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)

Canine haemangiosarcoma was studied retrospectively in 31 cases recorded among 2,871 dogs presented for necropsy (1.08%). The German Shepherd breed was more frequently represented than other breeds. Affected dogs were older than 5 years (mean 9.1 years). Nineteen were males. Presenting signs often included episodic lethargy and weakness, with depression, anorexia and mucosal pallor. Spleen and lungs were the most frequently affected sites. Haematological findings in 9 dogs with splenic or hepatic haemangiosarcoma included a mild to moderate normochromic anaemia, neutrophilia, thrombocytopaenia, poikilocytosis and increased target cells. Acanthocytes occurred in 90% of cases, schizocytes in 80% and keratocytes and metarubyricytes in 70%. Fibrin split products were increased in 2 of the 3 cases in which they were measured. The changes in erythrocyte morphology are considered to be useful diagnostic features of canine haemangiosarcoma.
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PMID:Clinical and haematological features of haemangiosarcoma in dogs. 403 24

Lethargy, marked muscle weakness and rigidity, a maximal temperature of 40 degrees C, and a maximal creatine kinase value of 17,240 IU/liter developed in a 36-year-old woman following treatment with several neuroleptics. Initial treatment with dantrolene was unsuccessful. The patient's condition improved gradually over a 10-day period with no specific therapy. Muscle biopsy revealed a contracture pattern diagnostic of malignant hyperthermia susceptibility, as well as abnormal sensitivity to fluphenazine. This report may be the first description of a patient with neuroleptic malignant syndrome in whom muscle biopsy response similar to that seen in malignant hyperthermia occurred and documents that dantrolene is not uniformly successful therapy for this syndrome.
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PMID:Neuroleptic malignant syndrome. Patient with unique clinical and physiologic features. 614 89

A 17 year old high school boy experienced fever and diarrhea, which subsided within 4 days by appropriate medications. Six days later, however, he developed unsteadiness and limb spasm. On the morning of admission, he was found to have drowsiness, dysarthria, gait disturbance and involuntary jerks. When he was brought to the hospital, he was lethargic but could follow simple verbal commands. Frequent involuntary movements manifested by facial grimacings, limb spasms and twitchings with dystonic features were seen. Decorticate posturing was readily elicited by painful stimuli. There was no meningeal irritation sign or gross sensory impairment. The deep tendon reflexes were symmetrically exaggerated with bilateral Babinski signs. Bilateral lateral rectus muscle weakness was found together with mild ptosis and upward gaze limitation. Nystagmus was not present and the funduscopic examination was normal. Immediately he was placed on anticonvulsants, steroid hormone, gamma-globulin and antibiotics as well. A brain CT scan and a CSF examination revealed no abnormality. Meanwhile he continued to show a progressive deterioration associated with fever and status epilepticus, and within 24 hours he lapsed into coma in decorticate posture. An EEG obtained at the 3rd hospital day was compatible with spindle coma. In spite of aggressive treatment he remained febrile and comatous. Therefore, vidarabine (adenine arabinoside) was initiated from the 3rd hospital day for 5 days. Then he began to groan and show frequent choreic movements. For the subsequent 2 weeks he made a slow recovery.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[A case of brain stem encephalitis with complete recovery (Bickerstaff's encephalitis)]. 620 73

Two anaesthetic techniques were assessed in 120 fit young women having non-emergency gynaecologial laparoscopy as in-patients. One group breathed halothane spontaneously via a face mask, and the second group were given neuromuscular blocking drugs and ventilation was controlled. There was no significant difference in intraoperative anaesthetic or surgical complications between the two groups although morbidity was greater in the intubated group when assessed 4 h after surgery. After 24 h there was no difference in postoperative morbidity. In an appendix to the study, 40 day-stay patients having the same operation under similar conditions were reviewed. After 24 h abdominal pain, lethargy and weakness were still present; 30% of the patients stated that they would prefer to be admitted overnight for a similar procedure in the future.
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PMID:Gynaecological laparoscopy: clinical experiences of two anaesthetic techniques. 623 62

Congenital adrenocortical unresponsiveness to ACTH is characterized by hyperpigmentation, muscular weakness, and episodes of hypoglycemia, with lethargy or coma and convulsion, and without signs or symptoms of salt wasting. Endocrinological evaluation reveals low levels of serum and urinary glucocorticoids, elevated levels of plasma ACTH and unresponsiveness to exogenous ACTH. On the other hand, aldosterone secretion or excretion is normal and is elevated during a low sodium diet. We reported on two patients with this syndrome. Case A, a 4 year-old-girl, showed skin hyperpigmentation, hypoglycemia, convulsion and coma. She was tall wlth a marked advance of bone age. Case B, a 4 year-old-boy, showed skin hyperpigmentation, fatigability and muscular weakness. Both of them revealed low urinary excretion of THE, THF, cortolone, and beta-cortolone and low levels of plasma cortisol. The levels of urinary glucocorticoids and plasma cortisol did not respond to ACTH administration. During a low sodium diet, urinary aldosterone excretion was elevated, urinary sodium excretion ws decreased, and the patients were able to conserve sodium normally. We also summerized other reported cases and discussed the etiology of this syndrome.
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PMID:[2 cases of congenital adrenocortical unresponsiveness to ACTH (author's transl)]. 625 Sep 21

