Drug interactions
Drug interactions are extensive, and are as follows:
Azathioprine and 6-mercaptopurine: Azathioprine is metabolised to 6-mercaptopurine which in turn is inactivated by the action of xanthine oxidase - the target of allopurinol. Giving allopurinol with either of these drugs at their normal dose will lead to overdose of either drug;  only one-quarter of the usual dose of 6-mercaptopurine or azathioprine should be given;
Didanosine: plasma didanosine Cmax and AUC values were approximately doubled with concomitant allopurinol treatment; it should not be co-administered with allopurinol and if it must be, the dose of should be reduced and the person should be closely monitored.Allopurinol may also increase the activity or half-life of the following drugs, in order of seriousness and certainty of the interaction:
Ciclosporin
Coumarin anticoagulants, such as warfarin (reported rarely, but is serious when it occurs)
Vidarabine
Chlorpropamide
Phenytoin
Theophylline
Cyclophosphamide, doxorubicin, bleomycin, procarbazine, mechlorethamineCo-administration of the following drugs may make allopurinol less active or decrease its half-life:
Salicylates and medicines that increase the secretion of uric acid
furosemide (see more on diuretics below)Co-administration of the following drugs may cause hypersensitivity or skin rash:
Ampicillin and amoxicillin
Diuretics, in particular thiazides, especially in renal impairment
Angiotensin-converting-enzyme inhibitors (ACE inhibitors)

Pharmacology
A common misconception is that allopurinol is metabolized by its target, xanthine oxidase, but this action is principally carried out by aldehyde oxidase. The active metabolite of allopurinol is oxipurinol, which is also an inhibitor of xanthine oxidase. Allopurinol is almost completely metabolized to oxipurinol within two hours of oral administration, whereas oxipurinol is slowly excreted by the kidneys over 18–30 hours.
Chronic neutrophilic leukemia (CNL) is a rare myeloproliferative neoplasm that features a persistent neutrophilia in peripheral blood, myeloid hyperplasia in bone marrow, hepatosplenomegaly, and the absence of the Philadelphia chromosome or a BCR/ABL fusion gene. Signs and symptoms
The most common clinical finding is hepatosplenomegaly. Pruritus, gout, and mucocutaneous bleeding are occasionally seen. Cause
The cause of CNL is currently unknown. An association between CNL and multiple myeloma has been suggested based on the observation of myeloma in 20% of CNL cases. However, a clonal genetic abnormality has not been detected in these myeloma-associated cases of CNL, raising the possibility that the neutrophilia is a reaction due to the neoplastic myeloma cells. The postulated cell of origin is a limited-potential, marrow-derived stem cell. Genetics
The majority (90%) of cases have not had detectable cytogenetic abnormalities. Most importantly, the Philadelphia chromosome and other BCR/ABL fusion genes are not detected. Diagnosis
Laboratory findings
Peripheral blood neutrophilia (> 25 x 109/L) with myeloid precursors (promyelocytes, myelocytes, metamyelocytes) comprising less than 5% of leukocytes. Sites of involvement
Peripheral blood, bone marrow, spleen, and liver are most common, but any organ or tissue can be infiltrated by neutrophils. Bone marrow biopsy
On both the bone marrow aspirate and the core biopsy, a hypercellular marrow with an increased myeloid:erythroid ratio of 20:1 or greater. Myelocytes and neutrophils are increased, and blasts and promyelocytes are not increased. Due to the myeloproliferative nature of the disease, an increase in megakaryocytes and erythroid precursors may be observed, but dyspoiesis in not seen in any cell lineage. Also, reticulin fibrosis is rare.