If cost-effectiveness (quality-adjusted life years in return for expenditure) is taken as a guide, it is generally unclear whether thrombophilia investigations justify the often high cost, unless the testing is restricted to selected situations.Recurrent miscarriage is an indication for thrombophilia screening, particularly antiphospholipid antibodies (anti-cardiolipin IgG and IgM, as well as lupus anticoagulant), factor V Leiden and prothrombin mutation, activated protein C resistance and a general assessment of coagulation through an investigation known as thromboelastography.Women who are planning to use oral contraceptives do not benefit from routine screening for thrombophilias, as the absolute risk of thrombotic events is low. If either the woman or a first-degree relative has had thrombosis, the risk of developing thrombosis is increased. Screening this selected group may be beneficial, but even when negative may still indicate residual risk. Professional guidelines therefore suggest that alternative forms of contraception be used rather than relying on screening.Thrombophilia screening in people with arterial thrombosis is generally regarded as unrewarding and is generally discouraged, except possibly for unusually young patients (especially when precipitated by smoking or use of estrogen-containing hormonal contraceptives) and those in whom revascularization, such as coronary arterial bypass, fails because of rapid occlusion of the graft. Treatment
There is no specific treatment for thrombophilia, unless it is caused by an underlying medical illness (such as nephrotic syndrome), where the treatment of the underlying disease is needed.
And that if this were the case, then the mechanism remains unclear.Administration of nitrous oxide anesthesia can precipitate subacute combined degeneration in people with subclinical vitamin B12 deficiency, while chronic nitrous oxide exposure can cause it even in persons with normal B12 levels. Posterior column dysfunction decreases vibratory sensation and proprioception (joint sense). Lateral corticospinal tract dysfunction produces spasticity and dorsal spinocerebellar tract dysfunction causes ataxia. Cause
In general, the most common cause of this condition is a deficiency of vitamin B12. This may be due to a dietary deficiency, malabsorption in the terminal ileum, lack of intrinsic factor secreted from gastric parietal cells, or low gastric pH inhibiting attachment of intrinsic factor to ileal receptors.Vitamin E deficiency, which is associated with malabsorption disorders such as cystic fibrosis and Bassen-Kornzweig syndrome, can cause a similar presentation due to the degeneration of the dorsal columns. Diagnosis
Serum vitamin B12, methylmalonic acid, Schilling test, and a complete blood count, looking for megaloblastic anemia if there is also folic acid deficiency or macrocytic anemia. The Schilling test is no longer available in most areas.MRI-T2 images may reveal increased signal within the white matter of the spinal cord, predominantly in the posterior columns and possibly in the spinothalamic tracts. Treatment
Therapy with vitamin B12 results in partial to full recovery where SACD has been caused by vitamin B12 deficiency, depending on the duration and extent of neurodegeneration. References


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