Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0023380 (lethargy)
 5,697 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Idiopathic hypoparathyroidism was diagnosed in five young to middle-aged cats of mixed breeding. Three of the cats were male and two were female. Historic signs included lethargy (n = 5), anorexia (n = 5), muscle tremors (n = 4), weakness (n = 4), generalized seizures (n = 3), ataxia (n = 3), mental dullness or disorientation (n = 3), panting (n = 2), pruritus (n = 1), ptyalism (n = 1) and dysphagia (n = 1). Weakness (n = 4), dehydration (n = 2), cataracts (n = 2), hypothermia (n = 1), and bradycardia (n = 1) were found on physical examination. Results of electrocardiography revealed a prolonged Q-T interval in two cats. Results of initial laboratory tests revealed profound hypocalcemia and severe hyperphosphatemia with normal renal function. The diagnosis of hypoparathyroidism was made on the basis of the history, clinical signs, and results serum biochemical testing (i.e., severe hypocalcemia and hyperphosphatemia); in two cats, the diagnosis was also confirmed by histologic examination of parathyroid glands. Initial treatment included intravenous administration of 10% calcium gluconate and oral administration of large loading doses of calcium and vitamin D (dihydrotachysterol). Successful long-term management with dihydrotachysterol and calcium was achieved in all cats. The final dosage of dihydrotachysterol required to maintain normocalcemia in the five cats ranged from 0.004 to 0.04 mg/kg/day (mean = 0.015 mg/kg/day). Long-term calcium supplementation was given to three of the cats in dosages ranging from 29 to 53 mg/kg/day (mean = 42 mg/kg/day) of elemental calcium. One cat died after 28 months of therapy from widely metastatic hemangiosarcoma; the other three cats are still alive and well after 5 to 37 months of treatment.
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PMID:Idiopathic hypoparathyroidism in five cats. 202 14

An episode of pulmonary arteritis and sclerosis in twenty 5- to 6-month-old dairy calves was investigated. Sixteen of the calves died acutely, without marked premonitory signs of disease. Four calves evaluated clinically had lethargy, pallor, weakness, tachycardia, tachypnea, and jugular venous distention. Cardiac catheterization performed in 3 of the calves revealed pulmonary hypertension; 1 of these calves survived. Necropsy findings in 19 calves included pale lungs and excess free fluid in the pleural and abdominal cavities. In addition, 13 of 19 calves had a dilated and thin-walled right ventricle; 4 of the calves had right-sided cardiac hypertrophy, and 2 had dilatation of the pulmonary artery. Microscopically, pulmonary arteritis and sclerosis of the small to medium-sized arteries were evident in all calves submitted for necropsy. A lung biopsy specimen from a surviving calf had similar lesions. Centrilobular hepatic necrosis was found in 17 of 19 calves. Investigation of the disease episode, including feed analysis for toxins and serologic and microbiological studies of clinically affected calves and clinically normal in-contact penmates, failed to reveal any associated risk factor. The pulmonary arterial changes in the calves were similar to lung lesions in rats fed monocrotaline.
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PMID:Pulmonary hypertension in a group of dairy calves. 202 38

Juliflorine (CAS 76202-00-1), an antibacterial and antidermatophytic alkaloid, was studied for its toxicity in mice, rabbits, chicks, chick embryos and vero cell line. In mice LD50 was determined as 17.46 mg/kg; in rabbits 33.11 mg/kg; in chicks 24.104 mg/kg; and in chick embryos 18.284 mg/kg. In rabbits the subsequent injection of non-lethal doses (10 mg/kg) through the same route induced swelling, induration, inflammation and tissue degeneration (around injected area) with sterile abcess. Topically 1% juliflorine in polyethylene glycol-400 was found non-toxic but higher concentrations (less than or equal to 2.5%) produced irritation and inflammation; the severity of reaction was dose dependent. In vero cell-line juliflorine was found toxic at greater than or equal to 5 micrograms/ml. Injected animals showed lethargy, prostration and weakness (dose dependent) but recovered after some days, while newly hatched chicks, from injected eggs with higher dose, did not survive after 48 to 72 h. Internal organs (liver, kidney, brain, etc.) of dead, sick and healthy animals were examined and found normal.
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PMID:Toxicological studies of the antimicrobial alkaloid juliflorine. 204 77

