Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0002871 (anemia)
 52,094 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Pleural effusion in 37 horses, including 15 acutely affected and 22 chronically affected, was found to be due to a variety of causes, including lymphocarcoma, pulmonary granulomas, coccidioidomycosis, equine infectious anemia, pulmonary abscesses, chronic pneumonia, and primary septic pleural effusion. Age, breed, or sex predilection was not found. Horses with chronic disease had weight loss, increased respiratory rate, dull respiratory sounds in the ventral portion of the thorax, and varying degrees of anorexia. Many horses were anemic. Those acutely affected had respiratory distress or signs of colic and many were anorectic. Most horses with acute primary disease had small volumes of pleural fluid. Culture and cytologic examination of pleural fluid and tracheal washings revealed the causative organism in some instances, but in a number of "primary" cases there were negative results on bacterial culture. The latter cases must be differentiated from other causes of chronic weight loss in the horse.
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PMID:Pleuritis and pleural effusion in the horse: a study of 37 cases. 57 21

Serum zinc concentrations are decreased in patients with a variety of clinical disorders including cirrhosis, nephrotic syndrome and renal insufficiency. Urinary zinc excretions are increased in the first two disease states. Symptoms of acute zinc deficiency (anorexia, dysfunction of smell and taste, and mental and cerebellar disturbances) and chronic zinc deficiency (growth retardation, anemia, testicular atrophy, and impaired wound healing) are common in these patients. It remains unresolved whether these disease states are indicative of true symptomatic or asymptomatic zinc deficiency or merely reflect a decrease in available zinc binding proteins. The low serum zinc concentrations and high urinary zinc excretions in patients with nephrotic syndrome do not appear to be due to loss of zinc bound to urinary proteins. Studies in dogs indicate increased serum and urine concentrations of certain amino acids(cysteine, histidine) greatly increase urinary zinc excretions. Studies are now underway to determine if the hyperzincuria and hypozincemia of cirrhosis, nephrotic syndrome and hyperalimentation can be explained by an increase in these urinary amino acids.
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PMID:Zinc metabolism in renal disease and renal control of zinc excretion. 60 38

A suicidal 67-year-old woman with manic-depressive psychosis took an overdose of asprin, amitriptyline and diazepam. The initial effects were pyrexia, tachycardia, hyperpnea, metabolic acidosis, electrocardiographic changes, hypoprothrombinemia, gastritis, and pancreatitis. Four to six weeks later, she was examined because of persistent abdominal pain with mausea, anorexia anemia, and possibly a malabsorption syndrome. An exploratory laparotomy was performed. The surgeon found several previous adhesions, a small intestinal volvulus, and a nodular pancreas. This suggested previous perforation of the small bowel from enteritis, causing a "blind-loop" syndrone. The invilved section of the small bowel was resected. With appropriate treatment, the patient is well three months after operation.
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PMID:Unusual abdominal complications of a suicidal overdose of analgesic and psychotropic drugs in an elderly patient. 61 54

internal abdominal abscesses in 25 horses, including 8 horses that died or were euthanatized, were found to be caused by Streptococcus equi, Streptococcus zooepidemicus, or Corynebacterium pseudotuberculosis. Breed or sex predilection was not found. Although horses of all ages were affected, those under 5 years of age were more commonly affected. Nearly all of the horses had a history of respiratory catarrh or lymphadenitis. Horses with internal abdominal abscesses also had intermittent, prolonged colic or chronic weight loss. Most horses had increased rectal temperature, increased heart and respiratory rates, and varying degrees of anorexia. Chronic depression anemia, increased plasma fibrinogen concentration, increased total plasma protein with hypergammaglobulinemia, and hypoalbuminemia were prominent clinicopathologic findings. Results of rectal examination or surgical exploration often revealed an abdominal mass. Peritoneal fluid from 14 horses was examined, and the protein content was greater than 2.5 g/dl, with increased numbers of neutrophils. Culture results were negative in all 14 cases, although bacteria were seen intracellularly in 5 cases. Long-term (2- to 6-month) antimicrobial therapy with procaine penicillin G resulted in clinical resolution in most of these animals.
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PMID:Internal abdominal abscesses in the horse: a study of 25 cases. 62 Nov 78

Pseudohyperparathyroidism was diagnosed in a mature stallion presented for anorexia, weight loss, pollakiuria and constipation. Laboratory findings included hypercalcemia, hypophosphatemia, anemia and isosthenuria. Thoracocentesis indicated an exfoliating squamous cell carcinoma. At necropsy, a squamous cell carcinoma of the stomach with metastases to the abdominal and thoracic cavities was diagnosed. No osseous metastases were found. No gross or microscopic renal lesions were noted. Bone tissue showed arrested resorption, and the parathyroid gland was atrophic.
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PMID:Gastrict carcinoma with pseudohyperparathyroidism in a horse. 63 16

Serum zinc conentrations are decreased in patients with a variety of clinical disorders including cirrhosis, nephrotic syndrome and renal insufficiency. Urinary zinc excretions are increased in the first two disease states. Symptoms of acute zinc deficiency (anorexia, dysfunction of smell and taste and mental and cerebellar disturbances) and chronic zinc deficiency (growth retardation, anemia, testicular atrophy and impaired wound healing) are common in these patients. It remains unresolved whether these low serum zinc concentrations in these disease states are indicative of true symptomatic or asymptomatic zinc deficiency, or merely reflect a decrease in available zinc-binding proteins, as well over 90% of serum zinc is bound to protein in normal subjects. The correlation between serum zinc and albumin concentrations, reportedly the major zinc-binding protein, is unimpressive. Studies of serum and urine binding of added radiozinc65 using Sephadex G-200 gel column chromatography and polyacrylamide gel electrophoresis suggest most of the radiozinc is bound to a protein with a molecular weight near albumin (68,000). Polyacrylamide gel electrophoresis suggests this might be a prealbumin. The low serum zinc concentration in the patient with nephrotic syndrome does not appear to be due to loss of zinc bound to urinary protein.
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PMID:Serum concentrations and urinary excretions of zinc in cirrhosis, nephrotic syndrome and renal insufficiency. 66 9

