Preeclampsia represents one of the most frequent complications of pregnancy. Damage of the endothelial layer lining the blood vessel wall is thought to play an important role in the pathophysiology of preeclampsia, accordingly, mild hyper homocysteinaemia has been reported to be more prevalent among preeclamptic women. Homocystine is a naturally occurring sulphur containing amino acid resulting from demethylation of methionine. The accumulation of homocysteine and its metabolites is caused by a disruption of any of the required enzymes or cofactors involved in the pathways of methionine metabolism. These abnormalities could arise from genetic predisposition and/or nutritional and environmental factors. The most common cause of homocysteinemia, encompassing 95% of the patients, is a deficiency in the cystathionine B-synthase (CBS) enzyme, defective methylcobalamin synthesis, or abnormality in methylene tetrahydrofolate reductase (MTHFR).Homocysteine is responsible for endothelial cell damage leading to proatherogenic effects, thromboembolic effects, hypoperfusion of placenta, and overproduction of free radicals. In pregnancy homocystenemia has been implicated with recurrent miscarriage,pre-eclamsia, placental abruption, IUGR, preterm delivery. We present a unique case of massive abruption and IUD. A 34 year old G4 P1 + 2 with an uneventful antenatal period presented at 36 weeks with antepartum haemorrhage, massive abruption and intrauterine demise diagnosed on admission. Postpartum investigations of note were elevated urate at 394, red cell distance width of 19.2, and Homocystine level of 17.7 mmol/l(mild Homocystinemia). Review of literature indicated plasma levels over12 mol/L should be treated aggressively with vitamin supplementation. We had therefore initiated therapy with B12, B6, folic acid to normalise homocysteine levels.
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