Figure 1 Image of the Week, 9/7/14

Discussion in 'Article Discussions' started by CaffeinatedSquirrel, Sep 6, 2014.

  1. CaffeinatedSquirrel

    CaffeinatedSquirrel Married into Medicine
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    See the images and case details here.

    This patient has hypertrophic pulmonary osteoarthropathy, a rare syndrome defined by the presence of clubbing and periosteal proliferation of the tubular bones.

    Did you guess correctly? Comment and discuss below.

    See more cases like this on Figure 1.
     
    #1 CaffeinatedSquirrel, Sep 6, 2014
    Last edited: Sep 6, 2014
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  3. absolutjag9

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    From UptoDate: Hypertrophic pulmonary osteoarthropathy: defined by the presence of clubbing and periosteal proliferation of the tubular bones associated with lung cancer or other lung disease. Clinically, HPO is characterized by a symmetrical, painful arthropathy that usually involves the ankles, knees, wrists, and elbows. The metacarpal, metatarsal, and phalangeal bones may also be involved.

    Among patients with lung cancer, HOA is most frequently associated with adenocarcinoma and least frequently with small cell carcinoma.

    You detect this via bone scintiography. Pts often complain of clubbing and pain in ankles. HPO can also occur primary, rather than secondary as seen in this man's bone scan.

    Clubbing and HOA appear to be different manifestations of the same disease process. It is thought that localized activation of the platelet-endothelial cells, with the subsequent release of fibroblast growth factor(s) (eg, platelet-derived growth factor), plays an important role in the pathogenesis of HOA. The frequent association with lung disease raises the possibility that circulatory bypass of the lung may play an important role. One hypothesis is that megakaryocytes escape the normal fragmentation to platelets in the lung and reach the distal extremities where they release growth factors .

    Another hypothesis involves tumor production and release into the circulation of a factor that promotes features of HOA such as vascular proliferation, edema formation, and new bone formation. One candidate is vascular endothelial growth factor (VEGF). Two case reports of patients with lung cancer and HOA noted elevated circulating concentrations of VEGF, with evidence of tumor production of VEGF. In one case, a marked decline in VEGF followed resection of tumor and was temporally correlated with the disappearance of the skeletal abnormalities.

    Subsequent to these observations, the pathogenesis of primary HOA was elucidated and raised the question of whether the central abnormality in primary HOA, elevations in circulating prostaglandin E2, may play a pathogenetic role in secondary HOA.


     

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