Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0003090 (arthrodesis)
 8,374 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We report 33 cases of venous thrombosis of the limb, in children aged 15 years or less (average age is 10 years old): 22 acute thrombophlebitis have been treated, 11 children shown post-phlebitic disease. The thrombus was found, most of the time, in the iliac and/or femoral vein. Acute complications were seen in 30% of our cases, and 25% treated children reviewed, had post-phlebitic sequelae. Congenital disease of hemostasis (deficiency of antithrombin III, protein C or S) must be detect before anticoagulant start, because such deficiency influence the treatment and the prognosis. There is non indication for preventive treatment, because of the rarity of spontaneous thrombophlebitis by children. Nevertheless, we can draw an "high risk" population: antecedent of phlebitis, antecedent of congenital disease of hemostasis, antecedent of thrombophlebitis by parents below 40 years old, thrombogenic disease (homocystinuria), vertebral arthrodesis.
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PMID:[Thromboembolic complications in pediatric orthopedics. Multicentric collection of 33 case reports]. 262 Mar 85

Temporomandibular joint (TMJ) ankylosis is a significant problem in Asian countries and the most common etiology is trauma to the mandibular condyle. Other less common etiologies are infection, forceps delivery trauma and rheumatoid arthritis. Many hypotheses are given to explain the pathogenesis. All the proposed hypotheses revolve around trauma to the joint and subsequent healing causing ankylosis. This is however true for only few patients, most of the others do not progress to ankylosis after trauma to TMJ irrespective of seeking treatment or not. In this paper, we try to answer the question that why only a minor subset of condylar injuries progress to ankylosis and why others do not? The hypothesis follows a report of 4 cases that had bilateral TMJ ankylosis with extrahepatic portal venous obstruction (EHPVO) secondary to protein C deficiency. It is postulated that hypercoagulability/reduced fibrinolytic activity in these as well as non-EHPVO patients with TMJ ankylosis cases may have predisposed them to the development of joint ankylosis. The possible mechanism is explained and correlated with other causes of TMJ ankylosis and known facts of protein C deficiency/activated protein C resistance.
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PMID:Temporomandibular joint ankylosis: is hypercoagulable state of blood a predisposing factor? 2391 May 58