Clubbed fingers: the claws we lost?

Brouwers, Ad; Vermeij-Keers, Chr.; Zoelen, E.J.J. van; Gooren, L. J. G.

doi:10.1016/s0306-9877(03)00300-1

Cited by 7 publications

(4 citation statements)

References 15 publications

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“…The pathogenesis of digital clubbing is not known, however, fibroblasts proliferation and fibrillogenesis are the main focus of the fibrotic process, resulting in increased amount of collagen fibers [3] [8] [9]. Other suggested mechanisms include, dysregulation of the matrix molecules synthesized by the fibroblast with increased matrix deposits and increased synthesis of decorin in protein [8] [10], the higher levels of plasma growth hormone in patients than in controls [11], the return of the embryonic claw that was lost during evolution [12], and the release of platelets-derived growth factor by the trapped megakaryocytic and platelets and vascular endothelial growth factor in response to arterial hypoxaemia and subsequent increased vascularity, permeability and connective tissue changes [13].…”

Section: Discussionmentioning

confidence: 99%

Hypertrophic Osteoathropathy without Pachyderma in a Nigerian: A Case Report

Umar¹,

Adebayo²,

Abdullahi³

et al. 2015

WJCD

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Hypertrophic osteoathropathy is characterized by triad of digital clubbing, periostosis, and pachyderma. We report the case of a young male Nigerian with asymptomatic idiopathic digital clubbing with neither skin changes nor periosteal reaction. He presented to our hospital with swelling of fingers and toes of about six years' duration. All his fingers and toes were clubbed with drumstick appearance, no swelling or tenderness of the wrists, elbows, ankles or knees and no skin changes. The laboratory findings were normal. Primary hypertrophic osteoathropathy without pachydermia was entertained when neither skin changes nor periostosis were found. Although primary hypertrophic osteoathropathy without skin involvement is rare, effort should be made to search for secondary causes.

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Section: Discussionmentioning

confidence: 99%

Hypertrophic Osteoathropathy without Pachyderma in a Nigerian: A Case Report

Umar¹,

Adebayo²,

Abdullahi³

et al. 2015

WJCD

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“…Brouwers et al hypothesized that clubbing is the return of the embryonic claw. Disease by altering cytokines levels can activates the "dormant" genes and so clubbing appeared [2]. Martinez-lavin et al [3] suggest that the fibroblast growth factor as well as the vascular endothelial growth factor (VEGF) may be responsible for the fibroblast proliferation and collagen deposition.…”

Section: Discussionmentioning

confidence: 99%

Clubbing/Pseudoclubbing only in Fingernails Previously Affected by Psoriasis

Antonucci¹,

Tengattini²

2012

J Clin Exp Ophthalmol

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We report a case of fingernails clubbing in a 55-year-old man suffered since the age of 40 from cutaneous psoriasis. The patient had no clubbing before and had no familial cases of clubbing. Cardiological and pneumological visits revealed no abnormalities. All laboratory tests were within normal limits and X-rays excluded the presence of pachyodermoperiostosis. We made the diagnosis of atypical clubbing exclusively in the fingernails previously affected by psoriasis. It may be that a common mechanism lies at the root of these two phenomena.The patient had no enlargement of the distal phalanx before (unfortunately we don't have photo) and had no familial cases of clubbing. Cardiological and pneumological visits revealed no abnormalities. All laboratory tests were within normal limits. The patient underwent X-rays that excluded the presence of pachyodermoperiostosis. Capillaroscopy of the fingers with the enlargement of the distal phalanx showed alterations in the capillarity pattern like splayed and arborized loops and plexus. We made the diagnosis of clubbing/pseudoclubbing exclusively in the fingernails previously affected by psoriasis. Till now the ACH has been treated with acitretina 25 mg daily with good results but the enlargement of the distal phalanx persists at the 6 months follow-up visit. DiscussionThe mechanism for the development of clubbing is not clear, and several hypotheses have been proposed. Brouwers et al. hypothesized

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“…[90] Brouwers et al . [91] hypothesized that clubbed digits resemble the human embryonic fingers and toes, and may represent the return of the embryonic claw that we have lost during evolution. Pathologic condition by altering hormone levels in the blood, activates the “dormant” genes and resulting in the development of clubbing.…”

Section: Pathogenesis Of Clubbingmentioning

confidence: 99%

Digital clubbing

2012

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Digital clubbing is an ancient and important clinical signs in medicine. Although clubbed fingers are mostly asymptomatic, it often predicts the presence of some dreaded underlying diseases. Its exact pathogenesis is not known, but platelet-derived growth factor and vascular endothelial growth factor are recently incriminated in its causation. The association of digital clubbing with various disease processes and its clinical implications are discussed in this review.

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Clubbed fingers: the claws we lost?

Cited by 7 publications

References 15 publications

Hypertrophic Osteoathropathy without Pachyderma in a Nigerian: A Case Report

Hypertrophic Osteoathropathy without Pachyderma in a Nigerian: A Case Report

Clubbing/Pseudoclubbing only in Fingernails Previously Affected by Psoriasis

Digital clubbing

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