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Query: UMLS:C1762617 (weakness)
 37,932 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Dose-response relationships between blood lead levels and toxic effects have been evaluated in 160 lead workers in two smelters and a chemicals plant. Blood lead levels ranged from 0.77 to 13.51 mumol/litre (16-280 microgram/dl). Clinical evidence of toxic exposure was found in 70 workers (44%), including colic in 33, wrist or ankle extensor muscle weakness in 12, anaemia (Hgb less than 8.69 mumol/litre (Hb/4) or 14.0 gm/dl) in 27, elevated blood urea nitrogen (greater than or equal to 7.14 mmol/litre or 20 mg/dl) in 28, and possible encephalopathy in two. No toxicity was detected at blood lead levels below 1.93 mumol/litre (40 microgram/dl). However, 13% of workers with blood lead levels of 1.93 to 3.81 mumol/litre (40-79 microgram/dl) had extensor muscle weakness or gastrointestinal symptoms. Anaemia was found in 5% of workers with lead levels of 1.93-2.85 mumol/litre (40-59 microgram/dl), in 14% with levels of 2.90 to 3.81 mumol/litre (60-79 microgram/dl), and in 36% with levels greater than or equal to 3.86 mumol/litre (80 microgram/dl). Elevated blood urea nitrogen occurred in long-term lead workers. All but three workers with increased blood urea nitrogen had at least four years occupational lead exposure, and nine had received oral chelation; eight of this group had reduced creatinine clearance, and eight had decreased renal concentrating ability. These data support the establishment of a permissible biological limit for blood lead at a level between 1.93 and 2.90 mumol/litre (40-60 microgram/dl).
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PMID:Occupational lead poisoning in the United States: clinical and biochemical findings related to blood lead levels. 50 43

Twenty-two young cows died or were euthanatized after intoxication associated with ingestion of redroot pigweed (Amaranthus retroflexus) growing in marginal grass pasture. After several days of weakness and posterior incoordination, the cattle became recumbent but remained alert. Pertinent clinical laboratory findings included increased blood urea nitrogen content and marked proteinuria. At necropsy, perirenal edema and toxic tubular neprosis were seen.
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PMID:Perirenal edema and toxic nephrosis in cattle, associated with ingestion of pigweed. 118 28

Critical illness, surgery and hypocaloric feeding are accompanied by a high rate of total body nitrogen loss. Loss of body protein, occurring despite adequate nutrition, results in increased incidence of infection, poor wound healing, skeletal muscle weakness and increased mortality. Growth hormone (GH) administration together with nutritional support attenuates protein catabolism. This review focuses on normal GH physiology and the administration of GH in adult catabolic patients.
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PMID:Growth hormone: secretion and administration in catabolic adult patients, with emphasis on the critically ill patient. 149 2

A 55-year-old woman was admitted to our hospital, complaining of general malaise, muscular weakness, anorexia and weight loss. She had a history of ingesting of a certain germanium (Ge) compound over the preceding 19 months, with a total dose of 47 g as Ge element. She was found to have renal failure (blood urea nitrogen, 44 mg/dl; serum creatinine, 2.6 mg/dl) without abnormal findings in urinalysis, and muscular and nervous damage. Initially, polymyositis was diagnosed and prednisolone administered. However, no improvement was seen, and neuromuscular symptoms and signs steadily worsened, ending in death. Microscopic study of the kidney showed that lipofuscin granules increased in the cells of the thick ascending limb of Henle's loop to the distal convoluted tubule accompanying mild tubular atrophy and that some of the tubules of these segments had vacuolar degeneration or desquamation. No apparent glomerular and vascular changes were observed. High Ge content was found in serum, urine and various tissues, e.g., spleen, liver, kidney, adrenal gland and myocardium, while in controls Ge could not be detected in sera, urine or tissues. We also review case reports about Ge toxicity, and discuss the pathogenesis of renal failure induced by Ge compounds.
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PMID:Nephrotoxicity of germanium compounds: report of a case and review of the literature. 158 20

