Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0023418 (leukemia)
 93,477 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

An 82-year-old woman developed acute neuropsychiatric signs (confusion, disorders of speech and vision) together with ataxic gait and left hemiparesis mainly affecting the lower limb. For 10 years she had been known to have chronic lymphatic leukaemia (CLL) which had not hitherto needed treatment. The patient had an exceptionally high leucocyte count (1,300,000/microliters), most of the cells being morphologically atypical lymphocytes. The computed tomogram of the skull showed a marginal zone infarct with a hypodense focus in the area of the right middle and posterior cerebral arteries, extending from the cortical to subcortical zones almost as far as the posterior horn. This was interpreted as a leukostasis syndrome with cerebral infarction due to rapid progression of the CLL. Significant reduction of leucocyte count with considerable improvement in clinical signs was achieved after three doses of vincristine and prednisone together with one cycle of COP (cyclophosphamide, vincristine, prednisone) therapy. Although the leucocyte count is not an important criterion in planning the therapy of CLL, in the event of rapidly increasing leucocytosis it is important to begin cytoreductive treatment in good time so as to avert the leukostasis syndrome.
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PMID:[The leukostasis syndrome with a cerebral infarct in rapidly progressing chronic lymphatic leukemia]. 188 54

A 7-month-old, entire female, domestic shorthair cat was referred to our behavioural service owing to soiling in the house and a play-related problem. The owners' complaints were that the cat had never used the litter tray, and it did not know how to play. After reviewing the behavioural history, a problem of substrate preferences acquisition was suspected with regard to the elimination problem. During the consultation, the physical examination was unremarkable, but the neurological examination revealed a moderate and hypermetric ataxic gait, and a bilateral lack of menace response. Some degree of visual impairment was suspected. The problem was located in the central nervous system (CNS); specifically, an intracranial and multifocal problem was diagnosed. After a complete work-up (complete ophthalmological examination, complete blood count and a complete biochemistry panel, feline immunodeficiency virus/feline leukaemia virus test, thorax radiographs, abdominal ultrasound, brain magnetic resonance imaging [0.2 T], cerebrospinal fluid analysis and a urinary metabolic screen test), a degenerative CNS problem was suspected. No treatment was prescribed for the neurological problem. Regarding the problem of soiling in the house, reward-based training with a clicker was used, and the cat partially improved in a few weeks. Three months later, the cat was referred to the neurology service in status epilepticus. A symptomatic treatment was prescribed, with a mild response. After 2 years of treatment and a progressive worsening, the cat was euthanased. Necropsy revealed spongiform polioencephalomyelopathy. In order to rule out prion aetiology a PrPsc inmunohistochemistry assay was performed, and the results were negative. Congenital spongiform polioencephalomyelopathy (CSP) was diagnosed. We strongly suggest that the cat's behavioural clinical signs were caused by the CSP, causing learning impairment. To the best of our knowledge, this would be the first case in which a congenital degenerative disease affected a cat's capability to learn, leading to behavioural signs as the main complaint of the owners, even before neurological signs are detected by the owners.
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PMID:A case of spongiform polioencephalomyelopathy in a cat with a history of behavioural problems. 2849 81