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)

The prognostic significance of a battery of clinical, laboratory, and histological indicators was assessed in relation to mortality risk in a 1-year study of 253 patients with alcoholic liver disease, of whom 51 died within such time. The relative risk associated with each abnormality was calculated. A number of abnormalities was found to be statistically associated with a higher risk of death. Among the clinical abnormalities, these were: collateral circulation, edema, ascites, encephalopathy, spider nevi, anorexia, and weakness. Among the laboratory tests, these were: albumin, bilirubin, hemoglobin, abnormal prothrombin time, and alkaline phosphatase. Two hundred and sixteen of these patients had liver biopsies in which the quantifiable abnormalities were scored. Among the histological findings, the alterations significantly related to mortality were necrosis, Mallory, and inflammation, while the presence of cirrhosis per se did not influence the mortality risk. The relative risk factors for mortality associated with the histological alterations were lower than those derived from clinical or laboratory measurements. The advantage of using only clinical and laboratory items to derive a global, quantitative expression of severity is discussed. The relative mortality risks provided a means of calculating a "unit of severity" for each clinical and laboratory abnormality. A combined clinical and laboratory index (CCLI) results when these mortality-risk units are added. Such a combined index had a quasi-linear relationship with the risk of mortality for the complete population. This method compared well with severity scores derived from computerized, linear step-wise discriminant function (SDF) analysis and from a logistic regression (LR) analysis. The factors chosen to have independent prognostic significance by the SDF analysis were: encephalopathy, albumin, prothrombin time, and hemoglobin, while only encephalopathy, albumin, and hemoglobin were chosen by the LR analysis. Within a range of values, LR can provide a good discrimination in relation to mortality, similar to that observed for the CCLI in its complete range. However, there are some advantages to the CCLI method vs. the LR or SDF analyses. The CCLI is less susceptible to being unduly influenced by a nonspecific effect of treatment on the items chosen than the SDF and LR analyses, as the CCLI contains a large number of factors. Obtaining a single-severity score such as the CCLI is of value in: (a) assessing the effectiveness of treatment modalities; (b) analyzing the success of randomization; (c) separating cohorts of different severity, and (d) comparing new liver tests, histological abnormalities, or specific biological events with the severity of alcoholic liver disease.
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PMID:Assessment of prognostic factors in alcoholic liver disease: toward a global quantitative expression of severity. 662 18

The histologic and histochemical features of palatine muscles from 53 horses were studied; 25 of the horses were racehorses that had upper airway obstruction associated with dorsal displacement of the soft palate and 28 of the horses did not have any respiratory disorders and served as controls. Pathologic features observed included myonecrosis, phagocytosis, mononuclear cell infiltration of perimysial connective tissue, alkaline phosphatase-positive myofibers, and myofibers with cytoarchitectural changes that included irregular staining of the intermyofibrillar sarcoplasm and sarcoplasmic masses. These histopathologic features were judged to be indicative of myositis. Those features were found in both control horses and horses with dorsal displacement of the soft palate; however, their prevalence was higher in horses with dorsal displacement of the soft palate. For the control horses as well as the horses with dorsal displacement of the soft palate, the inflammatory changes were more prevalent in older horses. The finding of myositis suggests that palatal muscle weakness may contribute to the development of dorsal displacement of the soft palate; however, the myositis might have been secondary to trauma associated with displacement of the soft palate. We could not distinguish between these 2 possibilities. A large number of horses with dorsal displacement of the soft palate also had concurrent pharyngeal lymphoid hyperplasia. Extension of the mucosal inflammatory changes associated with pharyngeal lymphoid hyperplasia into the underlying palatine muscle might have accounted for the myositis.
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PMID:Palatal myositis in horses with dorsal displacement of the soft palate. 662 86

