Background. Assessment methods for atopic dermatitis (AD) are not standardized, and therapeutic studies are difficult to interpret. Aims. To obtain a consensus on assessment methods in AD and to use a statistical method to develop a composite severity index.Methods. Consensus definitions were given for items used in the scoring system (extent, intensity, subjective) and illustrated for intensity items. Slides were reviewed to address within and between-observer variability by a group of 10 trained clinicians, and data were statistically evaluated with a two way analysis of variance. Two variants of an assessment system were compared in 88 patients at 5 different institutions. Data were analyzed using principal-component analysis. Results. For 5 intensity items studied (erythema, edema/papulation, oozing/crusts, excoriations, lichenification), within- and between-observer variability was good overall, except for edema/papulation which was difficult to assess with slides. In the series of 88 patients, principal-component analysis allowed to extract two unrelated components: the first one accounting for 33% of total variance was interpreted as a ‘severity’ component; the second one, accounting for 18% of variance, was interpreted as a ‘profile’ component distinguishing patients with mostly erythema and subjective symptoms and those with mostly lichenification and dryness and lower subjective symptoms. Of the two evaluation systems used, the one using the rule of nine to assess extent was found more workable than the one using a distribution × intensity product. A scoring index (SCORAD) combining extent, severity and subjective symptoms was mathematically derived from the first system and showed a normal distribution of the population studied. Conclusion. The final choice for the evaluation system was mostly made based on simplicity and easy routine use in outpatient clinics. Based on mathematical appreciation of weights of the items used in the assessment of AD, extent and subjective symptoms account for around 20% each of the total score, intensity items representing 60%. The so-designed composite index SCORAD needs to be further tested in clinical trials.
A newly developed ELISA was used to detect and quantify the presence of a soluble form of intercellular adhesion molecule-1 (sICAM-1) in the circulation of healthy individuals compared with patients with psoriasis vulgaris. Seventeen psoriatic patients were studied. The extent of skin lesions was rated by the psoriasis area and severity index (PASI). Seventeen age- and sex-matched healthy individuals served as controls. Serum levels were measured by an ELISA technique utilizing an anti-ICAM-1 murine monoclonal antibody bound to the solid phase, and a second, peroxidase-conjugated monoclonal antibody reacting with sICAM-1. Serum levels in controls were 358.8 +/- 87.9 ng/ml sICAM-1, and 480.5 +/- 133.6 ng/ml in psoriatics (mean +/- SD; P = 0.02). In psoriasis, sICAM-1 levels were found to be directly proportional to the PASI score (y = 363.002 + 8.525x, R = 0.55, P = 0.021). These data suggest that the concentration of sICAM-1 in serum increases during psoriatic inflammation. The origin and function of sICAM-1 in psoriasis remain to be defined.
Chloroquine is known to exacerbate psoriasis. Since immunological stimuli are considered to be important for the pathogenesis of psoriasis, we compared the effects of chloroquine on cell-mediated immunity in 15 healthy control individuals and 15 patients with psoriasis. We employed the spontaneous and phytohemagglutin (PHA)-induced uptake of 3H-thymidine to measure lymphocyte proliferation. Chloroquine was added to the cultures at concentrations ranging from 0.022 to 220 μM. We found that both spontaneous and PHA-driven lymphocyte proliferations were significantly lower in patients with psoriasis (p < 0.002). The spontaneous blastogenesis in both controls and patients remained stable under chloroquine. In PHA-driven cultures in controls, 0.022––2.2 μM chloroquine had no effect, higher concentrations of the drug suppressed proliferation. In patients, 22 μM chloroquine surmounted the suppression of the PHA-induced proliferative response found in controls; moreover, 2.2––0.022 μM chloroquine increased lymphocyte proliferation by > 300% (p < 0.002). Our data indicate that in psoriasis the lower lymphocyte transformation is abnormally stimulated by the addition of pharmacological doses of chloroquine.
The purpose of this study was to measure soluble CD 14 (sCD14) molecules in the skin and in serum of patients with psoriasis. CD 14 is a newly discovered cell surface marker on monocytes that is shed after cell activation. The following procedures were used: suction blisters were raised over the abdominal skin of 9 healthy control individuals and 8 patients with psoriasis. Serum of 17 healthy controls and 17 patients with psoriasis was collected. sCD14 was determined in suction blister fluid and serum by the ELISA technique. The clinical status of psoriasis was rated by the psoriasis area and severity index (PASI score). We found that sCD14 levels in suction blisters of healthy skin (1,050 ± 236 ng/ml, mean ± SE) were similar to those of nonlesional psoriatic skin (841 ± 113 ng/ml). By contrast, control serum contained 2,687 ± 167 ng/ml, but psoriatic serum 4,059 ± 388 ng/ml sCD14 (p = 0.001, Wilcoxon test). Linear regression analysis revealed that serum sCD14 levels and the PASI score of patients did not correlate. We conclude that there is an abnormal monocyte stimulation in blood but not in nonlesional skin in psoriasis that is independent from the clinical status expressed by the PASI score.
Although a number of skin diseases are characterized by the presence of an increased number of phagocytes in their lesions, the effects of alcohol on phagocytic functions are not clearly understood. Therefore, we measured the influence of ethanol and acetaldehyde on the generation of oxygen radicals, chemotaxis and the release of lysosomal enzymes from human phagocytes. We added 0.03%-3% ethanol and 0.005%-0.25% acetaldehyde to cell cultures. We found that both ethanol and acetaldehyde suppressed the generation of oxygen radicals from granulocytes and monocytes; the ID50 was achieved at concentrations of approximately 0.25% for ethanol and 0.03% for acetaldehyde. A significant inhibition of granulocyte chemotaxis was first noted with 0.063% ethanol and 0.016% acetaldehyde. Ethanol and acetaldehyde inhibited the release of the lysozyme of monocytes at concentrations of greater than 0.75% and greater than 0.03% respectively, but granulocytes were unaffected; the release of beta-glucuronidase and lactate dehydrogenase remained stable. Due to the high volatility of the agents, especially acetaldehyde, under the experimental procedures employed, the actual concentrations of the agents were probably lower and similar to those measured in vivo. Our results indicate that defined phagocytic functions are strongly inhibited by concentrations of ethanol and acetaldehyde which are associated with moderate to severe inebriation.
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