Cases reported "Leukopenia"

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11/255. parvovirus B19 causing leucopenia and neutropenia in a healthy adult.

    A 27-year-old healthy female presented with a prolonged and intermittent febrile illness. She was found to have leucopenia, neutropenia and thrombocytopenia, but a normal haemoglobin. The patient recovered spontaneously and convalescent serology 1 month later was positive for specific parvovirus B19 IgM and IgG. parvovirus B19 infection was confirmed by detection of viral dna by dot blot hybridization in a specimen of blood taken during the acute illness. A review of the previously reported cases of parvovirus B19-induced leucopenia in normal adults is presented. parvovirus B19 should be considered in the differential diagnosis of leucopenia and neutropenia in healthy adults. ( info)

12/255. Strong alpha beta and gamma delta TCR response in a patient with disseminated mycobacterium avium infection and lack of NK cells and monocytopenia.

    Infection with atypical mycobacteria occurs mainly in patients with a compromised cellular immune system, in particular in those with a defective T cell or monocyte function. Here we analyzed the specific immune response of an adolescent hiv-negative patient with disseminated mycobacterium avium infection and fatal varizella zoster virus infection. The patient presented with dysplastic hematopoesis of all cell lineage's and a bicytopenia of erythrocytes and leukocytes, but a hematological malignancy could not be found. We found a peripheral lymphopenia and monocytopenia, as well as a lack of NK-cells and B-cells. lymphocytes consisted of 95% T cells, which contained up to 40% of TCR gammadelta CD4-CD8-T-cells (mainly TCR gamma9delta2), few monocytes and B-cells. Approximately 50% of CD3 T-cells showed a CD57 NK-like phenotype. Functional analysis of PBMC revealed a good antigen-specific T cell function if antigen-presenting cells were supplemented from a HLA-matched donor. Moreover, a strong M. avium specific cytotoxicity mediated by TCR alphabeta T-cells could be found in vitro and even ex vivo. In contrast, NK-killing was absent. No evidence for a defect in IL-12 or IFN-gamma production and signaling were found. The data indicate that a strong alphabeta and gammadelta T cell immunity tries to compensate for a deficient monocyte and NK cell function in this patient. ( info)

13/255. Marked cyclic leukocytosis-leukopenia in chronic myelogenous leukemia.

    A spontaneous oscillation of the white blood cell count was observed in a 58 year old man with chronic myelogenous leukemia (CML). Similar cyclic variations were noted in the platelet and reticulocyte counts with no apparent alterations in marrow cellularity to account for such changes. Since direct correlation was noted between white blood cells, platelets, and reticulocyte counts versus spleen size, it suggests that splenic hemopoiesis may be responsible for these cyclic changes. A possible inverse relationship between colony-stimulating factor (CSF) activity and the white blood cell count was noted, suggesting that CSF may be the humoral agent controlling granulocyte production. A direct correlation between the white blood cell count and serum unsaturated vitamin B12 binding capacity (UBBC) and lysozyme was also noted and further supports the concept that the latter two are measures of the granulocyte pool and metabolism. An inverse relationship between CSF activity and the UBBC suggests that these may be two different entities. Finally a modified form of standard chemotherapy may be effective in inducing remission in cases of CML with marked cyclic leukocytosis-leukopenia. ( info)

14/255. Juvenile rheumatoid arthritis presented with thrombocytopenia.

    leukopenia and thrombocytopenia are rare findings in systemic onset juvenile rheumatoid arthritis (S-JRA), and if present, bone marrow (BM) examination is necessary to exclude malignant diseases. We report here a 13.5-year-old boy with S-JRA who had severe thrombocytopenia and mild leukopenia, without arthritis, at the onset of the disease. BM was hypercellular with increased numbers of myeloid precursors and megakaryocytes. After treatment with acetylsalicylic acid, leukocyte and platelet counts returned to normal levels, and after two months chronic arthritis developed. ( info)

15/255. Olanzapine appears haematologically safe in patients who developed blood dyscrasia on clozapine and risperidone.

    We report a 2-year experience with olanzapine treatment (20 mg daily) in a 65-year-old male patient with treatment-resistant paranoid schizophrenia, who had previously developed leucopenia and neutropenia first on clozapine and, subsequently, also on risperidone. Olanzapine seems to be safe in this patient, since no major decreases of haematological parameters were observed. The only exception was a brief decrease of leucocyte and neutrophil (but not erythrocyte or platelet) counts during influenza-like viral infection. However, the control of psychotic symptoms on olanzapine is not as good as on clozapine. ( info)

16/255. coccidioidomycosis in compromised hosts. Experience at Stanford University Hospital.

