The exact dose and duration of administration will depend on the nature and dosage of other cytotoxic drugs given in conjunction with LANVIS.
LANVIS is variably absorbed following oral administration and plasma drug levels may be reduced following emesis or intake of food.
LANVIS can be used at various stages of treatment in short term cycles. However it is not recommended for use during maintenance therapy or similar long term continuous treatments due to the high risk of liver toxicity (see Precautions and Adverse Reactions).
Induction therapy: For adults, the usual dosage of LANVIS is between 60 and 200 mg/m2 body surface area per day.
For children, similar dosages to those used in adults, with appropriate correction for body surface area have been used.
Elderly patients: There are no specific dosage recommendations in elderly patients (See Dosage in renal or hepatic impairment as follows). LANVIS has been used in various combination chemotherapy schedules in elderly patients with acute leukaemia at equivalent dosages to those used in younger patients.
Dosage in renal or hepatic impairment: Consideration should be given to reducing the dosage in patients with impaired hepatic or renal function.
TPMT-deficient patients: Patients with inherited little or no thiopurine S-methyltransferase (TPMT) activity are at increased risk for severe thioguanine toxicity from conventional doses of thioguanine and generally require substantial dose reduction. The optimal starting dose for homozygous deficient patients has not been established (see Monitoring under Precautions and Pharmacology: Pharmacokinetics under Actions).
Most patients with heterozygous TPMT deficiency can tolerate recommended thioguanine doses, but some may require dose reduction. Genotypic and phenotypic tests of TPMT are available (see Monitoring under Precautions and Pharmacology: Pharmacokinetics under Actions). Consideration should be given to reducing the dosage in patients with impaired hepatic function.
Patients with NUDT15 variant: Patients with inherited mutated NUDT15 gene are at increased risk for severe thiopurine toxicity, such as early leukopenia and alopecia, from conventional doses of thiopurine therapy and generally require substantial dose reduction. Patients of Asian ethnicity are particularly at risk, due to the increased frequency of the mutation in this population. The optimal starting dose for heterozygous or homozygous deficient patients has not been established.
Genotypic and phenotypic testing of NUDT15 variants should be considered before initiating thiopurine therapy in all patients (including paediatric patients) to reduce the risk of thiopurine-related severe leukocytopenia and alopecia, especially in Asian populations (see Pharmacology: Pharmacokinetics under Actions).