Hypercalcemia is a potentially lethal endocrine disorder occurring in 10% to 20% of cancer patients at some time during the course of their disease. Clinical manifestations vary in severity, depending on the degree and duration of hypercalcemia, rapidity of onset, patient's age, performance status, sites of metastases, previous antineoplastic therapy, and the presence of hepatic or renal dysfunction. The clinical features of hypercalcemia are protean and affect multiple organ systems, resulting most prominently in neurologic, gastrointestinal, renal, cardiovascular, and musculoskeletal morbidity. Recognition of the disorder requires a high index of suspicion because many of its symptoms, such as nausea, anorexia, weakness, fatigue, lethargy, and confusion, are non-specific and, in the patient with a malignancy, can result from other complications of the primary disorder. If identified appropriately as being related to hypercalcemia, such symptomatology is potentially reversible with treatment. Whereas in the ambulatory general medical population the most common cause of hypercalcemia is primary hyperparathyroidism, in cancer patients and hospitalized patients in general, the most common cause is malignancy. Hypercalcemia in cancer patients is, in most cases, due to advanced metastasized disease. Diagnostic tests are useful in the differential diagnosis of hypercalcemia, and such tests, together with an accurate history and careful clinical observation, permit the best therapeutic approach to an individual patient.
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PMID:Clinical manifestations of cancer-related hypercalcemia. 218 49

Herpes simplex virus (HSV) is regarded as an agent that selectively affects temporal and frontal lobes with necrosis and hemorrhage, and no case of herpes simplex encephalitis (HSE) with white matter lesion in a diffuse fashion has previously been reported. A 2-year-old boy developed high fever, right hemi-convulsions and lethargy. Computed tomography (CT) showed wedge-shaped areas of high density in the left frontal region, whereas, cerebral angiography disclosed no vascular abnormality. T1-weighted magnetic resonance imaging (MRI) demonstrated cortical changes which were similar to those illustrated by CT. However, T2-weighted images depicted further spread high intensities of the lesion. The patient's symptoms spontaneously disappeared before an antiviral drug, acyclovir, was administered. After the significant increase of HSV antibody titers in serum and cerebro-spinal fluid (CSF) established a definite diagnosis, acyclovir was intravenously given at a daily dosage of 30 mg/kg for a period of 6 days in order to prevent the recurrence of HSE. Two months later, T2-weighted MRI visualized a diffuse lesion of increased signal intensities involving the white matter of both hemispheres, while both CSF protein and myelin basic protein were significantly elevated. Despite of these changes of the white matter, our patient developed a few symptoms such as mild speech disturbance, slight weakness of the right upper limb and sialorrhea. Although the mechanism of these changes in the white matter remains obscure, it is postulated that a direct invasion of HSV to the white matter, an immunological disorder following HSV infection and a side effect of acyclovir could have triggered a reversible process of demyelination of the cerebral white matter.
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PMID:[A case of herpes simplex encephalitis with cerebral white matter lesion after acyclovir administration]. 222 88

A porcine strain of Pasteurella multocida (serotype D:3) produced a toxin causing turbinate atrophy (TA) in pigs. The toxin (TAT), processed on a high performance liquid chromatography size exclusion column, eluted as a single peak (molecular weight of about 160,000) containing trace amounts of endotoxin (lipopolysaccharide, LPS; protein:LPS, 85:1). The eluted fraction migrated on sodium dodecyl sulfate polyacrylamide gels as a single band. It could be prevented from dissociating into two prominent polypeptides by addition of a protease inhibitor. A single dose (2.0 to 79.0 micrograms/kg) of TAT given to pigs intravenously was lethal. Doses from 0.02 to 1.0 microgram/kg caused transient clinical signs of porcine systemic toxicosis with reduced appetite, generalized weakness, depression, lethargy, weight loss, and in some instances, death. Intradermal doses of TAT (greater than or equal to 0.1 microgram/site) produced hemorrhagic areas within four hours. Systemically, TAT causes bilateral TA, lymphopenia, liver dysfunctions, and possible renal impairment. Affinity of TAT for cells of epithelial origin was demonstrated in mice given 125I-TAT. In vitro, TAT stimulated DNA and protein syntheses of peripheral blood lymphocytes and suppressed syntheses in turbinate and kidney cell cultures without being cytolytic. Biological effects of TAT were eliminated by exposure to either heat, trypsin or anti-TAT antibody.
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PMID:Host response to Pasteurella multocida turbinate atrophy toxin in swine. 230 67

