From the Editor…METHODOLOGY
This research assessed (a) the clinical presentation of PRP and (b) the clinical response to therapy at two teaching hospitals in Boston, Massachusetts. In addition, researchers wanted to determine the role of systemic agents (acitretin, cyclosporine and methotrexate) and biologic agents (Humira, Remicade, Enbrel and Amevive).
The first step was to identify all patients with PRP seen by a dermatologist from January 2000 through December 2011 at the Brigham and Women’s Hospital and Harvard Medical School.
Next, they harvested data on disease presentation, treatment and clinical response.
For purposes of the study, clinical response was defined as a relationship from a baseline. There were three possibilities:
❏½ no clinical response
❏½ partial clinical response (<75% improvement)
❏½ marked clinical response (❏‰¥75% improvement)
I wonder how they make that assessment? As an “active” PRP patient (August 2012-April 2014), I though of myself as just “getting better”. It would have never occurred to me to assign a number to that improvement. Perhaps it’s something dermatologists learn in medical school.
RESULTS
The article reports: “Of 176 patients identified, 40 had a diagnosis of PRP, 38 of whom received this diagnosis based on clinical and pathological findings.”
Editor’s Note: So, what happened to the 136 who were initiatively “identified” had a diagnosis of PRP? I will contact Brooke Eastham, one of the researchers I met at the American Academy of Dermatology annual meeting in Denver, CO (March 2014) and update this paragraph.
The article continues: “There were 36 patients with adult type 1 PRP (of whom 3 had associated polyarthritis and 6 required hospitalization), 3 with juvenile type 4, and 1 with juvenile type 5. There was no sex predominance, and the majority of patients were white. The mean age of adult and childhood onset was 57 and 5 years, respectively, with a two-year mean disease duration.”
The “lay language police: report that polyarthritis is any type of arthritis that involves five or more joints simultaneously.
Here’s where the article gets serious;
❏½ Partial to marked clinical response: 14 patients who were only given a topical corticosteroid.
❏½ Partial clinical response: 3 patients who received narrowband UV-B, UV-A1, and bath psoralen plus UV-A.
❏½ No clinical response: One patient received standard psoralen plus UV-A therapy without benefit.
TABLES
There are two informative tables associated with the article. They are worth reviewing if only to reconfirm the mantra of the PRP community: What works for one doesn’t work for all. Table 1 – Patients receiving Systemic Agents Without Progression to Biologic Agents and Table 2 – Patients Receiving Biologic Agents
❏½ Patients who received acitretin, methotrexate, methotrexate plus acitretin, mycophenolate mofetil, or cyclosporine (Table 1 and Table 2): 25
❏½ Patients received biologic agents, which were frequently used concomitantly with additional therapy (Table 2): 10
❏½ Patients with no clinical response to alefacept (Amevive): 2
❏½ Patients treated with tumor necrosis factor (TNF) antagonists had partial to marked clinical response. The mean interval between initiation of TNF inhibition and notable clinical response was 5.7 weeks.
LIMITATIONS
Researchers are always required to note the limitations of research. In this case:
❏½ The retrospective nature of their data
❏½ Small sample size
❏½ The possibility of spontaneous resolution as opposed to therapeutic effect.
The PRP community agrees with their overall assessment that “additional systematic investigation is necessary to determine which patients with PRP may respond to individual therapeutic options.”
Good grief – it looks like we are back to the PRP community mantra: What works for one doesn’t work for all.