Hyper homocysteinemia is a risk factor for arterial and venous thrombosis. It is asserted that in deficiency of vitamin B12 will increase thrombotic incidences due to increase in homocysteine and upon substituting the vitamin, this risk decreases (¹). However, this situation is not clear and there are a lot of conflict views.

The prevalence of hyperhomocysteinemia in the general population is estimated to be approximately 1%, although it may vary from area to area (²). It could be caused by both genetic and acquired conditions, including folate and cobalamin deficiency (³).

Homocysteine is metabolized by one of two divergent pathways: one of them is remethylation in which homocysteine produces methionine, this reaction is catalyzed by methionine synthase, cobalamin is the precursor of methylcobalamin, which is the cofactor for methionine synthase (Figure 3).

Although studies demonstrated that hyperhomocysteinemia is an independent risk factor for premature arteriosclerotic disease in the coronary, cerebral, and peripheral arteries (⁴, ⁵), but there a lot of conflict regarding venous thrombosis, in spite of that recent meta-analyses support the notion that hyperhomocysteinemia is an independent risk factor for venous thrombosis (⁶, ⁷). Brattström et al. (⁸) found no significant difference in plasma homocysteine concentrations between 42 patients with VTE and healthy control subjects, although the male patients showed a tendency toward higher plasma homocysteine than male control subjects. In contrast, Bienvenu et al. (⁹) demonstrated a significant association between fasting plasma homocysteine and VTE, and Falcon et al. (¹⁰) reported a high prevalence of hyperhomocysteinemia in patients less than 40 years of age who had VTE. Tore Amundsen et al, demonstrate that hyperhomocysteinemia is not a frequent cause of DVT (¹¹). Ducros et al, showed that Mild or moderate hyperhomocysteinemia does not seem to be a strong determinant in VTE (¹²).

With such conflicting studies we report these three cases with secondary hyperhomocysteinemia secondary to nutritional deficiency of cobalamin. our patients had no apparent risk factors for venous thrombosis other than the hyperhomocysteinemia, all of them had cobalamin deficiency and all are poor with low socioeconomic state, vegans for religious cause and their diet were deficient in meat and other B12 source like egg, milk etc. The vitamin B12 deficiency seen in our patient was considered not to be pernicious anemia, based on the fact that there was no evidence of atrophic gastritis and an absence of antiparietal cell antibodies.

In conclusion we think homocysteine is independent risk factor for deep venous thrombosis in patient with cobalamin deficiency, especially vegetarian and this may related to other associated factor which we have to look for.

None declared.