Interferon beta-1b

In 1993 the drug interferon beta 1 (UK: Betaferon/US: Betaseron) was approved by the FDA for use in MS patients to help reduce clinical symptoms. It is one of only a few drugs to be officially approved for the treatment of MS. In 1996 its use was approved in the UK.

The body naturally manufactures interferon when the immune system is weak. Interferon is a substance produced in cells infected with viruses. Its purpose is to prevent the growth of other kinds of virus, so that the person with one kind of virus infection is unlikely to develop another at the same time. MS patients appear to produce less interferon than healthy controls (Proc Natl Acad Sci USA, 1979; 76: 476-80).Surprisingly, even the medical press have been sceptical about the use of this powerful drug, which is similar, but not exactly like, naturally occurring interferon. Indeed, the BMJ recently referred to it as a "high risk" strategy, condemned its licensing in the UK on the basis of a single, small clinical trial (BMJ, 1996; 313: 1159) and reminded doctors that we remain totally ignorant of the long term side effects of the drug. Other recent trials have shown disappointing results (J Neurol, Neurosurgery and Psychi, 1996; 61: 239-41).

Synthetic interferon beta-1b has a different chemical structure than human interferon beta and has been shown to result in increased antibody responses (Lancet, 1996, 347:967). Other reported side effects include flu like symptoms, inflammation and pain at the injection site, allergic reaction, nausea, headache, confusion, menstrual disorders and sweating (Ann Neurol, 1993; 34: 310). Patients may also experience serious adverse effects, including abnormal liver function tests and severe even suicidal depression. One suicide and four attempted suicides were observed in the study during the three year long trial (Neurology, 1993; 43: 655-61 also 43: 662-7; Lancet, 1996; 347: 1417). Because of this, pharmaceutical companies have now synthesized interferon beta-1a which, it is claimed, is closer to the human form (Annals of Neurol, 1996; 39: 285-94), though this conclusion seems more hopeful than foregone.