LETTERS The physician scientist, peer review, and creativity To the Editor: Two recent publications l ,2 define a faculty recruitment problem facing academic health sciences centers, that is, the decrease in number of physician scientists active in clinical research. Both articles propose solutions for funding salaries and research support for physician scientists; however, the academic supports suggested have the crucial restraint of scientific peer review. By its very nature, the creation of new concepts necessitates confrontation. This leads to intellectual polarization between those holding older concepts and those proposing new theories. Thus, in the early development of new ideas, the greatest deterrent to the creative process is the scientific establishment, which is historically nonsupportive to most new ideas that question the validity of established concepts. 3 The second deterrent to neophyte physician scientists is the need for personal salary support, time for investigative endeavors, and research funds. Each of the proposed mechanisms to reverse the decline of the number of active physician scientists places the control of academic positions and research funds for physician scientists in the hands of those in the administrative structure of the academic centers or national scientific organizations. The scientific leadership of these groups tends to be conservative and steeped in older concepts perceived as stable, productive areas for research. 4 These leaders also favor for support those who matured under their tutelage and who share their concepts. New ideas in the beginning have little or no information about their validity. In addition, their credibility is further reduced when proposed by relatively unknown scientists. Administrators with limited financial resources in scientific institutions prefer to place their research funds in "guaranteed research," which they perceive has a minimum of associated controversy and a high potential for success. In the past economic climate of academic medical centers and before profit-oriented managed care, many physician scientists in academic centers used revenues from their clinical work to support their research. This economic circumstance freed them from the control of their scientific peers and fostered creativity. The new economics of managed patient care in the past two decades have not only reduced revenues from patient care, but the control of these revenues has been diverted to health maintenance organizations, central administrations of health science centers, or combinations of both. Because academic health science centers have had insufficient finances to support the wide range of their
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academic responsibilities, they have become increasingly dependent on revenues from patient care for their continued survival and have demanded more revenueproducing clinical work from their faculty physicians. Thus administrators in academic centers have not only reduced faculty time for research but they have taken patient care revenue and dedicated its use for education and limited, prioritized, institutional research goals. A consequence of the new economic climate in academic health science centers in the United States has been the demise of a highly successful model for funding innovations. To support uninhibited creativity without the inhibition of peer review, we need to re-establish the economic means to allow physician scientists to use significant amounts of the funds they generate from patient care for their health research projects. It would require administrators of academic health centers to reduce their increasing dependence on revenues from patients' fees and procure other resources to accomplish their institutional educational objectives. In the past, physician scientists with innovative controversial ideas not sanctioned by their scientific peers had to have independent resources to pursue their research. This historic economic model of physician scientists who funded their research from clinical practice fees offered a unique, productive, uninhibited support system for creativity. I am not confident that the proposed models,I,2 which depend on scientific peer and administrative controls, will duplicate our past laissez-faire creative freedom. Ramon M. Fusaro, MD, PhD Creighton University 984360 Nebraska Medical Center Omaha, NE 68198-4360 E-mail address:
[email protected] REFERENCES 1. Sontheimer RD, Werth VP. Whither the patient-oriented researcher? J Am Acad Dermatol1998;39:109-l3. 2. Goldstein JL, Brown MS. The clinical investigator: bewitched, bothered, and bewildered-but still loved. J Clin Invest 1997;99:2803-12. 3. Lillehei CWO New ideas and their acceptance: as it has related to preservation of chordae tendinea and certain other discoveries. J Heart Value Dis 1995;4(suppl 2):S106-14. 4. NIH peer review: time for some changes [editorial]. Nature Biotechnol1998;16:395.
Skin Signs of Systemic Disease To the Editor: It is now common practice for authors to reply to reviews of their books when they believe factuJournal of the American Academy of Dermatology
Journal of the American Academy of Dermatology Volume 40, Number 5, Part I
al errors have been made. In the review of the third edition of my book Skin Signs of Systemic Disease by Thiers in the October 1998 issue of the Journal (vol 39, p 665), the proposition is made that the delay of 2 years from submission of the manuscript to actual publication leads invariably to much of the material being dated. As an example the reviewer cites the fact that the connection between human herpesvirus 8 and Kaposi's sarcoma is not made in the chapter on AIDS. In fact, it is made in that chapter (p 183) and again in Chapter 2 (p 123, references 294a [1996] and 295 [1995]) in which the entire story of this novel herpesvirus in all forms of Kaposi's sarcoma is discussed. Because the bulk of the references may be from the early 1990s does not mean that the material is dated because the latest publications on any subject are not necessarily better than those published earlier. In fact, every subject was reviewed for the latest and best references as of 1996 when the manuscript was submitted and, if found, they were included. The actual publication of the book was October 1997. Unfortunately, it is the conceit of modem man to believe that only the latest information is correct and that all previous scientific or humanistic contributions, whether publications or illustrations, are no longer relevant. Irwin M. Braverman, MD Professor of Dermatology Department of Dermatology School of Medicine Yale University 333 Cedar St PO Box 208059 New Haven, CT 06502-8059
UVA therapy for scleroderma To the Editor: UVA I (340-400 nm) radiation has recently been reported to be effective in the treatment oflocalized scleroderma. 1,2 Its mechanism of action appears to be the direct stimulation of collagenase production by dermal fibroblasts. Unfortunately, the cost of UVA I light sources is prohibitive. But in their original work Petersen, Hansen, and Craig3 irradiated fibroblast cultures with standard UVA fluorescent bulbs (320-400 nm) and noted stepwise increases in collagenase messenger RNA production, suggesting to us that standard UVA might be effective as well. Using a Dermalite metal-halide light box with standard UVA filters, we have now treated one patient with localized scleroderma and another with systemic scleroderma with encouraging results. Case 1 was an ll-year-old Caucasian boy with a lifelong history of localized scleroderma on the left lower eyelid. Because of increasing eyelid retraction, low-
Letters 787 dose UVA therapy was begun using the same general protocol as Kerscher et al.I The lesion was spot-treated with 20 J/cm2 4 times weekly for 6 weeks, then once weekly for 6 weeks. Within 1 week the lesion had noticeably softened and the lid retraction reversed. The lesion continued to clear during the 12 weeks of therapy with significant softening, tanning, and thinning of the skin. At 3 months' follow-up, the lesion is quiescent with no lid retraction. Case 2 was a 42-year-old Thai woman with a history of progressive systemic sclerosis for 3 years with diffuse skin sclerosis associated with intractable pruritus, severe decreased range of motion of the arms and hands associated with joint contractures and claw hands, and severe perioral involvement impeding eating. Positive laboratory findings included an antinuclear antibody titer of I :640 with a nucleolar/homogeneous pattern, +Scl-70, and +Jo-1. D-Penicillamine and relaxin therapy were without benefit. In June 1998 we initiated whole-body UVA therapy 3 times per week at 20 J/cm 2. Within 3 weeks she noticed marked alleviation of her pruritus and facial sclerosis. Within 2 months the skin on her abdomen and thighs had noticeably softened. Because of the dramatic improvement in both these patients, we now advocate considering a trial ofUVA for all new patients with scleroderma following the protocol of Kerscher et al,1 substituting standard UVA for their UVA I' It is our reasoning that, if started at the earliest sign of sclerosis, standard UVA may arrest and reverse some of the cutaneous manifestations of scleroderma. James W. Steger, MD Jeanette H. Matthews, MD Department of Dermatology Naval Medical Center San Diego, CA 92134-5000 REFERENCES 1. Kerscher M, Volkenapdt M, Gruss C, Reuther T, Kobyletzki G, Freit~g M, et al. Low-dose UVA, phototherapy for treatment of localized scleroderma. J Am Acad DermatoI1998;38:21-6. 2. Stege H, Berneburg M, Humke S, Klammer M, Grewe M, Grether-Beck S, et al. High-dose UVA, radiation therapy for localized scleroderma. J Am Acad Dermatol 1997;36:938-44. 3. Petersen MJ, Hansen C, Craig S. Ultraviolet A irradiation stimulates collagenase production in cultured human fibroblasts. J Invest Dermatol 1992;99:440-4.
Reply To the Editor: This brief observation is important because UVA I irradiation devices indeed are highly expensive and therefore not accessible to most dermatologists.! Steger and Matthews advocate treating scleroderma at the earliest sign of sclerosis with stan-