Treatment of severe clozapine-induced neutropenia with granulocyte colony-stimulating factor (G-CSF)

1998 ◽  
Vol 172 (1) ◽  
pp. 82-84 ◽  
Author(s):  
B. Sperner-Unterweger ◽  
I. Czeipek ◽  
S. Gaggl ◽  
D. Geissler ◽  
G. Spiel ◽  
...  
Keyword(s):  
Severe Neutropenia ◽  
Pharmacological Intervention ◽  
Concomitant Treatment ◽  
Granulocyte Colony Stimulating Factor ◽  
Clozapine Treatment ◽  
Therapeutic Results ◽  
Clinical Consequences ◽  
History Of ◽  
Paranoid Type ◽  
Stimulating Factor

BackgroundA 17-year-old boy suffering from a severe schizophrenic disorder of the paranoid type and mental retardation did not respond to treatment with typical antipsychotics, whereas under clozapine treatment he showed a favourable response. Discontinuation of clozapine led to an acute psychotic relapse. During clozapine treatment the patient developed severe neutropenia.Method and ResultsDue to the history of unsatisfactory response to traditional antipsychotics, clozapine treatment was continued despite white blood cell (WBC) decline. Concomitant treatment with G-CSF was followed by a rapid normalisation of WBC.ConclusionsThis case report is not intended to challenge the clinical practice of discontinuing clozapine upon the development of neutropenia/agranulocytosis, but rather to stimulate further research in the pathophysiology and clinical consequences of a clozapine rechallenge after a WBC decline, especially in patients with a rather complex symptomatology where no sufficient therapeutic results can be achieved with any other pharmacological intervention than clozapine.

Severe Pancytopenia Following Single Dose Methotrexate In Psoriasis: A Rare And Potentially Lethal Manifestation

2020 ◽  
Vol 15 ◽  
Author(s):  
Ajeet Singh ◽  
Ritul Choudhary ◽  
Namrata Chhabra ◽  
Satyaki Ganguly ◽  
Vinay Rathore
Keyword(s):  
Single Dose ◽  
Plaque Psoriasis ◽  
Granulocyte Colony Stimulating Factor ◽  
Chronic Plaque Psoriasis ◽  
Toxic Side Effect ◽  
Plaque Erosion ◽  
Dose Methotrexate ◽  
History Of ◽  
Severe Pancytopenia ◽  
Stimulating Factor

: Methotrexate is an antimetabolite anticancer drug frequently used in the treatment of extensive chronic plaque psoriasis. Psoriatic plaque erosion is a rare toxic side effect of single-dose methotrexate and is described as a sign of the impending pancytopenia. Here, we report a case of a 48-year-old male, presented with multiple oral and genital erosions, fissuring over palm and soles for 5 days. His laboratory tests revealed severe pancytopenia and nephropathy. He had a history of chronic plaque psoriasis for which he took a single dose of 15 mg methotrexate. During the hospital stay, the patient needed folate antagonist, granulocyte colony stimulating factor (G-CSF), intravenous fluids, blood transfusions, and platelet transfusions. He recovered within 12 days of admission.

The Utility of Granulocyte Colony Stimulating Factor in Patients Receiving Chimeric Antigen Receptor T-Cell Therapy with Axicabtagene Ciloleucel

Blood ◽  
2020 ◽  
Vol 136 (Supplement 1) ◽  
pp. 23-25
Author(s):  
Jason N Barreto ◽  
Corina J Doleski ◽  
Justin R Hayne ◽  
Matthew A Hathcock ◽  
Tuan A Truong ◽  
...  
Keyword(s):  
T Cell ◽  
Research Funding ◽  
Severe Neutropenia ◽  
Granulocyte Colony Stimulating Factor ◽  
T Cell Therapy ◽  
Car T Cell ◽  
Car T ◽  
Baseline Characteristics ◽  
Stimulating Factor ◽  
Neutropenic Episode

