Molgramostim to treat SS-sickle cell leg ulcers

Pieters, RonaldC.; Rojer, RobertA.; Saleh, A.W.; Saleh, AlejandroE.C.; Duits, AshleyJ.

doi:10.1016/s0140-6736(95)90629-0

Cited by 53 publications

(31 citation statements)

References 1 publication

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“…All were cured, but the dripped dose of molgramostim was higher than our study and the treatment applied once daily [5]. The second series relied on subcutaneous injections at the ulcer margins, leading to the healing of 2/4 ulcers after 2 months [6]. …”

Section: Discussionmentioning

confidence: 99%

Topical Effectiveness of Molgramostim (GM-CSF) in Sickle Cell Leg Ulcers

Méry

Girot²,

Aractingi³

2004

Dermatology

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Background: Leg ulcers are a frequently neglected, severe complication of sickle cell disease (SCD), responsible for significant altering quality of life. The management of leg ulcers remains disappointing. Local application of recombinant human granulocyte-macrophage colony-stimulating factor has been shown to be effective in several types of chronic wound healing. Methods: We report 5 homozygous sickle cell patients with 14 leg ulcers lasting from 1 month to 6 years, treated with topical dripping of molgramostim solution. Results: Healing was obtained for 9/14 ulcers, with no local or systemic adverse reactions. Comments: Molgramostim solution appears to be an adequate therapy for SCD leg ulcers but a more conclusive evaluation will depend on larger series of patients and other types of formulations for topical applications could be even more effective in the future.

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Section: Discussionmentioning

confidence: 99%

Topical Effectiveness of Molgramostim (GM-CSF) in Sickle Cell Leg Ulcers

Méry

Girot²,

Aractingi³

2004

Dermatology

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“…Additionally, acute VOCs and acute chest syndrome are associated with high leukocyte and neutrophil counts (33). Furthermore, other reports of rapid onset of painful crises, acute chest syndrome, and death after administration of G-CSF or GM-CSF (47)(48)(49) suggest that leukocytes and neutrophils are directly involved in the pathophysiology of SCD. Both leukocytes and endothelial cells carry functional ETRs.…”

Section: Figurementioning

confidence: 99%

Endothelin receptor antagonism prevents hypoxia-induced mortality and morbidity in a mouse model of sickle-cell disease

Sabaa¹,

Franceschi²,

Bonnin³

et al. 2008

J. Clin. Invest.

124

129

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Patients with sickle-cell disease (SCD) suffer from tissue damage and life-threatening complications caused by vasoocclusive crisis (VOC). Endothelin receptors (ETRs) are mediators of one of the most potent vasoconstrictor pathways in mammals, but the relationship between vasoconstriction and VOC is not well understood. We report here that pharmacological inhibition of ETRs prevented hypoxia-induced acute VOC and organ damage in a mouse model of SCD. An in vivo ultrasonographic study of renal hemodynamics showed a substantial increase in endothelin-mediated vascular resistance during hypoxia/reoxygenation-induced VOC. This increase was reversed by administration of the dual ETR antagonist (ETRA) bosentan, which had pleiotropic beneficial effects in vivo. It prevented renal and pulmonary microvascular congestion, systemic inflammation, dense rbc formation, and infiltration of activated neutrophils into tissues with subsequent nitrative stress. Bosentan also prevented death of sickle-cell mice exposed to a severe hypoxic challenge. These findings in mice suggest that ETRA could be a potential new therapy for SCD, as it may prevent acute VOC and limit organ damage in sickle-cell patients.

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“…In early reports, severe or fatal crises have occurred in SCD patients administered with either GM-CSF or G-CSF to treat leg ulcer, mobilize hematopoietic stem cells, or correct neutropenia. [15][16][17][18] More recently, a patient was reported to have a rare co-existence of SCD and severe congenital neutropenia, exhibiting significantly alleviated disease manifestations compared with his siblings. However, when the patient received G-CSF to treat neutropenia, the course of the disease dramatically worsened.…”

Section: Neutrophils In Scdmentioning

confidence: 99%

Neutrophils, platelets, and inflammatory pathways at the nexus of sickle cell disease pathophysiology

Zhang

Manwani

et al. 2016

Blood

331

339

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Sickle cell disease (SCD) is a severe genetic blood disorder characterized by hemolytic anemia, episodic vaso-occlusion, and progressive organ damage. Current management of the disease remains symptomatic or preventative. Specific treatment targeting major complications such as vaso-occlusion is still lacking. Recent studies have identified various cellular and molecular factors that contribute to the pathophysiology of SCD. Here, we review the role of these elements and discuss the opportunities for therapeutic intervention.

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Molgramostim to treat SS-sickle cell leg ulcers

Cited by 53 publications

References 1 publication

Topical Effectiveness of Molgramostim (GM-CSF) in Sickle Cell Leg Ulcers

Topical Effectiveness of Molgramostim (GM-CSF) in Sickle Cell Leg Ulcers

Endothelin receptor antagonism prevents hypoxia-induced mortality and morbidity in a mouse model of sickle-cell disease

Neutrophils, platelets, and inflammatory pathways at the nexus of sickle cell disease pathophysiology

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