In clinical studies and postmarketing reports, the side effects seen in 1% or more of the patients were as follows:

Gastrointestinal system: nausea, vomiting, abdominal pain, and diarrhea
Central nervous system: headache
Whole body: fever, phlebitis or thrombophlebitis, complications at the intravenous cannulation site (e.g. induration), unspecified pain, flu-like syndrome, myalgia, chills, and paresthesia
Respiratory: dyspnea
Renal: increased plasma creatinine
Hematological: anemia
Electrolytes: hypokalemia
Liver: increased liver enzymes (asymptomatic)
Hypersensitivity: rash, facial edema, pruritus
Other: tachycardiaAdditionally, infrequent cases of symptomatic liver damage, peripheral edema and swelling, and hypercalcemia have been seen. One case of anaphylaxis (severe allergic reaction) has also been noted. Resistance
Resistance in C. albicans has been described, but is currently still rare. The mechanism is probably a point mutation in the (1→3)-β-D-glucan synthase gene. Drug interactions
Cyclosporin: see under hepatic effects
Tacrolimus: potential pharmacokinetic interactions
Other systemic antimycotic agents: with amphotericin B, itraconazole and mycophenolate, no interactions have been seen
Inducers of drug clearance (e.g. carbamazepine, phenytoin, rifampin, dexamethasone): consider 70 mg intravenous as maintenance dose instead of 50 mg

Duration of treatment
The mean duration of therapy in previous studies was 34 days. Some patients were even healed by a one-day treatment. However, a few patients were treated for as long as 162 days and tolerated the drug well, indicating that longtime use may be indicated and tolerated favourably in complicated cases of aspergillosis. Generally, the duration of treatment is dictated by the severity of the disease, the clinical response, and the improvement of immunocompetence in immunocompromised patients. Dosage
An initial dose of 70 mg by intravenous infusion is given followed by 50 mg intravenous daily.
Antithrombin III deficiency (abbreviated ATIII deficiency) is a deficiency of antithrombin III. This deficiency may be inherited or acquired. It is a rare hereditary disorder that generally comes to light when a patient suffers recurrent venous thrombosis and pulmonary embolism, and repetitive intrauterine fetal death (IUFD). Hereditary antithrombin deficiency results in a state of increased coagulation which may lead to venous thrombosis. Inheritance is usually autosomal dominant, though a few recessive cases have been noted. The disorder was first described by Egeberg in 1965. The causes of acquired antithrombin deficiency are easier to find than the hereditary deficiency.The prevalence of antithrombin deficiency is estimated at ~0.02 to 0.2% of the general population, and 1-5% of patients with venous thromboembolism. There is an elevated risk of thrombosis, whereby 50% patients with AT deficiency were found to have venous thromboembolism by age 50. Cause
Diagnosis
A clinical suspicion for antithrombin deficiency can be made in patients with: 1. recurrent venous thromboembolic disease, 2. childhood thrombosis, 3. thrombosis in pregnancy. Testing for antithrombin activity can confirm deficiency if the levels are less than 70%. Deficiency can result from genetic predisposition or from acquired causes such as: acute thrombosis, disseminated intravascular coagulopathy, liver disease, nephrotic syndrome, asparaginase deficiency, oral contraception/estrogens. Genetic testing for abnormalities of the SERPINC1 gene can be done to evaluate further. Management
In patients with antithrombin deficiency, they may develop resistance to unfractionated heparin, especially with continuous infusions. If large quantities of unfractionated heparin are required e.g. greater than 35000 units per day, this would point towards resistance.