Several studies have demonstrated a decreased cytokine production in patients with cancer. Likewise, there is some evidence showing that tumor markers may play a role in immunoregulation. In this work, we have studied the in vitro production of IL-1β, IL-6 and TNF-α in whole-blood cell cultures of 10 healthy subjects after polyclonal activation with lipopolysaccharide of Salmonella enteridis and phytohemagglutinin in the presence or absence of three markers, AFP, CEA and PSA. Each sample was incubated for 48 h at 37°C in a humidified atmosphere of 5% CO2. Subsequently, cytokine levels in the supernatant were determined. AFP did not significantly affect the production of the three cytokines compared to the basal value obtained on adding PBS. In contrast, CEA significantly increased the production of IL-6 (p <0.001) and TNF-α (p = 0.002), while PSA significantly decreased IL-1β (p <0.001), IL-6 (p = 0.031) and TNF-α (p <0.0001) production. These results suggest a possible role of CEA and PSA in the production of these cytokines.
A series of 20 patients with granular lymphocyte proliferative disorders (GLPD) is reported. The criterion of inclusion was presence of persistent (> or = 6 months) granular lymphocytosis in the absence of any causative illness. Diagnoses made upon analytical control in half the patients of splenomegaly (25%) and hepatomegaly (25%) were infrequent. Clinical course was nonprogressive in 17/20 patients, but two developed high-grade NHL several years later and one showed progressive disease. Actuarial probability of survival at 5 years was 85%. Granular lymphocyte morphology was relatively homogeneous, and peripheral blood counts were preserved in the most patients. Bone marrow lymphocytic infiltration was low, as assessed by bone marrow aspiration and/or biopsy. Eosinophilia was an outstanding feature in eight cases. Ultrastructurally, all cases showed parallel tubular arrays; cytoplasmic granules and numerous short microvilli were noticed. The lymphoid phenotype was heterogeneous, the most common being CD2+CD3+CD4-CD8+, but six patients (30%) were CD4+ with variable expression of natural killer-associated antigens. Chromosomal analysis was abnormal in 4/10 patients [trisomy 19, t(5;6); inv(14) and inv(10)]. The study of beta-chain of the T-cell receptor revealed clonal rearrangements in 14 (78%), restricted to CD3+ patients (92%). In vitro culture of myeloid precursors showed decreased CFU-GM in 5/6 patients. Virological studies for HTLV-I and II were negative. In conclusion, the presence of a clonal proliferation was not correlated with the clinical course or an associated disease.
In this short report we describe a patient with human parvovirus B19 (HPV B19)-induced transient pancytopenia. Parvovirus virions were seen by electron microscopy in both erythroid and granulocytic precursors. Erythroid cells are not the only targets in these cases. We draw attention to this disorder so that physicians involved with hematological disorders and transplantation be more aware of this infection.
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