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Background Primary aldosteronism is recognized as the most frequent cause of secondary hypertension. Screening for primary aldosteronism by determination of the aldosterone-to-renin ratio (ARR) is much more frequently performed in current practice. However, most antihypertensive medications interfere with ARR determination, and although verapamil and α-adrenergic blockers are considered sufficiently neutral, the specific drugs which should be discontinued before ARR screening are a matter of debate. Our objective was to evaluate the possible interference of a new progestin with antimineralocorticoid activity (drospirenone) on the determination of ARR and the diagnosis of primary aldosteronism. Methods and Results We describe an instance of a false-positive laboratory diagnosis of primary aldosteronism (by both screening and confirmatory test) in a normotensive 34-year-old healthy woman taking Yasmin (drospirenone + ethinylestradiol) (Shering S.p.A., Milan, Italy). Subsequent ARR values during Yasmin therapy changed during the menstrual cycle (days 7, 14, 21, and 28 were tested), reaching values above the screening ARR threshold that led to a suspicion of primary aldosteronism just before menses. In contrast, during a drug-free menstrual cycle, the ARR remained constantly below the screening ARR threshold. Conclusions We report for the first time that drospirenone may interfere with laboratory screening and confirmatory testing for the diagnosis of primary aldosteronism. As a consequence, this drug should be withdrawn in hypertensive women investigated for secondary hypertension. Although drospirenone was demonstrated to possess antihypertensive properties when taken as postmenopausal hormonal replacement therapy, its use for contraceptive purposes needs to be more carefully investigated.

Background: There is a debate in the recent literature about the effect of Helicobacter pylori eradication on platelet count in patients with idiopathic thrombocytopenic purpura (ITP). In order to clarify this controversial issue, we performed a systematic review with meta-analysis of the available literature. Methods: The meta-analytic comparison was focused on the difference in the platelet count increase between the experimental arm (H. pylori-infected patients who responded to eradication therapy) and each control arm (H. pylori-infected patients who failed to respond to eradication therapy; H. pyloriinfected patients who did not receive eradication therapy and H. pylori-negative patients) and was expressed as weighted mean difference (WMD). Moreover, in order to explain the heterogeneity, a meta-regression model was fitted with arm-level covariates. Results: Data involving 788 ITP patients were collected from 17 articles (16 studies with a prospective cohort design and 1 randomized trial). There was a statistically significant difference in the increase in platelet count in patients in whom eradication was successful compared with control groups [WMD, 40.77 3 10 9 /L (95% CI, 20.92‐60.63) compared with untreated patients; 52.16 (95% CI, 34.26‐70.05) compared with patients who failed eradication and 46.35 (95% CI, 27.79‐64.91) compared with H. pylori-negative patients]. Moreover, in the meta-regression model, the success of H. pylori eradication was highly significant as an explanatory variable for platelet count increase. Conclusions: Our analysis shows a strict correlation between H. pylori eradication and increase in platelet count. However, due to intrinsic limits in the design of the studies analysed, further evidence from randomized clinical trials is required to confirm the effect of eradication treatment on platelet count.

Background: Apolipoprotein C-III (apo C-III) is a marker of cardiovascular disease risk associated with triglyceride (TG)-rich lipoproteins. The T−455C polymorphism in the insulin-responsive element of the APOC3 gene influences TG and apo C-III concentrations. Long-chain n-3 polyunsaturated fatty acids (PUFAs) contained in fish have well-known apo C-III-lowering properties.Methods: We investigated the possibility of an interactive effect between the APOC3 gene variant and erythrocyte n-3 PUFAs, suitable markers of dietary intake of fatty acids, on apo C-III concentrations in a population of 848 heart disease patients who had coronary angiography.Results: In the population as a whole, apo C-III concentrations were significantly inversely correlated with total erythrocyte PUFAs, but the correlation was not significant when only −455CC homozygous individuals were taken into account. In the total population and in subgroups with the −455TT and −455CT genotypes, the relative proportions of individuals presenting with increased apo C-III (i.e., above the 75th percentile value calculated on the entire population after exclusion of individuals taking lipids-lowering medications) decreased progressively as the n-3 PUFA and docosahexaenoic acid concentrations increased. The opposite situation was observed in the homozygous −455CC subgroup, in whom increasing erythrocyte n-3 PUFA and docosahexaenoic acid concentrations were associated with higher proportions of individuals with high apo C-III. A formal interactive effect between genotype and n-3 PUFAs was confirmed even after adjustment for possible confounding variables [age, sex, body mass index, smoking, coronary artery disease (CAD)/CAD-free status, or use of lipid-lowering medications] by logistic models.Conclusion: Patients homozygous for the −455C APOC3 variant are poorly responsive to the apo C-III-lowering effects of n-3 PUFAs.