A patient with carcinoma of the prostate, extensive bony metastases, and osteomalacia is reported. The diagnosis of osteomalacia was suspected because of generalized weakness and bone pains, hypocalcemia, hypophosphatemia, and raised alkaline phosphatase. It was documented by low 1,25-dihydroxyvitamin D level. Furthermore, it was confirmed by improvement in patient's symptomatology and normalization of serum calcium and phosphorus after treatment with 1,25-dihydroxyvitamin D3 (Rocaltrol).
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PMID:Osteomalacia associated with prostatic cancer and osteoblastic metastases. 668 13

Hepatic function tests were performed on 48 dogs that had been given primidone, phenytoin, or a combination of anticonvulsant drugs for 6 months or longer. Except for histories of seizures, 44 of the dogs were healthy at the time the tests were performed. Abnormal test results were observed most frequently in dogs given only primidone and in dogs given combinations of anticonvulsant drugs. The test results that were abnormal most often were those for alanine transaminase and alkaline phosphatase activities, and sulfobromophthalein excretion. The dosage of anticonvulsant drug was found to modify certain test results. Statistically significant positive correlations were found between the dosage of primidone and serum alanine transaminase activity and between the dosage of phenytoin and serum alkaline phosphatase activity. Four of the dogs were examined because of signs of weakness and anorexia and 2 also had ascites. Three of the 4 dogs were euthanatized 2 to 49 days after admission with clinical signs compatible with hepatic failure, and cirrhosis of the liver was confirmed at necropsy. The fourth dog died at home and was not necropsied. Four of the remaining 44 dogs that apparently were healthy at the time of examination had abnormalities in hepatic biochemical test results that were comparable with those in the 4 dogs with clinical illness. We concluded that, although results of hepatic biochemical tests frequently may be abnormal in dogs given anticonvulsant drugs long-term, severe hepatic injury is observed less often.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Compromised hepatic function in dogs treated with anticonvulsant drugs. 669 76

Patients with end-stage renal failure develop osteodystrophy in part due to defective production of 1,25-dihydroxycholecalciferol by the kidney. We treated eight adults with chronic renal failure and osteodystrophy with 1,25-dihydroxycholecalciferol (calcitriol) for 30-44 months. Seven of these patients were also symptomatic with bone pain and/or muscle weakness. Striking amelioration of muscle weakness occurred, and bone pain was considered to be significantly improved in four of seven patients. Hypercalcemia was noted in all the patients, necessitating a reduction in the daily dose of calcitriol to a range of 0.125 to 0.5 microgram/day. While serum alkaline phosphatase fell during therapy, serum iPTH did not show any significant change. Bone mineral content improved in four patients, though it still remained below normal. Radiographic changes of osteodystrophy showed definite improvement in only three.
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PMID:Long-term therapy of uremic osteodystrophy in adults with calcitriol. 689 93

The toxic effects of PR toxin were observed in mice, rats, anesthetized cats and isolated rat auricle preparations. In mice and rats the toxic effects included abdominal writhing, decrease of motor activity and respiratory rate, weakness of hindleg and ataxia. In mice, the i.p. LD50 was 5.8 mg/kg. In mice, rats and cats PR toxin given i.p. caused ascites fluid an edema in the scrotum and lungs, and i.v. injection caused edema in the lungs, giving rise to a large volume of pleural and pericardial fluid. In rats, at the LD50 dose level (11.6 mg/kg, i.p. and 8.2 mg/kg, i.v.), the water content in the lungs was increased, but in the skin it was decreased. Blood K+, hematocrit, red blood cell, white blood cell, hemoglobin, uric acid, cholesterol, blood urea nitrogen and alkaline phosphatase concentrations were all increased, while the total protein and albumin contents were decreased after i.p. injection of PR toxin. High content of protein was found in the pleural fluid and fluid due to ascites. In anesthetized cats the blood pressure and respiratory rate were progressively decreased and the heart rate was reflexly increased after i.p. injection. The i.v. injection produced a multiple response on the arterial blood pressure, but with a progressively decreasing heart rate. Arrhythmias were observed in the late shock stage in the case of i.p. or i.v. injection. In the isolated rat auricle preparations contractile force was more affected that heart rate. We conclude that PR toxin produced acute toxic effects in animals via an increase of capillary permeability and a direct damage to the lungs, heart, liver and kidney.
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PMID:Acute toxicity of PR toxin, a mycotoxin from Penicillium roqueforti. 708 52