Background: Infection during the period of neutropenia following chemotherapy represents a major cause of morbidity and mortality in patients with malignancy.(Freifeld, et al, 2011, Baden LR, et al, 2012) Several guidelines recommend granulocyte colony stimulating factor (GCSF) to reduce the duration and severity of chemotherapy-induced neutropenia and abate infection risk.(Lyman, et al 2018, Aapro, et al, 2011, Smith, et al, 2015). Optimal GCSF administration following chimeric antigen receptor (CAR) T-cell therapy remains undefined and requires characterization. Methods: The Mayo Institutional Review Board approved this retrospective, single-center study. Electronic medical records for patients prescribed axicabtagene ciloleucel were reviewed until disease relapse, death, or a maximum of 60 days after infusion. Baseline characteristics and laboratory values were abstracted prior to lymphodepleting chemotherapy. GCSF support was originally prescribed when the absolute neutrophil count (ANC) declined below 500 cells/mm3 and discontinued when the ANC exceeded 1000 cells/mm3 (neutropenia) for 2 consecutive days. A practice change was made where GCSF was recommended only in those with febrile neutropenia and an increased concern for infection. The primary endpoint was the difference in the total days of neutropenia for patients receiving and not receiving GCSF. Secondary outcomes compared total days of severe neutropenia, number of neutropenia episodes, infection rates by GCSF use, and outcomes by protocol change. Neutropenia and severe neutropenia were defined as an ANC below 500 cells/mm3 and 100 cells/mm3, respectively. Updated data with more patients will be presented at the conference. Results: The 60 included patients had a median age of 59 (IQR: 44, 63) years, 38 (63%) were male and 53 (88%) were Caucasian. Significantly fewer patients were prescribed GCSF according to infection-related concerns compared to ANC-based indication, 18% vs. 94%, p<0.001. Because only 3 subjects received GCSF based on infection-related concerns, results based on GCSF use versus no use is shown here. GCSF was prescribed to 35 (58%) patients for a median of 8 (IQR: 6, 12) doses with a median cumulative dosage of 3840 mcg (IQR 2100-5400) and median time to first dose of 3 days (IQR: 1, 4) post CAR T-cell infusion. Table 1 displays additional baseline characteristics and laboratory parameters according to GCSF support utilization. GCSF prescribed: Table 2 displays outcomes by GCSF use. Total days of neutropenia were similar between groups (13 vs. 16, p=0.52) with a trend towards significantly fewer days of severe neutropenia when prescribed GCSF (6 vs. 9, p=0.129). Patients prescribed GCSF were more likely to experience multiple episodes of neutropenia (83% vs. 43% p=0.002) with a significantly greater median number of episodes (3 vs. 1, p=0.002) when compared to those not prescribed GCSF. GCSF use significantly decreased the median days of the first neutropenia episode (6 vs. 12, p=0.001). There was a trend for decreased median days of severe neutropenia in the first episode with GCSF (5.0 vs. 8.0, p=0.236). Figure 1 displays a trend towards a lower overall risk of infection (HR 0.55, 95%CI: 0.16-1.87, p=0.34) and lower risk of bacterial infection (HR: 0.49, 95% CI: 0.18-1.31, p=0.15); however, these were not statistically significant. Conclusion: Patients prescribed GCSF according to ANC-based indication were significantly more likely to experience multiple neutropenia episodes; however, duration of first neutropenic episode and days of severe neutropenia during the first neutropenic episode were significantly reduced. Interestingly, the total days of neutropenia and severe neutropenia were similar between groups. It is possible that using the parameter of ANC more than 1000 cells/mm3 for 2 consecutive days is not the optimal criteria for stopping GCSF. Risk of overall and bacterial infection was lower with ANC-based initiation of GCSF, although non-significant likely due to small sample size. The potential benefit for using CSF and the optimal timing after CAR T-cell infusion requires further, rigorous, prospective investigation. Disclosures Ansell: ADC Therapeutics: Research Funding; Trillium: Research Funding; Affimed: Research Funding; Regeneron: Research Funding; AI Therapeutics: Research Funding; Takeda: Research Funding; Seattle Genetics: Research Funding; Bristol Myers Squibb: Research Funding. Bennani:Purdue Pharma: Other: Advisory Board; Kite/Gilead: Research Funding; Affimed: Research Funding; Verastem: Other: Advisory Board. Lin:Kite, a Gilead Company: Consultancy, Research Funding; Vineti: Consultancy; Sorrento: Consultancy, Membership on an entity's Board of Directors or advisory committees; Gamida Cells: Consultancy; Takeda: Research Funding; Merck: Research Funding; Legend BioTech: Consultancy; Juno: Consultancy; Bluebird Bio: Consultancy, Research Funding; Celgene: Consultancy, Research Funding; Novartis: Consultancy; Janssen: Consultancy, Research Funding.

