By: Dr. Jeff Donovan
Preliminary Study in 3 Patients
Alopecia areata is an autoimmune hair loss condition that affects about 2% of the population. Treatments include a variety of immunosuppressive treatments. Hair transplantation is not an option for this type of hair loss condition.
Researchers from Columbia University in New York have uncovered a potentially new treatment for alopecia areata: an oral cancer drug known as ruxolitinib.
In a well designed study, the investigators first showed first that the drug was effective in a mouse model of alopecia areata. After showing it worked it mice, the researchers then tested the drug in three patients with alopecia areata. All three patients experienced hair growth in just a matter of a few months. Although the study was performed in only a small number of patients, it opens the door for further study of this medication.
What is Ruxolitinib?
Ruxolitib is a type of cancer drug. It is not a new drug and in fact is already on the market to treat an uncommon bone marrow cancer called myelofibrosis as well as a few other conditions. The drug belongs to a group of medications that inhibits signals within immune cells called the JAK kinase.
Ruxolitinib is currently prescribed by cancer physicians and patients who use the drug need to be carefully monitored. It can cause a drop in blood counts, and can increase the chance of bleeding and bruising. Some patients are more prone to infections while on the medication. Rarely other side effects such as irritation of the heart and liver, weight gain and elevated cholesterol levels can occur.
Further studies are needed to determine if the cancer drug ruxolitinib is safe and effective for patients with alopecia areata before determining if it should or should not be prescribed to larger numbers of patients. Certainly, results from the first three patients are encouraging.
1. Study article: Xing et al. Alopecia areata is driven by cytotoxic T lymphocytes and is reversed by JAK inhibition. Nature Medicine. Published online Aug 17 2014
2. Original source: