Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C1762617 (weakness)
 37,932 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Nine dogs with primary gastrointestinal disease had clinical and laboratory findings resembling hypoadrenocorticism. The dogs had histories of anorexia, weakness or lethargy, diarrhea, vomiting, and weight loss. Hypothermia, dehydration, and emaciation also were detected on physical examination. Hyponatremia, hyperkalemia, and abnormally low Na/K ratios were found on laboratory evaluation, but results of ACTH-response tests were not compatible with hypoadrenocorticism. The primary diagnoses were trichuriasis and salmonellosis in 2 dogs, trichuriasis in 5 dogs, and perforated duodenal ulcer in 2 dogs. Most dogs responded to medical or surgical treatment of their primary gastrointestinal disease, and the original electrolyte abnormalities resolved. These findings emphasize the importance of the ACTH-response test in the diagnostic evaluation of dogs with clinicopathologic findings similar to those of hypoadrenocorticism.
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PMID:Clinicopathologic findings resembling hypoadrenocorticism in dogs with primary gastrointestinal disease. 299 Nov 78

Psittacine inclusion body hepatitis (also known as Pacheco's parrot disease) was believed to be responsible for fatal necrotizing hepatitis and splenitis in a variety of psittacine birds from a private aviary. Splenic cells and degenerative hepatocytes around the outer zone of necrotic areas had margination of nuclear material and large intranuclear inclusion bodies. Clinical signs consisted of weakness, anorexia, vomiting, loose feces, and slight ruffling of feathers. The source of the infection was undetermined, but could have been associated with 3 Patagonian conures within the aviary. Patagonian conures are well-recognized as clinically normal carriers. The outbreak was limited by strict quarantine and disinfection of the aviary for 14 days.
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PMID:Psittacine inclusion body hepatitis in an aviary. 299 45

A unique case of inflammatory malignant fibrous histiocytoma of the large bowel is presented. This lesion occurred in the colon of an elderly man suffering from weakness, anemia, anorexia, and weight loss. A right hemicolectomy was performed, and six months later, on follow-up, he was found to be well. The literature on visceral involvement by malignant fibrohistiocytic tumors is reviewed.
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PMID:Primary inflammatory malignant fibrous histiocytoma of the colon. 301 30

Carbaryl, a widely used insecticide, is reputed to have a wide safety margin. It can induce acute cholinesterase poisoning, which is rapidly reversible on discontinuation of exposure. Long-term sequelae from long-term exposure have not previously been described in humans. This report describes the experience of a 75-year-old man who had long-term excessive exposure to carbaryl and in whom a debilitating syndrome, including headaches, memory loss, proximal muscle weakness, muscle fasciculation, muscle cramps, and anorexia with marked weight loss, developed. At the time of diagnosis, serum pseudocholinesterase levels were low, and his major symptoms resolved on termination of exposure. Late clinical features were sleep apnea and progressive development of a peripheral neuropathy. The difficulty in diagnosing the cause of a group of relatively nonspecific symptoms raises the question of whether chronic carbaryl neurotoxicity might be occurring more frequently than previously suspected.
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PMID:Subacute neurotoxicity following long-term exposure to carbaryl. 308 76

Eighteen patients with solid tumours were treated with human recombinant interferon-gamma at escalating dose levels starting at 1 X 10(6) units/m2 per infusion and rising through 3 X 10(6), 6 X 10(6), 9 X 10(6) and 22 X 10(6) to a maximum of 110 X 10(6) units/m2 per infusion. The IV infusions were given three times a week over a 4-week period. Side effects were seen in all patients, but were mild except at the highest dose. Acute dose-related effects included pyrexia, tiredness, thirst, chills and rigors. Chronic dose-related effects included anorexia, lethargy, weakness, disorientation, a trace of proteinuria and minimal rises in liver enzymes. In addition, effects were observed which were not related to dose. These included headache, nausea and vomiting, backache, myalgia, flatulence and a mild, transient reduction in neutrophils and erythrocytes. At the highest dose level dose-limiting toxicity was observed, consisting in severe tiredness and anorexia, hypotension, disorientation and changes on the electrocardiograph. Overall, toxicity was similar to that seen with preparations of interferon-alpha, except that no tolerance to the effects of interferon-gamma was noted. We observed less hepatic and haematological toxicity, but also recorded flatulence, handcramps and electrocardiograph changes, which have not been reported with interferon-alpha. When given according to this regimen, doses of 22 X 10(6) units/m2 per infusion of recombinant interferon-gamma were generally well tolerated by the patients.
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PMID:A toxicity study of recombinant interferon-gamma given by intravenous infusion to patients with advanced cancer. 309 8