scholarly journals Monocytopenia in clozapine-induced agranulocytosis: insights into pathophysiology and treatment

2019 ◽  
Vol 12 (1) ◽  
pp. bcr-2018-226016 ◽  
Author(s):  
Rajvi Patel ◽  
Ateaya Lima ◽  
Christopher Burke ◽  
Mark Hoffman
Keyword(s):  
Absolute Neutrophil Count ◽  
Monocyte Count ◽  
Granulocyte Colony Stimulating Factor ◽  
Colony Stimulating Factor ◽  
Gm Csf ◽  
The Third ◽  
Colony Forming Unit ◽  
History Of ◽  
The Impact ◽  
Stimulating Factor

A 26-year-old man with history of schizophrenia was admitted for neutropaenia. He was started on clozapine 3 months prior to admission. As a result he had weekly monitoring of his blood counts and on day of admission was noted to have an absolute neutrophil count (ANC) of 450 cells/μL. He was admitted for clozapine-induced agranulocytosis. Clozapine was held and the patient was started on granulocyte colony-stimulating factor (G-CSF) filgrastim and received two doses without any signs of ANC recovery. On further review, it was noted that the absolute monocyte count (AMC) was also low and tracked with the trend of ANC. We then theorised that the impact of clozapine was on a haematopoietic precursor (colony-forming unit granulocyte-macrophage, CFU-GM) which gives rise to both monocytic and myeloid lineages. Therefore, sargramostim GM-CSF was started. After two doses, the ANC and AMC started trending up and by the third dose, both counts had fully recovered. He was discharged from the hospital and there are no plans to rechallenge with clozapine. Thus, we demonstrate a case of monocytopenia accompanying clozapine-induced agranulocytosis with successful use of GM-CSF. At least in this case, the target of the clozapine injury appears to be the CFU-GM, explaining the rapid and full response to GM-CSF after lack of response to G-CSF.

Evaluation of neutropenia-related outcomes in Hodgkin's lymphoma patients with moderate or severe neutropenia who received ABVD chemotherapy without using granulocyte-colony stimulating factor

2019 ◽  
Vol 26 (4) ◽  
pp. 929-932
Author(s):  
Alparslan Merdin ◽  
Merih Kızıl Çakar ◽  
Mehmet Sinan Dal ◽  
Duygu Mert ◽  
Jale Yıldız ◽  
...  
Keyword(s):  
Neutrophil Count ◽  
Significant Relationship ◽  
Hodgkin’S Lymphoma ◽  
Lung Toxicity ◽  
Hodgkin's Lymphoma ◽  
Severe Neutropenia ◽  
Granulocyte Colony Stimulating Factor ◽  
Colony Stimulating Factor ◽  
Stimulating Factor ◽  
Abvd Chemotherapy

