CORRESPONDENCE J
one m e c h a n i s m for this is hypertension. 4-6 As soluble E-selectin is also raised in hypertension, 7 we m a y have e x p e c t e d TM to be increased as well. We were t h e r e f o r e surprised at the recent findings by Cacoub et al, 1 w h o found low levels of this m a r k e r in p r i m a r y p u l m o n a r y hypertension and precapillary pulm o n a r y hypertension, but raised levels in postcapillary hypertension. As the authors suggest, changes in TM levels m a y be a prim a r y o r s e c o n d a r y event, or m a y be related to renal or liver function, and have interesting impliKristine L. MacDonald, MD, MPH cations for vascular cell biology in hypertension. Michael T. Osterholm, PhD, MPH One w a y forward would be to PhiUip K. Peterson, MD c o m p a r e TM levels with those of 1. MacDonald KL, Osterholm MT, LeDell KH, et ah other established m a r k e r s of enA case-control study to assess possible triggers Patrick B. Hart, MD dothelial d a m a g e such as vWf, as and cofactors in chronic fatigue syndrome. Am J Maryville, Missouri this group have done on previous Med. 1996;100:548-554. occasions, s'9 Indeed, high vWf lev2. Hickie I, Lloyd A, Wakefield D, Parker G. The psychiatric status of patients with chronic fatigue syn- 1. Ervin F. Strategic business planning for internal els have also b e e n d e m o n s t r a t e d medicine. Am J Meal. 1996;101:95-99. drome. Br J Psych. 1990;156:534-540. in p u l m o n a r y hypertension; 10,~1 3. Rodin G, Voshart K. Depression in the medically 2. Drucker P. Management Tasks, Responsibilities, this is not surprising as the pulPractices. New York: Harper & Row; 1974. ill: an overview. Am J Psychiatry. 1986;143:696m o n a r y vasculature has signifi705. cant influences on p l a s m a vWf 4. BatesDW, Schmitt W, BuchwaldD, et al. Prevalence Manuscript submitted November 4, 1996, and levels. In p r i m a r y p u l m o n a r y hyof fatigue and chronicfatiguesyndromein a primarycare accepted December 17, 1996. practice. Arch Intern Med. 1993;153:2759-2765. p e r t e n s i o n , histological evidence 5. Vercoulen JHMM, Swanink CMA, Zitman FG, et of injury to p u l m o n a r y endothelial PLASMA al. Randomised, double-blind, placebo-controlled cells has also b e e n associated study of fluoxetine in chronic fatigue syndrome. Lan- THROMBOMODULIN IN with elevations of p l a s m a vWf, ATHEROSCLEROSIS AND cet. 1996;347:858-861. thus contributing to the risk of 6. Demitrack MA, Date JK, Straus SE, et al. Evi- ITS RISK FACTORS dence for impaired activation of the hypothalamict h r o m b o s i s and a hemodynamipituitary-adrenal axis in patients with chronic fatigue To the Editor: cally-induced increase in the ensyndrome. J Clin Endocrinol Metab. We read with interest the recent dothelial release of vWf. 11 1991;73:1224-1234. While Cacoub et al 1 mention 7. Bell DS. Chronic fatigue syndrome update: find- p a p e r b y Cacoub et all demonthat their levels of TM failed to ings now point to CNS involvement. Postgrad Meal. strating low levels of sTm in pa1994;96:73-81. tients with p u l m o n a r y hyperten- correlate with those of endothsion. As endothelial cell damage d i n - l , w e w o n d e r if further data Manuscript submitted November 12, 1996 and m a y be the primary event in ath- f r o m this group reporting estabaccepted November 14, 1'996. erosclerosis, 2 then m a r k e r s of vas- lished endothelial cell markers, cular insult m a y provide clues such as vWf, or other p a r a m e t e r s STRATEGIC BUSINESS PLANNING FOR INTERNAL a b o u t the d e v e l o p m e n t of this dis- of endothelial damage in pulmoease f r o m its established risk fac- n a r y hypertension m a y be m o r e ilMEDICINE tors. Three possible m a r k e r s in- luminative. Finally, we are declude v o n Willebrand factor lighted that their finding of lower To the Editor: Instead of providing internal (vWf), soluble E-selectin, and sol- levels of TM in females confirms medicine with a timely and useful uble t h r o m b o m o d u l i n (TM), in- our o w n recent report.12 Gregory Y.H. Lip, MD strategic business plan, Dr. F. Ri- creasing levels suggesting endoUniversity Department of chard Ervin a p p e a r s content to re- thelial cell injury or damage, 8'4 Medicine, City Hospital, hash h o a r y mythology. 1 Strategic I n c r e a s e d vWf is an established Birmingham, England planning has been defined as the feature in atherosclerosis, and additional studies are needed to determine whether ghic0corticoid deficiency can account for sympt o m s p r e s e n t in patients with CFS, and w h e t h e r s y m p t o m s c a n be imp r o v e d through ameliorating the deficiency. Immunologic, neurotransmitter, and hypothalamic-pituitary axis abnormalities have all b e e n described in patients with CFS. 7 The interrelationship b e t w e e n these abnormalities, the pathophysiology of s y m p t o m s associated with CFS, and the triggers of the s y n d r o m e still require further study. ,~
use of selected m e a n s in predetermined w a y s to attain desired results. 2 The m o s t likely result of Dr. Ervin's m e a n s - - h i s campfire stories a b o u t family p h y s i c i a n s - would be to drive m o r e wedges of misunderstanding b e t w e e n internists and family physicians. Good will, cooperation, and clear thinking are w h a t are needed, n o t further Balkanization. P e r h a p s Dr. Ervin's article can b e used to p r e p a r e medical students w h o are planning careers in generalism for the snide r e m a r k s they m a y h e a r from s o m e academic medical faculty. As a business strategy, Dr. Ervin's plan m a y provide short-term feelings of superiority for a few, but little longrange direction for internal medicine.
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