The systemic manifestations accompanying erythema nodosum can be differentiated from those associated with the precipitating infectious process and from coincident disease processes. Erythema nodosum itself is characterized by (a) skin lesions at pressure sites, (b) malaise, fever and occasionally chills, (c) arthritis (70 per cent) and (d) over-reactivity of tissue. Tissue hypersensitivity is most pronounced at sites of trauma, at sites of specific skin testing, and in the lymphoid system draining infections in the pharynx and lung. Common infections of the respiratory tract most often antedate attacks of erythema nodosum. In New England, a beta-hemolytic streptococcus infection is a common causative factor, and tuberculosis is an unusual causative factor. In endemic areas, coccidioidomycosis is a common cause of erythema nodosum. The most important coincidental disease process is rheumatic heart disease. Rarely is it a sequel of erythema nodosum. Other "collagen diseases" may coexist with erythema nodosum. Erythema nodosum is its own most common complication. Follow-up studies indicate that over half of the patients have a subsequent attack, and a certain number have recurrent episodes for months to years. The management of erythema nodosum is expectant. In each case the cause should be found and treated. Steroid treatment is rarely justified, and should be used only after tuberculosis and other treatable entities have been ruled out.

Arthritis↗

PubMed1955

The acceleration and inhibition of migration of human leucocytes in vitro by plasma protein fractions.

A new method is described for the quantitative study of leucocyte migration. Blood drawn into a capillary tube is centrifuged, forming a buffy coat. The migration of the leucocytes from the buffy coat into the plasma is measured by means of an ocular micrometer. While there is a great deal of variation from one normal individual to another in the migration rates of leucocytes those of each individual show relatively little variation in migration from day to day (Table I). In all cases of illness studied, the average migration rates fall within the normal range, but there was a wider variation in the day to day migration rate than obtains in normal healthy individuals (Tables II and III). From experiments in which the cells with typically "slow" and "fast" migration rates were tested in both the "slow" and "fast" plasmas, it could be concluded that while the cells invariably have some influence on the migration rate, the major factors influencing leucocyte migration reside in the plasma (Table V). Experiments in which the plasma proteins were fractionated according to the method of Lever et al. indicated the presence of a system of proteins which regulate leucocyte migration. A heat-labile (56 degrees C. for 30 minutes) component of fraction II was able to accelerate leucocyte migration, while fraction III acted as an inhibitor (Tables IX and X).

Blood Proteins↗

PubMed1955

Correlations between plasma protein fractions, antibody titers, and the passive transfer of delayed and immediate cutaneous reactivity to tuberculin PPD and tuberculopolysaccharides.

GUINEA PIGS SENSITIZED WITH TUBERCLE BACILLI DEMONSTRATE A DUAL ALLERGIC RESPONSE MEDIATED BY TWO CHEMICALLY DISTINCT PLASMA FRACTIONS: 1. Antibody to tuberculopolysaccharide is located exclusively in fraction II (gamma globulin). This fraction will passively transfer systemic anaphylaxis and urticarial type skin reactivity to tuberculopolysaccharide, and contains the Middlebrook-Dubos antibody. 2. Antibody to tuberculoprotein is contained exclusively in a new plasma fraction called fraction IV-10. By Cohn's Method X, fraction IV-10 is a part of fraction IV (alpha globulin) and to a lesser extent V (albumin). This fraction will passively transfer to normal guinea pigs a delayed type skin sensitivity to tuberculin PPD which is maximal between 18 and 30 hours, and it contains the Boyden antibody. When fractions II and IV-10 are combined, the antibody to tuberculopolysaccharide inhibits the passive transfer of delayed type reactivity. Combination of these two fractions does not alter their separate in vitro hemagglutinating properties. Adsorption of IV-10 with Boyden sensitized cells removes its ability to transfer delayed type tuberculin sensitivity. Adsorption of II with Middlebrook-Dubos-sensitized cells removes its capacity to effect passive transfer of immediate type reactivity to tuberculopolysaccharides.

Animals↗

PubMed1955