Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0033036 (APC)
10,214 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Resistance to activated protein C (RAPC) has been described recently as a cause of trombophilia; this may justify up to 50% of thromboembolic disease without predisposing cause in patients under 45 years. A 29 years-old male with a previous deep venous thrombosis (DVT) in the lower left limb three years earlier, developed a DVT in the right lower limb after a trauma of the knee that required immobilization, was associated to pulmonary thromboembolism diagnosed by gammagraphic methods. The phlebographic study showed femoro-iliaco-caval venous thrombosis. The proband's father and a younger brother had a previous history of thrombotic episodes. The following tests, were performed in the proband and relatives: prothrombin time, aPTT, thrombin time, fibrinogen, (Von Clauss), antithrombin III (chromogenic), protein C and protein S (coagulometry and ELISA), plasminogen (chromogenic) and lupus anticoagulant (ITT, dRVVT, aCL). RAPC was evaluated in two different samples. The proband study was performed under oral anticoagulation treatment (OAT). Control groups were: 21 blood donors and 12 OAT patients. The results showed a decreased response to APC in the proband (ratio 1.5) and relatives: father (1.4), brothers (1.5 and 1.5), while the mother was within the normal range (> or = 2). In normal controls and OAT patients the ratio was over 2. No other abnormalities were detected in the assays performed. It is concluded that RAPC is the cause of this familial trombophilia. RAPC should be included in the evaluation study of trombophilia.
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PMID:[Familial thrombophilia due to resistance to activated protein C]. 798 58

Sequential treatment scheme has been developed to overcome resistance problem in H. pylori eradication and favorable results have been obtained. This study compared the results of standard triple therapy with a sequential schema consisting of pantoprazole, amoxicillin, clarithromycin, and metronidazole in a high anti-microbial resistance setting. This retrospective study included subjects that underwent standard or sequential eradication treatment after a diagnosis of biopsy-documented H. pylori infection. Patients either received pantoprazole 40 mg bid, amoxicillin 1000 mg bid and clarithromycin 500 mg bid (PAC) for 10 days, or pantoprazole 40 mg bid and amoxicillin 1000 mg bid (PA) for the first 5 days of the treatment period and were then given pantoprazole 40 mg bid, clarithromycin 500 mg bid, and metronidazole 500 mg bid (PCM) in the remaining 5 days. Eradication was tested using urea breath test. The two treatment groups did not differ with regard to H. pylori eradication rate for both ITT population (63.9% versus 71.4% for standard and sequential therapy respectively, P = 0.278) and per protocol population (65.9% versus 74.1% for standard and sequential therapy respectively, P = 0.248). Although a sequential treatment appears to represent a plausible alternative, our findings suggest that alternative schedules may be required in certain populations to achieve higher success rates.
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PMID:Sequential therapy versus standard triple therapy in Helicobacter pylori eradication in a high clarithromycin resistance setting. 2523 29