Chronic myeloid leukaemia and sickle cell disease: could imatinib prevent vaso‐occlusive crisis?

Stojanovic, Katia Stankovic; Thiolière, Brigitte; Garandeau, Elzbzieta; Lecomte, Isabelle; Bachmeyer, Claude; Lionnet, François

doi:10.1111/j.1365-2141.2011.08670.x

Cited by 31 publications

(20 citation statements)

References 7 publications

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“…The present case series suggests for the first time the presence of MCAS as a factor in the morbidity of poor-phenotype SCA. As hypothesized by Vincent et al 9 and others, 45 , 46 several patients in the present series seem to have been significantly helped by therapy targeted at MC mediator production or action. Although it is interesting that current high-end estimates of the portion of the general population harboring MCAS (14%–17%) 41 , 42 roughly correspond to the portion of the SCA population suffering a poor phenotype of SCA, specific prospective studies will be needed to confirm the portion of the SCA population truly harboring MCAS.…”

Section: Discussionsupporting

confidence: 73%

Mast Cell Activation Syndrome as a Significant Comorbidity in Sickle Cell Disease

Afrin

2014

The American Journal of the Medical Sciences

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Section: Discussionsupporting

confidence: 73%

Mast Cell Activation Syndrome as a Significant Comorbidity in Sickle Cell Disease

Afrin

2014

The American Journal of the Medical Sciences

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“…Although the evidence is limited, clinical observations support a role for mast cells in chronic and acute pain in SCD. In a case report, a patient with SCD having multiple VOCs per year stopped having VOCs with imatinib treatment . On discontinuation of imatinib, VOCs recurred.…”

Section: Mast Cell Activity In Pain In Sickle Cell Diseasementioning

confidence: 99%

Mast cell‐neural interactions contribute to pain and itch

Gupta

Harvima

2018

Immunological Reviews

205

189

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Mast cells are best recognized for their role in allergy and anaphylaxis, but increasing evidence supports their role in neurogenic inflammation leading to pain and itch. Mast cells act as a "power house" by releasing algogenic and pruritogenic mediators, which initiate a reciprocal communication with specific nociceptors on sensory nerve fibers. Consequently, nerve fibers release inflammatory and vasoactive neuropeptides, which in turn activate mast cells in a feedback mechanism, thus promoting a vicious cycle of mast cell and nociceptor activation leading to neurogenic inflammation and pain/pruritus. Mechanisms underlying mast cell differentiation, activation, and intercellular interactions with inflammatory, vascular, and neural systems are deeply influenced by their microenvironment, imparting enormous heterogeneity and complexity in understanding their contribution to pain and pruritus. Neurogenic inflammation is central to both pain and pruritus, but specific mediators released by mast cells to promote this process may vary depending upon their location, stimuli, underlying pathology, gender, and species. Therefore, in this review, we present the contribution of mast cells in pathological conditions, including distressing pruritus exacerbated by psychologic stress and experienced by the majority of patients with psoriasis and atopic dermatitis and in different pain syndromes due to mastocytosis, sickle cell disease, and cancer.

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“…The mechanism of mast cell's role in sustained hyperalgesia is based on the studies in sickle mice. However, two separate clinical studies on sickle patients show that the use of imatinib, a known mast cell inhibitor, significantly reduced painful episodes in patients with SCD [ 25 , 26 ]. Another case report showed that a sickle patient who died following an overdose of fentanyl was on fentanyl for more than 18 months and had pruritis and sickle crises type of pain for 2 days as well as ACS and respiratory depression secondary to fentanyl overdose [ 27 ].…”

Section: Complex Pathophysiology Of Scd Is Intertwined With Painmentioning

confidence: 99%

Morphine for the Treatment of Pain in Sickle Cell Disease

Gupta

Msambichaka

Ballas

et al. 2015

The Scientific World Journal

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Pain is a hallmark of sickle cell disease (SCD) and its treatment remains challenging. Opioids are the major family of analgesics that are commonly used for treating severe pain. However, these are not always effective and are associated with the liabilities of their own. The pharmacology and multiorgan side effects of opioids are rapidly emerging areas of investigation, but there remains a scarcity of clinical studies. Due to opioid-induced endothelial-, mast cell-, renal mesangial-, and epithelial-cell-specific effects and proinflammatory as well as growth influencing signaling, it is likely that when used for analgesia, opioids may have organ specific pathological effects. Experimental and clinical studies, even though extremely few, suggest that opioids may exacerbate existent organ damage and also stimulate pathologies of their own. Because of the recurrent and/or chronic use of large doses of opioids in SCD, it is critical to evaluate the role and contribution of opioids in many complications of SCD. The aim of this review is to initiate inquiry to develop strategies that may prevent the inadvertent effect of opioids on organ function in SCD, should it occur, without compromising analgesia.

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Chronic myeloid leukaemia and sickle cell disease: could imatinib prevent vaso‐occlusive crisis?

Cited by 31 publications

References 7 publications

Mast Cell Activation Syndrome as a Significant Comorbidity in Sickle Cell Disease

Mast Cell Activation Syndrome as a Significant Comorbidity in Sickle Cell Disease

Mast cell‐neural interactions contribute to pain and itch

Morphine for the Treatment of Pain in Sickle Cell Disease

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