Cyclosporin-A-treated renal allograft recipients have demonstrated an improved graft survival rate, when compared to that of patients treated with conventional azathioprine and steroid therapy. Cyclosporin-A has been used for immunosuppressive therapy after renal transplantation at the National Taiwan University Hospital since November 1985. Since then, the one-year graft survival rate has been 78%, and the patient survival rate is 91%. At our service, acute rejection is confirmed mainly by an increase in the serum creatinine level of 0.5 mg% per day and a subsequent return of kidney function to normal after pulse steroid therapy. Twenty patients receiving cyclosporin-A and suffering from acute rejection episodes were chosen for comparison with 18 patients receiving conventional azathioprine and steroid therapy. Compared to conventional therapy, the classical systemic manifestations of rejection, such as malaise, lethargy, apathy, general weakness, vague discomfort, increase in body weight, swelling of graft with tenderness, were all more mild and less frequent in the cyclosporin-A-treated group. Episodes of rejection appeared earlier and the duration of rejection was shorter than in those of the conventional group. The urinary sodium concentration and the ratio of urine urea nitrogen to blood urea nitrogen were reliable references during the acute rejection episode in the conventional group, but it cannot be used as indices in the cyclosporine group. These findings can help us understand the changes which occurred in acute rejection in patients who receive renal transplantation during the cyclosporine era.
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PMID:Clinical manifestations of acute rejection in renal allograft recipients receiving cyclosporin-A therapy. 168 Sep 67

We attempted to define the site of muscle action accounting for the apparent muscle weakness occurring with postoperative fatigue. A model of the normal pathway of muscle contraction is presented. A series of studies, designed to separate the elements of the pathway, was performed on 38 patients undergoing major abdominal surgery. Central fatigue was measured with Christensen's analogue, voluntary strength by grip strength, perceived effort by grading the difficulty of a set work load, involuntary muscle function by ulnar nerve stimulation, and muscle bulk represented by total body nitrogen, measured by in vivo neuron activation analysis. Fatigue increased for the first 2 weeks after operation, was back to pre-operative levels within 1 month, and improved further at 3 months. Grip strength fell after operation and returned to pre-operative levels within 3 months. Perceived effort rose after operation and returned to pre-operative levels by 3 months. Involuntary muscle function was unaffected by operation. Similarly, total body nitrogen fell in the first 2 weeks after operation but was improved on baseline levels at 3 months. However, there was no consistent correlation between the movement patterns of any of the muscle parameters and fatigue. The results suggest that fatigue after surgery is not accompanied by any muscular defect, and that the apparent muscular weakness is probably a secondary phenomenon to the central fatigue.
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PMID:Postoperative fatigue: a prospective physiological study of patients undergoing major abdominal surgery. 192 79

Vanadate at a dosage level of 0.9 mg V/kg per day produced acute toxic signs in rats when injected subcutaneously for 16 days. These signs were weakness, loss of appetite, dehydration, significant reduction in body weight, nose bleeding, and death. The pathological and biochemical changes were most severe in kidney tissue. The kidney lesions were bilateral and multifocal. At two days, degenerative and necrotic changes of the tubular and glomerular epithelium, thickening of glomerular membrane, vascular congestion, and edema were observed. At five days, proliferation of tubular epithelial and interstitial cells was observed. At 12 days, the cellular proliferation in both cortex and medulla was significantly greater. Fibrosis was observed at glomerular tuft, preglomeruli, pretubules, and interstitium (cortex and medulla). At 25 days, the collagen deposition reached the highest level in all regions, cellular proliferation decreased, and thickening of the arteriolar wall became prominent. The renal lesions were coupled with changes in the levels of protein, RNA, DNA, and hydroxyproline. At 40 days, the kidney showed signs of recovery. Blood urea nitrogen levels were significantly elevated at 2-25 days post-treatment. Stained tissue sections from liver, lung, heart, spleen, thymus, lymph nodes, testes, and adrenal glands of the treated rats were examined microscopically and appeared normal. Biochemically, significant changes (p less than .05) in protein, RNA, DNA, and hydroxyproline were also observed in these organs. At lower dosage (0.6 mg V/kg per day for 16 days), similar but less severe pathological and biochemical changes in kidneys and other organs were observed. At 0.3 mg V/kg per day for 16 days, the changes in the tissues were detected only at the biochemical level. These results indicate that the toxic effects of vanadium are cumulative and that vanadium-produced fibrosis in tissues is dose-dependent.
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PMID:Time and dose-response study of the effects of vanadate on rats: morphological and biochemical changes in organs. 248 72