CD3O is a member of the tumor necrosis factor (TNF) receptor family, originally described as a marker for Hodgkin and Reed-Sternberg cells in Hodgkin's disease, which has been found to be preferentially expressed by T cells producing Th2-type cytokines. The presence of CD3O expression was assessed by both immunohistochemistry and reverse transcriptase-polymerase chain reaction in the target organs of patients with Th1- or Th2-dominated disorders. CD3O expression was found in neither the gut of patients with Crohn's disease nor in the gastric antrum of Helicobacter pylori-infected patients, where there was high interferon-γ (IFN-γ) expression. In contrast, high CD3O expression in the apparent absence of IFN-γ expression was observed in the skin of patients with systemic sclerosis or chronic graft versus host disease (GVHD), which can be considered Th2-dominated disorders. Moreover, high levels of soluble CD3O were found in the serum of both systemic sclerosis and GVHD patients but not in the serum of patients suffering from multiple sclerosis, a Th1-dominated disorder. Thus, CD3O expression appears to be preferentially associated with Th2-type responses not only in vitro but also in vivo.

Fluorescence in situ hybridization (FISH), using repetitive alpha satellite probes to chromosomes 9 and 17, was performed on 27 paraffin-embedded bladder specimens from 18 Egyptian patients affected with bilharzial carcinoma. Fluorescence in situ hybridization results in the carcinomas and benign mucosa of patients with schistosomiasis were compared with flow cytometric DNA ploidy and cell cycle assays. These results demonstrate the feasibility of this technique for studies of these archival specimens, and suggest early onset of chromosomal aberrations in histologically benign mucosa of schistosomal cystitis with progression during the development of bladder cancer. On the basis of these data, monosomy 9 may be an early chromosomal change in urothelium of the bilharzia-infested bladder, and a predictor of incipient carcinoma in patients with bilharzial cystitis.

SUMMARY There is evidence that both cellular and humoral components of the immune response are required for viral clearance to occur in chronic hepatitis B. Recent studies demonstrated that CD30 molecule, a member of the tumour necrosis factor superfamily of membrane cytokine receptors, is expressed on, and released as a soluble molecule (sCD30) by activated T cells producing T helper 2 (Th2) cytokines, which modulate antibody responses. To better characterize the immunoregulatory mechanisms in chronic hepatitis B virus (HBV) infection, sCD30 values were evaluated by an ELISA in 90 hepatitis B surface (HBsAg)-positive patients with chronic hepatitis, selected on the basis of active viral replication and biochemical activity. At presentation abnormal levels (>20 U/ml) of sCD30 were detected in 57 (63%) out of 90 patients with chronic hepatitis B, and median value was significantly higher in this group of patients compared with that of healthy HBsAg carriers (26.7 versus 10.5 U/ml, P

SUMMARY CD30 has been suggested to play a role in HIV infection. In this study the serum concentration of soluble CD30 (sCD30) was determined by an ELISA essay on samples collected from patients with acute primary HIV-1 infection during the acute phase (n = 17) and after seroconversion (n = 13). sCD30 during acute infection was consistently elevated (137·58 ± 120·33 versus 6·4 ± 5·4 U/ml (mean ± s.d.) in normal controls; P

