Cases reported "Agranulocytosis"

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1/188. Genetic determinants of drug-induced agranulocytosis: potential risk of olanzapine?

    Whether or not olanzapine causes bone marrow toxicity is still a matter of debate. In spite of pre-marketing and post-marketing clinical trials, and although there have been no cases in animals of olanzapine-induced neutropenia or agranulocytosis, the risk of bone marrow toxicity cannot be excluded. The present paper addresses the following questions: what is the potential background of drug-induced agranulocytosis? Are there any case reports supporting the view that olanzapine has relevant bone marrow toxicity? What strategies might be helpful in identifying the pathological mechanisms underlying this side effect?
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2/188. captopril-induced toxic epidermal necrolysis and agranulocytosis successfully treated with granulocyte colony-stimulating factor.

    captopril-induced bone marrow suppression is rare, except in certain high-risk patient populations. Severe exfoliative rashes have also been associated with captopril, but a combined presentation of toxic epidermal necrolysis and agranulocytosis has not been previously described. We report an unusual case of captopril-induced toxic epidermal necrolysis with agranulocytosis in a patient with no known risk factors. The bone marrow suppression was successfully treated using granulocyte colony-stimulating factor (G-CSF), and the white blood cell (WBC) count recovered within 3 days after starting therapy. This case underscores the early experience with captopril, which showed a strong correlation between high doses used to treat hypertension and bone marrow suppression.
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3/188. Congenital neutropenia. Report of a case and a biorationale for dental management.

    Congenital neutropenia is characterized by a marked decrease in or lack of circulating PMN's in children with no prior history of drug intake. The neutropenia is persistent and the clinical course is one of early onset of severe, recurrent, and eventually fatal infections. Bone marrow studies show a maturation arrest of neutrophilic precursors. Because of their greatly increased susceptibility to infection, patients with congenital neutropenia present a difficult dental management problem. A case of congenital neutropenia has been presented, as well as a biorationale for dental treatment. On the basis of reports in the literature, the following recommendations for the management of patients with congenital neutropenia are made: 1. The prevention and control of infection and the interception of dental disease before surgical intervention becomes necessary should be the overriding considerations in the management of patients with congenital neutropenia. 2. The carious breakdown of teeth should be prevented by the daily application of a 0.4 per cent stannous fluoride gel in addition to oral hygiene and limitation of sucrose intake. 3. Periodontal therapy should be palliative only, since alveolar bone loss is progressive despite frequent oral hygiene instruction and prophylaxis. The goal of periodontal therapy for patients with congenital neutropenia should therefore be a decrease in gingival inflammation to make the patient's mouth more comfortable and to slow down alveolar bone loss. Periodontal surgery is contraindicated. 4. bacteremia and subsequent septicemia should be prevented since a minor infection can become life threatening in patients with congenital neutropenia. The patient should rinse for 30 seconds and the gingival sulci should be irrigated with a phenolated antiseptic mouthwash prior to all dental manipulations of the soft tissue. This will significantly reduce the incidence of bacteremia. 5. Surgery should be avoided if at all possible because of the high risk of post-operative infection. All surgery sholld be performed in the hospital, and the patient should be given antibiotics as determined by his physician. Primary closure should be done with fine polyglycolic acid sutures to reduce the chance of infection. If postoperative infection can be prevented, wound healing will progress normally despite the complete absence of PMN's.
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4/188. fluconazole-induced agranulocytosis with eosinophilia.

    fluconazole is a commonly prescribed antifungal agent with a favorable safety profile. A patient experienced agranulocytosis and eosinophilia associated with the drug. Similar bone marrow-suppressive effect due to the azoles is rarely described in the English-language literature.
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5/188. Chronic neutropenia: Response to plasma with high colony-stimulating activity.

    A child with repeated infections was immunologically normal but was found to have neutropenia with periodic elevations of the absolute mature polymorphonuclear count at 21-day intervals. Immediately following the PMN rise, bone marrow morphology and in vitro cultures demonstrated a maturation arrest at the myelocyte stage with an increase in proliferative capacity. His cycle was not altered by infusions of normal plasma or by injections of epinephrine or typhoid vaccine. Infusion of 10 ml/kg of "stimulated" plasma from donors reactive to TV, obtained 60 minutes following immunization, resulted in an out-of-phase rise in PMN cells and clinical improvement. in vitro assays, using normal or patient marrow, detected high levels of colony-stimulating activity only in those plasma samples that were effective in the patient. These observations support a role of CSA as a physiologic regulator of granulopoiesis in man.
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6/188. Granulopoiesis in infantile genetic agranulocytosis. in vitro cloning of marrow cells in agar culture.

