Cases reported "Agranulocytosis"

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1/607. Olanzapine treatment after clozapine-induced granulocytopenia in 3 patients.

    BACKGROUND: How to best treat psychotic patients who have had past clozapine-induced agranulocytosis or granulocytopenia remains a problem. case reports: We report 3 patients with chronic schizophrenia who had previously stopped clozapine due to hematologic side effects. The patients evidenced improvement with olanzapine that equated to 16- to 31-point decreases in rating scale scores during 1-year follow-up without any hematologic abnormalities. CONCLUSION: The results suggest that olanzapine may be useful in treating patients with clozapine-induced granulocytopenia without the risk of recurrence of hematologic side effects. ( info)

2/607. Severe transient pancytopenia associated with procainamide ingestion.

    A 73-year-old woman was found to have clinically significant pancytopenia in association with procainamide hydrochloride ingestion. The syndrome, resembling systemic lupus erythematosus, which has been reported to develop in patients treated with this agent, is characterized by mild to moderate anemia and mild to moderate granulocytopenia. Severe granulocytopenia in patients taking procainamide and unrelated to a lupus syndrome has not previously been reported in association with significant thrombocytopenia. The clinical severity of this patient's presentation, suggesting an aleukemic leukemia, and its complete remission after cessation of procainamide administration occasional this report. ( info)

3/607. 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? ( info)

4/607. Olanzapine-induced agranulocytosis.

    The antipsychotic drug olanzapine was developed to reduce the risk of haematotoxicity. We report a case of agranulocytosis induced by olanzapine. ( info)

5/607. Cohen syndrome: two new cases in siblings.

    Cohen syndrome is a rare genetic disorder consisting of truncal obesity, hypotonia, mental retardation, characteristic facial appearance and ocular anomalies. Other diagnostic clinical features include narrow hands and feet, low growth parameters, neutropenia and chorioretinal dystrophy. We describe the similarities in the clinical and developmental profile of two siblings with Cohen syndrome, providing evidence for autosomal recessive inheritance in this condition. CONCLUSION: The diagnosis of Cohen syndrome should be suspected in mentally retarded children with the above characteristics. neutropenia and ocular anomalies with high-grade myopia and chorioretinal dystrophy are also considered important findings and can aid in the clinical diagnosis especially at an early age. ( info)

6/607. 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. ( info)

7/607. 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. ( info)

8/607. The platelets in preleukemia and myelomonocytic leukemia. Ultrastructural cytochemistry and cytogenetics.

    light and electron microscopic studies of platelets from 16 patients with myelomonocytic leukemia or "preleukemia" revealed major morphologic alterations in 15 and minor ones in 1. Although variable in severity from case to case, the changes present followed a distinct pattern. In most cases there were two platelet populations, one morphologically normal and one morpholigically abnormal. The most salient changes pertained to size (giant forms), shape (the platelets being rounded and probably spheroidal), decrease or absence of the microtubules, and increase in immature elements. A striking feature was the variation in size and shape of the granules, with truly giant forms (up to 2.5 mum) being present. In cytogenetic studies in 14 cases, there was no correlation between the chromosomal changes and the various types of platelet anomalies. ( info)

9/607. 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. ( info)

10/607. 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. ( info)
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