Interleukin-6 as a predictor of cardiovascular events in troponin-negative non-ST elevation acute coronary syndrome patients.

AIM: Risk stratification in acute coronary syndrome without ST-segment elevation (NSTE-ACS) and troponin-negative remains a challenge. We evaluated the value of interleukin-6 (IL-6) and amino-terminal pro-B-type natriuretic peptide (NT-proBNP) in the prognosis assessment of low-moderate risk NSTE-ACS and troponin-negative, and whether these biomarkers could improve the predictive performance of the established thrombolysis in myocardial infarction (TIMI) risk score. METHODS: A total of 212 low-moderate risk patients with NSTE-ACS and troponin-negative were prospectively studied. Clinical follow up at 6 months was performed for adverse endpoints. RESULTS: A total of 28 patients (13.5%) presented adverse clinical events. Those with adverse clinical events were associated with higher levels of IL-6 [8.58 (5.13-20.95) ng/l vs. 6.12 (4.16-9.14) ng/l, p = 0.043] and NT-proBNP [275.3 (108.6-548.2) ng/l vs. 126.8 (55.97-430.20) ng/l, p = 0.046]. In moderate risk group, we observed a higher event rate in patients with troponin-negative but elevated levels of IL-6 (p = 0.024). Only elevated IL-6 (> 12.40 ng/l) was an independent predictor of adverse outcomes [hazard ratios: 3.62, 95% confidence interval (CI) 1.69-7.75, p = 0.001]. The addition of IL-6 and history of ischaemic heart disease (IHD) to TIMI risk score significantly improved both the discrimination (integrated discrimination improvement, p = 0.003) and reclassification (Clinical Net reclassification improvement, p = 0.010) of the model for adverse events. CONCLUSIONS: Interleukin-6 is an independent predictor of adverse events in low-moderate risk patients with NSTE-ACS and troponin-negative. Its use identifies a higher risk population in moderate-risk patients. This provides together with history of IHD a better discrimination and reclassification beyond that achieved with clinical risk variables from TIMI risk score in these patients.

Soluble TNFα receptor type I and hepcidin as determinants of development of anemia in the long-term follow-up of heart failure patients.

BACKGROUND: Anemia is common in patients with chronic heart failure (CHF) and is associated with a worse prognosis. This study aims to identify the biological mechanisms which reflect evolutionary changes in the hemoglobin concentrations in heart failure patients who are still not anaemic. METHODS: Fifty-nine patients (54 ± 14 years, 83% males) with CHF (LVEF 28 ± 10%), who did not have anemia, and had not received any previous transfusions, were included. The parameters studied were: iron metabolism (ferritin, iron, transferrin, soluble transferrin receptor (sTfR), hepcidin); inflammation (C-reactive protein, soluble TNFα receptor I (sTNFRI), interleukin 6); and myocardial stress (NT-proBNP, high sensitivity TnT, growth differentiation factor 15). All parameters were measured on inclusion and 1 year after inclusion. RESULTS: Baseline hemoglobin (g/dL) was 14.7 ± 1.5 and at 1 year of follow-up it showed a significant decrease of -0.4 (RIC: -0.7 to -0.06) (p=0.02). At baseline, only the sTNFRI was a predictor of a decrease in hemoglobin 1 year later (p=0.007). During follow-up, the increase in sTNFRI (p=0.002, r=-0.39) and hepcidin (p=0.006, r=-0.35) were both associated with a decrease in hemoglobin. Similarly, the patients who became anemic (13%) had higher levels of hepcidin (p=0.001) and sTNFRI (p=0.008). The remaining parameters did not show any relationship with the evolution in the hemoglobin. CONCLUSIONS: In CHF patients without anemia, the increase in the inflammatory state (sTNFRI) and the following deterioration in the iron metabolism (hepcidin) were the main determinants of a decrease in hemoglobin and the appearance of anemia in the long term follow-up period.

Circulating cytokine concentrations in tuberculosis and other chronic bacterial infections.

Cytokines are a group of hormone-like polypeptides that play a variety of regulatory roles in host defense against infection. Because of the possible different involvement of these mediators in bacterial infections and tuberculosis, enzyme immunoassay was used to measure comparatively the plasma levels of the proinflammatory cytokines interleukin-1 beta (IL-1beta), tumor necrosis factor alpha (TNF-alpha), interleukin-6 (IL-6) and interferon gamma (IFN-gamma) in 25 immunocompetent patients divided into two groups: in 12 patients clinical and microbiological diagnosis showed a chronic bacterial infection and 13 patients had pleuropulmonar tuberculosis. After resolution of the infectious disorders (> or = 3 months), these measurements were repeated for each patient. High levels of IL-1b, TNF-alpha and IL-6 were observed at study entry, but no significant difference was found between the groups. In contrast, plasma levels (mean +/- SEM) of IFN-gamma were significantly higher in patients with tuberculosis when compared with the bacterial group (0.753 +/- 0.201 vs 0.325 +/- 0.105 IU/ml; P = 0.020). This different pattern of plasma proinflammatory cytokines could be ascribed to a prevaling role of the mediators of so-called Th-1 immune response (IFN-gamma) in host defense against infection with Mycobacterium tuberculosis.

