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At least 19 recordsLinked to original sources
PubMed1994

[Granulocyte colony-stimulating factor treatment (G-CSF) of antithyroid drug-induced granulocytopenia: granulocyte count measurement after 4 hours of G-CSF injection is useful for the detection of recovery from granulocytopenia].

The primary objective of this study was to ascertain the usefulness of granulocyte count measurement after 4 hours of granulocyte colony-stimulating factor (G-CSF) injections for the detection of recovery from granulocytopenia. Four Graves' patients with antithyroid drug-induced granulocytopenia (granulocyte count between 500 and 1000/mm3) and three Graves' patients with antithyroid drug-induced agranulocytosis (granulocyte count < 500/mm3) each received a daily dose of 75 mu g of G-CSF administered subcutaneously. In all granulocytopenic patients, after 4 hours of G-CSF injection the granulocyte counts increased to 5623, 4050, 8923 and 4647/mm3, and the granulocyte count after 24 hours of G-CSF injection was 3008, 4634, 4854, 4200/mm3. In one of the three agranulocytic patients, the granulocyte count increased from 238/mm3 to 5982/mm3 after 4 hours of G-CSF injection, and the granulocyte count after 24 hours of G-CSF injection was 4800/mm3. Although the granulocyte counts before G-CSF injection of the remaining two agranulocytic patients were 138 and 126/mm3, the granulocyte counts after 4 hours of G-CSF injection were 837 and 59/mm3 and those after 24 hours of G-CSF injection were 817 and 0/mm3. These results indicated that granulocyte count measurement after 4 hours of G-CSF injection was useful for detecting the recovery from granulocytopenia and agranulocytosis.

Adolescent↗
PubMed1997

Usefulness of granulocyte count measurement four hours after injection of granulocyte colony-stimulating factor for detecting recovery from antithyroid drug-induced granulocytopenia.

This prospective study was designed to investigate the usefulness of granulocyte count measurements 4 hours after injection of granulocyte colony-stimulating factor (G-CSF) for detecting recovery from antithyroid drug (ATD)-induced granulocytopenia or agranulocytosis. Granulocyte and white blood cell counts were measured 4 hours and 24 hours after patients with ATD-induced granulocytopenia had been given an injection of 75 micrograms of G-CSF (1.1 to 1.9 micrograms/kg; 1.5 +/- 0.2 micrograms/kg [mean +/- standard deviation]). Thirty-seven patients were studied and divided into three groups based on their initial granulocytopenic granulocyte count: 28 with mild (granulocyte count 0.501 to 1.0 x 10(9)/L), 6 with moderate (granulocyte count 0.101 to 0.5 x 10(9)/L), and 3 with severe (granulocyte count less than 0.1 x 10(9)/L) ATD-induced granulocytopenia. Twenty-five of the 28 patients with mild granulocytopenia and 4 of the 6 patients with moderate granulocytopenia were found to have recovered from the granulocytopenia both 4 hours and 24 hours after injection, and their granulocyte counts remained normal thereafter. However, the other 3 patients with mild granulocytopenia, 2 patients with moderate granulocytopenia, and all 3 patients with severe granulocytopenia had not recovered by either 4 or 24 hours after the G-CSF injection. Despite daily G-CSF injections, the granulocyte continued to decrease in most cases. It took 2 to 11 days for these counts to recover from granulocytopenia. These results indicate that granulocyte count measurement 4 hours after injection of G-CSF is useful for detecting recovery from ATD-induced granulocytopenia or agranulocytosis and for predicting disease severity. Accordingly, its measurement enables physicians to make an appropriate decision about whether a patient with ATD-induced granulocytopenia should be treated in the hospital or in the outpatient clinic.

Adolescent↗
PubMed1983

Pneumococcal sonicate-induced biphasic granulocytopenia and its dissociation from pulmonary leukostasis. The contribution of pneumococcal products and complement to early and late granulocytopenic phases.

