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 report a 47-year-old Japanese man who was a human T-cell leukemia virus type 1 (HTLV-1) carrier with strongyloidiasis, and who was born in an area endemic for both Strongyloides stercoralis ( S. stercoralis) and HTLV-1. He presented with edema of both legs. Laboratory examination on admission revealed hypoalbuminemia, and S. stercoralis rhabditiform larvae were found by stool microscopy. Purulent meningitis, which was suspected to be due to disseminated strongyloidiasis, developed during the first and second treatment for S. stercoralis infection. After the meningitis was alleviated, hydrocephalus with gait disturbance developed, and these features were attenuated by a ventriculo-peritoneal shunt. Impaired immunity and increased HTLV-1 proviral load, with an increased titer of HTLV-1 antibody, were observed in this patient. These results suggest that HTLV-1 proviral load and/or antibody titer of HTLV-1 can be used for the identification of carriers who are at increased risk of developing severe strongyloidiasis among those patients who are infected with both S. stercoralis and HTLV-1.
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PMID:Severe strongyloidiasis complicated by meningitis and hydrocephalus in an HTLV-1 carrier with increased proviral load. 1469 60

Human brucellosis is an important animal transmitted disease of man. Although, the cases have been recorded all over the world, the prevalence is higher in developing countries. Lack of sufficient knowledge about the disease among the physicians, its under-diagnosis or misdiagnosis and absence of effective prevention and management strategies are attributed to the widespread of the disease. Increase in the occurrence of animal brucellosis has also resulted indirectly in an increase in the prevalence of human infection. Absence of characteristic clinical symptoms, chronic nature of the infection and difficulty in isolation of the causal agent from the patients make the diagnosis of the disease more difficult. The serological tests employed for diagnosing human brucellosis vary in terms of their sensitivity and specificity. Therefore, a combination of serological tests is desirable. Currently no vaccine is available against human brucellosis, which could check the spread of the disease effectively. It is suggested that clinicians investigate the cases of pyrexia of unknown origin (PUO) for brucellosis. It is desirable that specimens from cases of tuberculosis, typhoid, rheumatoid arthritis, urogenital infections, kala-azar, cirrhosis, bacterial endocarditis, leukemia and filariasis should also be screened for brucellosis in man. The cases of meningitis of unestablished etiology as the cases of human brucellosis are often misdiagnosed as cases of typhoid or tuberculosis.
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PMID:Human brucellosis: review of an under-diagnosed animal transmitted disease. 1471 Aug 61

Candidal meningitis is a rare infectious disease that usually leads to substantial morbidity and mortality. We present a case of candidal meningitis refractory to systemic antifungal therapy (amphotericin B and fluconazole). A 63-year-old female with lymphoblastic lymphoma and myelodysplasia with leukemia transformation developed prolonged fever and headache on the seventh day following intrathecal prophylactic chemotherapy. A lumbar puncture showed neutrophilic pleocytosis, and a cerebrospinal fluid culture yielded Candida albicans. The clinical course was complicated by brain edema, subarachnoid hemorrhage, and hydrocephalus. Parenteral therapy with amphotericin B alone or amphotericin B in combination with fluconazole or intrathecal administration of amphotericin B failed to eradicate C. albicans in the cerebrospinal fluid. After 7 days of caspofungin therapy, however, the cerebrospinal fluid became sterile and the patient gradually regained consciousness. She was discharged 1 month after completing 4 weeks of caspofungin therapy. There were two critical issues we thought to be relevant to the favorable outcome of this case. First, isolation of C. albicans was achieved by inoculating enriched liquid medium with cerebrospinal fluid. Second, there is a potential therapeutic benefit of caspofungin in treating a fungal infection of the central nervous system.
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PMID:Refractory candidal meningitis in an immunocompromised patient cured by caspofungin. 1558 51

Leukemia affects the central and peripheral nervous system. Neurologic complications are a consequence of direct leukemic infiltration, as occurs with leukemic meningitis, and due to complications of either antileukemic treatment (thrombocytopenic or disseminated intravascular coagulation-related intracranial hemorrhage, steroid myopathy, vinca alkaloid peripheral neuropathy) or immune compromise (Herpes zoster shingles or Aspergillus meningitis).
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PMID:Leukemia and the nervous system. 1561 Jun 89

