Pseudolymphoma

Although some clinicians have used the term pseudolymphoma interchangeably with anticonvulsant HSR, pseudolymphoma applies only to patients who have both clinical and histological features suggestive of lymphoma. It is not considered a premalignant state. The syndrome occurs after one week to two years of exposure to the drug . Within seven to 14 days of drug discontinuation, the symptoms generally resolve. Management of drug-induced pseudolymphoma often involves no treatment other than withdrawal of the offending agent. Long term follow-up is necessary to rule out the possibility of pseudopseudolymphoma.

Numerous case reports in the literature describe pseudolymphoma in association with either phenytoin or carbamazepine therapy. A case of nodular, drug-induced pseudolymphoma of the skin following carbamazepine therapy is also described. Mycosis fungoides-like lesions have also been associated with pheny-toin and carbamazepine administration.

It is unknown whether cross-reactivity exists between the anticonvulsants. In one patient who developed mycosis fungoides-like lesions, withdrawal of phenytoin and initiation of phenobarbital and carbamazepine resulted in complete regression of skin lesions. However, because pseudolymphoma shares the symptomatology of the anticonvulsant HSR, it is recommended that all aromatic anticonvulsants be avoided in patients who develop pseudolymphoma. cialis professional online

Pseudopseudolymphoma

This term ‘pseudopseudolymphoma’ describes a small number of patients who, after withdrawal of phenytoin following pseudolymphoma and resolution of symptoms, later develop malignant lymphoma.

Lymphoma

Long term phenytoin therapy has been associated with small intestinal lymphoma, hairy cell leukemia, Hodgkin’s disease , non-Hodgkin’s lymphoma, multiple myeloma and mycosis fungoides . Discontinuation of phenytoin did not result in tumour regression. It is unknown whether phenytoin acts as an inciting agent on a dormant malignancy, allows expression of an oncogene, or predisposes patients to malignant change by its persistent antigenic stimulation.