The pathogenesis of pneumococcus (PNC)-induced granulocytopenia is unclear. We studied its relationship to pulmonary leukostasis and the possible roles of PNC constituents and complement. Nonviable PNC was infused into normal and 99% C3-depleted rabbits. PNC challenge induced both granulocytopenia and pulmonary leukostasis in normal animals; complement-depleted animals displayed granulocytopenia without pulmonary leukostasis. Therefore an intact complement system was not essential to the granulocytopenia, whereas pulmonary leukostasis was complement-dependent. Rabbits infused with serum, plasma, or nonpyrogenic normal saline, each after in vitro incubation with PNC, developed significant granulocytopenia (p less than 0.001, p less than 0.01, and p less than 0.001, respectively) with maximal mean percent decreases of -98%, -97%, and -91%, respectively. When the animals were sacrificed at 3 hr, no pulmonary leukostasis was found. The granulocytopenia persisted for 3 hr after infusion of either PNC-exposed serum or plasma, whereas the granulocytopenia induced by PNC-exposed saline was of less than or equal to 1 hr duration. If serum or plasma complement was inactivated prior to PNC incubation, subsequent infusion also induced significant granulocytopenia of less than 1 hr duration (p less than 0.05 and p less than 0.01). PNC-exposed saline that was subsequently heat-treated induced this same early (less than or equal to 1 hr) granulocytopenia (p less than 0.05). Control animals infused with serum, plasma, or saline unexposed to PNC displayed neither granulocytopenia nor pulmonary leukostasis. Therefore neither prior in vitro complement inactivation nor heat treatment after PNC incubation prevented the early granulocytopenic phase; in vitro complement inactivation totally aborted the late phase. The complement-independent, heat-stable early granulocytopenic phase was further investigated. Its granulocytopenia-inducing activity did not require the presence of PNC capsular polysaccharide and was resistant to trypsin treatment. With ultrafiltration, its molecular weight was 100,000 to 300,000. Thus PNC-induced granulocytopenia is a multifactorial phenomenon involving both complement-dependent and complement-independent mechanisms as well as contribution by PNC constituents or by-products.

Agranulocytosis↗
PubMed1993

Granulocyte colony-stimulating factor treatment of antithyroid drug-induced granulocytopenia.

The primary objective of this study was to ascertain the effectiveness of granulocyte colony-stimulating factor in the treatment of antithyroid drug-induced granulocytopenia of varying degree. Sixteen patients with Graves' disease with antithyroid drug-induced granulocytopenia (granulocyte counts < 1.0 x 10(9)/L) each received a daily dose of 75 micrograms of granulocyte colony-stimulating factor administered subcutaneously. Within 24 hours of the first injection, the granulocyte count increased (0.6 to 12.3 x 10(9)/L) in all 10 patients with mild granulocytopenia (granulocyte counts between 0.5 and 1.0 x 10(9)/L) and all three with moderate granulocytopenia (granulocyte counts < 0.5 x 10(9)/L). The three remaining patients with severe granulocytopenia (agranulocytic), whose granulocyte counts were zero, did not recover from granulocytopenia until the 6th, 7th, and 14th days of treatment with granulocyte colony-stimulating factor. Examination of bone marrow taken at the onset of the disease in all three agranulocytic patients showed a prominent decrease in granulocytic series, while identical examination in six of eight patients with mild to moderate granulocytopenia showed close to normal granulocytic series. There was no elevation of serum granulocyte colony-stimulating factor concentration in four patients with mild granulocytopenia and one with moderate granulocytopenia at the onset of their disease, whereas those of the remaining three patients with severe granulocytopenia (agranulocytic) increased at onset of agranulocytosis. This information led us to conclude that: (1) granulocyte colony-stimulating factor is effective in the treatment of antithyroid drug-induced mild to moderate granulocytopenia and (2) in severe agranulocytic cases, granulocyte colony-stimulating factor is not effective. Accordingly, we were again reminded of the importance of early diagnosis and treatment of antithyroid drug-induced agranulocytosis.

Adult↗
PubMed1995

Granulocytopenia after combined therapy with interferon and angiotensin-converting enzyme inhibitors: evidence for a synergistic hematologic toxicity.

