Digital clubbing and hyperthrophic osteorthropathy: The underlying mechanisms

Shneerson, John M.

doi:10.1016/0007-0971(81)90043-7

Cited by 83 publications

(27 citation statements)

References 98 publications

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“…Martinez-Lavin and colleagues [I 15,l 161 have made the persuasive case that when a careful examination is made, patients with cyanotic congenital heart disease often have radiologically evident bone and joint changes, even in the absence of symptoms. 'Clubbing and HOA may not represent distinct entities; our data suggest that they may be stages in an evolving, more generalized process of new bone formation or hypertrophy followed by osteolysis or atrophy affecting many parts of the skeleton' [38]. Nonetheless, there are some differences.…”

Section: Hypertrophic Osteoarthropathy (Hoa)mentioning

confidence: 64%

“…These include reduced ferritin [37], prostaglandins, bradykinin, and serotonin [38], cytokines [39] including tumour necrosis factor [40], purine nucleotides (adenosine triphosphate, especially), vasoactive intestinal peptide [3 11, oestrogens [2], and growth hormone [41,42,43]. In these cases there has usually been considerable overlap of blood concentration of the suspect material between clubbed and unclubbed patients [38,42,44,45]. Furthermore, such theories do not provide any plausible reason for clubbing distal to infected arterial aneurysms or for generalized clubbing in sub-acute bacterial endocarditis.…”

Section: Previous Theories To Explain Clubbingmentioning

confidence: 99%

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The aetiology of clubbing and hypertrophic osteoarthropathy

Dickinson

1993

Eur J Clin Investigation

133

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Abstract. The evidence is reviewed for the hypothesis that clubbing and hypertrophic osteoarthropathy are due to the peripheral impaction of megakaryocytes and platelet clumps in the fingers and toes, to which this particulate matter has passed in an axial stream. The normal pulmonary vascular bed retains these large particles, which fragment before entering the systemic circulation. A right-to-left shunt allows them to bypass the pulmonary vascular bed. A preliminary histological report of platelet clumps seen at necropsy in nail bed capillaries of clubbed fingers supports the hypothesis. Platelets contain and release platelet-derived growth factor, whose known effects could explain all the pathological changes in clubbing. In addition to explaining why clubbing should occur in cyanotic congenital heart disease, clubbing in sub-acute bacterial endocarditis and distal to infected arterial grafts and aneurysms can be understood in terms of platelet clumps breaking off valves or arterial walls, and passing distally. Clubbing in liver disease is associated with multiple small pulmonary arteriovenous anastomoses which allow large particles through. Hypertrophic osteoarthropathy probably shares the same mechanism, and is mainly attributable to PDGF release; but there may also be altered platelet function and an additional growth factor derived from the lungs.

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Section: Hypertrophic Osteoarthropathy (Hoa)mentioning

confidence: 64%

Section: Previous Theories To Explain Clubbingmentioning

confidence: 99%

The aetiology of clubbing and hypertrophic osteoarthropathy

Dickinson

1993

Eur J Clin Investigation

133

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“…10 reports of the syndrome are that vagotomy results in almost immediate symptomatic relief"l and radiological regression of the periosteal changes in six to 12 weeks10 and that blood flow in the calf and forearm is increased and decreases if the underlying cause is removed.12 It seems reasonable to regard the vagal stimulation as the "afferent" limb connecting centrally with a possible neurotransmitter that mediates the "efferent" limb. Vasoactive intestinal peptide is a non-adrenergic non-cholinergic neurotransmitter whose release from the porcine pancreas is mediated by electrical vagal stimulation.1' It is an extremely powerful peripheral vasodilator,'4 and its release by vagal stimulation might possibly account for the observed increase in blood flow in the calf and forearm.…”

Section: Discussionmentioning

confidence: 99%

Hypertrophic osteoarthropathy in cystic fibrosis.

Braude¹,

Kennedy²,

Hodson³

et al. 1984

BMJ

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“…The pathogenesis of clubbing is not yet fully understood and the theoretical explanations were explored by Shneerson (1981), Dickinson and Martin (1987), and by Atkinson and Fox (2004). They have postulated that growth factors, especially cytokines related to megakaryocytes, may be involved in the process and can accumulate at sites of the abnormalities.…”

Section: Introductionmentioning

confidence: 99%

Clubbed fingers: Radiological evaluation of the nail bed thickness

et al. 2008

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It is established that there is an increase in soft tissue of the clubbed digits as demonstrated on previous histopathological examinations. In the present study, the nail bed thickness was assessed and measured on plain radiographs of index fingers in two groups of patients: one group with lung disease and fingers clubbing and one group of normal controls. A vertical x-ray beam was used with a focus-film distance of 1.0 m, with the index finger placed in lateral view directly over the film, without anti-diffusion grid. Three investigators, blinded to prevent bias measured the thickness of soft tissues between the nail root and the terminal phalanx on the radiographs. This method was used to evaluate a group of 85 clinically clubbed (hyponychial angle > 192.0 degrees) adult patients with lung disease and a control group of a 100 normal adult individuals with no clubbing (hyponychial angle < 188.0 degrees). The mean nail bed thickness in the patients with clubbing (n = 85) was 3.88 +/- 0.55 mm (3.00-5.50 mm). In comparison, in the normal subjects (n = 100), the mean was 2.38 +/- 0.27 mm (1.75-3.10 mm), revealing a significant difference (P < 0.001). Only two normal individuals presented nail bed thickness >or=3.0 mm. A good interobserver agreement on the measurements was found (P > 0.900). The radiographic evaluation of the nail bed thickness was easily performed, with good interobserver concordance. It is possible to distinguish between clubbed from nonclubbed fingers, in vivo, using plain radiograph.

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Digital clubbing and hyperthrophic osteorthropathy: The underlying mechanisms

Cited by 83 publications

References 98 publications

The aetiology of clubbing and hypertrophic osteoarthropathy

The aetiology of clubbing and hypertrophic osteoarthropathy

Hypertrophic osteoarthropathy in cystic fibrosis.

Clubbed fingers: Radiological evaluation of the nail bed thickness

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