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)

Involvement of CNS with leukemic cells is well recognized complication of acute lymphatic leukemia (ALL) in childhood, but with recent improvements in systemic treatment and longer survival the incidence of this complication has increased in adults. Neurological symptomatology in patients with CNS leukemia is due to meningeal infiltration, but sometimes also to diffuse and nodular cerebral infiltration. Between January 1991 and December 1994, 36 patients suffering of acute leukemia, 28 with ALL, and 8 with acute myeloid leukemia (AML) were demonstrated to have neuroleukemia by the following criteria: (1) the presence at lumbar puncture (LP) pleocytosis and blast cells on CSF sediment (without positive bacteriologic and fungal cultures), and (2) the presence of neurological symptoms and signs. All 36 patients had 46 episodes of CNS involvement. All patients had neurological examinations during every episode, and according to the neurological abnormalities were classified into four categories. LP was performed in all, and CSF sediments obtained by sedimentation in Sayk's chambers, were routinely stained by MGG and cytochemical stains to detection of leukemic cells (Fig. 1). EEG was done during 21 episodes, CT scan during 15. We divided patients into four groups according to the most prominent neurological symptoms and signs. First was the group included 23 episodes (50%), (18 ALL, 5 AML), where symptoms and signs of meningeal irritation predominated, mimicking the clinical picture of meningitis. This meningeal syndrome can sometimes produce differential diagnostic problems with CNS infections, when CSF examination is of primary importance. Second was the group of 9 patients (6 ALL and 3 AML) with 10 episodes (21.74%) where cranial nerve symptoms and signs-predominated, or were exclusively present. Most frequently affected were bulbomotors, facials and opticus. Third group consisted of 8 ALL patients (8 episodes, 17.39%) with dominant spinal root symptomatology, caused by pathological infiltration of either spinal roots or meninges surrounding them. This group includes also one patient with mononeuritis multiplex and the other with painful polyneuropathy. All patients in this group had pain on straight leg raising, but we stress here that all patients from other groups had positive Lazarevitsh's sign, too. So, it can be a good differential diagnostic parameter for distinguishing toxic medicamentous polyneuropathy from leukemic poliradiculoneuropathy. Fourth group included 5 patients (5 episodes, 10.87%). 4 ALL and 1 AML, where cerebral symptoms, such as seizures, hemiparesis and psychoorganic syndromes were prominent. CSF was obtained during all episodes by lumbar puncture. The protein concentration ranged from 21-3180 mg/dl, and was above normal (45 mg/dl) during 28 episodes. Mild hypoglycoracchia was present during 16 episodes. Cell count ranged from 11-4816 cells/cm3, malignant cells were identified during all episodes with same morphological and cytochemical characteristics of identified type of leukaemia. It has been established that the most valuable diagnostic procedure in CNS leukemia is CSF examination, and detection of blasts is sufficient for diagnosis. All other procedures like EEG, myelography and CT have only supplemental diagnostic significance. Finally, in this study we showed that neurological symptomatology in patients with acute leukemia is not dependent of the type of leukemia, moreover different types of AL can have same neurological manifestations. As others, we sometimes used the term CNS leukemia in this paper, although it is clear that meninges and peripheral nervous system are most often involved. This is the reason why we suggest that neuroleukemia, or NS leukemia should be used as more appropriate expressions.
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PMID:[Neuroleukemia in adults]. 910 25

