Smoking is very closely related to Buerger’s disease and smoking history is one of the criterion for diagnosing the disease. In general if the patient absolutely abandons smoking the course of the disease will be invariably benign, but if smoking continues any treatment will ultimately be futile. Though "passive smoking" has adverse effect on cardiovascular system, non smokers should never develop the disease. Active smokers can be indentified by measuring levels of continine, the major metabolite of nicotine in urine. Since all smokers do not develop the disease an immunopathogenesis is considered probable. It has been proposed in Japanese that presence of a gene linked to some HLA antigens might control the susceptibility to the disease.
Socioeconomic conditions, work environment may also play in etiology as the disease is seen more in out door and manual workers. Hypercoagulable state has been observed in association with the disease. Hepatitis B Virus and rickettssiosis may contribute to pathogenesis, but this role is uncertain.
Buergers disease is an inflammatry occlusive disease which involves all layers of medium sized and small arteries of the extremitiles. Involved superficial veins bear a close resemblance to those in the affected artery. Majority of the patients develop critical limb ischemia with trophic lesions are distal to ankle, the anklebrachial doppler index could be normal in early stage. Toe pressures can be measured and if it is less than 30 mm Hg, the healing of ulcers is unlikely. The disease though commences peripherally, may gradually extend proximately occluding the larger arteries.
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