Leptomeningeal carcinomatosis is defined as malignant infiltration of the pia matter and arachnoid membrane. Leukaemias and lymphomas, lung, breast cancer and melanoma are the primary tumours commonly associated with leptomeningeal carcinomatosis. Diagnosis is based on compatible symptoms and signs, cytological evidence of malignancy in the cerebrospinal fluid, and neuroimaging studies. Treatment is largely palliative (median survival 2-4 months). Patients with lympomatous or leukaemic meningitis, chemosensitive tumours such as breast cancer, low tumour burden, minimal neurological deficits, good performance status and controllable systemic disease survive longer with occasional long-term responses. Available treatment options include focal radiation therapy to CNS sites of bulky, symptomatic or obstructive meningeal deposits, intrathecal cytotoxic therapy and systemic chemotherapy. No evidence of superiority of intrathecal treatment compared with best palliative care (including radiation therapy and systemic treatment) is available from clinical trials. Novel treatment approaches include intrathecal liposomal Ara-C, the development of new cytotoxic compounds, signal transduction inhibitors and monoclonal antibodies for intrathecal or systemic use. Until data from multi-centre randomised trials are available, rationalisation of therapy should be done by stratifying patients to prognostic groups. High-risk patients will only survive for a few weeks and are better managed with supportive measures, whereas low-risk patients justify vigorous cerebrospinal fluid-directed treatment combined with radiation therapy and systemic chemotherapy.
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PMID:Management of leptomeningeal malignancy. 1595 66

A 70-year-old woman was diagnosed with B-cell-type chronic lymphocytic leukemia (B-CLL) in May 2001. Initial white blood cell (WBC) count was 37 x 10(9)/l and most of the cells were mature small lymphocytes. Surface antigen analysis of these lymphocytes revealed positive reactions for CD19, 20, 25, 5, and lambda-light chain. Despite her Rai stage-0 status, various treatments were ineffective, including cyclophosphamide; fludarabine; 6-mercaptopurine; a combination of vincristine, cyclophosphamide, prednisolone, and adriamycin; and etoposide. Her WBC count increased, ranging from 150 to 450 x 10(9)/l, with marked splenomegaly, and symptoms of meningitis, such as headache, ophthalmalgia, hearing disturbance, and abnormal behavior, being manifested. The WBC count in the cerebrospinal fluid was elevated to 134/microl. The surface phenotype of these cells was identical to that of circulating lymphocytes, indicating meningeal involvement of leukemia, a rare complication in B-CLL. At the time of this WBC elevation, 24% of circulating lymphocytes had prominent nucleoli, indicating progression of the disease to CLL/prolymphocytic leukemia. Her symptoms disappeared after repeated intrathecal injections of methotrexate and dexamethazone. After four courses of treatment of the refractory B-CLL with rituximab, an anti-CD20 monoclonal antibody, the WBC count returned to normal levels and the splenomegaly disappeared. She is currently well, with sustained remission, as of April 2004.
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PMID:Excellent response of chemotherapy-resistant B-cell-type chronic lymphocytic leukemia with meningeal involvement to rituximab. 1624 65

Geotrichum capitatum, now known as Blastoschizomyces capitatus, can be responsible for several opportunistic infections (systemic infection or localized at lungs, liver, kidney, encephalitis or meningitis) in an immunocompromised host, especially in those patients affected by leukaemia or under immunosuppressive therapies. A 66-year-old woman with polimyosite under steroid and immunosuppressant therapy was hospitalized in ICU for an acute respiratory distress with moderate hypoxaemia and normocapnia. Pulmonary X-ray revealed a bilateral pneumonia. Hypoxaemia became severe 48 hours later and the patient underwent mechanical ventilation and empirical antibiotic therapy. Blood cultures, urine cultures and serological tests were negative, while yeast was identified by Gram's stain of bronchoaspirate. Before identifying the yeasts Fluconazole was added to therapy. At day 5 the clinical conditions remained severe and Candida spp were excluded: so Fluconazole was switched to liposomal Amphotericin B. At day 8 B. capitatus was identified. At day 26 the patient died of refractory respiratory insufficiency. B. capitatus infection is infrequent and its prognosis is severe, with a high mortality rate (>50%). Microbiological diagnosis requires time to characterize the yeast. At present no standard therapy is available although some authors report a good susceptibility to Amphotericin B and Voriconazole (100%), according to NCCLS guidelines.
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PMID:[Pulmonary infection caused by Blastoschizomices capitatus]. 1639 22