An experimental animal model of meningeal leukemia was developed in the nude rat, rnu/rnu, using the human-derived acute lymphoblastic leukemia cell line HPB-ALL. Anesthetized rats were placed in a modified stereotaxic frame and then injected intrathecally, at the level of the cisterna magna, with human leukemic cells. Cerebrospinal fluid and tissue samples from brain, spinal cord, heart, liver, kidney, spleen, bone marrow, and cervical lymph nodes were subjected to histopathologic examination and molecular genetic screening by clonotype primer-directed polymerase chain reaction (CPD-PCR). Ninety-three percent of animals (n = 14) developed signs of meningeal irritation leading to death 30 to 63 days postinjection (median, 36.0 days, mean, 38.7); death occurred between 30 and 39 days in 77% of all animals. Leukemic cells progressively infiltrated the pericerebellar and pericerebral subarachnoid space and infiltrated the Virchow-Robin (perivascular) space. The infiltrating meningeal leukemia closely resembled the pathologic presentation in the human condition. By CPD-PCR, leukemic cells were first detected in cerebrospinal fluid (CSF) on day 4 postinjection, were variably present over the ensuing 17 days, and were consistently detected after day 21. At terminal stages, CPD-PCR tissue surveys showed leukemic DNA in all brains and spinal cords and rarely in cervical lymph nodes, but leukemic DNA was not detected in any other tissue screened. Leukemic meningitis was reliably produced with a predictable survival time. Intrathecal administration of leukemic cells was an efficient means of transmitting leukemic meningitis and it compartmentalized the disease to the central nervous system (CNS), eliminating potential complications of systemic illness. The use of human-derived cell lines may render this model more relevant to the development of future therapeutic strategies to treat leukemia and lymphoma that invade the CNS.
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PMID:An experimental model of human leukemic meningitis in the nude rat. 920 65

The authors studied complications associated with intraventricular chemotherapy in patients with leptomeningeal metastases (LM). One hundred twenty consecutive patients with LM (71 females and 49 males) ranging in age from 10 to 72 years (median 42 years) were treated with involved-field radiotherapy and intraventricular chemotherapy using an Ommaya reservoir and intraventricular catheter system. The diagnosis of LM was determined by a combination of clinical presentation (114 patients); cerebrospinal fluid cytological studies (100); or neuroradiographic studies (42). Systemic tumor histological findings included breast (34 patients); non-Hodgkin's lymphoma (22); melanoma (16); primitive neuroectodermal tumors including medulloblastoma (10); glial neoplasms, leukemia, small cell lung, nonsmall cell lung, and colon (six each); prostate and kidney (three each); and gastric cancers (two). Sixteen patients, all with non-Hodgkin's lymphoma, also had acquired immune deficiency syndrome. Patients received one to four (median two) chemotherapeutic drugs and underwent a total of 1110 cycles of intraventricular chemotherapy (median 10). Intraventricular chemotherapy administration and diagnostic Ommaya reservoir punctures totaled 4400, with a median of 46 per patient. Complications included aseptic/chemical meningitis (52 patients); myelosuppression due to intraventricular chemotherapy (21); catheter-related infections (nine); unidirectional catheter obstruction (six); intraventricular catheter malpositioning (two); Ommaya reservoir exposure (two); leukoencephalopathy (two); and chemotherapy-related myelopathy (one). There were no treatment-related deaths; however, seven patients (6%) required additional surgery for either catheter repositioning (two) or reservoir removal (five). Seven patients with catheter-related infections were treated successfully with intraventricular and systemic antibiotic drugs, thereby preserving the Ommaya system. The authors conclude that Ommaya reservoirs are convenient and pharmacologically rational systems for administering intraventricular chemotherapy. Overall, serious complications requiring surgery are infrequent (6%) and most often secondary to catheter infections, Ommaya reservoir exposure, or initial catheter malpositioning. In the majority of instances, catheter infections may be managed medically, as may the most common complications of intraventricular chemotherapy including aseptic meningitis (43% of patients) and myelosuppression (18%).
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PMID:Complications associated with intraventricular chemotherapy in patients with leptomeningeal metastases. 964 98

Cryptococcus neoformans typically causes an insidious illness with symptoms related to meningitis or to lung involvement. This is the first reported sudden death due to cryptococcosis, which occurred in a child with leukemia that was in remission. The child had suddenly looked seriously ill and cried with abdominal pain and then died within 25 minutes. Disseminated cryptococcal infection of the lungs, heart, and pancreas was an unexpected finding at autopsy. This clinical experience raises the question whether fungal infections should now be considered in immunosuppressed patients who have an apparent septic collapse.
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PMID:Sudden death due to disseminated cryptococcosis in a child with leukemia in remission. 940 18

