Cases reported "Acute Disease"

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1/6279. leukostasis followed by hemorrhage complicating the initiation of chemotherapy in patients with acute myeloid leukemia and hyperleukocytosis: a clinicopathologic report of four cases.

    BACKGROUND: Pulmonary and cerebral leukostasis, or parenchymal hemorrhage in these organs, are well-known early complications developing in patients with acute myeloid leukemia (AML), particularly when myelomonocytic features, hyperleukocytosis, and/or a coagulation disorder are initially present. Commonly, these complications arise during increasing leukocyte counts (WBCs). methods: The authors describe four patients with AML and hyperleukocytosis who developed leukostasis followed by parenchymal hemorrhage. RESULTS: Bleeding in all patients occurred while their WBCs were decreasing following cytosine-arabinoside chemotherapy, and in the absence of disseminated intravascular coagulation or severe thrombocytopenia. Radiologic and histopathologic findings underscoring possible mechanisms are presented in the article. CONCLUSIONS: Alterations of cell adhesion associated with chemotherapy-induced blast lysis or cellular differentiation are possible factors contributing to this particular sequence (cytosine arabinoside-based chemotherapy, leukostasis, and subsequent hemorrhage). Prophylactic measures for managing this early complication of AML treatment include leukapheresis to reduce the WBC prior to the initiation of chemotherapy.
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2/6279. The changes in human spinal sympathetic preganglionic neurons after spinal cord injury.

    We have applied conventional histochemical, immunocytochemical and morphometric techniques to study the changes within the human spinal sympathetic preganglionic neurons (SPNs) after spinal cord injury. SPNs are localized within the intermediolateral nucleus (IML) of the lateral horn at the thoraco-lumbar level of the spinal cord and are the major contributors to central cardiovascular control. SPNs in different thoracic segments in the normal spinal cord were similar in soma size. SPNs in the IML were also identified using immunoreactivity to choline acetyltransferase. Soma area of SPNs was 400.7 15 microm2 and 409.9 /-22 microm2 at the upper thoracic (T3) and middle thoracic (T7) segments, respectively. In the spinal cord obtained from a person who survived for 2 weeks following a spinal cord injury at T5, we found a significant decrease in soma area of the SPNs in the segments below the site of injury: soma area of SPNs at T8 was 272.9 /-11 microm2. At T1 the soma area was 418 /-19 microm2. In the spinal cord obtained from a person who survived 23 years after cord injury at T3, the soma area of SPNs above (T1) and below (T7) the site of injury was similar (416.2 /-19 and 425.0 /-20 microm2 respectively). The findings demonstrate that the SPNs in spinal segments caudal to the level of the lesion undergo a significant decrease of their size 2 weeks after spinal cord injury resulting in complete transection of the spinal cord. The impaired cardiovascular control after spinal cord injury may be accounted for, in part, by the described changes of the SPNs. The SPNs in spinal segments caudal to the injury were of normal size in the case studied 23 years after the injury, suggesting that the atrophy observed at 2 weeks is transient. More studies are necessary to establish the precise time course of these morphological changes in the spinal preganglionic neurons.
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3/6279. Acute rheumatic fever with three major criteria: polyarthritis, carditis and chorea. A case report.

    An eight-year-old girl is presented with three major criteria of acute rheumatic fever: polyarthritis, carditis and chorea. The diagnosis was confirmed with a history of pharyngitis 15 days prior to admission and with the findings of positive acute phase reactants such as elevated erythrocyte sedimentation rate (ESR) and c-reactive protein (CRP), elevated anti-streptolysin-O (ASO) titration, and clinical findings of polyarthritis, carditis and chorea. Patient responded well to salicylate and phenobarbital treatment. The rare association of these three major criteria in acute rheumatic fever is emphasized.
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4/6279. central nervous system T-cell lymphoproliferative disorder in a patient with chronic active Epstein-Barr virus infection.

    PURPOSE: central nervous system (CNS)-T cell lymphoproliferative disorder (T-LPD) developing during the course of chronic active Epstein-Barr virus (CAEBV) infection is reported. patients AND methods: CAEBV was diagnosed in a 14-month-old boy with fever, cytopenia, hepatosplenomegaly, and abnormal high titers of anti-Epstein-Barr virus (EBV) antibodies. At 8 years of age, he had a splenectomy because of progressive disease. RESULTS: After 27 months of clinical remission, muscle weakness and paresthesia developed. magnetic resonance imaging of his brain showed spotty T2 prolongation in left parietal, bilateral frontal, and temporal white matter with meningeal enhancement. brain biopsy revealed the cerebral infiltration of CD3 , CD4 , CD8-, CD45RO , CD56-, and EBV-encoded rna 1 cells. CONCLUSIONS: The CNS involvement of EBV-associated T-LPD is a rare but serious complication in CAEBV without known underlying immunodeficiency.
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5/6279. Acute leukemia with the phenotype of a natural killer/T cell bipotential precursor.

