complementing existing diagnostic, therapeutic, and preventive strategies.
The magnitude of metabolic adaptation to malnutrition is still debated and few studies have investigated the phase of recovery from malnutrition. The aim of the present work was to determine whether refeeding was associated with adaptive changes in 1) energy expenditure, 2) maximal capacity for oxidizing lipids, and 3) whole-body protein turnover. Eleven malnourished patients with nonneoplastic gastrointestinal diseases were studied by using indirect calorimetry and L-[1-13C]leucine infusion while being infused with lipid-rich total parenteral nutrition (TPN). The same study was performed before initiation of TPN and after a mean gain of 6.5 kg body wt. In absolute values, resting energy expenditure (REE) increased after refeeding (4.05 +/- 0.85 compared with 4.60 +/- 1.05 MJ/d). Change in REE adjusted for fat-free mass (FFM) correlated significantly with change in body weight (r = 0.850, P = 0.01) and change in body fat (r = 0.798, P = 0.01) but not with change in FFM (r = -0.06, NS). Lipid oxidation decreased significantly after body weight gain (0.93 +/- 0.28 compared with 0.50 +/- 0.37 mg.kg-1.min-1). When expressed per kg FFM, protein turnover and breakdown increased significantly during body weight gain. Moreover, the change in protein turnover correlated with the rate of change in FFM, suggesting that FFM accretion requires increased interorgan exchange of amino acids. Our data suggest that in patients similar to those studied here and during recovery from malnutrition, the degree of change in adjusted REE during refeeding is correlated with change in fat mass and not with change in FFM, and that there is a decrease in oxidation of infused lipids. These mechanisms may contribute to body fat repletion and regulation during weight gain.
Advances in the physical and biological sciences have in recent years led to a rapidly increasing use of radioactive agents in clinical medicine. The distinctive properties of these agents have made them invaluable for a large variety of unique in vivo and in vitro diagnostic tests. In order to help the clinician employ such tests productively and realistically, we have attempted to review the present status of radiosotopes with regard to gastrointestinal diseases. Emphasis has been placed not only on their value but also on their limitations; the degree of safety for in vivo application has also been briefly considered.
Endoscopic ultrasonography provides detailed images of gastrointestinal structures by means of high frequency ultrasound transducers placed within the gastrointestinal tract. In this paper, the authors describe various systems and discuss their clinical potential and indications for use. Endoscopic ultrasonography allows imaging of various small pathological lesions in the visceral wall and adjacent structures, such as the mediastinum, pancreas and distal parts of the bile duct. Experience in endoscopy and ultrasonography is necessary for a proper management of the technique.
PURPOSE OF REVIEW: Although our general understanding of food hypersensitivity has improved in recent years, gastrointestinal food protein-induced diseases still pose diagnostic and therapeutic dilemmas. RECENT FINDINGS: Food allergy in children and adults may involve any part of the gastrointestinal tract. Clinical presentations include protein-induced enterocolitis syndrome, enteropathy and proctocolitis, as well as eosinophilic gastroenteritis and related disorders. For many of these conditions, our understanding of the pathophysiology is incomplete. Manifestations are mostly non-IgE mediated, and skin prick testing and measurement of food-specific IgE antibody levels are of limited diagnostic value. Atopy patch testing may be of benefit in identifying food items associated with late-onset gastrointestinal reactions. A definitive diagnosis of gastrointestinal food allergy, however, still relies on formal food challenges. Depending on the clinical presentation, gastrointestinal biopsies may be required. In infancy, hypoallergenic formula or maternal elimination diets have been shown to effectively control the gastrointestinal manifestations of food allergies. Growth parameters and micronutrient levels need to be carefully monitored while on elimination diets for prolonged periods. In older children and adults with eosinophilic gastrointestinal disorders, the response to dietary restriction is variable. Corticosteroids may be required to control symptoms in those who failed to respond to hypoallergenic diets. In eosinophilic esophagitis, steroids can be administered topically in the form of swallowed aerosols. Leukotriene receptor antagonists and other novel therapies may be useful as steroid-sparing agents. SUMMARY: Early diagnosis and treatment of food protein-induced gastrointestinal diseases may prevent significant nutritional complications. Further research is needed to develop diagnostic tools for these mainly cell-mediated disorders.