We have noted two morphologically distinct types of atypical lymphocytes (AL) in the cerebrospinal fluid (CSF) of adult patients with meningitis: one, which we designate type-I AL, with multilobulated nuclei resembling those of the abnormal cells in adult T-cell leukaemia (ATL); and another, type-II AL, characterized by large lymphocytes with basophilic cytoplasm and nuclei containing coarse chromatin. Type-I AL were detected in 25 of 39 patients (64%) with enteroviral and in 11 of 109 (11%) with aseptic meningitis presumed to be caused by other viruses, but not in meningitis resulting from Cryptococcus neofirmans (n = 14), Mycobacterium tuberculosis (n = 19) or acute bacterial infection (n = 49). Type-I AL were not seen in herpes zoster (n = 15) aseptic meningeal reactions (n = 15), or in leptomeningeal carcinomatosis (n = 14). Type-II AL were often present in meningitis of various aetiologies and in aseptic meningeal reactions, but not in leptomeningeal carcinomatosis. The presence of type-I AL in the CSF was found to be indicative of enteroviral meningitis with the highest predictive value (69%), while type-II AL had a lower diagnostic positive predictive value in meningitis of the five aetiologies above. Type-I AL immunostained for CD4, while type-II AL were stained for CD8. The presence of type-I AL in CSF strongly suggests enteroviral meningitis, which warrants careful follow-up without antifungal, antituberculous or antibacterial agents. However, type-I AL, which are likely to be virally transformed lymphocytes, must be distinguished from ATL cells, which frequently involve the meninges.
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PMID:Diagnostic value of atypical lymphocytes in cerebrospinal fluid from adults with enteroviral meningitis. 975 98

We present a case of tuberculous meningitis in a patient with acute myelogenous leukemia. The patient was in complete remission; he had persistent lymphopenia and CD4+ T lymphocytopenia. Diagnosis was complicated by the chronic and subacute nature of symptoms; some originally thought to be secondary to depression and chemotherapy related toxicity. Treatment was further complicated by the unusual phenomenon of paradoxical progression of disease while on appropriate therapy. This case illustrates the importance of consideration of mycobacteriosis in the differential diagnosis of chronic unexplained fever complicating treatment for acute leukemia. The natural history and essential aspects of diagnosis and treatment of CNS tuberculosis are reviewed. The clinical significance of unexplained CD4+ T lymphocytopenia and chronic lymphopenia in patients with leukemia is also discussed.
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PMID:Tuberculosis meningitis in a patient with acute myelogenous leukemia. 1019 37

To clarify the role of beta-phenylethylamine (PEA) in pediatric neurological disorders, we have measured the cerebrospinal fluid (CSF) levels of PEA in 12 children with aseptic meningitis--6 were in the acute phase and the other 6 were in the recovery phase--and 5 children with Rett Syndrome (RS). The findings were compared with those obtained from 13 age-matched children with leukemia as child controls and from 10 adults patients without any neurological symptoms and signs as control. In the control group, the CSF PEA level was negatively correlated with age until 200 months (17 years) old. The mean PEA levels in meningitis and RS were significantly lower than that of child controls (p < 0.03). The alteration in the CSF levels of PEA may be related to transient changes in the dopaminergic tone in aseptic meningitis and neurological impairment, especially in the dopaminergic neurons in RS.
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PMID:Developmental aspects of cerebrospinal fluid levels of beta-phenylethylamine and it's role in pediatric neurological disorders. 1031 9

