Cases reported "Agranulocytosis"

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1/37. 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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2/37. Treatment of antithyroid drug-induced agranulocytosis by granulocyte colony-stimulating factor: a case of primum non nocere.

    A 48-year-old woman who was treated for thyrotoxicosis with methimazole developed agranulocytosis. The methimazole was stopped and treatment with subcutaneous granulocyte colony-stimulating factor (G-CSF) was initiated. Administration of the drug for 8 days did not effectively shorten the recovery period compared with the average reported in the literature without the drug, and may have triggered additional iatrogenic complications. A search of the literature yielded 15 instances of severe antithyroid-drug-induced granulocytopenia (ATDIA) (granulocyte count of less than 0.1 x 10(9)/L) treated with G-CSF. Of the 16 patients, including the 1 reported here, only 3 displayed significant shortening of the agranulocytic period after treatment. We conclude that routine therapeutic application of G-CSF in afebrile severe ATDIG is not justified, and in some cases may generate a cascade of iatrogenic adverse events.
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3/37. Fournier's gangrene after hemorrhoidectomy: association with drug-induced agranulocytosis. Report of a case.

    An unusual case of Fournier's gangrene after hemorrhoidectomy and drug-induced agranulocytosis, as the predisposing condition, is described. The patient had severe granulocytopenia that was attributed to the recent use of dipyrone. Together with hemodynamic resuscitation, broad-spectrum antibiotic and recombinant human granulocyte colony-stimulating factor were started. Wide surgical excision of all the gangrenous tissues, in addition to laparoscopic formation of a defunctioning sigmoid loop colostomy, was performed. The white blood cell count rose steadily and the patient experienced a rapid recovery. We emphasize that radical surgery must be accompanied by pharmacologic interventions for a successful outcome in such cases.
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4/37. Rapid improvement of psoriasis vulgaris during drug-induced agranulocytosis.

    The role of neutrophils in psoriasis has long been discussed. We report a patient with long-standing psoriasis vulgaris who showed rapid improvement during agranulocytosis caused by ticlopidine. The patient did not develop any new psoriatic lesions for several days, although neutrophils increased daily after the administration of ticlopidine was stopped. The day after the peripheral blood neutrophil count recovered, several psoriatic plaques reappeared. The correlation of psoriatic activity with peripheral blood neutrophil counts suggests that a certain number of neutrophils may be required to initiate and maintain psoriasis.
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keywords = drug-induced
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5/37. Reversible granulocytopenia in association with riluzole therapy.

    OBJECTIVE: To report a case of severe neutropenia developing in association with riluzole 200 mg/d. CASE SUMMARY: A 63-year-old woman with amyotrophic lateral sclerosis (ALS) presented with nausea, anorexia, and fever two weeks following inadvertent dose escalation of riluzole from 100 to 200 mg/d. Granulocytopenia was diagnosed and evaluation for a possible causative infectious process was negative; riluzole was considered a possible offender. Blood counts returned to normal with discontinuation of riluzole and administration of filgramstim. DISCUSSION: riluzole is a glutamate release inhibitor used in the treatment of ALS, a devastating, progressive neurodegenerative disorder affecting motor neurons. A variety of adverse effects have been described with riluzole therapy, most commonly dizziness and gastrointestinal disorders. In this patient, multiple investigations failed to reveal an infectious cause or other drug-induced cause for the granulocytopenia. CONCLUSIONS: Granulocytopenia has been reported as an adverse effect of riluzole but is not a complication well known to clinicians, and there are no detailed reports published in the literature. In this patient, several lines of evidence raise the possibility of a causal relationship between riluzole and granulocytopenia.
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keywords = drug-induced
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6/37. invasive pulmonary aspergillosis in a puerperant with drug-induced agranulocytosis.

