Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0003123 (anorexia)
 13,794 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

An experiment including 20 lambs aged 3.5--4 months was performed with the aim to study the clinical and paraclinical characteristics of experimental nematodirosis. The lambs were divided into 4 groups each consisting of 5 animals. Experimental invasion with N. spathiger larvae was effected once per os as follows:group I--with 5000, group II--with 10 000, group III--with 30 000 larvae, and group IV was used as control. It was established that the course of nematodirosis is typical with well expressed clinical symptoms in group III -- diarrhoea, loss of appetite, nervous symptoms, oligochromemia, erythropaenia, leucocytosis, lymphocytosis, eosinophyly, acidosis, reduced carotene and total protein. Calcium and magnesium vary within the normal range while phosphorus content is reduced. The prepatent period is within the range of the 15th to the 22nd day. The first clinical symptoms appear in most cases before the first eggs in the feaces are observed. Clinical symptoms haematological changes are correlated with the number of larvae given.
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PMID:[Clinical and paraclinical studies in experimental nematodiriasis of lambs]. 54 94

Hypercalcaemia would seem to be rare during immobilisation, whilst osteoporosis and hypercalciuria are constant. In fact, it often goes unnoticed. The case presented here confirms its predominance in the adolescent male. The reason for immobilisation seems to be irrelevant. The clinical symptoms are very variable: polydipsia, nausea, headache, apathy, anorexia. Blood calcium levels are raised, up to 14 mg%. This hypercalcaemia is due to very marked bone loss in adolescents, secondary to hyper-resorption and a temporary stoppage in osseous formation. The differential diagnosis from primary hyperparathyroidism is sometimes difficult but is aided by laboratory and histological findings. The essential is to consider the possibility of immobilisation hypercalcaemia in the presence of any suggestive symptoms in an immobilised adolescent. Treatment includes a return to weight bearing, adequate water intake and the administration of phosphorus, calcitonin, furosemide, and corticosteroids.
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PMID:[Immobilisation hypercalcaemia (author's transl)]. 59 68

Two groups of weanling pigs, injected with 45Ca, were fed diets containing optimal calcium and phosphorus, and vitamin D3 at 1320 IU/kg feed in the control group, and 825,000 IU/kg feed in the test group. The groups were further subdivided with 2 pigs in each subgroup, with survival times of 1, 2, 3, 4, 7, and 14 days. Pigs fed the high level of vitamin D3 lost weight and anorexia, weakness, rough hair coat and labored breathing were observed. Hypercalcemia began at 12 hours and progressed rapidly after 2 days. Radioisotope sutdies interpreted in the light of histopathologic findings indicated that bone was the primary source of increased plasma calcium. Calcium was released at a rapid rate into blood from prelabeled bone which was undergoing necrosis; it was also removed from blood and deposited into bone at a slower rate due to decreased apposition. Histopathologic examination of bones from test pigs showed regressive changes in the osteocytes, chondrocytes and osteoblasts which bean within 1 day of treatment and resulted in evidence osteopenia within 7 days. Arrested osteocytic osteolysis led to the appearance of cementing lines and to chondroid core retention. Further regressive changes in the osteocytes resulted in osteocytic death and osteonecrosis with subsequent osteoclasia and osteopenia. Retardation and arrest of cartilage maturation as well as osteoblastic deficiency contributed to the osteopenia. The osteopenia was further evidenced by decreased specific gravity and ash content per unit volume of humerus. The initial negative effect on the osteocytes, chondrocytes and osteoblasts is attributed to a direct toxic effect of excessive dietary vitamin D3 since hypoparathyroidism and hypercalcitoninism, which occur secondarily to hypercalcemia, could not account for the rapid appearance of this effect, nor are they known to induce osteocytic death. The release of bone calcium and the resulting hypercalcemia in vitamin D3 toxicosis is therefore due to a direct toxic effect of the vitamin, or its metabolites, on the osteocyte resulting in osteonecrosis. It is not due to increased resorption as has been reported previously from both in vivo and in vitro investigations. Degeneration, with subsequent inflammation, but without calcification, was observed in the kidneys and in the lungs. Epithelial cells, basement membranes, and smooth muscle were affected. This conclusively demonstrates that degeneration is the primary soft tissue lesion in vitamin D3 toxicosis, and that the subsequent calcification is therefore dystrophic. Degenerative changes occurred in the parathyroid glands within 1 day of treatment resulting in necrosis, inflammation and atrophy within 4 days. Relative fibrosis was seen as the parenchyma receded. The parathyroid gland changes were considered a direct effect of vitamin D3 toxicity since they occurred with only mild hypercalcemia and since necrosis of parathyroid cells has not been demonstrated with hypercalcemia either in vivo or in vitro.
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PMID:Vitamin D toxicity. Initial site and mode of action. 66 94

