Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0030552 (paresis)
 5,831 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Studied were mass disease outbreaks on eight farms in calves intensively fed concentrate mixtures that were rich in phosphorus compounds. Clinically, there were selling and deformations of the joints with pains. The tarsal and carpal joints were chiefly involved. Kyphosis of the backbone, spastic paresis of the posterior part of the body as well as tetaniform spasms in the initial stage of the disease were also observed. Morphologically, the diseased animals manifested erosions and thinning of the joint cartilage, tearing of the Achilles tendon, and increased amounts of the joint fluid. The histologic study revealed edema of the cartilage cells, disorders in the structure of the hyalin cartilage, formation of cavities, and broadening of the lumen of the Haversian canals. In most cases the blood serum presented hyperphosphatemia (up to 15.67 mg% inorganic P) and relative or absolute hypocalcemia (up to 4.47 mg% Ca). On the farm both hypocalcemia and hypophosphatemia were observed. Good prophylactic results were obtained through correct Ca:P ratios in the diet that contained calcium additives as well as by the injection of vitamin D solutions, etc. It is believed that these cases should be referred to a distinctive form of rickets of a characteristic clinical course' the inadequate Ca:P ratios in the rations playing the main etiologic role. Subsidiary causes are probably vitamin D deficiency, restricted movement of the animals, and mechanical traumata caused by the animal's own bodyweight.
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PMID:[Study of disorders in calcium and phosphorus metabolism in the intensive fattening of young cattle]. 125 54

We report 10 patients with primary hypoparathyroidism. Age at onset varied from 7 months to 52 years (mean 28); 7 were female. Diagnosis was established at a mean of 4.1 years after the appearance of clinical manifestations. Unexplained hypocalcemia (mean 5.3 mg/dl) and hyperphosphatemia (mean 6.4 mg/dl) were present in all patients. Prevalent symptoms included tetany (9 patients), seizures (5) and hypocalcemic cataracts (4). Clinical manifestations may be grouped into 5 types 1) tetany; 2) seizures; 3) other neurologic disorders (basal ganglia calcification, pseudotumor of the brain, ataxia, nystagmus, hypertonus, paresis); 4) disorders of the lens including fully developed cataracts and 5) skin alterations like psoriasis and others. Some of these run on acute course (seizures, tetany), others a subacute one (skin alterations) while others are rather chronic (cataract and other neurologic disorders). Seizures and electroencephalographic disorders predominate in younger patients while tetany is more prevalent in older subjects.
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PMID:[Idiopathic hypoparathyroidism, a syndrome with various clinical expressions: analysis of 10 cases]. 251 14

Ponderosa pine needles cause abortion and a poorly described toxicosis when eaten by cattle. In previous trials, the abortifacient compound of pine needles was identified as isocupressic acid. At abortifacient doses, isocupressic acid caused no other toxicosis. However, other pine needle fractions, similar in composition to several commercially available rosin products, caused no abortion but were very toxic. The purpose of this study was to describe the toxicoses of ponderosa pine, compare its toxicity with other rosin and related pine products, and identify the toxin. Four groups of three pregnant beef cows each were treated with either ponderosa pine tips, rosin gum, dehydroabietic acid, or ground alfalfa. The cows treated with pine tips aborted, had retained placentas with endometritis, and developed both renal and neurologic lesions. The cattle treated with rosin gum or dehydroabietic acid did not abort but developed similar signs and lesions of intoxication. Clinical signs of intoxication included anorexia, mild rumen acidosis, dyspnea, paresis progressing to paralysis, and death. Clinical biochemical results, suggestive of renal, hepatic, and muscular disease, included azotemia, hypercreatinemia, hyperphosphatemia, proteinuria, and marked elevations of various serum enzymes. Histologically, all poisoned animals had nephrosis, vacuolation of basal ganglia neuropil with patchy perivascular and myelinic edema, and skeletal myonecrosis. The alfalfa-treated controls were normal. These findings suggest that ponderosa pine needles and tips are both abortifacient and toxic. Because the lesions caused by pine tips, rosin gum, and dehydroabietic acid are similar, toxicosis is most likely due to the diterpene abietane acids, common in all three.
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PMID:The toxic and abortifacient effects of ponderosa pine. 882 3

In recent years, there has been renewed interest in primary hyperaldosteronism, particularly because of its possible role in the progression of kidney disease. While most studies have concerned humans and experimental animal models, we here report on the occurrence of a spontaneous form of (non-tumorous) primary hyperaldosteronism in cats. At presentation, the main physical features of 11 elderly cats were hypokalemic paroxysmal flaccid paresis and loss of vision due to retinal detachment with hemorrhages. Primary hyperaldosteronism was diagnosed on the basis of plasma concentrations of aldosterone (PAC) and plasma renin activity (PRA), and the calculation of the PAC:PRA ratio. In all animals, PACs were at the upper end or higher than the reference range. The PRAs were at the lower end of the reference range, and the PAC:PRA ratios exceeded the reference range. Diagnostic imaging by ultrasonography and computed tomography revealed no or only very minor changes in the adrenals compatible with nodular hyperplasia. Adrenal gland histopathology revealed extensive micronodular hyperplasia extending from zona glomerulosa into the zona fasciculata and reticularis. In three cats, plasma urea and creatinine concentrations were normal when hyperaldosteronism was diagnosed but thereafter increased to above the upper limit of the respective reference range. In the other eight cats, urea and creatinine concentrations were raised at first examination and gradually further increased. Even in end-stage renal insufficiency, there was a tendency to hypophosphatemia rather than to hyperphosphatemia. The histopathological changes in the kidneys mimicked those of humans with hyperaldosteronism: hyaline arteriolar sclerosis, glomerular sclerosis, tubular atrophy and interstitial fibrosis. The non-tumorous form of primary hyperaldosteronism in cats has many similarities with "idiopathic" primary hyperaldosteronism in humans. The condition is associated with progressive renal disease, which may in part be due to the often incompletely suppressed plasma renin activity.
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PMID:Primary hyperaldosteronism, a mediator of progressive renal disease in cats. 1562 Aug 9