Parenteral nutrition in the management of a dog with lymphocytic-plasmacytic enteritis and severe protein-losing enteropathy.
(1/58)
Management of lymphocytic-plasmacytic enteritis in a dog with whipworm infestation, hypoproteinemia, and ascites is described. Short-term parenteral nutrition hastened normalization of serum proteins, resolution of diarrhea, and weight gain. A description of the potential benefits, limitations, and possible complications of parenteral nutrition in refractory inflammatory bowel disease is given. (+info)
Congenital nephrotic syndrome (NPHS1): features resulting from different mutations in Finnish patients.
(2/58)
BACKGROUND: Congenital nephrotic syndrome (NPHS1) is a rare disease inherited as an autosomally recessive trait. The NPHS1 gene mutated in NPHS1 children has recently been identified. The gene codes for nephrin, a cell-surface protein of podocytes. Two mutations, named Fin-major and Fin-minor, have been found in over 90% of the Finnish patients. In this study, we correlated the NPHS1 gene mutations to the clinical features and renal findings in 46 Finnish NPHS1 children. METHODS: Clinical data were collected from patient files, and kidney histology and electron microscopy samples were re-evaluated. The expression of nephrin was studied using immunohistochemistry, Western blotting, and in situ hybridization. RESULTS: Nephrotic syndrome was detected in most patients within days after birth regardless of the genotype detected. No difference could be found in neonatal, renal, cardiac, or neurological features in patients with different mutations. Nephrin was not expressed in kidneys with Fin-major or Fin-minor mutations, while another slit diaphragm-associated protein, ZO-1, stained normally. In electron microscopy, podocyte fusion and podocyte filtration slits of various sizes were detected. The slit diaphragms, however, were missing. In contrast to this, a nephrotic infant with Fin-major/R743C genotype expressed nephrin in kidney had normal slit diaphragms and responded to therapy with an angiotensin-converting enzyme inhibitor and indomethacin. CONCLUSIONS: The most common NPHS1 gene mutations, Fin-major and Fin-minor, both lead to an absence of nephrin and podocyte slit diaphragms, as well as a clinically severe form of NPHS1, the Finnish type of congenital nephrotic syndrome. (+info)
Wound healing in man: tensile strength of healing wounds in some patient groups.
(3/58)
The healing of test wounds was studied in 108 patients, in whom some impairment of wound healing was suspected. A 5 cm skin wound was performed in the forearm and the strength of the wound was tested after 5 days using the technique described by Sandblom and associates with two measurements in each wound. No differences in wound strength could be registered between the two wounds in each patient, between males and females nor in patients with malignant disease compared to other patients. Patients with low serum protein or serum albumin values had significantly weaker wounds than patients with normal protein values. Patients over 80 years of age had wounds somewhat weaker than those below 70, the difference having a statistical significance of 6%. The wound strength in patients was compared to values found elsewhere for wounds in rabbits, rats, and piglets. The pigs had much higher values than others, rabbits slightly stronger than and rats about equal to humans. (+info)
Effect of Helicobacter pylori infection and its eradication on nutrition.
(4/58)
AIMS: To investigate the effects of Helicobacter pylori infection and eradication on nutrition. METHODS: The body weight, height, blood pressure, gastric juice pH and fasting serum levels of glucose, total protein, albumin, total cholesterol and triglyceride were measured in H. pylori-positive and H. pylori-negative subjects, and the effect of eradication of H. pylori on these parameters was determined. The development of gastro-oesophageal reflux disease after treatment was also examined. Eight patients underwent a pancreatic function test before and after H. pylori eradication therapy. RESULTS: The incidence of hypoproteinaemia in H. pylori-positive subjects was significantly higher than that in H. pylori-negative subjects. After eradication of H. pylori, the gastric juice pH values were significantly decreased, and the body weight and serum levels of total cholesterol, total protein and albumin were significantly increased. The incidence of hyperlipidaemia significantly increased and that of hypoproteinaemia significantly decreased in the group with eradication. Pancreatic function improved significantly after eradication of H. pylori. No significant changes in these parameters were observed in the group without eradication. Obese patients had a higher risk of the development of gastro-oesophageal reflux disease after eradication of H. pylori infection. CONCLUSIONS: The eradication of H. pylori appears to improve some nutritional parameters. (+info)
Primary epitheliotropic intestinal T-cell lymphoma in a horse.