Renal failure in itself generates a state of malnutrition, due to three main causes: inadequate ingestion (anorexia, vomiting or diet insufficiencies), the existence of catabolic factors (proteins, acidosis, PTH) and extrarenal depuration (which provokes a lack of amino acids and vitamins). Artificial nutrition constitutes a series of measures that can be adopted to act upon each of the above causes. Adequate ingestion compared to inadequate ingestion can be performed orally (especially in chronic renal failure) by parenteral administration (preferable in acute renal failure) and enteral administration (complementary in both cases). The quantity and quality of adequate nutrients is non-dependent on the method of administration; 500 ml, of water should be administered plus diuresis, plus loss from other tracts; the mineral intake of sodium, potassium and phosphorus should be restricted; in the case of vitamins, these should be administered, especially the B and D complexes; there should be sufficient calories to constitute a hypercaloric diet (from 30-50 kg/day), at least 50% in the form of carbohydrates (hypertonic glucose, if administered intravenously, and dextrinolmaltose or starch if administered through the digestive tract) and at least 40% in the form of lipids (preferably of vegetable origin, rich in non-saturated fatty acids); proteins are the mainstay of nutrition in renal failure; thus, with a normal renal function or in dialysis, a dose of 1 g/kg/day is recommended; in chronic renal failure, 0.5 g/kg/day; in cases of renal failure not on dialysis, 0.3 g/kg/day, supplemented by essential amino acids or cetoacids (the effectiveness of the latter is still in dispute).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Artificial nutrition in kidney failure]. 176 Apr 78

The medical records of 7 hypercalcemic cats with primary hyperparathyroidism were evaluated. Mean age was 12.9 years, with ages ranging from 8 to 15 years; 5 were female; 5 were Siamese, and 2 were of mixed breed. The most common clinical signs detected by owners were anorexia and lethargy. A cervical mass was palpable in 4 cats. Serum calcium concentrations were 11.1 to 22.8 mg/dl, with a mean of 15.8 mg/dl calculated from each cat's highest preoperative value. The serum phosphorus concentration was low in 2 cats, within reference limits in 4, and slightly high in 1 cat. The BUN concentration was greater than 60 mg/dl in 2 cats, 31 to 35 mg/dl in 2 cats, and less than 30 mg/dl in 3 cats. Abnormalities were detected in serum alanine transaminase, aspartate transaminase, and alkaline phosphatase activities from 2 or 3 cats. Parathormone (PTH) concentrations were measured in 2 cats before and after surgery. The preoperative PTH concentration was within reference limits in 1 cat and was high in 1 cat. The PTH concentrations were lower after surgery in both cats tested. A solitary parathyroid adenoma was surgically removed from 5 cats, bilateral parathyroid cystadenomas were surgically resected in 1 cat, and a parathyroid carcinoma was diagnosed at necropsy in 1 cat. None of the cats had clinical problems with hypocalcemia after surgery, although 2 cats developed hypocalcemia without tetany, one of which was controlled with oral administration of dihydrotachysterol and the other with oral administration of 1,25 dihydroxyvitamin D. All 5 of the cta that underwent removal of an adenoma were alive at least 240 days after surgery.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Primary hyperparathyroidism in cats: seven cases (1984-1989). 181 72

A clinical trial, to evaluate the effects of a Chinese herbal drug, Rheum E and angiotensin converting enzyme inhibitor, Captopril on chronic renal failure (CRF), was conducted. Thirty cases with initial serum creatinine (Scr) levels of 344.8 +/- 114.0 mumol/L were allocated randomly to 3 groups: Rheum E treated group, Captopril treated group and Rheum E + Captopril group. A control group of 12 cases were on dietary therapy alone. During the 6-22 months of treatment, all the patients were kept on low-protein (0.6g/kg/d), and low-phosphorus (10mg/kg/d) diet. The results showed that the progression rate of renal failure, calculated by regression analysis of 1/Scr vs time, was found to be retarded after treatment with the increased regression coefficient (b value). Scr levels and blood urea nitrogen were kept stable or fell slightly. Albumin rose during the follow-up period (P less than 0.05) in the treated patients, being more marked in both Rheum E and Rheum E + Captopril groups. Uremic symptoms of nausea, anorexia improved in most of the treated patients. It is concluded that long-term low-dose Rheum E taken orally is beneficial to CRF. Its effect is better than that of Captopril. The regime of Rheum E and Captopril is a preferable choice in the long-term treatment for preventing progression of CRF.
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PMID:Clinical effects of rheum and captopril on preventing progression of chronic renal failure. 212 52