Advanced chronic hepatic disease was observed in 5 dogs that had received anticonvulsant drug therapy for 2 to 3 years. Clinical signs included anorexia, weakness, and restlessness, and 2 dogs also had ascites. There were remarkable increases in the serum activities of alanine aminotransferase, alkaline phosphatase, and gamma-glutamyl transferase. The total serum bile acid concentration was high in 3 of 4 dogs that were tested. Sulfobromophthalein excretion was delayed in all dogs. Histologic examination of liver specimens from 4 of the dogs demonstrated macronodular or micronodular cirrhosis.
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PMID:Hepatic cirrhosis associated with long-term anticonvulsant drug therapy in dogs. 711 8

Case report on a 48-year-old Swiss male living in Burundi who suddenly fell ill with vomiting and anorexia, followed by pappy stools, weakness and impotence. He presented with hepatomegaly, while sedimentation rate and alkaline phosphatase were both elevated. Stool examination revealed cysts and vegetative forms of Entamoeba histolytica, while amebic serology was negative. Treatment with ornidazole and later with diloxanide furoate was given. Sonography showed two cystoid areas in the right lobe of the liver. In the third sonographically guided fine-needle puncture both lesions were fully aspirated. Amebic serological tests were now positive for the first time. Six weeks later the sonogram showed a normal liver feature. The symptomatology and diagnosis of hepatic amebic abscess are discussed, with special reference to the important role of sonographically guided fine-needle puncture and drainage. Sonographic technique and differential diagnosis are briefly demonstrated.
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PMID:[Use of ultrasound, ultrasound-directed fine needle puncture and aspiration in amebic abscess of the liver. Case report and short overview]. 715 63

A new familial disorder, inherited as an autosomal dominant trait and characterized by dual features of neurologic degeneration and skeletal disorganization, is reported. The neurologic disease is a degenerative process of lower motor neurons and develops in middle age with progressive muscle weakness and ends in respiratory failure and premature death. Clinical examination, electromyography, and muscle biopsy with histochemical stains are diagnostic. The skeletal disorganization resembles Paget's disease of bone. It is characterized by polyostotic radiographic abnormalities, elevated serum alkaline phosphatase of bone origin, abnormal radioisotopic bone scan, elevated hydroxyprolinuria, and bone histology.
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PMID:A new familial disorder of combined lower motor neuron degeneration and skeletal disorganization. 718 74

Sixty-one patients with chronic renal failure and secondary hyperparathyroidism underwent total parathyroidectomy and parathyroid autograft. Symptoms relieved by parathyroidectomy included bone pain, pruritus, soft tissue calcification, muscle weakness and healing of fractures. Serum parathormone levels measured before and after operation in 48 patients returned to normal in all but two patients. Serum alkaline phosphatase levels also returned toward normal after operation, except in one patient with a retained parathyroid gland. Complete radiographic studies before and after operation were available in 30 of 61 patients. Twenty-three of 24 patients with osteitis fibrosa had evidence of healing, and in one patient no change occurred. Osteosclerosis noticed in 23 patients improved slightly in eight patients, did not change in 14 and became worse in one. Pathologic examinations revealed 45 patients to have diffuse hyperplasia and 16 nodular hyperplasia. There were two early postoperative deaths, in the first 30 days, and 16 late postoperative deaths, from four months to four years afterward. In no case did the operation contribute to death. Some patients required the administration of supplemental calcium after operation, but in no instance did profound hypocalcemia occur. No patient developed recurrent hyperparathyroidism.
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PMID:Treatment of secondary hyperparathyroidism in patients with chronic renal failure by total parathyroidectomy and parathyroid autograft. 724 22


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