Clubbing is associated with • Lung disease: •
Lung cancer •
Interstitial lung disease most commonly
idiopathic pulmonary fibrosis • Complicated
tuberculosis • Suppurative lung disease:
lung abscess,
empyema,
bronchiectasis,
cystic fibrosis •
Mesothelioma of the pleura •
Sarcoidosis • Heart disease: • Any disease featuring chronic
hypoxia •
Cyanotic heart defect (most common cardiac cause) •
Infective endocarditis •
Atrial myxoma (benign tumor) • Arteriovenous fistula or malformation • Gastrointestinal and hepatobiliary: •
Malabsorption •
Crohn's disease and
ulcerative colitis •
Cirrhosis, especially in
primary biliary cholangitis •
Hepatopulmonary syndrome, a complication of cirrhosis • Others: •
Graves' disease (autoimmune hyperthyroidism) – in this case, it is known as
thyroid acropachy • Familial and hereditary clubbing and "pseudoclubbing" (people of African descent often have what appears to be clubbing) • Vascular anomalies of the affected arm such as an
axillary artery aneurysm (in unilateral clubbing) • Primary hypertrophic osteoarthropathy Nail clubbing is not specific to
chronic obstructive pulmonary disease (COPD). Therefore, in patients with COPD and significant degrees of clubbing, a search for signs of bronchogenic carcinoma (or other causes of clubbing) might still be indicated.
Hypertrophic pulmonary osteoarthropathy of a patient with HPOA A special form of clubbing is
hypertrophic pulmonary osteoarthropathy (HPOA), known in continental Europe as Pierre Marie-Bamberger syndrome. This is the combination of clubbing and thickening of
periosteum (connective tissue lining of the bones) and
synovium (lining of joints), and is often initially diagnosed as
arthritis. It is commonly associated with lung cancer.
Primary hypertrophic osteoarthropathy Primary hypertrophic osteoarthropathy is HPOA without signs of pulmonary disease. This form has a hereditary component, although subtle cardiac abnormalities can occasionally be found. It is known eponymously as the
Touraine–Solente–Golé syndrome. This condition has been linked to mutations in the gene on the fourth chromosome (4q33-q34) coding for the enzyme
15-hydroxyprostaglandin dehydrogenase (HPGD); this leads to decreased breakdown of
prostaglandin E2 and elevated levels of this substance. ==Pathogenesis==