Long-term neuropsychological complications such as attention and concentration disturbances, poor school performance, hyperexcitability, and even leukoencephalopathy have been described in children after chemotherapy for acute lymphoblastic leukemia. Elevation of the cerebrospinal fluid level of tau protein, associated with neuronal axons, is a neurodegenerative marker. The aim of the study was to assess the level of cerebrospinal fluid tau protein in children with acute lymphoblastic leukemia. The study included 26 patients with acute lymphoblastic leukemia and 19 patients with clinical symptoms of cerebrospinal meningitis (reference group). Tau protein levels were determined by enzyme-linked immunosorbent assay. Cerebrospinal fluid total protein level was not elevated in any of the samples. The examination was performed at diagnosis, after induction treatment, during consolidation, and after reinduction, i.e. before maintenance therapy. Neither age nor sex had an effect on tau protein levels in both groups. The mean tau protein value at diagnosis was 244.84 +/- 98.96 pg/mL in the study group (norm 300 pg/mL) and produced no correlation with initial leukocytosis, lactate dehydrogenase activity, or organomegaly at this point. Dynamic analysis revealed a statistically significant increase in tau protein after induction treatment (431.25 +/- 232.50) as compared with its level at diagnosis (244.84 +/- 98.96, P < 0.008) and later during treatment. The levels of tau protein at various points of treatment did not differ statistically significantly between the groups, except for the values obtained after termination of remission induction. The observed metabolic changes in tau protein, which is a known marker of neuronal damage, indicate that some patients are at a greater risk of central nervous system disorders. This finding requires further studies, also in reference to other central nervous system proteins, and confirms the necessity of long-term follow-up of leukemia patients.
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PMID:Level of tau protein in children treated for acute lymphoblastic leukemia. 1664 96

We report a 49-year-old man who was a human T-cell leukemia virus type 1 (HTLV-1) carrier, born in Okinawa prefecture where both strongyloidiasis and HTLV-1 are endemic. He presented with fever, headache and urinary retention. On the basis of CSF examination and MRI findings, his condition was diagnosed as myelitis. He received methylprednisolone pulse therapy. He was transferred to our hospital due to severe paralytic ileus. Strongyloides stercoralis (S. stercoralis) was found in the duodenal stained tissue of a biopsy specimen. Ivermectin applied both orally and through enema were ineffective because of severe ileus and intestinal bleeding. Nine mg (200 microg/kg) of ivermectin solution was administered subcutaneously every other day for five days (total amount 45 mg). The S. stercoralis burden in the stool decreased and paralytic ileus gradually resolved. Three weeks after the resolution of S. stercoralis infection, purulent meningitis developed and acute obstructive hydrocephalus appeared. The hydrocephalus improved by ventricular drainage. Approximately three months after drainage, he died of incidental aspiratory pneumonia. Autopsy showed neither eggs nor larvae of S. stercoralis in the organs. In this case, the fourth reported case in the world, subcutaneous ivermectin injection was dramatically effective. We should consider a diagnosis of strongyloidiasis for any patient from Okinawa prefecture who was an HTLV-1 carrier presenting with unknown origin ileus after treatment of steroid therapy.
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PMID:[Fulminant strongyloidiasis successfully treated by subcutaneous ivermectin: an autopsy case]. 1838 29

We report a case of 15-year-old girl with T-cell acute lymphoblastic leukemia who had fever, neutropenia, and severe headache while receiving maintenance chemotherapy. Cerebrospinal fluid testing revealed a lymphocytic pleocytosis and no evidence of relapsed leukemia. Meningitis caused by lymphocytic choriomeningitis virus was identified serologically. The patient's course was complicated by hydrocephalus requiring ventriculoperitoneal shunt placement and by an intracranial hemorrhage. Lymphocytic choriomeningitis virus is a rare cause of aseptic meningitis that should be considered in the symptomatic immunocompromised patient with an appropriate exposure history.
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PMID:Meningitis caused by lymphocytic choriomeningitis virus in a patient with leukemia. 1901 81


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