Measurement of plasma aldosterone is increasingly required in clinical practice because primary aldosteronism (PA) is the most frequent secondary cause of hypertension (1)(2)(3)(4). Chemiluminescence-based (CL) assays are attractive alternatives to traditional RIAs for hormones such as aldosterone. We compared aldosterone results obtained with a new CL method (Nichols Advantage) and an RIA [Sorin Biomedical Diagnostics (SBD)] in blood samples from 236 hypertensive patients. Blood samples were collected and immediately stored in separate aliquots at −20 °C until analysis. For 104 of the samples from these patients, we also compared the SBD-RIA results with results from a second RIA method [Maia Adaltis (MA)]. We then used the CL assay and SBD-RIA to analyze samples obtained from 27 patients before and after inhibition testing (saline loading or fludrocortisone acetate) to confirm the diagnosis of PA. In all 27 patients, the inhibition test was performed because of a previous finding of an increased aldosterone-to-renin ratio (ARR). Aldosterone was assayed in 2 aliquots from the same sample of each patient, and mean values were used …

In this study the authors investigated the serum levels of the released soluble form of interleukin-2 receptor (sIL-2R) in patients with non-Hodgkin's lymphomas (NHLs). Data were evaluated in relationship to the morphologic and immunophenotypic heterogeneity of NHL at diagnosis and in progressive advanced diseases. Increased sIL-2R levels were found in most cases, when compared with levels observed in healthy controls. No obvious statistical correlation has been observed between sIL-2R values in different NHL subtypes as defined by current classifications. On the other hand, major significance was related to the extent of the disease. Very high values, comparable to those observed in hairy cell leukemia, were observed in a number of large cell NHLs complicating low-grade B-cell lymphoproliferations and in a single case of T-cell Kil+ NHL. The authors' findings suggest that the detection of sIL-2R in NHL may represent a good marker in improving risk assignment of single cases and/or for monitoring remissions and exacerbations during the treatment of cases with very high levels at diagnosis. Nevertheless, the observed overlap between groups on an individual case basis can render the clinical application of this marker problematic.

So far, enzyme histochemical examination has been applied, with few exceptions, either to tissue imprints or to cryostat sections of freshly collected samples. This procedure is not easily applicable in routine histopathologic examination. In this study, a simplified tissue embedding procedure is presented which can be performed using an automatic tissue changer. The paraffin embedded samples can be used for both conventional histopathologic examination and for demonstrating enzymes in sections. The enzymes studied (alkaline phosphatase, alpha-naphthyl acetate esterase, acid phosphatase, tartrate resistant acid phosphatase, ATPase, peroxidase, and chloroacetate esterase) gave comparable results in formalin-fixed cryostat sections and paraffin sections in both normal and pathologic lymphoid samples. The only exception was ATPase, which could not be demonstrated on paraffin-embedded material. The technic described has broad application in the analysis of lymphoid diseases.

Combinations of antibodies to membrane antigens and to terminal deoxynucleotidyl transferase (TdT) were used to study human thymocyte and bone marrow subpopulations and leukemia cells. Cortical thymocytes were TdT+ and expressed T-cell antigens (HuTLA+), a thymocyte-specific antigen (HTA-1+), and a leukocyte antigen (HLe-l++) but lacked detectable HLA-A,B,C and la (HLA-D) antigens. In contrast, medullary thymocytes were TdT-, HuTLA+, HTA-1-, HLe-l++. A small subpopulation of larger, probably immature, thymocytes were strongly TdT+, HuTLA+, la-, HTA-1-, HLe-l +/-. Many blast cells from cases of thymic acute lymphoblastic leukemia (Thy-ALL) showed the phenotype of this small subset, and only a proportion of Thy-ALL blast cells exhibited HTA-1 and HLe-l antigens as strongly as was observed on normal cortical thymocytes. In contrast, TdT+ cells observed in normal juvenile bone marrow were HuTLA, HTA-1-, HLA+, la+. This phenotype corresponded to the phenotype of the common form of ALL (non-T, non-B) and indicated that further studies are necessary to analyze the differentiation of bone marrow precursors to thymic cells.