(5/58)
A 17-year-old Quarterhorse gelding with a clinical diagnosis of protein-losing enteropathy was submitted for necropsy following a 4-5-month duration of weight loss, decreased appetite, and hypoproteinemia. Gross findings included multiple 1-2-cm diameter ulcers on the luminal surfaces of the duodenum and ileum. Histologic examination revealed individual large, round cells infiltrating much of the mucosal epithelium of the duodenum, jejunum, ileum, and colon in addition to multifocal areas of ulceration. Similar round cells infiltrated Brunner's glands and expanded the submucosa beneath the foci of ulceration. Immunohistochemical staining indicated the round cell population was of T-lymphocyte origin. Several features of this equine neoplasm bear similarities to enteropathy-associated T-cell lymphoma in humans. (+info)
Molecular diagnosis of analbuminemia: a novel mutation identified in two Amerindian and two Turkish families.
(6/58)
BACKGROUND: Analbuminemia is a rare autosomal recessive disorder in which individuals have little or no circulating albumin, usually the most abundant plasma protein. We describe a new mutation associated with analbuminemia. METHODS: We studied four apparently unrelated patients who had congenital analbuminemia: two of Amerindian and two of Turkish origin. The 14 exons and the flanking intron sequences of the albumin gene were amplified by PCR and screened for mutations by single-strand conformational polymorphism and heteroduplex analysis. The mutated DNA fragments were sequenced directly. RESULTS: In all four cases, analbuminemia was caused by the same mutation, an AT deletion at nucleotides 2430-2431, the 91st and 92nd bases of exon 3. This novel defect, named Kayseri, produces a frameshift leading to a premature stop two codons downstream. The predicted translation product would consist of 54 amino acid residues. CONCLUSIONS: The AT deletion at nucleotides 2430-2431 is a novel mutation associated with analbuminemia. (+info)
Utilization of knockout mice to examine the potential role of gastric histamine H2-receptors in Menetrier's disease.
(7/58)
Menetrier's disease is characterized by giant gastric folds with foveolar hyperplasia and cystic dilatation, hypoproteinemia, and enhanced mucus secretion. The etiology remains unresolved and an effective treatment has yet to be established. Here we show that histamine H(2)-receptor deficient mice developed gastric pathophysiological changes resembling Menetrier's disease for up to 17 months of observation. Mutant mice were found to have an increased stomach weight, enlarged gastric folds with cystic dilatation, hypergastrinemia, hypoalbuminemia, increased mucus secretion and overexpression of mucosal transforming growth factor (TGF) alpha. Both a cholecystokinin (CCK)(2)-receptor antagonist and an epidermal growth factor (EGF)-receptor tyrosine kinase inhibitor significantly reduced the increase in stomach weight. It appears that lack or downregulation of histamine H(2)-receptors might be involved in the pathogenesis of Menetrier's disease. (+info)
Giant hypertrophic gastritis and acute hepatitis associated with cytomegalovirus infection.
(8/58)
A 38-year-old man developed prominent hypoproteinemia after acute elevation of serum transaminase levels. Giant hypertrophy of the gastric mucosa, a short serum albumin half-life, and the absence of massive hepatocyte necrosis established the diagnosis of protein-losing gastropathy. The hypoproteinemia, gastric fold hypertrophy and hepatitis remitted spontaneously within 4 months. A high antibody titer against cytomegalovirus suggested an association between the viral infection and the patient's disease. (+info)