ABSTRACT
These are natural inhibitors of coagulation, and deficiencies of any of these factors is referred to as thrombophilia. The identified main causes of thrombophilia are deficiencies of antithrombin III, protein C, or protein S, resistance to actived protein C associated with Factor V Leiden mutation, and inherited hyperhomocystinemia. Inherited and acquired thrombophilias may also contribute to pathophysiological processes involved in recurrent pregnancy loss, fetal death, intrauterine growth restriction, placental abruption, placental infarction, and pre-eclampsia. Various therapeutic protocols with low-molecular-weight heparin (LMWH) were used. because it is associated with a low incidence of osteoporosis and thrombocytopenia. We experienced the two cases of successful deliveries by Cesarean section following a successful pregnancy maintenance in thrombophilia. we administered LMWH to prevent thromboembolism. one patient was the primi-gravidarum, with inherited thrombophilia, who has the familial history of pulmonary embolism and deep vein thrombosis. the other was the multi-gravidarum, with acquired thrombophilia, who has the past medical history of pulmonary embolism.
Subject(s)
Female , Humans , Pregnancy , Abruptio Placentae , Antithrombin III , Cesarean Section , Factor V , Fetal Death , Heparin, Low-Molecular-Weight , Incidence , Infarction , Osteoporosis , Pre-Eclampsia , Pregnancy Maintenance , Protein C , Protein S , Pulmonary Embolism , Thrombocytopenia , Thromboembolism , Thrombophilia , Venous ThrombosisABSTRACT
We have reviewed the medical records of 4 pregnant patients with concomitant acute leukemia at our institution in conjunction with determining the delivery process in order to reduce complications associated with the delivery. Of the 4 patients, three cases were diagnosed as acute leukemia and the other as myelodysplastic syndrome. One experienced an incomplete abortion at gestational age of 10 weeks, after remission induction chemotherapy. The remaining three patients made delivery at full term by Cesarean section. Our observation indicated that Cesarean delivery was advisable for these three patients. Most of the patients had thrombocytopenia or anemia. Before the Cesarean section or dilatation or evacuation, transfusion was undertaken to prevent hemorrhage or severe anemia. In the cases of refractoriness to blood transfusion, a greater amount was transfused. After Cesarean section, some complications were reported such as fever, delayed wound repair, and vaginal bleeding. Based on the our observations, we are of the opinion that pregnant women with acute leukemia or myelodysplastic syndrome can be managed even in those cases where the state of leukemia is not in complete remission or chemotherapy-induced cytopenia is. And the proper measures are timely undertaken to prevent complications associated with delivery.
Subject(s)
Female , Humans , Pregnancy , Abortion, Incomplete , Anemia , Blood Transfusion , Cesarean Section , Dilatation , Drug Therapy , Fever , Gestational Age , Hemorrhage , Leukemia , Medical Records , Myelodysplastic Syndromes , Pregnant Women , Remission Induction , Thrombocytopenia , Uterine Hemorrhage , Wounds and InjuriesABSTRACT
BACKGROUND: Hyperhomocysteinemia is an independent risk factor for cerebrovascular disease. MTHFR 677TT genotype can induce hyperhomocysteinemia. However, the association between this 677TT genotype and ischemic stroke still remains controversial. This study was undertaken to determine whether MTHFR 677TT genotype was associated with certain subtype of ischemic stroke. METHODS: The case group consisted of 129 patients with ischemic stroke and the control group consisted of 157 healthy individuals. We checked their fasting plasma homocysteine levels and analyzed the C677T mutation in the MTHFR gene. The relative risk of MTHFR 677TT genotype was assessed by odds ratios using multivariate logistic regression. RESULTS: Homocysteine levels in plasma were significantly higher in ischemic stroke patients (10.386.44 mol/L) than in controls (8.002.40) (P<0.05). In small-artery disease (11.366.01), the same result was found (P<0.05). On the other hand, the prevalence of the homozygote mutation was not significantly higher in ischemic stroke patients (20.2%) than in controls (13.4%) (adjusted OR 1.39, 95% CI 0.65 to 2.96). The adjusted OR and 95% CI was 2.59 (1.08 to 6.25) for the TT genotype in patients with small-artery disease compared to controls. The 677TT genotype was increased in small-artery disease compared to large-artery disease (adjusted OR 7.60, 95% CI 1.66 to 34.77). CONCLUSIONS: Our findings suggest that the homozygous C677T mutation in the MTHFR gene is a risk predictor in the subtype of ischemic stroke, such as small-artery disease.
Subject(s)
Humans , Fasting , Genotype , Hand , Homocysteine , Homozygote , Hyperhomocysteinemia , Logistic Models , Odds Ratio , Plasma , Prevalence , Risk Factors , StrokeABSTRACT
PURPOSE: Hyperhomocysteinemia was observed in epileptic patients receiving anticonvulsants, especially homozygotes for mtehylenetetrahydrofolate reductase (MTHFR) gene 677C->T mutation. Hyperhomocysteinemia induce atherosclerosis, fetal anticonvulsant syndrome, etc. Therefore, we examined any other factors that might affect the level of homocysteine in epileptic patients. METHODS: We investigated the plasma total homocysteine level in 145 patients with epilepsy. And then we analyzed various factors (clinical findings, neuro-image finding, drugs, MTHFR gene, serum folate and vitamin B12 level) affecting the level of homocysteine. RESULTS: Among the various factors, male, present neurological deficits, frequent seizure attacks, MTHFR gene 677 TT genotype, polypharmacy, and conventional drug (phenytoin, carbamazepine, valproic acid, phenobarbital, primidone, benzodiazpines) than new drug (lamotrigine, vigabatrin, topiramate, oxcarbazepine zonisamide) were related with elevated homocysteine levels. CONCLUSION: We recommend monotherapy with new drugs and higher vitamin requirement in the male epileptic patients of MTHFR TT genotype with neurological deficits and frequent seizure attacks.
Subject(s)
Humans , Male , Anticonvulsants , Atherosclerosis , Carbamazepine , Epilepsy , Folic Acid , Genotype , Homocysteine , Homozygote , Hyperhomocysteinemia , Oxidoreductases , Phenobarbital , Plasma , Polypharmacy , Primidone , Seizures , Valproic Acid , Vigabatrin , Vitamin B 12 , VitaminsABSTRACT
We report a 48-year-old man with laryngeal cancer who received a massive cisplatin toxic overdose without intravenous prehydration through an error in prescription. He received 400 mg/m2 of cisplatin over a 4-day period. On day 4, he exhibited a broad range of cisplatin toxicities and emergency plasma exchange was started. From day 5 through 19, he underwent 9 cycles of plasma exchange and his plasma cisplatin concentration decreased from 2,470 ng/ml to 216 ng/ml. He completely recovered without any sequelae. No previous reports exist in the English literature of survival without complication after the administration of such a high cisplatin dosage without prehydration.
Subject(s)
Humans , Male , Antineoplastic Agents/poisoning , Cisplatin/poisoning , Middle Aged , Drug Overdose/therapy , Plasma ExchangeABSTRACT
No abstract available.
Subject(s)
Classification , von Willebrand Diseases , von Willebrand FactorABSTRACT
No abstract available.