A 56 year-old man presented with vertigo and the right sided weakness. Neurological examination revealed a lethargic man with good orientation to three spheres. His neck was supple. He had anisocoria, the right pupil being larger than the left by 1.5 mm with sluggish light reaction bilaterally. He had exotropia of the right eye in primary gaze. The abduction of both eyes were full with terminal horizontal nystagmus. The adduction of both eyes were quite limited in each eye. He had a limited upward gaze with poor convergence. These were interpreted as the syndrome of the medial longitudinal fasciculus (MLF) bilaterally. He had a depressed gag reflex on the right side with tongue deviation to the right. He had a mild weakness of the right side limb and also had the right sided hemihyperesthesia including his face to pain and temperature. Twenty four hours after the onset, the left brachial angiography revealed a complete occlusion of the rostral portion of the basilar artery without visualization of the posterior cerebral and superior cerebellar arteries bilaterally. CT scans three days after the onset revealed a low density area in the mid pons with extension rostrally up to the mesencephalon. Four days later he became quadriplegic with bilateral horizontal gaze palsy. No more internuclear ophthalmoplegia is noted on both sides. The midline location of the MLF in the pons, and the separate blood supplies by different paramedian branches of the basilar artery, form the anatomical explanation for the frequent unilaterality of vascular and bilaterality of demyelinating lesions. Bilateral MLF syndrome has been considered almost pathognomonic of multiple sclerosis.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Bilateral internuclear ophthalmoplegia in association with basilar artery occlusive disease]. 235 Sep 28

Weakness, lethargy, ataxia, lateral recumbency, limb paddling, tremors, salivation, and diarrhea were observed in newborn pigs on a commercial swine farm. Many pigs became moribund and died. All had been treated with an aerosol wound spray containing 2.5% chlorpyrifos. A controlled study was undertaken to determine whether the aerosol spray was the cause of these clinical signs. Pigs exposed to aerosol spray containing 2.5% chlorpyrifos at 3 hours (n = 4) and 6 hours (n = 3) after birth developed clinical signs similar to those on the farm; none survived. Pigs exposed at 24 hours (n = 5) after birth developed clinical signs consistent with those that had developed in pigs on the farm; 3 died and 2 survived. Of 3 pigs exposed to the same spray at 36 hours after birth, 1 developed tremors 7.5 hours later and diarrhea 9 hours later, then returned to normal.
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PMID:Toxicosis in newborn pigs associated with cutaneous application of an aerosol spray containing chlorpyrifos. 244 44

We have studied aminoglutethemide (AG) combined with hydrocortisone in 28 patients with advanced and refractory prostate carcinoma. All the patients had failed at least one endocrine therapy. Six patients received only one prior hormonal treatment. Five patients were off study within 3 weeks due to early death and toxicity, 14 had progressive disease, and 9 had stable disease. No objective partial remission was observed, but the nine stable patients had therapeutic benefit, with improvement in bone pain and performance status for a median duration of 153 days. Three patients withdrew because of postural hypotension, dizziness, weakness, and lethargy. The median survival of the entire group was 186 days (range 41-606 days). Our results suggest that aminoglutethemide and hydrocortisone can be an alternative treatment for patients with advanced and refractory prostate carcinoma.
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PMID:A study of aminoglutethemide and hydrocortisone in patients with advanced and refractory prostate carcinoma. 247 42

To study the overt toxicosis of intraperitoneally (IP)-administered single doses of cholecalciferol (D3), groups of male CF-1 mice (N = 12) were given graded doses of D3 in corn oil and observed for 21 days. There was a 2- to 4-day onset of signs, including ocular squinting, reluctance to move, lethargy, weakness, anorexia, hunched posture, rough haircoat, and dehydration. This was followed by tremors, coma, and death (large doses) or gradual recovery. Deaths occurred 3 days (larger doses) to 21 days after D3 injection. The linear regression of mortality probits on log10 dose was Y = 7.332X-10.653. The median lethal dose (LD50) of D3 and 95% confidence limits were 135.4 mg/kg (112.2-157.4 mg/kg). To screen potential antidotes against acute D3 toxicosis, groups of mice (N = 12) were given subcutaneous (SC) injections of various substances beginning 2 days after IP injection of a large dose of D3 (300 mg/kg). Substances were given once or twice daily in constant volumes of saline solution (66.8 ml/kg) for 7 days. Two control groups were given D3 but no treatment. They both had 91.7% mortality; their mean (+/- SD) survival time (MST: censored to 21 days observation) was 6.8 +/- 4.7 days and 10.3 +/- 7.0 days. Mortality and MST were not affected significantly (P greater than 0.05) by once-daily injection of saline solution, saline containing dexamethasone (DEX), or saline containing the following substances with or without DEX: ascorbate; citrate; dimercaptosuccinic acid; oxytetracycline; ZnSO4; or MgCl2.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Acute intraperitoneal cholecalciferol (vitamin D3) toxicosis in mice: its nature and treatment with diverse substances. 253 55


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