    invasive pulmonary aspergillosis (IPA) is an acute infection of aspergillus species to the lungs. It generally occurs in immunocompromised hosts, especially with neutropenia. We report a 30-year-old puerperant, who developed IPA from agranulocytosis. She had been treated for threatened labor with ritodrine and cefepime, one of which induced agranulocytosis. After vaginal delivery of twins, pneumonia emerged in the right lower lobe. She was diagnosed to have IPA according to the halo sign on computed tomography (CT) and positive circulating antibody against aspergillus, and was treated successfully with oral itraconazole followed by surgical resection. It is important to note that IPA might arise in otherwise immunocompetent hosts when neutropenia is long-standing.
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keywords = drug-induced
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7/37. ethosuximide induced agranulocytosis.

    agranulocytosis caused by ethosuximide is extremely rare in children. Drug-induced agranulocytosis is an unexpected side effect of a drug, and delay in diagnosis of agranulocytosis can result in a fatal outcome. We experienced a case of a 16-month-old male infant with down syndrome in whom fever appeared 16 days after the start of administration of ethosuximide and then severe pneumonia developed. Results of a blood test on admission showed a decreased leukocyte count of 1700/microl, and a hemogram showed that there were no granulocytes. The erythrocyte and thrombocyte counts were within normal ranges. The results of a bone marrow aspiration test showed that there was no production of any types of granulocytes. The patient required mechanical ventilation due to deterioration in his pneumonia and complication with disseminated intravascular coagulation, but the neutrophilic leukocytes began to increase from the 8th day after discontinuation of ethosuximide administration and start of treatment with granulocyte colony-stimulating factor, and the patient survived. The mechanism of onset in this case is thought to have been immunologic. Careful attention should be given to this type of agranulocytosis because of its sudden onset at 1-2 weeks after the start of administration of the causal drug. A drug-induced lymphocyte stimulation test was useful for diagnosis in this case, showing a positive reaction only for ethosuximide.
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ranking = 0.2
keywords = drug-induced
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8/37. Treatment of methimazole-induced severe aplastic anemia with recombinant human granulocyte-monocyte colony-stimulating factor and glucocorticosteroids.

    The in vivo response to recombinant human granulocyte-monocyte colony-stimulating factor (rHu GM-CSF) in facilitating the reconstitution of granulomonopoiesis was evaluated in a patient with Graves' disease who developed severe aplastic anemia during methimazole therapy. After 10 days of treatment with rHu GM-CSF, the neutrophil and monocyte counts rose to 1.65 x 10(9)/l and 0.41 x 10(9)/l, respectively. However, the patient was still dependent on erythrocyte and platelet transfusions. Two days after rHu GM-CSF withdrawal, the neutrophil count dropped off to 0.41 x 10(9)/l.rHu GM-CSF was reinitiated for 2 days along with glucocorticosteroids. With this combined therapeutic approach, the neutrophil count returned to normal and remained stable, and both Hb and platelet values began to improve. It is concluded that the combination of rHu GM-CSF and glucocorticosteroids can be used as a therapeutic option that may lead to beneficial results in drug-induced aplastic anemia.
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keywords = drug-induced
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9/37. Treatment of drug-induced agranulocytosis with recombinant GM-CSF.

    A 53-year male patient, treated for rheumatoid arthritis with sulphasalazine, developed a total agranulocytosis. When this state had prevailed for at least 10 d no bone marrow granulocyte progenitor cells were detectable. Intravenous GM-CSF treatment was initiated 5 d later, and the patient recovered within the next 6 d. GM-CSF treatment for severe agranulocytosis deserves further investigation.
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ranking = 0.8
keywords = drug-induced
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10/37. Prospective in vitro testing for drug-induced neutropenia in a patient requiring anti-malarial prophylaxis: confirmation of findings on exposure of patient to drug.

    A patient with moderate pancytopenia thought to be due to chloroquine ingestion was shown to have granulocyte progenitors (CFU-G) which were abnormally sensitive in vitro to chloroquine. As he required further anti-malarial prophylaxis, his marrow was prospectively tested in vitro with proguanil and its metabolite cycloguanil. The patient's CFU-G were also abnormally sensitive to these agents and predicted neutropenia was verified when the patient had a trial course of proguanil. We believe this is the first instance of in vivo confirmation of in vitro CFU-G drug sensitivities.
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ranking = 0.8
keywords = drug-induced
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