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)

We reviewed 63 cases of cytologically confirmed leptomeningeal metastases (LM). 31 (49%) had solid tumors 17 (27%) had leukemia and 15 (24%) had lymphoma. The most common presenting symptom was pain (76%) with radicular discomfort (58%), headache (32%), neck or back pain (17%). The predominant neurological signs were mental status abnormalities (49%), weakness (47%), seizures (14%). The mode of presentation varied with tumor type. Patients with leukemia (18%) and lymphoma (13%) tended to present frequently with LM without systemic involvement, or during periods of apparent remission (leukemia 35%, lymphoma 27%), while patients with solid tumors had established systemic metastases (90%) at time of presentation. Laboratory studies did not vary among the groups. 71% had positive cytology on the first lumbar puncture (LP) and only 8% required more than 2 LPs. The cell count was a poor predictor of positive cytology as 29% of LP's with positive cytology and 36% of all LP's had less than 4 cells/mm. We conclude that 1) LM presents with pain and seizures more frequently than has been previously recognized; 2) LM is frequently the mode of presentation in patients with leukemia and lymphoma and; 3) cytology is positive frequently in CSF specimens with normal cell counts and chemistries.
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PMID:Leptomeningeal metastases: comparison of clinical features and laboratory data of solid tumors, lymphomas and leukemias. 208 37

An 11-year-old girl being treated with DNA-recombinant growth hormone therapy presented with proximal limb weakness. Laboratory studies were negative. A few months later she presented with acute lymphoblastic leukemia (ALL). A diagnosis of carcinomatous neuromyopathy was made. After successful treatment of the leukemia the symptoms subsided and did not recur.
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PMID:A girl treated with growth hormone presenting with neuromyopathy as first sign of acute lymphoblastic leukemia. 209 12

Chronic granulocytic leukaemia (CGL) is the commonest leukaemia among adults in India. Case records of 183 CGL patients diagnosed between 1975 and 1985 were reviewed. The median age at diagnosis was 40.5 years. Most patients presented with weakness, fullness in the left upper abdomen and fever. Splenomegaly and hepatomegaly were present in 90% and 48% respectively. Patients were treated with oral, intermittent busulphan with monitoring of total leucocyte count. Overall, 87 patients expired, including 63 (72%) due to blast crisis. The median survival was 33 months from diagnosis and 44 months from the onset of symptoms.
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PMID:Chronic granulocytic leukaemia. A study of 160 cases. 162 26

The Cas-Br-E and ts-Mo BA-1 murine leukemia viruses (MuLV) induce a spongiform neurodegenerative disease with different clinical manifestations, namely, either hind limb paralysis (Cas-Br-E) or tremors, spasticity, and hind limb weakness (ts-Mo Ba-1). We constructed the chimeric NEBA-1 MuLV by replacing the long terminal repeat of Cas-Br-E MuLV with that of ts-Mo BA-1 MuLV. In SWR/J or CFW/D mice, NEBA-1 MuLV induced an ataxic neurological disease characterized by clinical signs different from those induced by both parents. Although NEBA-1 MuLV did not induce lesions in novel brain areas, the spongiform lesions were more severe in deep cerebellar nuclei and in the spinal cord than those found in paralyzed mice inoculated with Cas-Br-E MuLV. By in situ hybridization, we found that the distribution of the spongiform lesions closely correlated with the distribution of the infected central nervous system cells. In the spinal cord, a close correlation was found between the number of infected cells and the severity of the spongiform degeneration. Sequencing of the substituted ts-BA-1 MuLV fragment and comparison with homologous sequences of Cas-Br-E and Moloney MuLV showed differences mainly in the U3 tandem direct repeats. Our results show that a few modifications within the U3 long terminal repeat allow the virus to cause more severe lesions in some central nervous system regions and that the severity of the spongiform degeneration correlates with the level of viral replication.
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PMID:Substitution of the U3 long terminal repeat region of the neurotropic Cas-Br-E retrovirus affects its disease-inducing potential. 216 94

A 52-year-old human immunodeficiency virus type 1-seropositive bisexual black man was evaluated at UCLA because of the recent onset of progressive lower-extremity weakness. Initial neurologic examination showed that the patient's distal weakness was greater than his proximal weakness, with bilateral foot drop and electrophysiologic evidence of denervation in the distal lower extremities. Magnetic resonance imaging of the brain and spinal cord disclosed no abnormalities. Subsequent neurologic evaluation 8 months later showed a myelopathy, with progression of lower-extremity weakness, spasticity, and flexor spasms, and urinary incontinence, as well as the peripheral neuropathy noted previously. A second magnetic resonance imaging scan of the brain showed patchy foci of increased signal intensity in white matter and cortex, with mild generalized cerebral and cerebellar atrophy and no lesions in the spinal cord. Specimens of the patient's serum and cerebrospinal fluid contained antibodies to human immunodeficiency virus type 1. Additionally, specimens of his serum and cerebrospinal fluid were tested for antibody to human T-cell leukemia virus type I by Western blotting and radioimmunoprecipitation, and found to be positive for human T-cell leukemia virus type I gag, env, and tax antibodies. The primary cause of severe myelopathy in this patient may be infection with human T-cell leukemia virus type I rather than with human immunodeficiency virus type 1. Treatment with prednisolone resulted in improvement of the lower-extremity weakness, reduction in flexor spasms, and slower but significant improvement in urinary symptoms. Patients who are infected with human immunodeficiency virus type 1 and have unusual motor findings should be tested for concomitant human T-cell leukemia virus type I infection.
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PMID:A patient with progressive myelopathy and antibodies to human T-cell leukemia virus type I and human immunodeficiency virus type 1 in serum and cerebrospinal fluid. 232 40

