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1.  Granulocyte Macrophage Colony-Stimulating Factor in 66 Patients with Myeloid or Lymphoid Neoplasms and Recipients of Hematopoietic Stem Cell Transplantation with Invasive Fungal Disease 
Acta haematologica  2012;129(1):26-34.
Background/Aims
Adding granulocyte macrophage colony-stimulating factor (GM-CSF) may improve the response to antifungal therapy in immunosuppressed patients with invasive fungal disease (IFD).
Methods
We retrospectively assessed 66 patients in whom GM-CSF was given during antifungal therapy.
Results
Severe neutropenia (77%) and refractory/relapsed cancer (65%) were common in the group. Prior to GM-CSF therapy, 15% of patients received high-dose corticosteroids for a median of 30 ± 16 days (median cumulative dose [c.d.], 1184 ± 1019 mg), and 9 received steroids during GM-CSF therapy for a median of 16 ± 12 days (median c.d., 230 ± 1314 mg). Mild toxic effects were noted in 9% of patients; there were no cases of cardiopulmonary toxicity. All cause deaths were observed in 68% and 48% of patients died of progressive IFD. High-dose corticosteroids prior to GM-CSF (OR, 24; 95% CI, 2.21–264.9; P ≤ 0.009), GM-CSF started in the intensive care unit (OR, 10; 95% CI, 1.66–63.8; P ≤ 0.01), concurrent granulocyte transfusions (OR, 5; 95% CI, 1.27–16.8; P ≤ 0.02), and proven/probable IFD (OR, 4; 95% CI, 1–16.2; P ≤ 0.05) predicted antifungal treatment failure.
Conclusions
GM-CSF adjuvant therapy was tolerated without serous toxicity and antifungal treatment failure remained a challenge in patients treated with high-dose systemic corticosteroids.
doi:10.1159/000342121
PMCID: PMC3622475  PMID: 23038157
invasive fungal disease; granulocyte macrophage colony-stimulating factor; stem cell transplant; leukemia; combination antifungal agents; immune suppression
2.  Hypogonadism in Patients with Sickle Cell Disease: Central or Peripheral? 
Acta haematologica  2012;128(2):10.1159/000337344.
There is conflicting evidence in the literature on the etiology of hypogonadism in patients with sickle cell disease (SCD). A cross-sectional study was done to determine whether hypogonadism in male patients with SCD is due to primary testicular failure or secondary pituitary/hypothalamic dysfunction and assess the association between hypogonadism and serum ferritin levels. Hormonal assessment for serum concentrations of testosterone, follicle stimulating hormone (FSH) and luteinizing hormone (LH) was done for 34 men with SCD and their charts were reviewed for relevant clinical variables. Eight men (24%) were classified hypogonadal based on their serum testosterone levels. These men have significantly lower LH (p = 0.001) and FSH (p = 0.01) levels than normogonadal men, indicating a central etiology. There was no significant difference between hypogonadal and normogonadal men with respect to ferritin levels (p = 0.71). Our study indicates a central etiology of hypogonadism in patients with SCD. In this small study ferritin level was not significantly related to hypogonadism.
doi:10.1159/000337344
PMCID: PMC3864664  PMID: 22678347
Ferritin; Hemoglobinopathy; Hypogonadism; Testosterone
3.  Antioxidant-Mediated Effects in a Gerbil Model of Iron Overload 
Acta haematologica  2007;118(4):193-199.
Introduction
Iron cardiomyopathy is a lethal complication of transfusion therapy in thalassemia major. Nutritional supplements decreasing cardiac iron uptake or toxicity would have clinical significance. Murine studies suggest taurine may prevent oxidative damage and inhibit Ca2+-channel-mediated iron transport. We hypothesized that taurine supplementation would decrease cardiac iron-overloaded toxicity by decreasing cardiac iron. Vitamin E and selenium served as antioxidant control.
Methods
Animals were divided into control, iron, taurine, and vitamin E/selenium groups. Following sacrifice, iron and selenium measurements, histology, and biochemical analyses were performed.
Results
No significant differences were found in heart and liver iron content between treatment groups, except for higher hepatic dry-weight iron concentrations in taurine-treated animals (p < 0.03). Serum iron increased with iron loading (751 ± 66 vs. 251 ± 54 μg/dl, p < 0.001) and with taurine (903 ± 136 μg/dl, p = 0.03).
Conclusion
Consistent with oxidative stress, iron overload increased cardiac malondialdehyde levels, decreased heart glutathione peroxidase (GPx) activity, and increased serum aspartate aminotransferase. Taurine ameliorated these changes, but only significantly for liver GPx activity. Selenium and vitamin E supplementation did not improve oxidative markers and worsened cardiac GPx activity. These results suggest that taurine acts primarily as an antioxidant rather than inhibiting iron uptake. Future studies should illuminate the complexity of these results.
doi:10.1159/000109879
PMCID: PMC2892915  PMID: 17940334
Iron overload; Taurine; Heart; Liver; Antioxidants
4.  Safety and Efficacy of Combined Chelation Therapy with Deferasirox and Deferoxamine in a Gerbil Model of Iron Overload 
Acta haematologica  2008;120(2):123-128.
Introduction
Combined therapy with deferoxamine (DFO) and deferasirox (DFX) may be performed empirically when DFX monotherapy fails. Given the lack of published data on this therapy, the study goal was to assess the safety and efficacy of combined DFO/DFX therapy in a gerbil model.
Methods
Thirty-two female Mongolian gerbils 8–10 weeks old were divided into 4 groups (sham chelated, DFO, DFX, DFO/DFX). Each received 10 weekly injections of 200 mg/kg iron dextran prior to initiation of 12 weeks of chelation. Experimental endpoints were heart and liver weights, iron concentration and histology.
Results
In the heart, there was no significant difference among the treatment groups for wet-to-dry ratio, iron concentration and iron content. DFX-treated animals exhibited lower organ weights relative to sham-chelated animals (less iron-mediated hypertrophy). DFO-treated organs did not differ from sham-chelated organs in any aspects. DFX significantly cleared hepatic iron. No additive effects were observed in the organs of DFO/DFX-treated animals.
Conclusions
Combined DFO/DFX therapy produced no detectable additive effect above DFX monotherapy in either the liver or heart, suggesting competition with spontaneous iron elimination mechanisms for chelatable iron. Combined therapy was well tolerated, but its efficacy could not be proven due to limitations in the animal model.
doi:10.1159/000174757
PMCID: PMC2884393  PMID: 19018129
Deferasirox; Deferoxamine; Iron overload

Results 1-4 (4)