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)

Rostral and middle cranial fossa tumors affecting the optic chiasm and resulting in acute visual deficits were diagnosed in 7 dogs and 1 cat. Blindness and dilated nonresponsive pupils were the primary signs in all animals. Other concurrent neurologic deficits were either absent or were equivocal. Behavioral changes, including signs of depression and lethargy, were noticed in 1 dog and the cat subsequent to the onset of blindness. Retinal function was assessed as normal by electroretinography in all animals. The histologic necropsy diagnosis was pituitary carcinoma in 1 dog and the cat and paranasal sinus carcinoma with intracranial extension in 1 dog. A cytologic diagnosis of polycentric lymphosarcoma affecting the optic chiasm was diagnosed in 1 dog. In the remaining 4 dogs, results of computed tomographic imaging or endocrine function testing suggested pituitary gland neoplasia. Four dogs were treated with cobalt-60 radiation or chemotherapy. There was partial return of visual function in only 1 of the dogs treated with radiation.
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PMID:Acute blindness associated with intracranial tumors in dogs and cats: eight cases (1984-1989). 195 68

Acromegaly was diagnosed in 14 middle-aged to old cats of mixed breeding. Thirteen (93%) of the cats were male and one was female. The earliest clinical signs in the 14 cats included polyuria, polydipsia, polyphagia, all of which were associated with untreated diabetes mellitus. All developed severe insulin resistance within a few months; peak insulin dosages required to control severe hyperglycemia ranged from 20 to 130 U per day. Other clinical findings weeks to months after diagnosis included enlargement of one or more organs (e.g., liver, heart, kidneys, and tongue) (n = 14), cardiomyopathy (n = 13), increase in body size and weight gain (n = 8), nephropathy associated with azotemia and clinical signs of renal failure (n = 7), degenerative arthropathy (n = 6), and central nervous system signs (i.e., circling and seizures) caused by enlargement of the pituitary tumor (n = 2). The diagnosis of acromegaly was confirmed by demonstration of extremely high basal serum growth hormone concentrations (22 to 131 micrograms/l) in all cats. Computerized tomography disclosed a mass in the region of the pituitary gland and hypothalamus in five of the six cats in which it was performed. Two cats were treated by cobalt radiotherapy followed by administration of a somatostatin analogue (octreotide), whereas two cats were treated with octreotide alone. Treatment had little to no effect in decreasing serum GH concentrations in any of the cats. Eleven of the 14 cats were euthanized or died four to 42 months (median survival time, 20.5 months) after the onset of acromegaly because of renal failure (n = 2), congestive heart failure (n = 1), concomitant renal failure and congestive heart failure (n = 3), progressive neurologic signs (n = 2), persistent anorexia and lethargy of unknown cause (n = 1), the owner's unwillingness to treat the diabetes mellitus (n = 1), or unknown causes (n = 1). Results of necropsy examination in ten cats revealed a large pituitary acidophil adenoma (n = 10), marked left ventricular and septal hypertrophy (n = 7), dilated cardiomyopathy (n = 1), arthropathy affecting the shoulder, elbow, or stifle (n = 5), and glomerulopathy characterized by expansion of the mesangial matrix and variable periglomerular fibrosis (n = 10).
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PMID:Acromegaly in 14 cats. 240 66

A diagnosis of glioblastoma multiforme (GBM) was made for cerebral masses found at necropsy in two baboons (Papio cynocephalus anubis). Case 1 was an adult (6.18 years old) male baboon that suddenly died during a physical examination as part of a clinical evaluation for a leg lameness. Case 2 was an adult (5.95 years old) female baboon that stopped breathing during anesthesia for an magnetic resonance imaging to evaluate lethargy, weight loss, inappetence, and dilated pupils. Both animals had undergone total body irradiation with cobalt during a research protocol. The incidence of spontaneous brain tumors in nonhuman primates is low, but radiation-induced GBM lesions in rhesus macaques (Macaca mulatta) have been reported. A definitive diagnosis was made in these cases, using histopathologic criteria of cellular pleomorphism, high mitotic rate, regions of coagulation necrosis, and endothelial proliferation.
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PMID:Radiation-induced glioblastoma multiforme in two adult baboons (Papio cynocephalus anubis). 1525 81

The nootropic drug piracetam was investigated in various experimental models of epilepsy. Generally, piracetam exhibits no or only moderate anticonvulsant properties against generalized tonic or clonic seizures. However, in many cases it did increase the anticonvulsant effectiveness of conventional antiepileptics, as shown in the maximal electroshock seizure (MES) threshold test, the traditional MES test or in DBA/2 mice. A pharmacokinetic interaction does not seem to be responsible for this effect. In lethargic mice, a model of absence seizures, piracetam significantly decreased the incidence and duration of spike-wave discharges. Furthermore, in the cobalt-induced focal epilepsy model piracetam reduced the number of spikes/min and in the hippocampal stimulation model it increased the anticonvulsant potency of phenobarbital and phenytoin after single and repeated administration. In conclusion, the well tolerated piracetam itself did not show marked anticonvulsant effects in most screening tests, however, its co-medication with antiepileptic drugs improved seizure protection in various models which may bear potential clinical significance.
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PMID:Effects of piracetam alone and in combination with antiepileptic drugs in rodent seizure models. 1533 29

Cobalt can cause a distinctive, rapidly progressive and reversible depression of cardiac systolic function, which is readily distinguished from other causes of cardiomyopathy. Patients present with the subacute onset of severe heart failure, which is accompanied by hypotension and cyanosis, pericardial effusion, low voltage on the electrocardiogram, marked elevation of serum enzymes, and lactic acidosis. They typically have a history of lethargy, anorexia, and weight loss in the months preceding the illness and exhibit other evidence of cobalt's effects on the body (eg, polycythemia and goiter). The course of cobalt-related cardiomyopathy may be progressive and fatal, but those who survive and cease exposure generally demonstrate complete resolution of symptoms and recovery of cardiac function. Patients presenting with rapid onset of cardiomyopathy, who also exhibit polycythemia, pericardial effusion, or goiter should be evaluated for cobalt exposure. Exposure can be confirmed by the measurement of cobalt in the serum, but serum levels of the ion are not reliably predictive of clinical cardiotoxicity. The clinical emergence of cobalt cardiomyopathy seems to require the coexistence of one or more cofactors, particularly a low-protein diet, thiamine deficiency, alcoholism, and hypothyroidism. As the medicinal use of cobalt has waned and measures to reduce industrial exposure have been implemented, subacute cobalt-related cardiomyopathy had become rare. However, reports describing classical features of the disease have recently surged among patients with a malfunctioning cobalt-alloy hip prosthesis.
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PMID:Cobalt Cardiomyopathy: A Critical Reappraisal in Light of a Recent Resurgence. 2785 54