PURPOSE: The purpose of this study was to assess whether granulocytopenia observed in 3 of 38 patients with essential mixed cryoglobulinemia who were treated with low-dose interferon was due to the underlying disease or to synergistic toxicity of interferon with other drugs. PATIENTS AND METHODS: Adverse effects of interferon therapy were monitored in 38 patients affected with type II essential mixed cryoglobulinemia. Patients were treated with 3 million units (MU), daily or on alternate days, of recombinant interferon-alpha 2a (35 patients) or with natural interferon-beta (3 patients). The duration of treatment ranged between 6 and 15 months; the total duration of follow-up, including after therapy, ranged between 8 and 93 months. RESULTS: None of 35 patients treated with interferon alone developed significant hematologic alterations. In addition, none of 7 patients treated with angiotensin-converting enzyme (ACE) inhibitors alone showed hematologic toxicity. Three patients who were treated with a combination of interferon and ACE inhibitors developed severe granulocytopenia a few days after starting treatment. Granulocytopenia subsided within 1 to 2 weeks after suspending therapy. Resumption of treatment with this drug combination produced a granulocytopenia relapse in 1 patient. In these 3 patients, interferon treatment alone, or ACE inhibitor monotherapy, was not followed by granulocytopenia. CONCLUSION: Although severe hematologic toxicity rarely develops in patients treated with low-dose interferon, granulocytopenia occurred in all 3 of our patients with mixed cryoglobulinemia who were treated with a combination of low-dose interferon-alpha 2a and ACE inhibitors. Neither drug alone was toxic in any of our cryoglobulinemic patients, indicating a high risk of severe hematologic toxicity for this drug combination, at least in patients with this disease. Physicians should be aware of this danger when using interferon treatment in patients with this, or possibly other, disorder(s) that also require antihypertensive therapy.

Adult↗
PubMed1981

Reversal of hemodialysis granulocytopenia and pulmonary leukostasis: A clinical manifestation of selective down-regulation of granulocyte responses to C5adesarg.

The transient granulocytopenia of hemodialysis results indirectly from plasma complement activation by dialyzer cellophane membranes. The C5a(desarg) so produced can induce reversible granulocyte aggregation in vitro and in vivo, and we hypothesized that the pulmonary leukostasis responsible for the granulocytopenia results from embolization of aggregates formed under the influence of C5a(desarg) produced in the dialyzer. These studies were designed to measure C5a(desarg) generation during dialysis by granulocyte aggregometry and to determine the reason for the transience of the leukostasis. C5a(desarg) generation was equally evident throughout dialysis, persisting well after granulocytopenia had reversed, and dialyzer-induced complement activation was insufficient to produce significant depletion of plasma complement titers. That granulocyte deactivation might be responsible for the transience was suggested by the absence of the usual granulocytopenia in a patient with uniquely high levels of C5a(desarg) in his predialysis plasma. Granulocytes drawn from seven stable uremic patients after granulocytopenia had reversed exhibited a dose-related, selective and irreversible refractoriness to stimulation with C5a(desarg), but their responses to n-formyl-Met-Leu-Phe remained normal. Identical deactivation was produced in normal cells by short- or long-term exposure of C5a(desarg) in vitro. These studies suggest that C5a(desarg) is indeed generated by the dialyzer throughout hemodialysis and that the transience of the leukostasis and granulocytopenia is due to selective down-regulation of cellular responses to C5a(desarg)-a phenomenon that hitherto has been described only in vitro and that may be important in limiting the deleterious effects of adherent granulocytes on the endothelium in patients with intravascular complement activation.

Agranulocytosis↗
PubMed1989

Methylprednisolone inhibits granulocytopenia induced by infusion of complement-activated serum but not of complement-activated plasma in rabbits.

The effect of methylprednisolone was examined on complement-induced granulocytopenia in vivo following infusion of zymosan-activated autologous plasma or serum into rabbits. Methylprednisolone only inhibited granulocytopenia and thrombocytopenia when zymosan-activated serum or fibrinogen-depleted plasma were infused. It was ineffective at preventing granulocytopenia in animals infused with zymosan-activated plasma. Only zymosan-activated plasma contained fibrin monomers which could directly cause granulocytopenia independently of the generation of C5a. Hence, during complement activation in whole blood in vivo, little or no effect of methylprednisolone should be expected in preventing granulocytopenia.

Agranulocytosis↗
PubMed1997

Cyanamide-induced granulocytopenia.

