STOWE, VT. — Drug-aggravated dermatologic diseases are far more elusive and less common than cutaneous drug reactions, said Dr. Peter W. Heald at a dermatology conference sponsored by the University of Vermont.
To help unmask some of the dermatologic impostors, Dr. Heald, professor of dermatology at Yale University, New Haven, Conn., presented a series of clinical cases from his own practice along with management pearls gleaned from personal experience and recent literature.
Interferon-Induced Cytokine Psoriasis
Cytokine psoriasis—a subset of psoriasis with a unique clinical appearance and therapy profile—started appearing with some frequency around 1990, not coincidentally around the time treatment with interferon for hepatitis C became more common, Dr. Heald said. “Over the past decade, we've started seeing tons of patients who are 1–2 months into interferon therapy coming in with psoriasis that's just gone crazy. They have acute, irritated, oozing lesions, sometimes with pruritus and often associated with palmar lesions and acral dermatitis,” he said. Of interest, the psoriatic lesions are not local to the interferon injection sites, but rather are all over the body and, if the patient has or is prone to psoriatic arthritis, that will be induced or aggravated as well.
Although the exact underlying mechanism for this is not fully understood, psoriasis is thought to be an immune-mediated disease with a cytokine profile predominantly of the T helper cell, type 1 (TH1) subset. Presumably, interferon-α triggers psoriasis by activating dendritic cells and T cells involved in the pathogenesis of the condition, according to Dr. Heald. “I'm not a big believer in interferon inducing new cases;” it is more likely that interferon causes problems in people who are prone to psoriasis or who have a mild case, he said. “If you've got a condition where you've already got a TH1-mediated process going on in the skin, and you feed that interferon, it's going to cause problems.”
The plan for managing this type of psoriasis is to treat the patients while they are completing their course of interferon therapy. “The usual regimen is etanercept—I start them on 50 mg twice a week—with or without prednisone for rapid onset of relief,” Dr. Heald said. “In my experience, the response to etanercept for this type of psoriasis is even better than [it is for] regular psoriasis.” At the end of the interferon course, patients can be safely tapered off of the etanercept, he said.
An important consideration in the management of these patients, said Dr. Heald, is to involve the treating physician in the decision process. “Let them know that you are going to start treatment and that you're comfortable using the anti-tumor necrosis factor therapy.”
Lithium Psoriasis
“It's not an unusual scenario to see someone on lithium for bipolar disorder getting worsening psoriasis that persists even after 2 months of methotrexate,” Dr. Heald said. “Clinically, it's quite similar to interferon-exacerbated psoriasis in that it is tough and doesn't melt away quickly with standard treatments.”
While the mechanism for this condition is also not well understood, it is suspected that lithium influences the proinflammatory cytokines in the “psoriatic cytokine network,” according to Dr. Heald. As with hepatitis C patients receiving interferon, treating psoriasis in patients on lithium requires treating through the condition with methotrexate or a biologic drug.
A unique management difficulty has to do with the nature of the patient population. “You have to be particularly careful because many of these bipolar patients may be prone to suicide,” said Dr. Heald. “If the bipolar patient is at risk for noncompliance or at times has gone out of control, you should be in a situation where you're controlling the modality—whether by having a nurse give [the patient] the methotrexate or biologic agent or by bringing the patient in for infliximab infusions.”
ACE Inhibitor Psoriasis
Many individuals with psoriasis take angiotensin-converting enzyme (ACE) inhibitors without incident. In a small subset of patients, however, the antihypertensive medication has been linked to the induction or exacerbation of psoriasis. At one point, ACE inhibitors were associated with an increase in skin kinin levels, but a recent study suggests that the presence in some patients' families of an ACE insertion allele may confer susceptibility to the development of psoriasis and may be the precursor to ACE inhibitor psoriasis exacerbation (Br. J. Dermatol. 2004;151:792–5).
A typical patient with this condition “is someone whose psoriasis has been stable but becomes more widespread and pruritic within 6 months of initiation [of] ACE inhibitor treatment,” according to Dr. Heald. “Often there will also be small, thin lesions in places where the patient hadn't had them before.”