Objective To evaluate the possible neutropenia-related effects of administering adriamycin [doxorubicin], bleomycin, vinblastin, dacarbazine (ABVD) chemotherapy in Hodgkin’s lymphoma patients with moderate or severe neutropenia without granulocyte-colony stimulating factor supplementation. Methods This study evaluated neutropenia-related outcomes and the need for granulocyte-colony stimulating factor use during the periods between chemotherapy rounds. Forty-three rounds of ABVD chemotherapy were evaluated in the study. The outcomes that could be related to neutropenia were analyzed. In addition, rounds of ABVD chemotherapy given in the presence of severe neutropenia were compared with ABVD chemotherapy rounds given in the presence of moderate neutropenia in terms of neutropenia-related outcomes and the need for granulocyte-colony stimulating factor use. The study only included patients with classical Hodgkin's disease (lymphoma). Patients with a final neutrophil count of <1 × 103 cells/µL (<1000 cells/µL) prior to chemotherapy round and those receiving ABVD chemotherapy for Hodgkin’s lymphoma were included in the study. Results We observed that none of the patients with moderate neutropenia before the start of chemotherapy round needed granulocyte-colony stimulating factor, and four patients with severe neutropenia prior to the start of chemotherapy round required granulocyte-colony stimulating factor. However, there was no statistically significant relationship between the severity of neutropenia (in terms of moderate and severe) before chemotherapy and granulocyte-colony stimulating factor requirement after chemotherapy (p> 0.05). Furthermore, none of the patients included in the study had bleomycin-related lung toxicity during the treatment periods included in the study. Conclusion Administering ABVD chemotherapy to patients with moderate neutropenia seems to be safe.

scholarly journals S1. CLOZAPINE RECHALLENGE FOLLOWING NEUTROPENIA USING GRANULOCYTE COLONY-STIMULATING FACTOR: A QUEBEC CASE SERIES

2020 ◽  
Vol 46 (Supplement_1) ◽  
pp. S30-S30
Author(s):  
Laurent Béchard ◽  
Olivier Corbeil ◽  
Maude Plante ◽  
Marc-André Thivierge ◽  
Charles-Émile Lafrenière ◽  
...  
Keyword(s):  
Neutrophil Count ◽  
Demographic Data ◽  
Case Series ◽  
Granulocyte Colony Stimulating Factor ◽  
Colony Stimulating Factor ◽  
Treatment Resistant ◽  
Previous Response ◽  
Response Level ◽  
Clozapine Treatment ◽  
Stimulating Factor

Abstract Background Clozapine possesses unique efficacy profile in treatment-resistant schizophrenia but is associated with neutropenia and agranulocytosis, in respectively, 3% and 0.7% of exposed patients. Granulocyte colony-stimulating factor (G-CSF) has been used to allow clozapine continuation or rechallenge in such situation (1,2). Methods We aim to describe the use of G-CSF to maintain clozapine despite neutropenia or agranulocytosis in treatment resistant schizophrenia patients in Quebec province, Canada. A national clozapine hematological monitoring database was consulted to identify all patients who have had red event (neutrophil count &lt; 1,5 threshold) since 2004 in Quebec and was cross-referenced with hospital pharmacy software to identify patients who have received at least one dose of G-CSF while been exposed to clozapine All patients with an active cancer diagnosis while taking clozapine and G-CSF were excluded. A group of pharmacists specialized in psychiatry in Quebec was also contacted to ensure selecting all cases in the province. In additional to demographic data and clozapine and G-CSF details, Clinical Global Impression severity scale (CGI-S) was used to evaluate psychopathology severity during four critical turning points: before and after clozapine introduction, after agranulocytosis episode and after clozapine rechallenge. All data were collected retrospectively, using patient’s medical files, from January to July 2019. Results Eight (8) patients (5 males, 3 females), Caucasian, mean age 48 years old, with clozapine median exposition of 4.8 years, were identified. In 7/8 of those, G-CSF was used according to an “as required strategy”, i.e., whenever the patient’s neutrophil count dropped below a pre-determined threshold, varying according to patient between 0,8 à 1,5. In the other patient, a 3-weekly doses were preventively administered. Despite this, a mean number of 4 red events (ranging from 1 to 10 events) were subsequently observed in those patients, leading to clozapine cessation in 4/8 patients. One other patient responded to G-CSF but the clinical team felt uncomfortable to maintain clozapine in such circumstances. No complication (infection for instance) due to low neutrophil counts was observed nor any significant side effect related to G-CSF. However, in all these cases, while clozapine treatment was associated with clinically significant improvement of psychopathology (mean CGI-S decreased from 5.5 to 3.4), clozapine cessation led to an important psychotic deterioration (mean CGI-S of 6.2) at follow up. Fortunately, in patients successfully rechallenged (3/8), a strong clinical improvement was observed, with return to previous response level observed. Discussion To our knowledge, this is the largest case series of clozapine rechallenge using G-CSF and adds to the 39 already described cases in which G-CSF was concomitantly used with clozapine (1,2). While an “as required” strategy was mainly used here, a different prophylactic G-CSF use may have led to higher rates of clozapine maintenance, despite red codes, which provides the impetus for further studies. Reference

