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The biological association between chronic lymphocytic thyroiditis (CLT) and differentiated thyroid cancer (DTC) has not been elucidated yet. The aim of the study was to assess whether the presence of CLT exerts any influence on clinical or histological presentation of DTC. Nine hundred and seven consecutive patients with DTC treated in the years 1998–2016 were divided into two groups according to the presence or absence of concomitant CLT. The statistical differences were analysed. Out of 907 patients included in the study, 331 were diagnosed with DTC and CLT (studied group), while 576 patients with DTC but without CLT constituted a control group. The distribution of papillary and follicular thyroid cancer did not differ. In CLT group, the prevalence of pT1 was greater than for pT2–pT4 DTC (P= 0.0003; OR = 1.69, 95% CI 1.27–2.24) compared to controls (68.3 vs. 56.1%, respectively). The presence of multifocal lesions was similar. The thyroid capsule infiltration without extrathyroidal invasion (P< 0.0001; OR = 0.21, 95% CI 0.14–0.31) was more frequent in the studied group, unlike extracapsular invasion, which was significantly more often present in patients with DTC but without CLT (P= 0.004; OR = 1.66; 95% CI 1.17–2.34) as well as nodal involvement (P= 0.048; OR = 0.65, 95% CI 0.42–0.99). The collected data indicate a protective role of CLT in preventing the spread of the DTC. The presence of CLT might limit tumour growth to the primary site.

Cells from pleural effusions (28 malignant and 14 nonmalignant with reactive mesothelial cells) were examined in parallel by means of conventional cytology and multiparametric flow cytometry. The latter included the evaluation of DNA ploidy, the calculation of DNA index (DI), the determination of S phase fraction (SPF), and cell proliferation associated with Ki-67 antigen expression. Propidium iodide was used for the DNA staining, and fluorescein-conjugated monoclonal mouse antibodies were applied to the human Ki-67 antigen staining. The specimens were analyzed by the Becton Dickinson (BD) FACScan apparatus. 104 events were collected, and thereafter the obtained data were analyzed by the software Lysis II and CellFit (BD) for DNA and Ki-67 data analysis, respectively. Out of the 28 cases examined, 18 (64%) of the malignant effusions were aneuploid. All of the benign effusions were typically diploid. The average SPF of benign, malignant diploid, and malignant aneuploid cases was 6, 6, and 30 respectively. The comparison between SPF and DI in malignant cases showed a significant correlation (p < 0.001). The average of Ki-67-positive cells that were benign, malignant diploid, and malignant aneuploid were 11, 19, and 35, respectively. There was a significant correlation between Ki-67 expression, SPF (p < 0.05), and the percent of the aneuploid cell population (p = 0.01). The sensitivity of conventional cytology, the determination of DNA ploidy and of Ki-67 expression, was 80, 64, and 92%, respectively; specificity was 100% for cytology and DNA ploidy and 46% for Ki-67 expression. These data show that Ki-67 antigen expression is a potentially useful adjunct to cytometric DNA content analysis, determination of SPF, and conventional cytology in the diagnosis of malignant pleural effusions.

A reciprocal regulation between the expression of tumor necrosis factor (TNF)-alpha and interleukin (IL)-10, demonstrated in monocytes and mesangial cells, provides a rationale for new therapeutic approaches in glomerulonephritis (GN). Administration of IL-10 to mice with antibody- mediated GN attenuated the severity of glomerular lesions. Recently, however, it has been shown that the genetically determined predominance of Th1 or Th2 cytokines results in different glomerular responses to the same planted antigen, but in an equally severe impairment of renal function. We looked for the expression of IL-10 and TNF-alpha in 111 renal biopsy specimens with proliferative and nonproliferative forms of GN and in 10 control kidneys, by means of immunocytochemistry, in situ hybridization, or reverse-transcriptase polymerase chain reaction (RT- PCR). Six patients had acute endocapillary GN (AGN), 10 patients had pauci-immune GN due to microscopic polyangiitis (MP), 48 patients had immunoglobulin-A (IgA)-GN, 18 patients had idiopathic membranous GN (IMGN), 12 patients had minimal change disease (MCD), and 13 patients had focal segmental glomerulosclerosis (FSGS) and four other forms of GN. Antibodies against monocytes (CD14) and macrophages (CD68) were applied to attribute the expression of TNF-alpha and IL-10 to resident renal or infiltrating cells. We show that mRNAs for TNF-alpha and IL-10 are detected by RT-PCR and in situ hybridization in the normal kidney. A constitutive expression of TNF-alpha protein is observed in mesangial cells, smooth muscle cells in renal arteries, and in the interstitium. A trace immunoreactivity for IL-10 is restricted to arterial smooth muscle cells, distal tubular epithelial cells, and some interstitial cells. Upregulation of both cytokines is found in glomerular diseases. The expression of TNF-alpha increases in mesangial areas in MCD, IMGN stages I/II, and IgA-GN with minor glomerular abnormalities, that is, under conditions with a generally well-preserved glomerular structure. Conversely, marked glomerular proliferation in IgA-GN and, particularly, acute vascular lesions in MP, are accompanied by a significant upregulation of IL-10 (at the mRNA and protein level). Patients with nephrotic-range proteinuria show a significant increase in tubulointerstitial expression of IL-10, whereas the immunoreactivity for TNF-alpha reflects the extent of interstitial fibrosis. Thus, our results confirm previous suggestions that proinflammatory and antiinflammatory cytokines are produced in situ by resident renal cells and contribute to the natural course of human GN. (Am J Kidney Dis 1998 Jul;32(1):80-92)

Lymphocytes populations and DNA ploidy were analysed in 30 pleural effusions (12 nonmalignant and 18 malignant) by the use of flow DNA cytometry. The percentage of lymphoctes T, B, NK, cytotoxic, helper & activated was estimated. The changes in lymphocyte populations and DNA ploidy were compared in both malignant and benign pleural effusions. Malignant pleural effusions were divided into two groups according to aneuploid DNA contents. It was observed that DNA contents in malignant cells had no influence on lymphocyte B, cytotoxic & NK cells count. However, in pleural effusions with aneuploid population, the numbers of lymphocytes T, helper & activated were lower than in benign effusions.The results of this study may suggest that immunological response is decreased in malignant environment with aneuploid cells population.