    An acute leukemia with an unusual immunophenotype developed in a 17-year-old girl. At the initial presentation, extramedullary involvement was not evident, but with advancing disease, massive splenomegaly and an osteolytic rib tumor developed. The disease was aggressive and refractory to intensive chemotherapeutic regimens for myeloid and lymphoid malignancies, and the patient died 3 months after the initial presentation. The leukemic cells were of irregular shape and variable size; they had deeply indented or bi-lobed nuclei and relatively fine, azurophilic granules in their cytoplasm. They were positive for acid phosphatase and beta-glucuronidase in granular staining, but they were negative for myeloperoxidase. The leukemic cells had a unique immunophenotype: it was positive for T-cell antigens (CD1a, CD2, cytoplasmic CD3, CD4), myeloid antigens (CD13 and CD33), NK-cell antigen (CD56), CD19 and CD30. dna analysis revealed no gene rearrangement in the T-cell receptor beta, gamma and delta, or immunoglobulin heavy chain genes. The leukemic cells of our patient are thought to have arisen from the transformation of a putative precursor cell common to both the T- and NK-cell lineage in the bone marrow. The current literature on precursor NK-cell malignancy is reviewed, and its clinicopathological feature is discussed.
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6/6279. Acute traumatic proximal tibiofibular joint dislocation confirmed by computed tomography.

    High-quality AP and lateral radiographs of both knees are essential to confirm the diagnosis. Computed tomography may help resolve diagnostic uncertainty and enable earlier closed reduction to be performed. Moreover, CT scans may be more consistently reproducible than the varied quality of emergency radiographs. In this case, the relative severity of the patient's pain and suggestive radiographs led us to obtain CT scans, which confirmed the diagnosis and enabled early successful closed reduction.
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7/6279. Long-term follow-up of relapsed acute leukemia treated with immunotherapy after allogeneic transplantation: the inseparability of graft-versus-host disease and graft-versus-leukemia, and the problem of extramedullary relapse.

    Long-term outcome of 23 acute myeloid (AML, n=16) or lymphoblastic (ALL, n=7) leukemia patients who had received immunotherapy for treatment of persistent or recurrent disease 1.5-26 (median 4) months after allogeneic transplantation was studied to determine eventual survival. Immune manipulation comprised donor leukocyte infusion (n=18), interferon-alpha2b and/or interleukin-2 (n=15), and cyclosporine withdrawal (n=11) in various combinations. Graft-versus-host disease (GVHD) developed in 12 patients. Thirteen of 20 evaluable patients responded; 6 relapsing again. Eight patients died of toxicity, and 10 of progressive disease at 3-206 weeks (median 11). Five patients (3 AML, 2 ALL) are alive in remission with GVHD 2-46 months (median 23) after immunotherapy with Karnofsky scores of 70-100% (median 80). The overall survival of the whole group is 1-206 weeks (median 12), with an actuarial survival of 22% at 2 years. The development of GVHD was associated with superior survival in multivariate analysis (P=.007). Seven patients received immunosuppression because of the severity of GVHD (grade III/IV acute or extensive chronic): 3 died of GVHD, 3 improved but relapsed concomitantly, and 1 is alive in remission with extensive chronic GVHD. Four episodes of extramedullary relapse (granulocytic sarcomas) were seen in 3 patients with AML whose marrow remained in remission. We conclude that GVHD appears to be inseparable from graft-versus-leukemia in relapsed acute leukemia patients undergoing immunotherapy with a high proportion of patients dying due to toxicity or progressive disease, and isolated extramedullary relapse seems to be unusually common.
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8/6279. Clonally unrelated BCR-ABL-negative acute myeloblastic leukemia masquerading as blast crisis after busulphan and interferon therapy for BCR-ABL-positive chronic myeloid leukemia.

    We report a patient with philadelphia (Ph)-positive, BCR-ABL rearrangement positive, chronic myeloid leukemia (CML) with a prolonged chronic phase of 24 years who was first prescribed alpha-2 interferon 22 years after initial diagnosis. This therapy was tolerated poorly on account of thrombocytopenia, but an eventual major cytogenetic response was followed soon afterwards by transformation to terminal acute myeloid leukemia (AML). Cytogenetic studies indicated that the transformed myeloblasts were karyotypically normal and Ph negative. Although polymerase chain reaction (PCR) analysis of total leukemic mRNA remained BCR-ABL positive, other molecular studies, including Southern blotting and fluorescent in situ hybridization (FISH) analyses, showed that myeloblasts were BCR-ABL rearrangement negative. PCR-based clonality studies using an X-chromosome-linked restriction fragment polymorphism within the phosphoglycerate kinase gene (PGK1) further showed that the Ph-negative blast cells had a different clonal origin from the Ph-positive clone of chronic phase. We suggest that cases of underlying Ph-negative leukemic transformation in Ph-positive CML warrant further study and should be considered for trial of intensive remission induction therapy as appropriate for acute leukemia.
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9/6279. Severe panarteritis associated with drug abuse.

    A case of panarteritis with purpura fulminans, mononeuritis multiplex, gastrointestinal manifestation and presumably cardiac involvement in a previously healthy 22-year-old man with a history of drug abuse including cocaine, cannabinoids and methamphetamines is described. Histopathological examination of the gut led to the diagnosis of panarteritis without immune deposits. Antineutrophil antibodies were negative. Besides the drugs, no other possible cause of vasculitis was found. The patient recovered completely after 1 year. Drug abuse is a thus possible cause of severe extracerebral disabling vasculitis.
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10/6279. effect of kidney resection on blood pressure and plasma renin activity. Case report and clinical study.

    Acute transient hypertension following kidney trauma occurred in a 17-year-old youth due to increased activity of the renin/angiotensin system. The systemic blood pressure and plasma renin activity was also studied following elective kidney resection. In one group of patients the operation was performed with clamping of the renal vessels; in the other no clamping was performed. Only minimal changes in blood pressure and plasma renin activity was found in both groups.
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