Rapidly and extensively absorbed after PO administration. Protein binding: 50%. Widely distributed, including to CSF and erythrocytes. Metabolized in the liver to inactive metabolites. Primarily excreted in urine. Unknown if removed by hemodialysis. Half-life: 1.5 hr.
! A hypersensitivity reaction may be life threatening. Signs and symptoms include fever, rash, fatigue, intractable nausea and vomiting, severe diarrhea, abdominal pain, cough, pharyngitis, and dyspnea.
Selective costimulation modulator; inhibits T-cell activation by binding to CD80 and CD86 on antigen presenting cells, thus blocking the required CD28 interaction and inhibiting autoimmune T-cell activation.
Rheumatoid arthritis (RA), second-line reduction of signs and symptoms of moderate-to-severe active RA, monotherapy or in combination with other disease-modifying antirheumatic drugs (DMARDs) (e.g., methotrexate).
Rheumatoid Arthritis (moderate to severe) in patients who have had an inadequate response to one or more disease-modifying antirheumatic drugs
! Infections: should be cautious when considering the use of abatacept in patients with a history of recurrent infection, underlying conditions that may increase risks of infections, or chronic, localized infections. These patients should be monitored closely. If a patient develops a serious infection, the treatment should be discontinued.
Adjunct to aspirin and heparin therapy to prevent cardiac ischemic complications in patients undergoing percutaneous coronary intervention and those with unstable angina not responding to conventional medical therapy.
Active internal bleeding, arteriovenous malformation or aneurysm, cerebrovascular accident (CVA) with residual neurologic defect, history of CVA (within the past 2 yr) or oral anticoagulant use within the past 7 days unless PT is less than 1.2 times control, history of vasculitis, intracranial neoplasm, prior IV dextran use before or during PTCA, recent surgery or trauma (within the past 6 wk), recent (within the past 6 wk or less) GI or GU bleeding, thrombocytopenia (less than 100,000 cells/mcl), and severe uncontrolled hypertension.
Top can be applied dry or moistened with normal saline solution; blot on sterile gauze to remove excess solution, shape to fit with light finger compression; hold pressure until dry. Apply to bleeding surfaces. Material may be cut to appropriate size or secured in extraction sites with sutures.
Use as single drug or in combination with insulin or oral hypoglycemics (sulfonylureas, metformin) in type 2 diabetes (non–insulin-dependent diabetes mellitus [NIDDM]) when diet control is ineffective in controlling blood glucose levels.
Chronic intestinal diseases associated with marked disorders of digestion or absorption, cirrhosis, colonic ulceration, conditions that may deteriorate as a result of increased gas formation in the intestine, diabetic ketoacidosis, hypersensitivity to acarbose, inflammatory bowel disease, partial intestinal obstruction or predisposition to intestinal obstruction, significant renal dysfunction (serum creatinine level greater than 2 mg/dl)
A beta1-adrenergic blocker that competitively blocks β1-adrenergic receptors in cardiac tissue; high doses may competitively block both β1– and β2-adrenergic receptors. Reduces the rate of spontaneous firing of the sinus pacemaker and delays AV conduction. Exhibits mild intrinsic sympathomimetic activity (ISA) (partial beta-agonist activity).
Well absorbed from the GI tract. Bioavailability: approximately 40%. Protein binding: 26%. Undergoes extensive first-pass metabolism to active metabolite. Eliminated via bile and excretion into GI tract through intestinal wall, as well as partly excreted in urine. Removed by hemodialysis. Half-life: 3–4 hr (parent drug); 8–13 hr (metabolite).