IntroductIon Vitamin K antagonists (VKAs) including warfarin (most commonly used worldwide), acenocoumarol, and phenprocoumon are highly effective in the prevention and treatment of thromboembolic disorders. The effectiveness and safety of oral anticoagulation is critically dependent on maintaining the prothrombin time, expressed as the inter national normalized ratio (INR).The current guidelines recommend a target INR of 2−3 for long-term oral anticoagulation in the secondary prevention of venous thromboembolism (VTE) and ischemic stroke in patients with atrial fibrillation. 1 A dose of VKAs depends on several factors, predominantly diet and medications 2 , or individual features such as age and body weight 3. Genetic factors largely determine a dose of VKAs in patients regardless of the indication to anticoagulation. 4,5 Current evidence indicates that combined genotyping for the polymorphisms, CYP2C9*3 and −1639G>A or 1173C>T VKORC1 gene, predicts about 50% of the inter individual variability of the anticoagulation pharmacodynamic response. 6 The incidence of non-compliance among anticoagulated subjects has been estimated to be up to 30%. 7
A 58-year-old woman with an 8-year history of seropositive rheumatoid arthritis was admitted with right hemiparesis, history of seizures, fever, weight loss and headaches. Her blood tests revealed the presence of rheumatoid factor, elevated C-reactive protein and anti-cyclic citrullinated peptide antibodies (>200 RU/ml). Examination of cerebrospinal fluid demonstrated pleocytosis (118 cells/mm(3), predominantly lymphocytes) with elevated protein level (58 mg/dl); cultures were negative. Magnetic resonance imaging findings were suggestive for meningoencephalitis. Short course of high-dose corticosteroids and cyclophosphamide led to clinical improvement. Rheumatoid vasculitis was probably responsible for neurological symptoms.
Asthma therapy with monoclonal antibodies is a promising and effective approach for those with a severe and refractory type of disease. Although such a targeted therapy is considered to be safe, unusual complications may occur. We present a case of a 45 year-old female patient with severe allergic asthma and chronic spontaneous urticaria, who developed autoimmune polyendocrine syndrome type 2 (APS-2) after 26 months of omalizumab administration. The patient was diagnosed with primary adrenal insufficiency (Addison's disease) and Hashimoto's thyroiditis accompanied by autoimmune atrophic gastritis. According to our knowledge this is the first description of APS-2 that developed in conjunction with omalizumab treatment, although we have no evidence that the observed phenomenon indicated a cause-effect relationship to omalizumab.
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