Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0038362 (stomatitis)
 8,852 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

An experimental protein-calorie malnutrition was produced in weanling Sprague-Dawley rats. The model resembles human malnutrition with respect to weight loss, inanition, angular stomatitis, anemia, lymphopenia, hypoproteinemia with hypoalbuminemia, and marked thymic involution. In addition, systemic invasion by gram-negative rods was documented. However, no edema was produced, and animals did not survive for longer than six weeks on the protein-deficient diet. One percent glycogen was found to be a satisfactory nonprotein stimulus for induction of a peritoneal exudate consisting primarily of young macrophages. Electron microscopy showed that morphologic events of phagocytosis and degranulation proceeded normally in macrophages from protein-deficient animals. In addition, cell surface receptors for IgG were preserved under these experimental conditions. These data indicate that weanling rats may be employed as a small animal model for servere, fulminant protein-calorie malnutrition in humans.
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PMID:Antibacterial functions of macrophages in experimental protein-calorie malnutrition. I. Description of the model, morphologic observations, and macrophage surface IgG receptors. 9 98

The features of 41 proven or suspected cases of pancreatic glucagonoma and one possible case of renal glucagonoma have been reviewed. Glucagonoma is one form of islet cell neoplasm and involves pancreatic alpha cells. It may occur more frequently in women and is more likely to be malignant than insulinoma. Patients may present with glucose intolerance, an erythematous, eczematous dermatitis, glossitis, stomatitis, vaginitis and unexplained weight loss. Anemia, hypoproteinemia, hypoaminoacidemia and hypolipidemia may also be present. Malignant glucagonoma metastasizes frequently to liver. An evaluation for possible glucagonoma may be considered in a patient with the characteristic eczematous dermatitis, glossitis or stomatitis and glucose intolerance, an unusual or atypical history of diabetes mellitus, or hepatomegaly with other characteristics of glucagonoma. Initial evaluation may include measurement of fasting plasma glucagon concentration, and an oral glucose tolerance test with measurements of plasma glucose and glucagon levels. Extreme fasting hyperglucagonemia, and a paradoxical rise in plasma glucagon concentrations after glucose ingestion should strongly suggest the presence of glucagonoma. Radiographic demonstration of pancreatic glucagonoma is best carried out by celiac arteriography. Surgical excision of the tumor is the treatment of choice. Nonresectable lesions may respond to chemotherapy with streptozotocin. Treatment for the various dermatologic or metabolic complications of glucagonoma which include glucose intolerance, hypoproteinemia, hypocholesterolemia and anemia may not be satisfactory. Glucose intolerance is usually mild and may be adequately treated with dietary or insulin therapy. Rarely, glucagonoma with massive destruction of the pancreas or other factors may induce severe glucose intolerance. In contrast, the anemia, skin rash, and hypoproteinemia do not respond to conservative therapies tested thus far. Glucagonoma is a model for studying the importance of glucagon in causing the hyperglycemia of diabetes mellitus. Study of patients with glucagonoma does suggest that glucagon has some role in the etiology of hyperglycemia in diabetic states; however, as in studies on diabetes, investigations on glucagonoma do not demonstrate that glucagon has a primary role in producing severe glucose intolerance.
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PMID:Clinical and metabolic aspects of glucagonoma. 698 81

Steatitis due to vitamin E deficiency occurred in three 10-wk-old boat-billed herons (Cochlearius cochlearius) despite daily placement of a powdered vitamin supplement on the fish that was subsequently washed off by the parents. Physical findings included emaciation, yellow-brown subcutaneous nodules, a firm distended coelom, stomatitis, and yellow-white, submucosal pharyngeal nodules. Clinical pathology revealed heterophilic leukocytosis, anemia, hypoproteinemia, and low plasma alpha (alpha)-tocopherol levels (1.94 microg/ml and 2.14 microg/ml). Two of the chicks died of severe, diffuse pansteatitis and respiratory aspergillosis.
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PMID:Vitamin E deficiency and pansteatitis in juvenile boat-billed herons (Cochlearius cochlearius). 1048 50