Hyperglycemia induced by megestrol acetate in a patient with AIDS.

OBJECTIVE: To report a case of hyperglycemia induced by megestrol acetate in a patient with AIDS. CASE SUMMARY: A 28-year-old man with AIDS developed hyperglycemia requiring insulin therapy 5 days after beginning megestrol therapy. The hyperglycemia resolved with discontinuation of the agent and treatment with insulin, and recurred 2 years later, when megestrol acetate treatment was rechallenged. In this case the patient had developed hyperglycemia and pancreatitis 1 year before, related to pentamidine therapy. DISCUSSION: To our knowledge this is the first reported case of hyperglycemia that was induced by megestrol acetate as early as 5 days after beginning therapy and confirmed by rechallenge. The mechanism of action is unclear. CONCLUSIONS: Clinicians caring for patients with AIDS-related cachexia should be aware that megestrol acetate can cause a severe but reversible hyperglycemic state.

[Spectrum of the renal pathology in HIV infection: description of 85 autopsies and clinico-pathologic correlation]. / El espectro de la patología renal en la infección por el VIH: descripción de 85 autopsias y correlación clínico-patológica.

A descriptive cross-sectional study was conducted on the prevalence and histologic characteristics of renal lesions found in the autopsies of 85 patients with HIV infection: also, a retrospective analysis of clinico-biological characteristics in 56 of these patients in order to establish the factors associated with the histological findings. A total of 85 autopsies were made from 1985 to 1993; 50 autopsies (58.8%) showed renal changes: 23 (27%) infections, 13 (15.2%) acute tubular necrosis (ATN), 6 (7%) tumors, 5 (5.8%) intersticial nephritis (IN), 5 (5.8%) nephrocalcinosis (NC), 10 (11.7%) others. In an additional study: group IIc (n = 37, study group with nephropathy) had a higher incidence in the hepatitis B surface marker (HBsAg) than in group Ic (n = 19, control group, without nephropathy) (0 vs 10, p < 0.05). The presence of disseminated mycobacteriosis in the autopsy was significantly higher in the group with nephropathy than in the group without nephropathy (11 vs 1, p < 0.05). No consistent data were observed between the clinical diagnosis of nephropathy and autopsic findings. In summary, a high incidence of nephropathy was found in the autopsies of HIV infected patients, although it was not previously suspected. Renal lesions in autopsies of HIV infected patients had a tubular-intersticial predominance over glomerular lesions. The use of potentially nephrotoxic drugs, the presence of HBsAG, and some opportunist infections apparently influenced on the development of renal lesions among these patients.

[The polyangiitis overlap-Schönlein-Henoch purpura-PAN syndrome: a case of more than a rare association]. / Síndrome poliangeítico de solapamiento púrpura de Schönlein Henoch-PAN: un caso más de una rara asociación.

A fifty-four-years old male with palpable purpura, polyarthritis and nephritic syndrome is presented. The renal biopsy disclosed mesangial proliferation with IgA deposits. During hospitalization abdominal pain and upper digestive bleeding also presented. Digital angiography showed splenic artery microaneurysms. Then it's a new case of polyangiitis overlap with mixed features of Schönlein-Henoch purpura and polyarteritis nodosa. Differential diagnosis between several vasculitic associations in a patient is discussed.

[Sclerosing cholangitis, papillary stenosis and B-cell lymphoma in a patient with acquired immunodeficiency syndrome]. / Colangitis esclerosante, estenosis de papila y linfoma-B en un paciente con síndrome de inmunodeficiencia adquirida.

The case of a 31 year old man who had been intravenous drug abuser for years is reported. He was studied because of abdominal pain, jaundice, a weight loss of 10 kg, and the presence of a subclavicular mass. Biopsy of the mass demonstrated a high-grade B-cell non-Hodgkin's lymphoma, and the patient was classified in group IV-D of the human immunodeficiency virus infection because he had HIV serum antibodies and a reduced CD4/CD8 lymphocyte ratio. Although lymphoma had a good response to chemotherapy, persistent cholestasis led to liver and biliary evaluation. Sclerosing cholangitis and papillary stenosis were found. He has been followed for two years, without evidence of any secondary infectious disease associated to the acquired immunodeficiency syndrome.

Additional predictive value of serum unsaturated vitamin B12 proteins in multiple myeloma.

The distribution of serum cobalamin-binding proteins was studied in 30 patients with low-grade multiple myeloma and in 26 patients with high-grade myeloma. The mean total cobalamin concentration (holotranscobalamin I and II) was similar in both groups of patients. We found a marked rise in total unsaturated binding cobalamin capacity mainly due to an increase in apotranscobalamin II (apo-TC II) in patients with high-grade myeloma. There was also a positive correlation between serum beta-2-microglobulin (B2M) and apo-TC II in myeloma patients. Our results indicate that pretreatment measurement of serum apo-TC II could supplement B2M as a prognostic guide.