Three dogs with hypoadrenocorticism did not have characteristically abnormal serum concentrations of sodium, potassium, and chloride and had not been treated with glucocorticoids. Diagnosis was based on lack of adrenocortical response to exogenous adrenocorticotropic hormone. Clinical signs included lethargy, weakness, anorexia, vomiting, and weight loss. The case demonstrated that the diagnosis of canine hypoadrenocorticism should not be excluded on the basis of normal serum electrolyte values.
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PMID:Atypical hypoadrenocorticism in three dogs. 626

Naturally-occurring hyperadrenocorticism was diagnosed in an 11-year-old female Dachshund with signs of polydipsia, polyuria, pendulous abdomen, weakness, depression and lethargy, and laboratory test abnormalities comprising lymphocytopaenia, eosinopaenia, hypercholesterolaemia and increased plasma alkaline phosphatase concentration. While awaiting hormonal test results, an adrenocorticolytic drug (o,p'-DDD) was administered for 14 days, during which the patient deteriorated. Hormonal assays suggested a functioning adrenocortical tumour, but the poor condition of the patient precluded adrenalectomy. An adrenocortical carcinoma with hepatic metastases was found at necropsy.
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PMID:Functioning adrenocortical tumour in a dog. 628 91

Of cases of hyperadrenocorticism in small animals 80-85% are the result of adrenocortical hyperplasia. Middle-aged or older Poodles, Dachshunds, Boston Terriers and Boxers are most commonly affected, and cats rarely. Clinical signs include polydipsia, polyuria, alopecia, abdominal distension, lethargy, weakness, hepatomegaly, calcinosis cutis, testicular atrophy and anestrus. Hematologic and biochemical changes may include neutrophilia, lymphopenia, monocytosis, eosinopenia, increased blood levels of alkaline phosphatase, SGPT, cholesterol, Na and glucose, and decreased K and T4 levels. The high-dosage dexamethasone suppression test helps differentiate pituitary-dependent hyperadrenocorticism from that caused by adrenal tumors. The low-dosage dexamethasone suppression test, determination of plasma ACTH levels, and ACTH response test are additional diagnostic aids in the diagnosis of Cushing's disease. Medical treatment involves oral use of mitotane (o,p'-DDD) at 50 mg/kg/day for 7 days and prednisone or prednisolone at 0.05 mg/kg/day. Hypophysectomy has been used with only 5% mortality in cases of pituitary-dependent hyperadrenocorticism. Adrenalectomy is indicated in cases of adrenal neoplasia.
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PMID:Diseases of the adrenal cortex of dogs and cats. 633 May 21

Nadolol (N) titrated from 80 to 240 mg or bendroflumethiazide (B) 5 to 10 mg, or the combination (B + N), were randomly assigned double-blind to 365 men with pretreatment diastolic blood pressures (BP) of 95 to 114 mm Hg. After 12 weeks of treatment, a diastolic BP of less than 90 mm Hg was achieved in 49% who received N, 46% who received B and 85% who received B + N. With N, the diastolic BP decreased more in whites than in blacks; with B, this racial trend was reversed. Side effects were infrequent; the most common were impotence, lethargy, weakness and postural dizziness, which occurred more often with B than with N. Addition of hydralazine, 25 to 100 mg twice daily, controlled diastolic BP at a level of less than 90 mm Hg in approximately 60% of those previously uncontrolled. N, and especially B + N, provided an efficacious once-daily treatment for systemic hypertension, and addition of hydralazine was effective in most nonresponders.
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PMID:Efficacy of nadolol alone and combined with bendroflumethiazide and hydralazine for systemic hypertension. 635 51

Supravesical urinary diversion using a jejunal conduit may be associated with hyponatremia, hypochloremic-acidosis, hyperkalemia, azotemia, and a clinical picture of nausea, vomiting, dehydration, muscular weakness, elevated temperature, and lethargy. This syndrome is secondary to the loss of sodium chloride into the urine passing through the conduit and absorption of potassium and urea from it. Treatment and prevention of this syndrome consist of adequate supplements of sodium chloride and hydration. Intravenous hyperalimentation as the precipitating factor of a severe form of this syndrome and its successful management are described. The pathophysiology of the jejunal conduit syndrome is also discussed. Great selectivity and extreme caution are recommended with respect to the use of intravenous hyperalimentation in patients with jejunal conduits.
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PMID:The pathophysiology of the jejunal conduit syndrome and its exacerbation by parenteral hyperalimentation. 642 49


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