    A 3-year-old boy and a 2-year-old girl with infantile genetic agranulocytosis have been studied by in vitro cloning of bone marrow cells in agar culture. The patients display a normal concentration of colony forming cells and the morphological maturation is identical with that of control marrow cultured in vitro. The marrow cells of the patients show some degree of auto-stimulation indicating that endogenous production of colony stimulating factor is operating. As an inverse relationship is expected between the peripheral neutrophil count and the percentage of marrow colony forming cells in S-phase a high percentage was expected. On the contrary, we find that the percentage of colony forming cells in S-phase is extremely low indicating a genetic unresponsiveness of granulopoietic precursor cells to feed back regulation in infantile genetic agranulocytosis.
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7/188. ticlopidine-induced severe agranulocytosis after the placement of coronary artery stent--a case report.

    ticlopidine is an oral antiplatelet agent frequently utilized in the treatment of cerebrovascular disease. It is rarely associated with severe bone marrow suppression. A case of an elderly woman is reported who developed febrile agranulocytosis two months after commencing ticlopidine but who had a favorable outcome after cessation of that drug and treatment with granulocyte colony-stimulating factor (G-CSF). All patients should have regular monitoring of their blood counts during therapy with ticlopidine.
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8/188. G-CSF plasma levels in clozapine-induced neutropenia.

    BACKGROUND: Clinical reports emphasize the therapeutic usefulness of granulocyte colony-stimulating factor (G-CSF) in clozapine-induced granulocytopenia. Only sparse information exists, however, on the natural course of endogenous G-CSF plasma levels in this condition. methods: We monitored G-CSF and white blood cell (WBC) counts in a 73-year-old patient who developed granulocytopenia while being treated with clozapine for schizoaffective disorder. clozapine treatment was discontinued immediately, and G-CSF serum levels were determined repeatedly during the clinical course. RESULTS: Whereas WBC counts increased again within 6 days after discontinuation of clozapine, G-CSF level decreased significantly within the same period. The rapid decrease of endogenous G-CSF levels paralleled by a normalization of neutrophil count was interpreted as the result of an intact regulatory mechanism of granulocytopoesis. Therefore G-CSF therapy was not initiated. Owing to lack of therapeutic alternatives, it was decided to reintroduce clozapine. G-CSF levels decreased further, accompanied by an increase of WBCs, indicating stable bone marrow functioning. CONCLUSIONS: Based on this observation, we assume that the course of G-CSF and WBC counts indicated an abortive form of toxic bone marrow damage with subsequent recovery. We conclude that monitoring of G-CSF levels may serve as a useful tool in the follow-up of patients in whom clozapine-induced bone marrow damage is suspected.
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9/188. Congenital neutropenia: neutrophil proliferation with abnormal maturation.

    A child with congenital neutropenia was studied using bone marrow culture and ultrastructural and cytochemical techniques. The patient's marrow cells formed a large number of granulocytic colonies of normal size in culture, and her peripheral blood leukocytes produced adequate colony-stimulating factor. No serum inhibitors were identified. The patient's promyelocytes from direct marrow and culture appeared normal in ultrastructure, and primary granules, contained peroxidase and acid phosphatase activity. Myelocytes and rare segmented neutrophils from direct marrow specimens demonstrated atypical notched nuclei, myelin figures in Golgi lamellae and primary (azurophilic) granules, and no identifiable secondary (specific) granules. These data indicate an intrinsic neutrophil defect which allows normal proliferation of precursor cells, but results in abnormal granulogenesis and apparent inability to form secondary granules.
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10/188. agranulocytosis associated with initiation of famotidine therapy.

    OBJECTIVE: To report a case of agranulocytosis associated with initiation of famotidine. CASE SUMMARY: An 87-year-old white man was admitted to the internal medicine department of an acute care hospital because of fever and agranulocytosis (granulocyte count 0). Eight days prior to admission, famotidine therapy had been initiated. famotidine was discontinued and granulocyte-macrophage colony stimulating factor was administered, with concomitant recovery of the granulocyte count and subsequent development of a leukemoid reaction. DISCUSSION: According to the Naranjo probability scale, famotidine was the probable cause of agranulocytosis. This is a rare adverse effect of this medication; only a few other cases have been reported. CONCLUSIONS: Although agranulocytosis is a rare adverse effect of famotidine, the pharmacist and physician should be aware of this potentially fatal event. If any patient treated with famotidine develops fever, the clinician should consider, among other things, performing a white blood cell count.
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