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ScienceWeek
MEDICAL BIOLOGY: OBESITY, SMOKING, AND PSORIASIS
The following points are made by M.D. Herron et al (Arch Dermatol 2005:141;1527-1534)
1) Psoriasis is a common disease, affecting approximately 2% of the population.[1] That psoriasis might serve as a marker of cardiovascular risk, even if indirectly, would be important information for physicians. Three recent articles[2-4] suggest that patients with psoriasis vulgaris are frequently overweight or obese and smoke tobacco more frequently than patients with other skin diseases or in patients from the general population. The implications for caring for these patients go well beyond the dermatologic considerations.
2) The association between obesity and psoriasis has been suspected by clinicians for many years. A recent report[2] has confirmed the association between obesity and psoriasis and answers a number of important questions about that association. The prevalence of obesity in psoriasis patients at the University of Utah's dermatology clinic was nearly double that of the general population in Utah and also greater than the prevalence of obesity in the dermatology clinic population without psoriasis.[2] A report by McGowan et al[3] noted a higher frequency of overweight and obesity in nationally representative data sets of psoriasis patients compared with the nonpsoriatic population, although the study was not sufficiently powered to detect statistical significance.
3) Given evidence suggesting that psoriasis and obesity are linked, it is important to know whether obesity causes psoriasis or results from this skin disease. Herron et al[2] report that most patients had a normal body mass index at age 18 years and at onset of psoriasis, but 71% became overweight or obese at some point after acquiring psoriasis. The body mass index of psoriasis patients in this study was significantly greater than that of the Utah population (after controlling for sex and age) and also was greater than the dermatology clinic population without psoriasis. Similarly, the median body image score was normal at the onset of psoriasis, but increased to indicate overweight or obesity after psoriasis developed. The authors concluded that obesity is a consequence rather than a risk factor for psoriasis.
4) The authors conclude: Patients with psoriasis attending the University of Utah Dermatology Clinics were more likely to be obese and to smoke compared with nonpsoriatic patients and more likely to be obese compared with other large cohorts with psoriasis. Smoking appears to have a role in the onset of psoriasis, but obesity does not. The high prevalence of obesity and smoking in a psoriasis cohort has not been previously noted; if confirmed, it supports the prediction that a significant portion of patients with psoriasis will have the comorbid conditions and public health issues of those with obesity and smoke.[4.5]
References (abridged):
1. National Psoriasis Foundation. Psoriasis statistics. Available at: http://www.psoriasis.org/about/stats/. Accessibility verified December 9, 2005
2. Herron MD, Hinckley M, Hoffman MS, et al. Impact of obesity and smoking on psoriasis presentation and management. Arch Dermatol. 2005;141:1527-1534
3. McGowan JW, Pearce DJ, Chen J, Richmond D, Balkrishnan R, Feldman SR. The skinny on psoriasis and obesity. Arch Dermatol. 2005;141:1601-1602
4. Fortes C, Mastroeni S, Leffondré K, et al, for the IDI Multipurpose Psoriasis Research on Vital Experiences (IMPROVE) Study Group. Relationship between smoking and the clinical severity of psoriasis. Arch Dermatol. 2005;141:1580-1584
5. Naldi L, Chatenoud L, Linder D, et al. Cigarette smoking, body mass index, and stressful life events as risk factors for psoriasis: results from an Italian case-control study. J Invest Dermatol. 2005;125:61-67
J. Am. Med. Assoc. http://www.jama.com
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Related Material:
THE PLACEBO EFFECT IN EVALUATING PSORIASIS TREATMENT
The following points are made by P.I. Spuls et al (Arch Dermatol. 2004;140:338-344):
1) In measuring the specific effects of systemic therapeutic interventions, researchers keep in mind that the natural course of a disease as well as the placebo effects of an intervention can influence therapeutic outcome.(1) The natural course of psoriasis varies considerably from patient to patient. Variation may include chronic persistence of the lesions for many years, temporary remissions with or without exacerbation, and persistent or only temporary regression.(2) Endogenous and exogenous factors can initiate, aggravate, or provoke the clinical manifestations.
2) Placebo effects have been reported to influence treatment outcome in general in up to 35% of patients.(3) These effects include patient expectations, the attitude and instructions given by the treating physician, the treatment mode, and even the color of drugs.(4) The existence of variation in the natural course and the placebo effect are therefore good reasons for the inclusion of placebo control groups in clinical trials of new therapies and to blind patients and physicians from treatment allocation.
3) The influence of natural course and placebo on treatment outcome in psoriasis has been the subject of debate. In chronic plaque-type psoriasis, variations in clinical expression are considered to be limited. The need for placebo control groups is believed by many to be less urgent for this disease than it is for more variable diseases.(5)
4) Some data about the natural course of psoriasis and the percentage of patients with self-limiting psoriasis can be obtained from older epidemiologic studies. Farber et al (1968) reported that nearly 40% of the patients experienced at least once in their life an episode of complete remission. These results were based on patient questionnaires, without specifying the duration and extent of the psoriasis or factors influencing these episodes. In that review, 29% of the patients claimed that their psoriasis went into remission without physician-directed therapy. Krueger (1993) wrote that after the onset, psoriasis tends to wax and wane, but spontaneous remission is rare. Greaves and Weinstein (1995) wrote that psoriasis plaques can regress spontaneously without scarring after weeks, months, or years.
