Is obstructive sleep apnoea syndrome really one of the causes of secondary polycythaemia?

Solmaz, Soner; Duksal, Faysal; Ganidağlı, Sencer

doi:10.1179/1607845414y.0000000170

Cited by 20 publications

(23 citation statements)

References 9 publications

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“…However, a rapid change of oxygen tension from hypoxia to normoxia rectifies the hypoxia-induced RBC growth, preferentially eliminating the new RBC or neocytes, a process coined as neocytolysis ( Alfrey et al, 1997 ; Risso et al, 2007 ). This would be the reason that OSA patients, with significant cycles of severe hypoxia during sleep, do not present polycythaemia ( Solmaz et al, 2015 ; Song et al, 2017 ). We think this also would be the reason that CIH guinea pigs have identical haematocrit to normoxic control ones, in spite of a significantly higher level of EPO (214 vs. 141 mU/mL in C); the increased EPO level in CIH group should be considered as a HIF-mediated adaptive response to CIH.…”

Section: Discussionmentioning

confidence: 99%

Guinea Pig as a Model to Study the Carotid Body Mediated Chronic Intermittent Hypoxia Effects

et al. 2018

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Clinical and experimental evidence indicates a positive correlation between chronic intermittent hypoxia (CIH), increased carotid body (CB) chemosensitivity, enhanced sympatho-respiratory coupling and arterial hypertension and cardiovascular disease. Several groups have reported that both the afferent and efferent arms of the CB chemo-reflex are enhanced in CIH animal models through the oscillatory CB activation by recurrent hypoxia/reoxygenation episodes. Accordingly, CB ablation or denervation results in the reduction of these effects. To date, no studies have determined the effects of CIH treatment in chemo-reflex sensitization in guinea pig, a rodent with a hypofunctional CB and lacking ventilatory responses to hypoxia. We hypothesized that the lack of CB hypoxia response in guinea pig would suppress chemo-reflex sensitization and thereby would attenuate or eliminate respiratory, sympathetic and cardiovascular effects of CIH treatment. The main purpose of this study was to assess if guinea pig CB undergoes overactivation by CIH and to correlate CIH effects on CB chemoreceptors with cardiovascular and respiratory responses to hypoxia. We measured CB secretory activity, ventilatory parameters, systemic arterial pressure and sympathetic activity, basal and in response to acute hypoxia in two groups of animals: control and 30 days CIH exposed male guinea pigs. Our results indicated that CIH guinea pig CB lacks activity elicited by acute hypoxia measured as catecholamine (CA) secretory response or intracellular calcium transients. Plethysmography data showed that only severe hypoxia (7% O2) and hypercapnia (5% CO2) induced a significant increased ventilatory response in CIH animals, together with higher oxygen consumption. Therefore, CIH exposure blunted hyperventilation to hypoxia and hypercapnia normalized to oxygen consumption. Increase in plasma CA and superior cervical ganglion CA content was found, implying a CIH induced sympathetic hyperactivity. CIH promoted cardiovascular adjustments by increasing heart rate and mean arterial blood pressure without cardiac ventricle hypertrophy. In conclusion, CIH does not sensitize CB chemoreceptor response to hypoxia but promotes cardiovascular adjustments probably not mediated by the CB. Guinea pigs could represent an interesting model to elucidate the mechanisms that underlie the long-term effects of CIH exposure to provide evidence for the role of the CB mediating pathological effects in sleep apnea diseases.

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Section: Discussionmentioning

confidence: 99%

Guinea Pig as a Model to Study the Carotid Body Mediated Chronic Intermittent Hypoxia Effects

et al. 2018

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“…163 In addition, OSA severity correlates modestly with hematocrit level, 164 although the disease rarely leads to polycythemia. 165,166 Taken together, these findings suggest that there may be patients with OSA who have inadequate tissue oxygenation but more invasive assessments would be needed to confirm this hypothesis.…”

Section: Tissue Hypoxiamentioning

confidence: 95%

Metabolic dysfunction in obstructive sleep apnea: A critical examination of underlying mechanisms

Mesarwi

Sharma

Jun

et al. 2014

Sleep and Biological Rhythms

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It has recently become clear that obstructive sleep apnea (OSA) is an independent risk factor for the development of metabolic syndrome, a disorder of defective energy storage and use. Several mechanisms have been proposed to explain this finding, drawing upon the characteristics that define OSA. In particular, intermittent hypoxia, sleep fragmentation, elevated sympathetic tone, and oxidative stress – all consequences of OSA – have been implicated in the progression of poor metabolic outcomes in OSA. In this review we examine the evidence to support each of these disease manifestations of OSA as a unique risk for metabolic dysfunction. Tissue hypoxia and sleep fragmentation are each directly connected to insulin resistance and hypertension, and each of these also may increase sympathetic tone, resulting in defective glucose homeostasis, excessive lipolysis, and elevated blood pressure. Oxidative stress further worsens insulin resistance and in turn, metabolic dysfunction also increases oxidative stress. However, despite many studies linking each of these individual components of OSA to the development of metabolic syndrome, there are very few reports that actually provide a coherent narrative about the mechanism underlying metabolic dysfunction in OSA.

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“…Furthermore, IH resulting from sleep apnea was suspected to induce polycythemia. However, Solmaz et al recently suggested that OSA rarely causes secondary polycythemia ( 93 ). Similarly, King et al commented that OSA does not lead to clinically significant erythrocytosis ( 94 ).…”

Section: Potential Confounding Factors For Intermittent Hypoxic Trainmentioning

confidence: 99%

Intermittent Hypoxia in Childhood: The Harmful Consequences Versus Potential Benefits of Therapeutic Uses

Serebrovskaya

2015

Front. Pediatr.

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Intermittent hypoxia (IH) often occurs in early infancy in both preterm and term infants and especially at 36–44 weeks postmenstrual age. These episodes of IH could result from sleep-disordered breathing or may be temporally unrelated to apnea or bradycardia events. There are numerous reports indicating adverse effects of IH on development, behavior, academic achievement, and cognition in children with sleep apnea syndrome. It remains uncertain about the exact causative relationship between the neurocognitive and behavioral morbidities and IH and/or its associated sleep fragmentation. On the other hand, well-controlled and moderate IH conditioning/training has been used in sick children for treating their various forms of bronchial asthma, allergic dermatoses, autoimmune thyroiditis, cerebral palsy, and obesity. This review article provides an updated and impartial analysis on the currently available evidence in supporting either side of the seemingly contradictory scenarios. We wish to stimulate a comprehensive understanding of such a complex physiological phenomenon as intermittent hypoxia, which may be accompanied by other confounding factors (e.g., hypercapnia, polycythemia), in order to prevent or reduce its harmful consequences, while maximizing its potential utility as an effective therapeutic tool in pediatric patients.

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Is obstructive sleep apnoea syndrome really one of the causes of secondary polycythaemia?

Abstract: We think that OSA is very rarely the reason for secondary polycythaemia.

Cited by 20 publications

References 9 publications

Guinea Pig as a Model to Study the Carotid Body Mediated Chronic Intermittent Hypoxia Effects

Guinea Pig as a Model to Study the Carotid Body Mediated Chronic Intermittent Hypoxia Effects

Metabolic dysfunction in obstructive sleep apnea: A critical examination of underlying mechanisms

Intermittent Hypoxia in Childhood: The Harmful Consequences Versus Potential Benefits of Therapeutic Uses

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