We report a 64-year-old male with granulocytopenia and dermatitis due to cyanamide treatment. We administered cyanamide for alcoholism. After about one month he suffered from scaly erythema over his whole body and granulocytopenia (granulocyte; 140/microliter) with maturation arrest in bone marrow. After cessation of cyanamide and the start of granulocyte colony-stimulating factor administration, the skin eruption ameliorated gradually, and the peripheral blood granulocyte counts increased. Cyanamide showed positive results in the drug lymphocyte stimulation test (198%) and the patch test led to the diagnosis of granulocytopenia and dermatitis induced by cyanamide. After restarting glibenclamide and diazepam administration, his granulocytopenia did not reoccur. To our knowledge, this is the first report of a case with granulocytopenia induced by cyanamide.

Agranulocytosis↗
PubMed1977

The relationship of fever, granulocytopenia and antimicrobial therapy to bacteremia in cancer patients.

The relationship of fever, granulocytopenia, and antimicrobial therapy to bacteremia was studied retrospectively in 53 cancer patients. Severe granulocytopenia was present at the time blood cultures were positive in 27 to 31 episodes of bacteremia. Twenty-five episodes of bacteremia documented before the initiation of antimicrobial therapy in patients who were granulocytopenic and febrile. No bacteremia occurred in the absence of fever. Only two bacteremias occured while patients were receiving parenteral antimicrobials. Antimicrobial therapy was terminated 30 times in the presence of granulocytopenia and fever, and subsequent bacteremia occurred in 14 patients within 4 days. Patients who died with fungal disease did not receive more antibiotics than patients who died without fungal disease. These data suggest a rationale for long-term use of antimicrobial therapy in patients with persistent granulocytopenia and fever.

Adolescent↗
PubMed1978

Granulocytopenia in hospitalized patients: I. Prognostic factors and etiology of fever.

The clinical course of 126 hospitalized patients during 192 episodes of granulocytopenia and fever was studied. Fever was a regular accompaniment of granulocytopenia, occurring in 94 per cent of granulocytopenic episodes. The mean duration of granulocytopenia (less than 1,000/mm3) was 18 days, with fever (temperature greater than 38 degrees C) being present during 44 per cent of those days. Fever was present during 69 per cent of days with a granulocyte count less than 10/mm3. A presumed infection was present in 86 of 128 febrile granulocytopenic episodes in adults and in 19 of 64 febrile granulocytopenic episodes in children. A fungal infection was found in 11 patients; a viral infection in 23 patients. Bacteremia occurred during 44 granulocytopenic episodes with 16.8 bacteremias/1,000 days of granulocytopenia in adults and 12.7 bacteremias/1,000 days in children. The mortality was 33 per cent per granulocytopenic episode in adults and only 8 per cent per episode in children.

Adolescent↗
PubMedDate not supplied

[Treatment of clozapine-induced granulocytopenia with lithium (two observations)].

Despite the availability of new treatments, the antipsychotic effectiveness of clozapine has not been matched yet. Unfortunately, its regulation is limited by the side effects. The most detrimental is the hematologic toxicity (neutropenia and agranulocytosis) which requires a regular biological monitoring. Treatment with clozapine must be stopped in those cases of secondary granulocytopenia for about 3% of the patients. The current psychiatric drug lithium carbonate has an opposite effect: it can induce leukocytosis. Thus, lithium carbonate is administered in leukopenia, as well as in many hematologic and immunological diseases. However, few teams have used lithium in order to alleviate clozapine-induced granulocytopenia. We report here 2 patients who developed severe neutropenia (neutrophil count<1.5 yen 10 (9)/L) and for whom the use of lithium enabled us to continue the treatment by clozapine. The first patient had a granulocyte rate constitutionally low which rapidly decreased with clozapine. Thanks to the administration of lithium, he recovered quickly a normal blood cell count, which in fact was much higher than his normal rate. According to our research, it's the first time that lithium is reported to be so efficacious in a patient with such a low rate of granulocytes before treatment. It may be that clozapine is not used for those kinds of patients. The second patient developed granulocytopenia after one year of treatment with clozapine. The use of lithium increased so much the number of granulocytes that we continued the treatment with clozapine alone. After 4 months, there is no reappearance of granulocytopenia. We must take into account the partial and contradictory reports in the literature. However, if this result is confirmed, it could be of a high interest to extend the prescription of clozapine, the most effective current antipsychotic drug.

Adult↗
PubMed2000

Granulocyte colony-stimulating factor plasma levels during clozapine- and olanzapine-induced granulocytopenia.

