C5.10 Haematology and biochemistry

Polycythaemia should be confirmed as being secondary to COPD by blood gas measurement that demonstrates hypoxaemia. The possibility of sleep apnoea or hypoventi­lation should be considered if polycythaemia is present but oxygen desaturation or hypoxaemia on arterial blood gas tests are absent when the patient is awake.

Hyperthyroidism and acidosis are associated with breath­lessness. Hyperventilation states are associated with respira­tory alkalosis. Hypothyroidism aggravates obstructive sleep apnoea. Harrison et al 2014 performed a multicentre prospective study of exacerbations of COPD requiring hospital admission in 1343 patients with spirometry confirmed COPD. The authors reported the novel finding of an association between thrombocytosis (>400/mm3 on admission) and mortality. Thrombocytosis (after controlling for confounders) was associated with an increased 1 year all-cause mortality and an increased in hospital mortality (OR 1.53 (95% CI 1.03 to 2.29, p=0.030) and OR 2.37 (95% CI 1.29 to 4.34, p=0.005)) respectively (Harrison 2014) [evidence level III-2].

The prevalence of severe homozygous (ZZ) alpha1 antitrypsin deficiency has been estimated at between 1/4,348 and 1/5,139 in European populations (Blanco 2006). Available data from 15 cohorts in Australia and New Zealand suggest that the prevalence of affected individuals is around 1/4000 (de Serres 2002). Although 75 to 85% of such individuals will develop emphysema, tobacco smoking is still the most important risk factor for COPD even in this group. Targeted screening suggests between 1.0 – 4.5% of patients with COPD have underlying severe a1-AT deficiency (American Thoracic Society/European Respiratory Society 2003). The index of suspicion should be high in younger Caucasian patients with predominantly basal disease and a family history. The diagnosis can be made by measuring serum levels of alpha1 antitrypsin and if reduced, genotyping should be performed.