During a recent outbreak of Rhodesian sleeping sickness in the Lambwe Valley no asymptomatic Rhodesian sleeping sickness patients were found although 54% of the primary patients had mild symptoms and 9% were stuporous or comatose at presentation. The duration of symptoms was three months or less in 90% of the patients. Headache, weakness, joint and back pains and weight loss were claimed by at least 75% of the patients, while 82% of the females reported amenorrhoea and 70% of the males claimed impotency. Physical examination revealed lymphadenopathy in 86% but fever in only 36% of the patients, while chancres were found in only 16%. Patients had significantly lower levels of haemoglobin and thrombocytes than controls and their erythrocyte sedimentation rates were elevated. A comparison of both blood group and haemoglobin type between patients and controls yielded no significant differences. Fifty-seven per cent of the primary patients reporting mild symptoms had abnormal levels of leucocytes in their CSF. All relapse patients had abnormal CSF parameters. Levels of serum urea nitrogen were significantly elevated in patients, but SGOT, SGPT and total bilirubin were not. Levels of albumin and beta-globulin in patients were significantly lower than controls while gamma-globulin was elevated. Mean serum IgM levels in patients were elevated to nearly three-fold those of controls, but 35% of the individual patient values fell within the 95% range of control values. Some patients had extended prothrombin and thrombin times while fibrinogen levels were significantly elevated. No patients reported haemorrhage, and none was seen.
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PMID:Presenting features of Rhodesian sleeping sickness patients in the Lambwe Valley, Kenya. 261 98

An animal model for clinically observed clofibrate (p-chlorophenoxy isobutyrate, CPIB)-induced toxicity has been tested. It is demonstrated that propylthiouracil-induced hypothyroid-hyperlipidemic chick develops severe toxic manifestations following clofibrate administration. Toxic symptoms are characterized by listlessness, drowziness, and extreme muscular weakness. This is associated with elevation of blood urea nitrogen, creatine phosphokinase, uric acid and glutamic oxaloacetic transaminase. Histological examination of muscle specimen from chicks exhibiting toxic syndrome showed degeneration and vacuolization of muscle fibers. The biochemical and histological changes observed are quite similar to those reported in clinical practice in some patients given clofibrate. It is suggested that this chick model could be used to investigate the biochemical basis of clofibrate toxicity.
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PMID:Propylthiouracil-induced hypothyroid hyperlipidemic chick: a model for clofibrate-induced toxicity. 287 99

After routine cryptorchid castration, a 2-year-old Thoroughbred colt was admitted 72 hours later because of depression, abdominal distention, and pollakiuria, with production of small quantities of urine. A diagnosis of a ruptured bladder was made on the basis of a large volume of abdominal fluid and a disparity between the urea nitrogen and creatinine concentrations in the serum (70 mg/dl and 8.4 mg/dl, respectively) and in the abdominal fluid (154 mg/dl and 43 mg/dl, respectively). The colt had undergone surgical correction of a ruptured urinary bladder at 4 days of age, and a 5-cm tear through one of the previous scars was identified and repaired during exploratory celiotomy. The previous injury to the bladder was extensive and may have left an inherent weakness in the bladder wall. Evidence of adhesion formation or urethral obstruction was not found. The combination of a full bladder and the trauma associated with induction of anesthesia may have contributed to the recurrence of bladder rupture.
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PMID:Urinary bladder rupture in a two-year-old horse: sequel to a surgically repaired neonatal injury. 288 12


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