OBJECTIVE: Recent case studies suggest that impaired granulopoiesis, well-known to occur during clozapine treatment, may also be observed when olanzapine is administered. The underlying mechanisms are unknown, but haematopoietic cytokines such as granulocyte colony-stimulating factor (G-CSF) are likely to be involved. METHOD: We measured the plasma levels of G-CSF and of other cytokines longitudinally in a female patient who developed granulocytopenia twice, first during clozapine treatment and again when olanzapine was administered. RESULTS: G-CSF levels, but not those of other cytokines, closely paralleled granulocyte counts, yielding a significant positive correlation. G-CSF was not detectable in plasma when granulocytopenia occurred. Granulocytopenia resolved spontaneously despite continuing treatment with olanzapine. CONCLUSION: The present case suggests that clozapine and olanzapine both are able to induce transient granulocytopenia through a similar or common mechanism that does not involve a compensatory increase in G-CSF levels.

Adult↗
PubMed1992

Recombinant human granulocyte-colony-stimulating factor in the treatment of patients with chronic benign granulocytopenia and congenital agranulocytosis (Kostmann's syndrome).

Seven patients with chronic benign granulocytopenia and nine patients with congenital agranulocytosis, received consecutive seven-day courses of recombinant human granulocyte-colony stimulating factor at a starting dose of 50 micrograms/m2/day, subcutaneously. If there was no response the doses were increased to 300 micrograms/m2. All patients with chronic benign granulocytopenia responded rapidly at the minimum dose within 1-3 days after administration. By contrast, only three of the nine patients with congenital agranulocytosis responded within 1-7 days at this dose. Four patients with congenital agranulocytosis showed a response between days 7-19 at a dose of granulocyte-colony-stimulating factor 100-200 micrograms/m2 but in the remaining two cases no response was obtained. The administration of granulocyte-colony-stimulating factor was shown to be safe and effective also in reducing infectious episodes in these patients. Previously it was reported that granulocyte-colony-stimulating factor 10-30 micrograms/kg/day was effective for patients with congenital agranulocytosis. These results indicate that patients with congenital agranulocytosis may require much higher doses of recombinant human granulocyte-colony-stimulating factor than patients with chronic benign granulocytopenia and that the response to ordinary doses of recombinant human granulocyte-colony-stimulating factor may be useful in differentiating between chronic benign granulocytopenia and congenital agranulocytosis.

Adolescent↗
PubMed1982

Gram-positive bacteria-induced granulocytopenia and pulmonary leukostasis in rabbits.

Pneumococci have been shown to induce granulocytopenia and pulmonary leukostasis which might contribute to morbidity and mortality in pneumococcal sepsis. We studied whether other gram-positive species (groups A and B streptococci, Staphylococcus aureus, Bacillus cereus, and Clostridium perfringens) could also induce these phenomena. Rabbits were challenged with nonviable preparations of each species, and all five species induced profound granulocytopenia (mean decrease of 90%) and pulmonary leukostasis. In vitro studies of serum incubated with these species of bacteria showed a mean consumption of total hemolytic complement of 90%, a mean increase of chemotactic activity for granulocytes of 204%, and a mean augmentation of granulocyte adherence of 45% (compared with 18% for the control). Infusion of sonicate-exposed sera induced granulocytopenia in recipient rabbits. Thus, several nonviable gram-positive species can interact with serum to activate the complement system, generate C5a bioactivity, augment granulocyte adherence, and generate a neutropenia-inducing factor. These alterations may contribute to granulocytopenia or pulmonary leukostasis, which may play a role in the morbidity and mortality associated with gram-positive bacterial infections.

Agranulocytosis↗
PubMed1992

Dialysis granulocytopenia is preceded by an increased surface expression of the adhesion-promoting glucoprotein Mac-1.

We studied the expression of Mac-1 on granulocytes (flow cytometry) from 9 patients (27 examinations) during hemodialysis with cuprophane membranes (CuM). Samples were drawn before dialysis and from the arterial and venous lines at 5, 15 and 180 min. Granulocytopenia was most pronounced after 15 min of treatment. Mac-1 expression on granulocytes increased during dialysis, and a pronounced enhancement occurred across the dialyzer. Mac-1 expression on granulocytes increased 116% across the dialyzer at 5 min, and the degree of Mac-1 mobilization at 5 min correlated with the degree of subsequent granulocytopenia at 15 min. In in vitro experiments, granulocytes from healthy blood donors were incubated with plasma drawn from the arterial and venous lines at 5 min. Plasma drawn from the venous line at 5 min had a greater ability to mobilize Mac-1 than plasma from the arterial line (p less than 0.002). This difference correlated with the degree of granulocytopenia at 15 min (r = 0.76, p = 0.01). Pieces of a washed CuM were incubated in normal human serum (NHS) preparations for different times. Inactivation of the alternative pathway of complement activation (NHS-50 degrees) did not alter the generation of Mac-1-mobilizating capacity compared to NHS. In contrast, inactivation of the classical pathway (NHS-EGTA) decreased the early but not the late generation of Mac-1-mobilizating capacity. Our results indicate that the early mobilization and not the absolute expression of Mac-1 correlates with granulocytopenia, and that sera in vitro attain Mac-1-mobilizating capacity more rapidly when the classical pathway of complement activation is intact.

Aged↗
PubMedDate not supplied

Pilot study of daily ifosfamide 1 g/m2 until grade III granulocytopenia as second-line chemotherapy for anthracycline-pretreated advanced soft tissue sarcoma.

BACKGROUND AND AIMS: Second-line chemotherapy regimens for advanced soft tissue sarcomas after treatment failure or tumor relapse following anthracyclines are still investigational. The aim of the present study was to assess the activity of ifosfamide with a new schedule for patients with advanced soft tissue sarcoma failing to achieve remission or relapsing following anthracycline-containing regimens; it was attempted to individualize dosages and prevent excessive toxicity. STUDY DESIGN: A second-line chemotherapy regimen of ifosfamide 1 g/m2 daily, with drug withdrawal until the next cycle upon appearance of grade III granulocytopenia, was administered to 21 patients with advanced soft tissue sarcoma. All patients failed to achieve remission or relapsed following a first-line high-dose anthracycline regimen (epirubicin 180 mg/m2 or zorubicin 600 mg/m2 per cycle). The cycles were repeated every four weeks. RESULTS: The median number of cycles applied was three (range, 1-15). The ifosfamide dosage reached was 4-13 g/m2 per cycle, median 5 g/m2. A complete response was achieved in 1/21 patient (5%), no partial responses were observed, 4/21 patients (20%) had stable disease, and 16/21 (75%) had progressive disease. No difference in response and stable disease rates was observed between responders and non-responders to first-line chemotherapy. No difference in the ifosfamide dose reached was noted between patients receiving second-line chemotherapy directly following first-line therapy and those with a time interval between first- and second-line chemotherapy. The granulocytopenia grade III nadir lasted for a median of one day (range, 1-3) and other toxicities including hematological toxicity were mild and infrequent. CONCLUSIONS: In view of the swift regeneration from grade III granulocytopenia, continuation of the study with granulocytopenia grade IV as a limiting factor for ifosfamide dose escalation seems feasible, with the prospect of better efficacy without excessive toxicity.

Adult↗
PubMed1989

Granulocytopenia and thrombocytopenia associated with combination therapy of amphotericin B and low-dose flucytosine in a patient with cryptococcal meningitis.

A patient was admitted complaining of fever and headache. He was suspected of meningitis due to nuchal rigidity, and a lumbar puncture was performed. The patient was diagnosed as having cryptococcal meningitis, as Cryptococcus neoformans was found in an India ink preparation of the cerebrospinal fluid. Both amphotericin B and low-dose flucytosine (50 mg/kg/d) were concomitantly administered to the patient and his clinical symptoms improved. However, the combination therapy induced granulocytopenia and thrombocytopenia, which resolved after discontinuance of the drugs. Amphotericin B alone failed to cause granulocytopenia or thrombocytopenia. These results suggest that the mechanisms of granulocytopenia and thrombocytopenia may be toxic reactions to flucytosine in the azotemic state caused by amphotericin B. Our report emphasizes the need for clinicians to monitor for granulocytopenia and thrombocytopenia in patients receiving treatment with both amphotericin B and flucytosine, even when flucytosine is administered in a low dose.

Adult↗
PubMed2000

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.

Agranulocytosis↗