LETTERS to the EDITORAssociation between platelet microthrombi and finger clubbing
References (10)
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Megakaryocyte and platelet clumps as the cause of finger clubbing
Lancet
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Finger clubbing
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Finger clubbing and tumour necrosis factor &agr
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Is clubbing a growth disorder?
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Cited by (28)
Clubbing in patients with fibrotic interstitial lung diseases
2017, Respiratory MedicineCitation Excerpt :The exact cause of clubbing is unknown, though several theories have been proposed. The most plausible cause seems to be the “platelet” theory, which is supported by outcomes of various studies [9,21–24]. In this theory, clubbing is explained by a dysfunction of the fragmentation of megakaryocytes into platelets in the lungs.
Periostitis and Hypertrophic Pulmonary Osteoarthropathy: Report of 2 Cases and Review of the Literature
2009, Seminars in Arthritis and RheumatismCitation Excerpt :The imaging studies of clubbed fingers show increased blood flow. Pathologically, fingertip cutaneous vessels have diffuse endothelial hyperplasia with partial occlusion of the capillary lumen, a pericapillary lymphohistocytic infiltrate, hyalinosis, sclerosis with thickening/packing of collagen fibers, and sebaceous/eccrine hypertrophy (66). The vessels in the histologic sections of clubbed fingers are frequently dilated and contain platelet clusters (67).
Clubbing: An update on diagnosis, differential diagnosis, pathophysiology, and clinical relevance
2005, Journal of the American Academy of DermatologyCitation Excerpt :Patients with cyanotic heart disease and secondary HOA had a lower platelet count and higher mean platelet volume than control subjects, indicating larger platelets and less fragmentation of megakaryocytes in the lungs.62 Necropsy of clubbed fingers showed more platelet microthrombi than in control subjects, indicating more platelet activation.63 Patients with primary and secondary HOA had greater PDGF levels than control subjects and patients with lung disease without HOA.64
Pathogenesis of the glomerular abnormality in cyanotic congenital heart disease
2000, American Journal of CardiologyCitation Excerpt :It has been argued persuasively that right-to-left shunts deliver whole megakaryocytes from the systemic venous to the systemic arterial circulation where they may lodge in capillaries of the digits and periosteum, release PDGF and TGF-β, and cause clubbing and hypertrophic osteoarthropathy.27,28 Megakaryocytic nuclei have been found at necropsy in clubbed fingers of cyanotic patients.29 We present evidence that the nonvascular glomerular abnormality in CCHD may result from locally released PDGF and TGF-β in cytoplasmic granules of systemic venous megakaryocytes that are shunted into the systemic arterial circulation with their cytoplasm and fortuitously impact in glomerular capillaries.
Folic Acid improves Phenytoin Pharmacokinetics
1995, Journal of the American Dietetic Association