Parasite-free pony foals (n = 10) were infected orally with 1000,000 Parascaris equorum embryonated eggs. One pony foal each was euthanatized on days 1, 3, 5, 7, 11, 16, 23, 27, 42, or 80 after infection. Foals infected for more than 7 days showed signs of coughing, anorexia, rough coat, and weight loss. Cellular changes in the blood were mild anemia, marked eosinophilia, and leukopenia. Gross postmortem lesions included hemorrhage, edema, and white-to-yellow necrotic foci (0.5 to 1.00 mm) in lungs, liver, and bronchial and hepatic lymph nodes. Microscopically, the liver was hemorrhagic and had focal necrosis and eosinophilic granulomas. Eosinophilic lymphadenitis with edema was in the hepatic and bronchial lymph nodes. The lungs had focal areas of necrosis with hemorrhage and interstitial pneumonia with hyalinization of the alveolar walls. Larvae were first seen in the liver at postinfection hour 24 and in the lungs on postinfection day (PID) 11. Average length of larvae in the liver was 1 mm and 2.5 mm in the lungs. Larvae were not found in the liver after PID 11 or in the lungs after PID 42. The migratory pathway of P equorum was similar to that of Ascaris lumbricoides because the larvae migrated via lymph and blood vessels to the liver and then to the lungs. After migrating through the lungs, the larvae were coughed up and swallowed and then developed in the small intestine.
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PMID:Pathologic changes and pathogenesis of Parascaris equorum infection in parasite-free pony foals. 67 34

Chronic copper poisoning in a dairy herd fed supplementary copper is recorded. Most cows received 11 g of copper sulphate per day but high milk producers received 22.0 g and within 6 months, 3 of them became ill and died. The signs shown by the 3 cows were anorexia, decreased milk production, frequent recumbency and jaundice. Within 4 days of showing signs, the cows died. The autopsy findings were dehydration, anaemia, jaundice, liver damage and intestinal haemorrhage. Liver copper values varied from 1,250 to 2,410 ppm DM.
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PMID:Chronic copper poisoning in dairy cows. 68 67

The effectiveness of MFC (mitomycin C, 5-fluorouracil and cytosine arabinoside) therapy for nonresectable cancers and cancers recurring after surgery was investigated in 60 patients with solid cancers aged 26 to 69 years. Treatment was effective in 28 patients (47%) including seven (12%) who showed a very good response. Side effects included anorexia, vomiting, melena, anemia, decreased leukocyte and platelet counts, and impaired renal function. In particular, hemorrhage of the digestive tract should be watched carefully during MFC therapy. MFC therapy is suitable for solid tumors of the breast and digestive organs, especially with metastases to the lymph nodes. Response to treatment is generally seen after 6--10 doses. If there is no response at this time, treatment should be changed. In cases where induction of remission is successful, maintenance therapy should be continued keeping the frequency of administration to a minimum. Remission is readily induced with MFC therapy, but because of the problems of hemorrhage of the digestive tract, and bone marrow suppression, its use for outpatient treatment is not considered safe. Therefore, alternative treatment should be given for long term maintenance of remission. FAMT (5-fluorouracil, cyclophosphamide-endoxan, mitomycin C, chromomycin A3 -toyomycin) therapy is considered safe and suitable for maintenance therapy in outpatients. Three cases in which MFC therapy was very effective are described to illustrate the treatment program.
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PMID:Combination therapy with mitomycin C, 5-fluorouracil, and cytosine arabinoside for nonresectable malignant tumor in man. 73 30

Twenty-seven dogs with lead poisoning were admitted to the University of Pennsylvania Veterinary Hospital from July, 1963, to April, 1975. The major source of the lead was paint. A common history was ingestion of plaster or paint scrapings during room renovation. Most of the dogs were less than 1 year old and had clinical signs referable to the gastrointestinal or the nervous system, or both. The gastrointestinal signs, in order of frequency, were vomiting, anorexia, tender abdomen, diarrhea, and constipation. The neurologic signs, in order of frequency, were hysteria, convulsions, ataxia, blindness, and mydriasis. The finding of many nucleated erythrocytes without severe anemia was nearly pathognomonic for lead poisoning. Of 14 affected dogs subjected to abdominal radiography, 9 had evidence of ingested radiopaque material. A mean blood lead concentration of 18.8 mug/100 ml, with a range of 0 to 50 mug/100 ml, was found for 26 dogs that were hospitalized for problems unrelated to lead poisoning. Of the 27 dogs with lead poisoning, 22 had their blood analyzed for lead. This group had blood lead values ranging from 40 to 530 mug/100 ml. Seven of the affected dogs were monitored throughout their period of treatment with calcium ethylenediaminetetraacetate. The concentration of lead in the blood decreased quickly after the initiation of treatment but leveled off after 2 or 3 days. The initial rapid phase probably corresponded to the removal of weakly bound or extracellular lead, whereas the slow phase probably corresponded to strongly bound or intracellular lead.
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PMID:Lead poisoning in dogs at the University of Pennsylvania Veterinary Hospital. 81 31


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