W C Wong

It has been suggested that interleukin 1 (IL-1) may be elevated systemically after major burn injury. Several metabolic changes commonly observed in patients with burns can be attributed in part to elevated IL-1 production; these include temperature elevation, skeletal muscle proteolysis, and alterations in the production of certain serum proteins by the hepatocyte (e.g., albumin and acute phase reactants). In this article we describe a likely source of this elevated IL-1 activity: the burn wound. Fluid taken from blisters on thermally injured skin early after burn injury contains substantial amounts of IL-1. This activity is less apparent in certain blister fluid (BF) samples, probably because of the presence of an inhibitor(s) of lymphocyte proliferation. However, after gel filtration high-performance liquid chromatography, the IL-1 actively elutes at a molecular weight of 15,000 to 20,000 daltons and can be blocked with an antibody to IL-1. We suggest that the source of this IL-1 activity is the injured keratinocyte and that release of this IL-1 systemically is inevitable. We postulate that release of IL-1 from the wound into the systemic circulation accounts in part for the metabolic changes outlined above. Furthermore, since epidermal IL-1 is a potent T cell chemoattractant, we believe that burn wound IL-1 may affect sequestration of T cells near the burn wound, resulting in T cell lymphopenia.

Abstract Pediatric classical Hodgkin's lymphoma (cHL) is characterized by Hodgkin Reed‐Sternberg cells located in an inflammatory microenvironment. Blood biomarkers result from active crosstalk between these cells. One promising biomarker in adult cHL patients is “thymus‐and‐activation‐regulated chemokine” (TARC). The objectives of this study were to define normal TARC values in non‐cHL children and to investigate and correlate pretherapy TARC as diagnostic marker in pediatric cHL. In this multicenter prospective study, plasma and serum samples were collected of newly diagnosed cHL patients before start of treatment (n = 49), and from randomly selected non‐cHL patients (n = 81). TARC levels were measured by enzyme‐linked immunosorbent assay. The non‐cHL patients had a median plasma TARC value of 71 pg/mL (range: 18‐762), compared to 14 619 pg/mL (range: 380‐73 174) in cHL patients ( P < .001). TARC values had a high discriminatory power (AUC = .999; 95% confidence interval, .998‐1). A TARC cutoff level of 942 pg/mL maximized the sum of sensitivity (97.9%) and specificity (100%). TARC plasma levels were associated with age, treatment level, bulky disease, B‐symptoms, and erythrocyte sedimentation rate. TARC was found to be a highly specific and sensitive diagnostic marker for pediatric cHL. This noninvasive marker could be of great value as screening test in the work‐up for pediatric patients with lymphadenopathy.

A 67-year-old female who had a long history of autoimmune thrombocytopenic purpura on corticosteroid therapy was hospitalized because of worsening petechiae and bruises despite apparent normalization of the platelet count. Peripheral blood counts by automated blood cell analyzer (COULTER LH 750) showed: haemoglobin 158 g/l, platelet count 144 × 109/l and leucocyte count 11·4 × 109/l with neutrophilia. However, blood film examination showed a paucity of platelets with an estimated manual platelet count of only 12 × 109/l. Furthermore, the red cells showed the occasional presence of ‘punch-holes’ in their cytoplasm, sometimes resembling a ‘bite-cell’ (left panel). Careful scrutiny of the blood film showed the presence of aggregates of amorphous pale staining materials in the thicker areas, which were barely discernible in the lighter-stained and better-spread areas. A ‘punch-hole’ appearance resulted when the red cells were overlaid with such materials (right panel). A review of the clinical history showed that the patient was a chronic hepatitis C carrier and had recently developed cryoglobulinaemia. The cryoglobulin level was 10·1 g/l. The blood sample was then warmed to 37°C and tested again; the thrombocytopenia was confirmed by the automated blood cell analyzer. Blood film examination showed normalization of the red cell morphology and disappearance of the amorphous materials, confirming that the amorphous materials were cryoglobulin.

Introduction Pediatric classical Hodgkin’s lymphoma (cHL) is characterized by Hodgkin Reed-Sternberg (HRS) cells located in an inflammatory microenvironment. HRS cells and microenvironment communicate through active crosstalk. This results in secretion of blood biomarkers, which may serve as surrogate markers for lymphoma viability [1], [2]. One promising biomarker in adult patients with cHL is “Thymus and Activation-Regulated Chemokine” (TARC) [3], [4]. So far, TARC levels in pediatric cHL patients have not been reported. The objectives of this study were to investigate TARC as a diagnostic marker in pediatric cHL patients and to define normal TARC values in non-cHL children.