1. Chloramphenicol has been widely used in the treatment of serious infections including typhoid fever and meningitis. However, the drug is haemotoxic in man inducing firstly, a reversible, dose-dependent anaemia which develops during treatment, secondly, an often fatal aplastic anaemia with pancytopenia and acellular marrow, and thirdly, leukaemia. 2. We investigated the haemotoxicity of chloramphenicol succinate (CAPS) in female CD-1 mice in repeat dose studies, to compare the response with the reversible anaemia reported in man. Studies in male Wistar Hanover rats were also carried out. 3. CAPS was gavaged daily to mice at dose levels from 800 - 2000 mg/kg for seven days. Values were significantly reduced for reticulocytes at 1700 and 2000 mg/kg, and for erythrocytes (RBC), haematocrit (HCT), and haemoglobin (Hb) at 2000 mg/kg. Platelet and white blood cell (WBC) counts were unaffected. 4. Mice were dosed with CAPS at 1400 mg/kg for 10 days and sampled at 1, 4 and 15 days after the last dose. At day 1 post dosing, RBC, HCT and Hb values were significantly reduced, but returned to normal (or above normal) by day 4 or 15. 5. CAPS from 2000 - 4000 mg/kg was gavaged to rats daily for 19 days. Hb values were significantly lower at 3600 and 4000 mg/kg; reticulocytes were not reduced. WBC and platelet counts, in general, were unaffected. 6. Levels of apoptosis in marrow mononuclear cells were increased in CAPS-treated mice, but not in CAPS-treated rats. Serum biochemistry parameters, in general, showed few changes of toxicological significance. 7. We conclude that the administration of CAPS to CD-1 mice induced haematological changes showing close parallels with the chloramphenicol-induced reversible anaemia seen in man.
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PMID:Haemotoxicity of chloramphenicol succinate in the CD-1 mouse and Wistar Hanover rat. 1052 71

Three patients with acute leukaemia, who were severely neutropenic and iatrogenically immunosuppressed post-chemotherapy, developed rapidly fatal septicaemic shock and coma caused by Bacillus cereus (B. cereus). The illness was marked by two phases: a mild febrile illness lasting 6-14 h and accompanied by subtle symptoms of autonomic sympathetic nervous system overactivity, and a second short fulminant one, marked by high fever of 40-41 degrees C accompanied by major central nervous system disturbances, and ending with deep coma and brain stem dysfunction. One patient developed the sepsis in spite of 4 days of coverage with amikacin. In the other two patients, amikacin was commenced at the earliest phase of the infection, but failed to influence the outcome. This form of B. cereus sepsis in neutropenic patients seems to be caused by strains capable of causing bacteraemia and meningitis and has the ability to produce a substance that causes leptomeningeal and neuronal necrosis. Lack of early clinical and laboratory markers inevitably leads to death. Use of antibiotics effective against B. cereus and capable of achieving high concentrations in the cerebrospinal fluid. and identification and neutralization of the necrotizing substance may hopefully help to reverse this fatal illness.
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PMID:Fulminant septicaemic syndrome of Bacillus cereus: three case reports. 1060 35

We report a 49-year-old man who was an HTLV-I carrier with an immunodeficiency state and intracranial pyramidal tract lesion revealed by MRI. He was born in Hokkaido and was admitted to our hospital because of fluminant hepatitis. On admission, neurologic examination revealed exaggerated deep tendon reflexes including the jaw jerk; the plantar response was flexor. Laboratory examination revealed decrease in the number of lymphocytes and CD4-positive lymphocytes in the peripheral blood and CD4/CD8 ratio was consistently low, indicating the presence of cellular immunodeficiency state. Serum anti-HTLV-I antibody was markedly increased but he did not have HTLV-I associated myelopathy (HAM). He had no underlying disease which would cause immunodeficiency state such as adult T-cell leukemia (ATL) or HIV infection. We concluded that the HTLV-I carrier state induced his immunodeficiency. During the course, he developed retrobulbar neuritis. T2 weighted cranial MRI revealed high signal lesions in the bilateral corona radiata, posterior limb of the internal capsule, and the pontine base, corresponding to the location of the pyramidal tracts. His hospital course was complicated by opportunistic infections such as Pneumocystis carinii pneumonia, cytomegalovirus infections, and meningitis, and died of multiple organ failure 7 months after the admission. Cellular immunodeficiencies in ATL patients are well known. Intracranial central nervous system (CNS) lesions in HAM patients are also mentioned. Recently coincidence of ATL and HAM in the same patients has also been reported. Asymptomatic HTLV-I carriers may have a latent immunodeficiency state and/or CNS lesions. We shall have to be alert about the presence of such carriers.
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PMID:[A patient with marked immunodeficiency in an HTLV-I carrier: a case report]. 1083 33


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