scholarly journals Blood mononuclear cells from patients with severe congenital neutropenia are capable of producing granulocyte colony-stimulating factor

Blood ◽  
1991 ◽  
Vol 77 (6) ◽  
pp. 1234-1237 ◽  
Author(s):  
T Pietsch ◽  
C Buhrer ◽  
K Mempel ◽  
T Menzel ◽  
U Steffens ◽  
...  
Keyword(s):  
Mononuclear Cells ◽  
Leukemia Cell Line ◽  
Severe Neutropenia ◽  
Granulocyte Colony Stimulating Factor ◽  
Colony Stimulating Factor ◽  
Severe Congenital Neutropenia ◽  
Congenital Neutropenia ◽  
Blood Mononuclear Cells ◽  
Stimulating Factor

Abstract Severe congenital neutropenia (SCN) is a disorder of myelopoiesis characterized by severe neutropenia or absence of blood neutrophils secondary to a maturational arrest at the level of promyelocytes. We examined peripheral blood mononuclear cells (PBMC) of SCN patients who demonstrated normalization of their blood neutrophil counts in a phase II clinical study with recombinant human granulocyte colony-stimulating factor (rhG-CSF). When stimulated in vitro with bacterial lipopolysaccharides (LPS), PBMC of those SCN patients produced G-CSF activity, as judged by proliferation induction of the murine leukemia cell line, NFS-60. Western and Northern blot analysis showed G-CSF protein and G-CSF-mRNA indistinguishable in size from those of normal controls. We conclude that PBMC of the SCN patients tested are capable of synthesizing and secreting biologically active G-CSF in vitro.

Once Per Cycle Pegfilgrastim Versus Daily Filgrastim in Pediatric Patients with Ewing Sarcoma.

Blood ◽  
2004 ◽  
Vol 104 (11) ◽  
pp. 2919-2919
Author(s):  
Gerald Wendelin ◽  
Herwig Lackner ◽  
Wolfgang Schwinger ◽  
Petra Sovinz ◽  
Christian Urban
Keyword(s):  
Ewing Sarcoma ◽  
Pediatric Patients ◽  
Actinomycin D ◽  
Single Injection ◽  
Severe Neutropenia ◽  
Granulocyte Colony Stimulating Factor ◽  
Subcutaneous Injections ◽  
Comparable Effect ◽  
Chemotherapy Patients ◽  
Stimulating Factor

