Abnormal Proliferation of the Skin and Osseous Tissue at the Distal Parts of the Extremities
Clubbing and Hypertrophic Osteoarthropathy are Different Clinical Manifestations of the Same Disease Process
Pathogenesis Involves Activation of the Platelet-Endothelial Cells, with Subsequent Release of Fibroblast Growth Factor (Platelet-Derived Growth Factor)
Pathogenesis of Primary Hypertrophic Osteoarthropathy
Elevation in Circulating Prostaglandin E2 Due to Mutation in the HPGD gene Which Encodes 15-Hydroxyprostaglandin Dehydrogenase: this is the primary enzyme responsible for prostaglandin degradation
Pathogenesis of Secondary Hypertrophic Osteoarthropathy Associated with Lung Cancer (Possible Mechanisms)
Megakaryocytes May Escape the Normal Fragmentation to Platelets in the Lung, Reaching the Distal Extremities Where they Release Growth Factors
Tumor Production and Release of a Factor Which Induces the Manifestations of Hypertrophic Osteoarthropathy (Such as Vascular Proliferation, Edema Formation, and New Bone Formation)
Possible Increase in PGE2 (Similar to that Observed in Primary Hypertrophic Osteoarthropathy)
In Cystic Fibrosis: serum prostaglandin concentrations are higher in those with clubbing compared with those without clubbing
Unresectable Lung Cancer: overproduction of PGE2 has been demonstrated
Diagnosis
X-rays of Long Bones (Tibia, Fibula)
Demonstrates Characteristic Periosteal New Bone Formation