A recent letter to the editor of the Annals of the Academy of Medicine recently touched on the skin reaction Toxic Epidermal Necrolysis (TEN), a potentially-life threatening side effect of Levaquin (levofloxacin) and related drugs.

Toxic Epidermal Necrolysis is an autoimmune disease, a disease wherein the immune system malfunctions and attacks the patient’s own body. In the case of TEN, the immune system attacks the skin as it would an invading organism. TEN is a more severe form of Stevens Johnson Syndrome, a milder — though still potentially deadly — autoimmune reaction afflicting the skin.

In TEN, which can allegedly be caused by Levaquin (Levoflaxacin), the reaction is so severe that patches of skin all over the body die and slough off, leaving burn-like wounds. The damage so closely resembles large-area burns that most intensive care centers treating TEN patients are forced to move them to their burn wards. Nearly all cases of SJS and TEN are caused by a reaction to prescription and over-the-counter drugs.

Levofloxacin is among the drugs that have been alleged to cause TEN and SJS. Levofloxacin belongs to a family of antibiotics called the quinolones, a family of synthetic antibiotics. When quionlones were first invented, it was hoped that their artificial nature would mean that bacteria could not readily adapt to them, reducing the problems of resistance. While this has not been the case, the drugs have proven largely effective as antibiotics. However, they are not free of serious side effects, like the potential risk of SJS and TEN.

The letter to the editor of AAMS touched on the issue of TEN cases implicating Levofloxacin. While the letter stated that this side effect is rare, it stressed the seriousness of TEN.

Though the sample size was small, exactly half of all cases of TEN from 2002 through the present, 50 percent had died from the reaction. The normal mortality rate of TEN is approximately 35 percent, and the difference could be attributed to the small sample size. Additionally, the mortality of rate of TEN varies with the severity of the reaction.

The authors of the letter, Wan Lin Teo and Shiu Ming Pang, also describe a new treatment for treating TEN. Previously, treating TEN and SJS has proved complicated.

Other autoimmune diseases like Lupus and the Erythemias may respond to steroids, since these selectively turn down the immune system. However, this treatment has proved controversial. Studies cannot prove that it improves SJS and TEN, and may even make them worse.

At most, physicians are limited to supportive care, which means treating the symptoms and keeping the patient comfortable while the disorder runs its course. Often, this involves treating the patient with antibiotics to avoid opportunistic infections — except in cases where TEN was triggered by antibiotics like Levofloxacin in the first place.

Instead, the authors champion using immunoglobins, antibodies harvested from donor blood. The case report involved an older woman who received prior to treatment, a less-than 42 percent chance of survival, based on the fact that at one point 40 percent of her skin had died and fallen off. Also stacking the deck against the patient, she had developed secondary infections, including MRSA. However, once immunoglobins were administered, the patient began to improve, and was well enough for discharge 16 days later, with most of her skin growing back.

The authors closed out their paper by advising physicians to familiarize themselves with TEN and SJS. The fact that these reactions are relatively rare, coupled with the fact that their early symptoms mimic more common diseases, make physicians unlikely to diagnose them quickly. This can seriously impact the patient’s chance of survival, as the best treatment, according to the authors, is to remove the drug that triggered SJS or TEN in the first place.