Abstract The administration of the recombinant human granulocyte colony-stimulating factor (rhG-CSF) Filgrastim for reducing the duration of severe neutropenia after cytotoxic chemotherapy has become an important part of oncologic supportive care. Due to the short serum half-life Filgrastim has to be administrated daily by subcutaneous injections. Frequent injections however mark a problem in pediatric patients. Studies in adult patients have shown a comparable effect of the new long lasting rhG-CSF Pegfilgrastim which has to be administrated only once per cycle. In the current study the effects of Pegfilgrastim in pediatric patients were analysed. Five patients (10–16 years) with Ewing sarcoma were treated in a cross over study design alternately with Pegfilgrastim and Filgrastim following the EURO E.W.I.N.G. 99 protocol. Starting on day 4 after chemotherapy patients received Filgrastim 10μg/kg daily by subcutaneous injection until an absolute neutrophil count (ANC) >1000/μl after the expected nadir. Pegfilgrastim 100μg/kg was administrated on day 4 once per cycle subcutaneously. In 3 patients the stimulation with rhG-CSF was performed after each of the 6 preoperative VIDE-(Vincristin, Ifosfamide, Doxorubicin, Etoposide) cycles, in 2 patients after 8 postoperative VAI-(Vincristin, Actinomycin D, Ifosfamide), and in 2 patients after 7 postoperative VAC-(Vincristin, Actinomycin D, Cyclophosphamide) cycles of the EURO-E.W.I.N.G. 99 protocol. The duration of grade 4 neutropenia after single administration of Pegfilgrastim was 2,8 ±3,1 (0–10) days, after daily administration of Filgrastim 3,1 ± 2,7 (0–8) days. The number of days with a body temperature over 38 degrees and grade 4 neutropenia at the same time was 0,9 ±1,5 (0–6) after Pegfilgrastim and 0,9± 1,4 (0–4) after Filgrastim. Filgrastim had to be injected 6,7 ± 1,8 (3–10) times per cycle. Bone pain associated with Pegfilgrastim was noted in only one patient. Costs for Pegfilgrastim were 16% lower than for Filgrastim. We conclude that in pediatric patients with Ewing sarcoma the duration of severe neutropenia and number of days with febrile neutropenia after once per cycle Pegfilgrastim and daily Filgrastim are comparable. By using Pegfilgrastim the number of subcutaneous injections can be reduced to one single injection and costs can be lowered.

Recombinant Albumin-Partnering Technology: Development Of Balugrastim, a Novel Long-Acting Granulocyte Colony-Stimulating Factor

Blood ◽  
2013 ◽  
Vol 122 (21) ◽  
pp. 4854-4854 ◽  
Author(s):  
Noa Avisar ◽  
Laurie Pukac ◽  
Liat Adar ◽  
Steve Barash ◽  
Shane Clark ◽  
...  
Keyword(s):  
Half Life ◽  
Rational Design ◽  
Severe Neutropenia ◽  
Carrier Protein ◽  
Granulocyte Colony Stimulating Factor ◽  
Colony Stimulating Factor ◽  
Myelosuppressive Chemotherapy ◽  
Patients With Cancer ◽  
Long Acting ◽  
Stimulating Factor

Abstract Introduction Various strategies have been used to extend the half-life of therapeutic proteins, including genetic fusion with carrier proteins. One such carrier protein is human serum albumin (HSA), a benign protein with minimal intrinsic biologic activity that is naturally present in the circulation at a high concentration. It has a long half-life (≈19 days in humans) and is highly soluble. Recombinant HSA produced from yeast retains the beneficial stabilizing properties of HSA while minimizing the potential disadvantages of a serum-derived product. Balugrastim, a novel, long-acting recombinant protein composed of HSA and human granulocyte colony-stimulating factor (G-CSF), was developed for once-per-cycle subcutaneous (SC) administration to provide a novel option for the prevention of severe neutropenia in patients with cancer receiving myelosuppressive chemotherapy. The rational design of balugrastim, differences in its protein chemistry compared with pegfilgrastim, and the clinical and practical implications are presented here. Methods During the design phase of balugrastim, HSA was deemed an ideal candidate as a carrier protein because of its wide distribution in the body, long half-life, and low potential for affecting biological activity of G-CSF. A highly engineered proprietary yeast strain was chosen to achieve high levels of expression and quality. Balugrastim is manufactured using recombinant DNA technology in the yeast Saccharomyces cerevisiae in contrast to pegfilgrastim, which is a PEGylated form of a G-CSF expressed in the bacterium Escherichia coli and then modified by chemical conjugation to polyethylene glycol. Balugrastim was purified using a combination of ion exchange and affinity and chromatography techniques. For clinical testing, sensitive immunogenicity and serum concentration assays were developed for the product. Results The manufacturing process produces balugrastim, a 759-amino-acid monomeric protein with a molecular mass of ≈85 kDa. It is a single continuous polypeptide chain in which residues 1–585 correspond to HSA and residues 586–759 correspond to the amino acid sequence of human G-CSF, connected via a peptide bond. The purified protein is >95% pure as determined by N-terminal sequencing. The result is a highly homogeneous product. The manufacturing process is straightforward, requiring no reformulations, additional chemical modifications, or secondary manufacturing, and is a scalable, modular production system. Balugrastim has a pharmacodynamic profile comparable to that of pegfilgrastim. In a clinical trial comparing balugrastim with pegfilgrastim in patients with breast cancer, the half-life of balugrastim 40 mg SC administered once per cycle was 37.7 hours, maximum plasma concentration was 875 ng/mL, and mean area under the concentration–time curve over 144 hours was 60321 h•ng/mL, providing sustained activity in the therapeutic window and stable blood levels (Pukac, MASCC/ISOO, 2012). Corresponding values for pegfilgrastim 6 mg SC were 47.1 hours, 164 ng/mL, and 11554 h•ng/mL, respectively. In this study, and in a randomized phase III trial in patients with breast cancer, balugrastim was noninferior to pegfilgrastim, with a safety profile similar to that of pegfilgrastim and low incidence of immunogenicity (Gladkov, ASCO, 2011). Conclusions Albumin partnering is an established technology used to generate innovative, half-life extended products. This technology formed the basis for the rational design for balugrastim, a novel once-per-cycle G-CSF for the prevention of severe neutropenia in patients with cancer receiving myelosuppressive chemotherapy. The technology provides balugrastim with several advantages, including a consistent, high-quality product with low immunogenic potential and an extended half-life that permits once-per-chemotherapy cycle administration. The low viscosity of balugrastim permits small needle size (29 gauge). Balugrastim, developed as an alternative to pegfilgrastim, has been shown to be noninferior to pegfilgrastim in clinical trials. Disclosures: Avisar: Teva Pharmaceuticals, Inc: Employment. Pukac:Teva Pharmaceuticals, Inc: Employment. Adar:Teva Pharmaceuticals, Inc: Employment. Barash:Teva Pharmaceuticals, Inc: Employment. Clark:Teva Pharmaceuticals, Inc: Employment. Liu:Teva Pharmaceuticals, Inc: Employment. Bock:Teva Pharmaceuticals, Inc: Employment. Shen:Teva Pharmaceuticals, Inc: Employment.

Copper deficiency masquerading as myelodysplastic syndrome

Blood ◽  
2002 ◽  
Vol 100 (4) ◽  
pp. 1493-1495 ◽  
Author(s):  
Xylina T. Gregg ◽  
Vishnu Reddy ◽  
Josef T. Prchal
Keyword(s):  
Myelodysplastic Syndrome ◽  
Copper Deficiency ◽  
Severe Neutropenia ◽  
Granulocyte Colony Stimulating Factor ◽  
Colony Stimulating Factor ◽  
Billroth Ii ◽  
Morphologic Characteristics ◽  
Red Blood Cell Transfusions ◽  
Copper Therapy ◽  
Stimulating Factor

We describe a woman with severe neutropenia and dependency on red blood cell transfusions who had previously undergone Billroth II surgery and whose bone marrow (BM) showed morphologic characteristics typical of myelodysplastic syndrome (MDS) with ringed sideroblasts. She had transient reversal of anemia and severe neutropenia after therapy with erythropoietin and granulocyte colony-stimulating factor. Because of relapse while receiving growth factors, the patient was referred for allogeneic BM transplantation. A pretransplantation nutritional evaluation revealed severe copper deficiency, and her hematologic abnormalities resolved fully with copper therapy. This case shows that copper deficiency should be an integral part of the differential diagnosis of sideroblastic MDS, even in patients not requiring parenteral nutrition.

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