    To determine the frequency and clinical characteristics of infection with coccidioides immitis in immunosuppressed patients at Stanford University Hospital, clinical records of 14 years were examined. Thirteen cases met the diagnostic criteria. Half had Hodgkin's disease. In six the infection was disseminated; five of the six died early in the course of their infectious illness, frequently without diagnosis. Conclusions include: 1. The occurrence of coccidioidomycosis in immunosuppressed patients seen at institutions in or adjacent to the endemic area is not as rare as the literature suggests. 2. Dissemination is frequently explosive and the radiographic appearance of pulmonary involvement may appear late. Widespread pulmonary dissemination may occur within 24 hours after a negative x-ray. 3. Although the skin test loses its diagnostic value, the serology remains valid. Thus immunosuppressed patients with febrile illnesses (with or without radiographically evident pulmonary involvement) who have a history of travel to an endemic area should have serological examinations. 4. Lymphocytopenia correlates with risk of dissemination of coccidioidomycosis. 5. The administration of immunsuppressive chemotherapy correlates with such risk while radiotherapy and the malignant or non-malignant nature of the disease do not. ( info)

17/255. Immune cytopenias as the presenting finding in primary sjogren's syndrome.

    A diagnostic delay of several years in primary sjogren's syndrome is common, even in patients who present with sicca symptoms. It is much more likely in cases with prominent symptomatic extraglandular involvement. We report on three such patients who presented as Coomb's positive haemolytic anaemia, systemic symptoms with agranulocytosis and gingival bleeding due to immune thrombocytopenia, to alert clinicians to the fact that primary sjogren's syndrome may present as clinically significant immune-mediated cytopenia in the absence of sicca symptoms. sjogren's syndrome, a common autoimmune disorder, should be considered in the differential diagnosis of apparently 'idiopathic' cytopenias and actively sought by directed history, Schirmer test and autoantibody screening. ( info)

18/255. Olanzapine-induced leukopenia with human leukocyte antigen profiling.

    Olanzapine is an atypical antipsychotic medication frequently used in the management of psychotic states. While it has proved to be safe compared to clozapine with regard to haematotoxicity, because it has only been available for a few years, full documentation of its haematological side-effects remains incomplete. We report a case of olanzapine-induced leukopenia with associated neutropenia. Since clozapine-induced haematotoxicity has been associated with characteristic human leukocyte antigen (HLA) groups, HLA typing was determined in this patient. Following failure with typical antipsychotic medication, the patient received 10 mg/day of olanzapine. Three weeks later, he developed fever and a significant decrease in leukocyte count. Olanzapine was immediately discontinued. HLA typing was determined. The white cell count returned to normal and the fever, most probably secondary to the low white cell count, subsided with antibiotic treatment. HLA typing results were: A1 24, B7, B35, DRB1*15, DRB1*11, DRB3*01-03, DRB5*01-02. Olanzapine may induce serious leukopenia and neutropenia. HLA typing in this single patient demonstrated a distinct haplotype compared to that previously observed in clozapine-induced haematoxicity. ( info)

19/255. Trovafloxacin-associated leukopenia.

    OBJECTIVE: To report a case of trovafloxacin-associated leukopenia, which occurred in a trauma patient shortly after administration and resolved following discontinuation of the drug. CASE SUMMARY: A 79-year-old white man was admitted to Yale New Haven Hospital after sustaining partial amputation of his right lower leg by an industrial lawn mower. After successful resuscitation, he underwent complete right lower amputation and was treated with intravenous alatrofloxacin mesylate. He developed leukopenia that resolved after discontinuation of the drug. DISCUSSION: Trovafloxacin is a broad-spectrum synthetic fluoroquinolone used for a wide variety of bacterial infections. We report, for the first time in the English-language literature, a case of trovafloxacin-associated leukopenia. The leukopenia resolved promptly after discontinuation of the drug. This association is further supported by the exclusion of other potential causes for this adverse effect. CONCLUSIONS: leukopenia is a well-recognized adverse effect of several drugs. We report a case of trovafloxacin-associated leukopenia during treatment of a trauma patient. Healthcare personnel should be aware of this possible adverse reaction in patients treated with trovafloxacin. ( info)

20/255. Leucopenia induced by low dose clozapine in Parkinson's disease recedes shortly after drug withdrawal. Clinical case descriptions with commentary on switch-over to olanzapine.

    Four patients affected by severe Parkinson's disease developed leucopenia (900-1200 WBC) during treatment of psychosis (3) or untreatable insomnia (1) with clozapine (37.5-75 mg/day). clozapine withdrawal was followed by recovery of leucopenia (4000-6000 WBC) in two weeks with no need for the administration of leucokines. After 1-6 months olanzapine was administered (increasing the dose from 2.5 to 10 mg/day) to treat persisting disturbances, but the drug induced severe worsening of parkinsonism and also this drug had to be withdrawn. ( info)
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