Sarcocystis spp can cause poor growth, anorexia, fever, anemia, muscular weakness, nervousness, abortion, and even death in cattle. Lesions in the CNS of cattle infected with Sarcocystis spp are microscopic and relatively minor, compared with those in other organs. We report extensive encephalitis in a steer attributable to a Sarcocystis-like organism.
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PMID:Encephalitis caused by a Sarcocystis-like organism in a steer. 311 52

Toxicity studies with latex of Calotropis procera RBr were conducted in the black rat, Rattus rattus. The latex was fed through bait prepared from wheat flour, ground nut oil and sugar at concentrations of 5, 7.5 or 10% (W/W). The bait was fed up to mortality and for a maximum of 10 days. The signs produced were passivity, sluggishness, sedation, dyspnea, weakness, reduction in weight, anorexia, diarhhea, hematuria, bleeding from nose, eyes and anus, eye lens opacity, mild tetanic convulsions, collapse and death. The observed mortalities were 56.25, 68.75 and 87.5% with the respective doses. Histopathological studies showed: cloudy swelling of hepatocytes, inflammatory changes, Kupffer cell hyperlasia, cytoplasmic granulation, hepatocytolysis, compactness of lobular architecture, and occasional hemorrhage in the liver; cloudy swelling of convoluted tubular epithelium, inflammatory changes and hemorrhage in the kidney; erosion, increased mucus secretion, congestion and infiltration of lymphocytes in portions of the alimentary canal.
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PMID:The toxicity of Indian Calotropis procera RBr latex in the black rat, Rattus rattus Linn. 317 4

The etiology, clinical presentation, and management of hypophosphatemia are reviewed. Phosphorus is a major intracellular anion and plays an important role in many biochemical pathways relating to normal physiologic functions. Approximately 60 to 90% of the 1 to 1.5 g of daily dietary phosphorus intake is absorbed, and of that amount, about two thirds is excreted in the urine. The overall incidence of hypophosphatemia is about 2 to 3% of all hospitalized patients. Factors associated with hypophosphatemia include phosphate-binding antacid therapy, nasogastric suction, liver disease, sepsis, alcoholism, and acidosis associated with diabetic ketoacidosis. Patients receiving parenteral nutrient solutions were also at higher risk for hypophosphatemia before the routine supplementation of these formulations with phosphate. Patients with hypophosphatemia may be asymptomatic or may experience weakness, malaise, anorexia, bone pain, and respiratory arrest. The major systems involved include the neuromuscular, hematologic, and skeletal systems. Phosphorus-containing products used to treat hypophosphatemia are a combination of monobasic and dibasic phosphate salts. Therefore, it is essential to calculate doses in millimoles rather than milligrams or milliequivalents to more accurately reflect the phosphorus concentration and to avoid potentially serious dosage errors. Normal daily requirements are readily maintained by dietary sources of phosphorus such as milk products or may be supplemented by phosphate-containing products administered orally or intravenously. Since phosphorus is a key factor in many organ systems, it is essential to monitor serum phosphorus concentrations in patients at risk for hypophosphatemia.
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PMID:Management of hypophosphatemia. 328 Feb 19

Two dogs were examined because of anorexia, lethargy, muscle tremors, weakness, and seizures that were associated with an acute onset of hypocalcemia. Both dogs had histories of chronic hypercalcemia. Examination of the parathyroid glands revealed infarction of focal parathyroid adenomas, with atrophy of the remaining parathyroid glands. It was concluded that the acute onset of hypocalcemia was caused by infarction of functional parathyroid adenomas that were previously responsible for the cause of persistent hypercalcemia. Infarction of a parathyroid adenoma should be included in a list of differential diagnoses of acute hypocalcemia in the dog, especially if hypercalcemia has been diagnosed previously.
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PMID:Acute hypocalcemia associated with infarction of parathyroid gland adenomas in two dogs. 335 Jul 46

To evaluate the effects of chronic infection on skeletal muscle dimensions and contractile properties, we used a hamster model of visceral leishmaniasis, a parasitic infection of the reticuloendothelial system produced by Leishmania donovani (LD). To distinguish between effects of reduced caloric intake and infection per se, we also studied healthy control animals and noninfected animals subjected to caloric restriction. Three muscles were tested in vitro: plantaris, soleus, and diaphragm. Both caloric restriction and LD infection caused loss of body weight and reduced muscle cross-sectional areas and wet weights. The interventions had variable effects on in vitro contractile properties, the most pronounced being reduction in peak tension in response to tetanic stimulation. Tension loss was 35-45%, except for a loss of 65% in plantaris of LD-infected animals. We conclude that chronic LD infection affects skeletal muscles in both indirect and direct ways. 1) Reduced caloric intake due to anorexia decreases muscle size and active tension. Disuse probably enhances this effect in limb muscles. 2) Infection produces profound weakness of inactive fast-twitch muscle by unknown mechanisms.
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PMID:Effects of a chronic wasting infection on skeletal muscle size and contractile properties. 335 64


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