A 42-year-old female case of HTLV-I associated myelopathy (HAM) combined with adult T-cell leukemia (ATL) was reported. The patient noticed paresthesia in the soles at the age of 17, and gait disturbance and urinary retention at the age of 20. These symptoms progressed slowly. The patient showed indurations in both hypothenar regions and leukocytosis of 17,900/microliters in the peripheral blood at the age of 41. On admission to our hospital, she had spastic gait, muscle weakness of four extremities, increased deep tendon reflexes, pathologic reflexes, mild decreased of vibration sense and vesico-rectal disturbance. Anti-HTLV-I antibody (PA method) was increased to 1,024 fold in serum and 64 fold in spinal fluid. Thus, this patient was diagnosed as having HAM. In addition, leukocyte count in the peripheral blood was increased to 17,200/microliters including 33% atypical lymphocytes, and lymphocytes subset analysis showed 96.1% CD4+, 1.8% CD8+ and marked increase in CD4/CD8 ratio. Southern blot analysis of HTLV-I provirus DNA in the lymphocytes was of complete type with a monoclonal mode of integration. These findings indicated a diagnosis of ATL for this patient. HLA typing revealed A2, A11, Bw22, Bw46, Cw1, Cw3, being compatible with HAM type reported by Usuku et al. HAM and ATL were reported to be caused by an identical virus. However, there has been no case report of combination of the two diseases. Usuku et al proposed that the development of each disease was based on the differences in HLA haplotypes and HTLV-I-specific immune responsiveness.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[HTLV-I associated myelopathy (HAM) with adult T-cell leukemia (ATL)]. 279 8

Granulocytic sarcoma (GS) usually occurs during the course of, or as a presenting sign of myelogenous leukemia. Rarely it is found before peripheral blood or bone marrow evidence of leukemia is present. We describe a man who presented with low back pain and lower extremity weakness. He had spinal cord compression due to GS without evidence of leukemia. Only four such instances have been previously reported. Such aleukemic presentations of GS are frequently misdiagnosed. The chloroacetate esterase stain and electron microscopy are useful in demonstrating the myeloid origin of GS cells. GS lesions are probably best treated by localized radiation therapy and systemic chemotherapy.
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PMID:Granulocytic sarcoma presenting as an epidural mass with cord compression. 292 90

We have reported the first case of the Eaton-Lambert syndrome associated with leukemia in an adult, a 74-year-old woman with acute T cell lymphocytic leukemia and a mediastinal mass accompanied by weakness of the upper and lower extremities and pain in the lower extremities. Electromyographic studies were diagnostic of the syndrome. Treatment with guanidine hydrochloride resulted in clinical improvement of the neuromuscular disease, but the patient died of refractory leukemia.
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PMID:Eaton-Lambert syndrome in a patient with acute T cell lymphocytic leukemia. 305 24

A progressive neurodegenerative disease occurred following infection of mice with a temperature-sensitive (ts) isolate of Moloney (Mo) murine leukemia virus (MuLV), ts Mo BA-1 MuLV. This NB-tropic ecotropic MuLV, which was ts for a late function, induced a syndrome of tremor, weakness of the hind limbs, and spasticity following infection of several strains of laboratory neonatal mice, including NFS, C3H/He, CBA, SJL, and BALB/c. The latent period of 8 to 16 weeks was considerably longer than that observed for the acute paralytic diseases observed following neonatal infection with other ts Mo-MuLV, rat-passaged Friend MuLV, and some wild mouse ecotropic MuLVs. Spongiform pathology without inflammation and degeneration of neurons devoid of budding virions occurred in the cerebellar grey matter, brain stem, and upper spinal cord; but lower spinal cord anterior horn cells were less obviously affected than in other MuLV-associated neuroparalytic syndromes. ts Mo BA-1 MuLV differed from other ts Mo-MuLV mutants that are capable of inducing a neuroparalytic syndrome in that while infected nervous system tissue contained high levels of MuLV p30 and gp70, no evidence of precursor accumulation or abnormal processing of MuLV p30 or gp70 could be demonstrated. The localization of virus within the nervous system suggests that direct neuronal infection may not be the etiologic mechanism in this MuLV-induced neurodegenerative disease.
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PMID:Characterization of a progressive neurodegenerative disease induced by a temperature-sensitive Moloney murine leukemia virus infection. 373 86

A 61-year-old male receiving treatment for acute myelomonocytic leukaemia (AMML) developed weakness and sensory loss in the thumb, index and middle finger and half of the ring finger of the left hand as a result of a spontaneous haemorrhage into the carpal tunnel and forearm, an unusual cause of median nerve compression. These findings were confirmed by CT scanning and post-mortem examination. This is the first report of spontaneous haemorrhage occurring in a patient with AMML.
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PMID:Acute median nerve compression by haemorrhage from acute myelomonocytic leukaemia. 385 26


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