Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0023380 (lethargy)
 5,697 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Severe hypomagnesemia (0.8 mg/dl; reference range, 1.6 to 2.3 mg/dl), hypocalcemia, and protein-losing enteropathy were identified in a 5-year-old castrated male 3-kg (6.6 lb) Shih Tzu examined because of anorexia, lethargy, paresis, and abdominal distention. Histologic examination of intestinal biopsy specimens revealed lymphangiectasia and lymphocytic, plasmacytic, neutrophilic infiltrates. Initial treatment included administration of magnesium (0.80 mEq/kg [0.36 mEq/lb]) of body weight in a balanced electrolyte solution. This treatment resulted in normalization of the serum magnesium concentration (1.7 mg/dl); resolution of the lethargy, paresis, and tachycardia; and an increase in the serum parathyroid hormone and ionized calcium concentrations. Findings were consistent with secondary hypoparathyroidism attributable to hypomagnesemia. Magnesium concentration should be monitored in all dogs with gastrointestinal tract disease, especially those with protein-losing enteropathy, anorexia, and weakness.
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PMID:Secondary hypoparathyroidism attributed to hypomagnesemia in a dog with protein-losing enteropathy. 1176 24

A 5-month-old Morgan filly was presented to the Atlantic Veterinary College with a history of lethargy, fever, depression, anorexia, and dependent ventral edema. Diagnostic tests revealed severe inflammation, hypoproteinemia, and thickened small intestinal loops. Protein-losing enteropathy caused by Lawsonia intracellularis was diagnosed and treated successfully with erythromycin-rifampin.
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PMID:Protein-losing enteropathy caused by Lawsonia intracellularis in a weanling foal. 1261 60

A 46-year-old woman was admitted to the hospital with complaints of chronic diarrhoea, vomiting and severe muscle weakness. Clinical examination showed a lethargic, malnourished, dehydrated patient with ascites and bilateral leg oedema. Laboratory evaluation revealed mild normochromic normocytic anaemia and severe hypoproteinaemia with hypoalbuminaemia. Upper gastrointestinal endoscopy showed a thickened, friable duodenal mucosa with multiple erosions. Colonoscopy revealed nodular, pseudopolypoid lesions with patchy erosions in the left hemicolon. Haematoxylin-eosin stained sections from biopsies of endoscopically abnormal bowel segments showed multi-focal aggregates of large, histiocyte-like cells with abundant pale cytoplasm in the lamina propria. These cells were negative on PAS, Ziehl-Neelsen, Giemsa and toluidine blue stains. Their immunophenotype was CD68 (+), c-kit/CD117 (+) and mast cell tryptase (+), which is consistent with mast cells. A trephine biopsy showed diffuse replacement of the bone marrow by atypical, monomorphic, frequently spindle-shaped mast cells. No associated haematopoietic malignancy was detected. The final diagnosis was aggressive systemic mastocytosis with involvement of the gastrointestinal tract complicated by protein-losing enteropathy. This association has not been reported previously. The patient has been treated with prednisolone and interferon-alpha and has since recovered.
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PMID:Aggressive systemic mastocytosis complicated by protein-losing enteropathy. 1684 41

A 13-year-old Quarterhorse mare had a 6-month history of diarrhea, progressive weight loss, and lethargy. At presentation the mare was hirsute, had hyperhidrosis, and abnormal fat distribution in addition to severe diarrhea. A presumptive clinical diagnosis of protein-losing enteropathy and pituitary pars intermedia dysfunction was made. T-cell lymphoma was diagnosed in a rectal biopsy specimen. The owner elected to euthanize the mare because of poor prognosis and the severity of the disease. At necropsy, the mare had hypertrichosis and the pituitary gland was diffusely enlarged. Histologically, neoplastic lymphocytes infiltrated the gastrointestinal mucosa, mesenteric lymph nodes, and the pituitary gland. In addition, there was hyperplasia of the pituitary gland pars intermedia. Pituitary adenoma was not present. Hypertrichosis in this case could have been triggered by a combination of adenomatous hyperplasia of pars intermedia and lymphoma resulting in disruption of the hypothalamic dopaminergic tone or disruption of the hypothalamic thermoregulatory center.
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PMID:Hypertrichosis in a horse with alimentary T-cell lymphoma and pituitary involvement. 1745 49

This study reports the results in 34 dogs with protein-losing enteropathy (PLE). Rottweilers and Yorkshire Terriers were overrepresented. Most obvious clinical signs and laboratory findings were diarrhea (91 %), weight loss (74 %), anorexia (56 %), lethargy (51 %), ascites (18 %), ascites without gastrointestinal signs (9 %), hypoalbuminemia (<12 g/l, 65 %) and hypocholesterolemia (51 %). Ultrasonographic findings included intestinal wall thickening in 71 %, abnormal echogenicity in 68 %, and no abnormalities in 29 %. The most important endoscopic findings were diffuse and profound dilation of villi in 35 %, a more granular appearing mucous membrane in 32 % and a "rice-grain" appearing villus dilation in 12 %. In 21 % of the dogs the mucous membrane was considered unremarkable. Histologically, 62 % had lymphangiectasia, in 86 % of these associated with moderate to severe inflammatory infiltrates, and in 71 % associated with dilatation of intestinal crypts. In 68 % of the dogs lesions in intestinal crypts were found, 35 % of these without lymphangiectasia. In 12 % of the dogs the histological findings failed to explain intestinal protein loss. This study shows the important prevalence of crypts' lesions in protein-losing enteropathy.
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PMID:[Protein-losing enteropathy of non neoplastic origin in the dog: a retrospective study of 34 cases]. 2023 16

Non-IgE-mediated gastrointestinal food-induced allergic disorders (non-IgE-GI-FAs) account for an unknown proportion of food allergies and include food protein-induced enterocolitis syndrome (FPIES), food protein-induced allergic proctocolitis (FPIAP), and food protein-induced enteropathy (FPE). Non-IgE-GI-FAs are separate clinical entities but have many overlapping clinical and histologic features among themselves and with eosinophilic gastroenteropathies. Over the past decade, FPIES has emerged as the most actively studied non-IgE-GI-FA, potentially because of acute and distinct clinical features. FPIAP remains among the common causes of rectal bleeding in infants, while classic infantile FPE is rarely diagnosed. The overall most common allergens are cow's milk and soy; in patients with FPIES, rice and oat are also common. The most prominent clinical features of FPIES are repetitive emesis, pallor, and lethargy; chronic FPIES can lead to failure to thrive. FPIAP manifests with bloody stools in well-appearing young breast-fed or formula-fed infants. Features of FPE are nonbloody diarrhea, malabsorption, protein-losing enteropathy, hypoalbuminemia, and failure to thrive. Non-IgE-GI-FAs have a favorable prognosis; the majority resolve by 1 year in patients with FPIAP, 1 to 3 years in patients with FPE, and 1 to 5 years in patients with FPIES, with significant differences regarding specific foods. There is an urgent need to better define the natural history of FPIES and the pathophysiology of non-IgE-GI-FAs to develop biomarkers and novel therapies.
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PMID:Non-IgE-mediated gastrointestinal food allergy. 2595 13