This study has been done to evaluate serum calcium, phosphorus (P), magnesium, parathyroid hormone (PTH), calcitonin (CT), and cyclic adenosine monophosphate (cAMP) in recently diagnosed pulmonary tuberculous patient, (n = 61) and the results were compared with the healthy control group (n = 22). Twenty four hours urine was collected for estimation of these electrolytes as well as cAMP. Nephrogenous cAMP (NcAMP) was calculated. Serum Ca and PTH were significantly reduced in TB groups, but CT was elevated. Serum Mg, P and cAMP as well as urinary Ca and Mg in TB groups were similar to that of the control group. Urinary P, cAMP NcAMP were increased in patient groups compared with the control. The reduced serum Ca could be due to impaired intestinal absorption of Ca, or deficient intake as a result of anorexia, decreased plasma albumin, decreased active metabolites of vitamin D or elevated CT. The rise in serum CT in TB might be due to increased CT secreted from the bronchial K-cells. Increased NcAMP might be due to the associated increase in serum antidiuretic hormone (ADH). The elevated urinary P in TB could be attributed to tissue breakdown, decreased serum PTH or increased CT.
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PMID:Calcium homeostasis in untreated pulmonary tuberculosis. I--Basic study. 216 2

As part of a study of the pathology and pathogenesis of bovine ephemeral fever virus infection 44 cattle were infected by the intravenous injection of virulent virus. Thirty-eight animals responded clinically and detailed haematological and serological data were obtained from 10 of them. Inappetence was the only clinical sign observed before the onset of fever. The temperature response was characteristically biphasic, with the second peak occurring 12 to 24 hours after the first. The only consistent haematological response was an increase in the numbers of circulating neutrophils with a concurrent decline in the numbers of mononuclear leucocytes. There were no detectable changes in plasma or blood volume, packed cell volume, red cell count, haemoglobin concentration, serum calcium, magnesium, phosphorus and creatinine concentrations, or aspartate aminotransferase activity. Viraemia was demonstrated on either the first or second day of clinical disease and lasted for at most 48 hours. Low levels of neutralising antibody could be detected within one or two days after the cessation of viraemia. Six antibody-free animals did not respond clinically to injection with virulent virus, and did not develop detectable viraemia or a serum neutralising antibody response.
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PMID:Clinical response of cattle to experimental infection with bovine ephemeral fever virus. 230 90

The harmful effect of iron excess was studied in an experiment using fifteen adult sheep. The animals were divided into three groups of 5 each. The sheep of the group I were kept as controls, those of the group II and III were supplemented with iron in doses of 80 and 40 mg/kg body weight (BW)/24 h respectively. The animals of group II died after a period of 3-7 weeks showing anorexia, loss of weight, diarrhoea, depression and symptoms of circulatory and respiratory failure. From the animals of group III one died after 13 weeks, with symptoms of pulmonary oedema, while the other 4 survived for 22 weeks, together with the animals of the control group. The iron-supplemented animals presented increased values of Serum Iron (SI), Total Iron Binding Capacity (TIBC), percent Transferring Saturation (% SAT), Alanino aminotransferase (ALT), serum Alkalin Phosphatase (SAP), Serum Urea Nitrogen (SUN) Creatinine, Phosphorus and decreased values of serum Copper concentration. These parameters were greater in group II. The iron concentration in the liver, spleen, myocardium and kidneys was also much higher than in the controls. The histological examination revealed degeneration of the liver, spleen, myocardium and kidneys in both groups, while cells overloaded with hemosiderin were seen in the third group only. In conclusion, it was shown that chronic intoxication may occur in sheep overdosed with iron. The toxic dose of iron ranged between 40 and 80 (mg/Kg body weight) per day and was close to 40 mg, when iron was administered in the soluble from FeCl3.6H2O.
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PMID:Iron toxicity in sheep. 253 32

An 8-year-old sexually intact male llama was euthanatized because of obstruction of the penile portion of the urethra and rupture of the urinary bladder. Clinical signs of obstruction included anorexia, lethargy, teeth grinding, straining to defecate, inability to urinate, and tense abdomen. Laboratory findings included anemia, leukocytosis with left shift, high serum urea nitrogen, creatinine, and phosphorus concentrations, and low serum chloride concentration. Necropsy revealed ruptured urinary bladder and acute fibrinous peritonitis. A firm, gray, nonmineralized urethral plug occluded the penile portion of the urethra for a distance of 14 cm in the midpenile region, distal to the sigmoid flexure of the penis. The urinary bladder mucosa and the urethra had microscopic evidence of chronic inflammation. Escherichia coli, Klebsiella sp, and alpha-streptococci were isolated from the urethral plug.
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PMID:Urethral obstruction in a male llama. 259 47


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