5) The authors report a study to determine the outcome in placebo-treated patients with plaque-type psoriasis. The study involved an online search of MEDLINE and EMBASE until January 2001 and the Cochrane Library (2001, issue 1), supplemented by references, reviews, guidelines, and textbooks. The authors conclude that the effect of treatment in placebo groups varies across studies in an unpredictable way, and that to evaluate the variability, improvement of the standardization of study designs, entry criteria, and outcome measures is necessary in psoriasis trials.
References (abridged):
1. Kleijnen J, de Craen AJ, van Everdingen J, Krol L. Placebo effect in double blind clinical trials: a review of interventions with medications. Lancet. 1994;344:1347-1349
2. Braun-Falco O, Plewig G, Wolff HH, Winkelman RK. Erythematous and erythematosquamous skin diseases. In: Braun-Falco O, Plewig G, Wolff HH, Burgdorf WHC, eds. Dermatology. Berlin-Heidelberg, Germany: Springer-Verlag; 1991:403-466
3. Beecher HK. The powerful placebo. JAMA. 1955;159:1602-1606
4. De Craen AJ, Roos PJ, de Vries AL, Kleijnen J. Effect of colour of drugs: systematic review of perceived effect of drugs and of their effectiveness. BMJ. 1996;313:1624-1626
5. Rawlinson MC. Truth-telling and paternalism in the clinic: philosophical reflections on the use of placebos in medical practice. In: White L, Tursky B, Schwartz GE, eds. Placebo: Theory, Research, and Mechanisms. New York, NY: Guilford Press; 1985:403-418
Archives of Dermatology http://pubs.ama-assn.org
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OBESITY AND THE RISK OF HEART FAILURE
The following points are made by S. Kenchaiah et al (New Engl. J. Med. 2002 347:305):
1) Heart failure is a major health problem that is increasing in scope.(1) Despite recent therapeutic advances, morbidity and mortality after the onset of heart failure remain substantial.(1) Consequently, prevention of heart failure through identification and management of risk factors and preclinical phases of the disease is a priority.(2) In this context, several studies have evaluated body-mass index (the weight in kilograms divided by the square of the height in meters) as a risk factor for left ventricular remodeling and overt heart failure. In these investigations, obesity has been consistently associated with left ventricular hypertrophy and dilatation,(3-5) which are known precursors of heart failure. Whereas extreme obesity has been associated with heart failure, data are limited regarding the influence of overweight and lesser degrees of obesity on the risk of heart failure. Accordingly, the authors investigated the relation of body-mass index with the risk of heart failure in a community-based sample.
2) The authors investigated the relation between the body-mass index and the incidence of heart failure among 5881 participants in the Framingham Heart Study (mean age, 55 years; 54 percent women). During follow-up (mean, 14 years), heart failure developed in 496 subjects (258 women and 238 men). After adjustment for established risk factors, there was an increase in the risk of heart failure of 5 percent for men and 7 percent for women for each increment of 1 in body-mass index. As compared with subjects with a normal body-mass index, obese subjects had a doubling of the risk of heart failure. For women, the hazard ratio was 2.12 (95 percent confidence interval, 1.51 to 2.97); for men, the hazard ratio was 1.90 (95 percent confidence interval, 1.30 to 2.79).
3) The authors conclude that in their large, community-based sample, increased body-mass index was associated with an increased risk of heart failure. The authors suggest that given the high prevalence of obesity in the US, strategies to promote optimal body weight may reduce the population burden of heart failure.
References (abridged):
1. American Heart Association. 2002 Heart and stroke statistical update. Dallas: American Heart Association, 2001
2. Hunt SA, Baker DW, Chin MH, et al. ACC/AHA guidelines for the evaluation and management of chronic heart failure in the adult: executive summary: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Committee to Revise the 1995 Guidelines for the Evaluation and Management of Heart Failure). J Am Coll Cardiol 2001;38:2101-2113
3. Messerli FH, Sundgaard-Riise K, Reisin ED, et al. Dimorphic cardiac adaptation to obesity and arterial hypertension. Ann Intern Med 1983;99:757-761
4. Hammond IW, Devereux RB, Alderman MH, Laragh JH. Relation of blood pressure and body build to left ventricular mass in normotensive and hypertensive employed adults. J Am Coll Cardiol 1988;12:996-1004
5. Lauer MS, Anderson KM, Kannel WB, Levy D. The impact of obesity on left ventricular mass and geometry: the Framingham Heart Study. JAMA 1991;266:231-236
New Engl. J. Med. http://www.nejm.org
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