Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0042963 (vomiting)
 31,883 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

An unusual central nervous system (CNS) manifestation in a 18-year-old male with Ki-1- positive anaplastic large-cell lymphoma is presented. The diagnosis of Ki-1 lymphoma was first confirmed by the distinct pleomorphic morphology, expression of Ki-1 (CD30) antigen on neoplastic cells and the specific chromosome translocation, t(2;5)(p23;q35). Although young age is thought to be a good prognostic factor in this disease, the course in our patient was very aggressive. At presentation, there was already extensive extranodal involvement, with malignant cell found in the pleural cavity and bone marrow. In spite of rapid shrinkage of whole-body lymph nodes and a decrease in malignant pleural effusion soon after starting chemotherapy, headaches and vomiting ensued in the following days. A computerized tomography scan of the brain showed poor corticomedullary differentiation without definite mass lesions, and numerous malignant cells were found in the cerebrospinal fluid (CSF). Although intrathecal methotrexate was given, the patient died following the sudden onset of acute hydrocephalus. CNS involvement in Ki-1 anaplastic large-cell lymphoma is very rare and most cases present as focal mass lesions in the brain parenchyma. Leptomeningeal seeding of the lymphoma cells with acute hydrocephalus contributing directly to death has never been reported. The experience from this case suggests that CNS involvement may present in variable forms in Ki-1 lymphoma and may be an important cause of mortality in young patients, especially those in advanced stages of the disease. Early detection of CNS involvement by CSF investigation or even prophylactic CNS therapy may be mandatory in these patients.
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PMID:Leptomeningeal seeding with acute hydrocephalus--unusual central nervous system presentation during chemotherapy in Ki-1-positive anaplastic large-cell lymphoma. 863 43

We retrospectively reviewed the medical records of neonates with chromosomal abnormalities and epilepsy who had been admitted to the neonatal intensive care unit (NICU) and followed up at the outpatient clinic of Dokkyo University School of Medicine. Chromosomal anomalies were diagnosed in 128 of 5789 patients admitted from 1978 through 2001. Seventy-one neonates had trisomy 21, 29 had trisomy 18, 8 had trisomy 13, and 20 had other chromosomal anomalies. Seizures occurred in five patients with trisomy 21 and in one patient each with trisomy 18, 6q-, 13q-, 21q-, and mosaicism trisomy 13. Two patients with 4p- [Wolf-Hirschhorn syndrome] were admitted to the NICU, but were not followed up at our outpatient clinic. The boy with 6q- (46,XY,-6, +der(6)t(6;11)(q25.1;q23.3)mat) had agenesis of the corpus callosum and multiple congenital anomalies as well as intractable epilepsy. The girl with 13q- (46, XX, t(2,4)(q24.2;p14), del (13)(q21.2q31.2)) had infantile spasms at 12 months, which were well controlled with nitrazepam and vitamin B6. The girl with mosaic trisomy 8q; (46, XX, der(8) (qter-->q11.2::p23.3-->qter)/46, XX), was not born at our hospital, but showed unique clinical features. She had intractable epilepsy characterized by episodes of vomiting and staring with astatic seizures. Computed tomography of the brain revealed bilateral calcification in the globus pallidus, associated with bursts of high-amplitude slow waves on electroencephalography. One of the two patients with del(15)(q12)[Angelman syndrome] had giant-amplitude visual evoked potential, suggesting hyperexcitability of the visual cortex.
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PMID:An analysis of epilepsy with chromosomal abnormalities. 1602 55