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What causes secondary erythrocytosis?

Article by:

Christopher D Nguyen
Affiliations
  • Division of Pulmonary and Critical Care Medicine, Department of Medicine, Stanford University, Palo Alto, CA, USA
  • Stanford Sleep Medicine Center, Department of Psychiatry, Stanford University, Palo Alto, CA, USA
Jon-Erik C. Holty

Affiliations

  • Division of Pulmonary and Critical Care Medicine, Department of Medicine, Stanford University, Palo Alto, CA, USA
  • Pulmonary, Critical Care and Sleep Medicine Section, VA Palo Alto Health Care System, Palo Alto, CA, USA
  • Center for Health Policy (CHP/PCOR), Stanford University, Palo Alto, CA, USA

Correspondence

  • Corresponding author. Pulmonary, Critical Care and Sleep Section, VA Palo Alto Healthcare System, 3801 Miranda Ave. (MC 111P), Palo Alto, CA 94304, USA.

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Highlights

Clinically significant erythrocytosis appears uncommon in those with suspected/confirmed OSA. \

OSA presence and severity is not associated with hematocrit or significant erythrocytosis.

Both awake and nocturnal-hypoxemia are associated with clinically significant erythrocytosis.

Thus, nocturnal oximetry may be warranted in those with unexplained erythrocytosis.

Abstract

Background

The current literature suggests a relationship between obstructive sleep apnea (OSA) severity and hematocrit. However, the degree that OSA contributes to clinically significant erythrocytosis is uncertain. The aim of this study is to evaluate this association in a large study sample controlling for multiple confounders.

Methods

We evaluated consecutive subjects with suspected untreated OSA using multivariate analysis to test the associations between apnea-hypopnea index (AHI) and hematocrit. Subjects were evaluated with sleep studies, comprehensive sleep questionnaires, and detailed electronic medical record reviews to document their medical comorbidities, and demographic and laboratory information.

Results

1604 consecutive veterans (age 57.6 ± 13.4 years, 92% male) were included in the analysis with 77.4% diagnosed with OSA. However, few included subjects (1.6%) had clinical erythrocytosis. OSA severity defined by AHI was not associated with hematocrit or clinically significant erythrocytosis. Rather, awake oxygen saturation (-0.17 points, p < 0.001) and mean nocturnal oxygen saturation (-0.08 points, p = 0.04) were inversely proportional to hematocrit (per standardized Z-score). Other factors including active tobacco, increased alcohol ingestion and exogenous testosterone therapy were associated with higher hematocrit. Although AHI was not predictive of erythrocytosis, having severe OSA was predictive of nocturnal hypoxemia (adjusted OR 7.4, p < 0.001).

Conclusions

Hematocrit levels and presence of erythrocytosis appear not associated with OSA severity, but rather with hypoxemia as measured by awake and to a lesser extent mean nocturnal oxygen saturation. Nocturnal oximetry may provide diagnostic utility in the evaluation of unexplained secondary polycythemia and polysomongraphy may be warranted in those with unexplained nocturnal hypoxemia and erythrocytosis.