Elsevier

The Lancet

Volume 338, Issue 8762, 3 August 1991, Pages 313-314
The Lancet

LETTERS to the EDITOR
Association between platelet microthrombi and finger clubbing

https://doi.org/10.1016/0140-6736(91)90452-UGet rights and content

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  • Clubbing in patients with fibrotic interstitial lung diseases

    2017, Respiratory Medicine
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    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 Rheumatism
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    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 Dermatology
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    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 Cardiology
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    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
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