Clinicopathologic features of adult EBV-associated B-cell lymphoproliferative disease

In the present study, 21 cases of adult/late-onset EBV-associated lymphoproliferative disease (AELPD) with an uncertain malignant potential were investigated with regard to their histomorphology, immunophenotype, clonal rearrangement of the heavy chain (IgH) and T-cell receptor (TCR) genes and clinical course.The cases were histomorphologically reevaluated and assigned to one of three morphological groups: mononucleosis-like, Hodgkin-like, or polymorphous. In addition, cases with or without detectable necrosis were investigated for differences in clinical outcome.Overall survival was highest in the group with Hodgkin-like morphology (4/4 patients), followed by patients with mononucleosis-like phenotype (4/5 patients surviving). Cases with polymorphous morphology showed the poorest survival rates with 7/12 patients dead of disease (58%). 4/6 patients with histologically detectable necrosis died (66%), but only 4/15 patients without necrosis (27%). 11/21 cases with AELPD showed clonal rearrangement for IgH (n?=?4), TCR (n?=?5) or IgH?+?TCR (n?=?2). 5/11 patients with clonal rearrangement died (45%), and this percentage was similar in all of the three subgroups.In conclusion, the present study shows that polymorphous morphology and detection of necrosis in AELPD are frequently linked to a fatal clinical course, whereas Hodgkin-like morphology seems to be associated with a more favourable prognosis. Clonal rearrangement of IgH or TCR is frequent in AELPD, but prognosis is unpredictable from this feature.     

Association of uric acid with mortality in patients with stable coronary artery disease

ObjectiveThe association between uric acid and cardiovascular disease is poorly studied. We undertook this study to assess whether uric acid level predicts clinical outcome in patients with stable coronary artery disease (CAD) treated with percutaneous coronary intervention (PCI).Materials/MethodsThis study included 8149 patients with stable CAD who underwent PCI. Uric acid was measured before angiography. The primary end point was 1-year mortality. Quartiles of quartiles of uric acid were: 1.49 to < 5.49 mg/dl (1st quartile; n=2032 patients), 5.49 to < 6.40 mg/dl (2nd quartile; n=1981 patients), 6.40 to < 7.50 mg/dl (3rd quartile; n=2093 patients) and 7.50 to 21.90 mg/dl (4th quartile; n=2043 patients).ResultsThere were 196 deaths during the 1-year follow-up. The numbers of deaths (Kaplan-Meier estimates) according to uric acid quartiles were: 35 deaths (1.8%) in the 1st quartile, 30 deaths (1.6%) in the 2nd quartile, 45 deaths (2.2%) in the 3rd quartile and 86 deaths (4.3%) in the 4th quartile (unadjusted hazard ratio [HR]=1.60, 95% confidence interval [CI] 1.38-1.86, P < 0.001 for each standard deviation [SD] increase in the logarithmic scale). After adjustment for traditional cardiovascular risk factors, renal function and inflammatory status, the association between uric acid and 1-year mortality remained significant (adjusted HR=1.26, 95% CI 1.07-1.48; P=0.005 for each standard deviation increase in the logarithmic scale). Uric acid improved predictivity of the multivariable model regarding mortality (P=0.040).ConclusionsElevated level of uric acid is an independent predictor of 1-year mortality in patients with stable CAD treated with PCI.     

Prognostic value of uric acid in patients with acute coronary syndromes

The association between uric acid and cardiovascular disease is incompletely understood. In particular, the prognostic value of uric acid in patients with acute coronary syndromes who undergo percutaneous coronary intervention has not been studied. This study included 5,124 patients with acute coronary syndromes who underwent percutaneous coronary intervention: 1,629 with acute ST-segment elevation myocardial infarction, 1,332 with acute non-ST-segment elevation myocardial infarction, and 2,163 with unstable angina. The primary end point was 1-year mortality. Patients were divided into quartiles according to uric acid level as follows: quartile 1, 1.3 to <5.3 mg/dl; quartile 2, 5.3 to <6.3 mg/dl; quartile 3, 6.3 to <7.5 mg/dl; and quartile 4, 7.5 to 18.4 mg/dl. There were 450 deaths during follow-up: 80 deaths in quartile 1, 77deaths in quartile 2, 72 deaths in quartile 3, and 221 deaths in quartile 4 of uric acid (Kaplan-Meier estimates of 1-year mortality 6.4%, 6.2%, 5.6%, and 17.4%, respectively; unadjusted hazard ratio 3.05, 95% confidence interval 2.54 to 3.67, p <0.001 for fourth vs first quartile of uric acid). After adjustment for traditional cardiovascular risk factors, renal function, and inflammatory status, the association between uric acid and mortality remained significant, with a 12% increase in the adjusted risk for 1-year mortality for every 1 mg/dl increase in the uric acid level. Uric acid improved the discriminatory power of the predictive model regarding 1-year mortality (absolute integrated discrimination improvement 0.008, p = 0.005). In conclusion, elevated levels of uric acid are an independent predictor of 1-year mortality across the whole spectrum of patients with acute coronary syndromes treated with percutaneous coronary intervention.     

From Longitudinal Gastric Resection to Sleeve Gastrectomy—Revival of a Previously Established Surgical Procedure

Introduction  

Sleeve gastrectomy is becoming increasingly popular within bariatric surgery. Initially introduced as a component of complex interventions and later as part of a two-stage operation in high-risk patients, the procedure is now more common as one-stage operation and subject of avid scientific discussion. However, the concept of longitudinal gastric resection is not new. The procedure was already established in ulcer surgery but soon faded into insignificance. This article aims to trace the historical development of resection of the greater curvature with particular reference to its origin in ulcer and bariatric surgery. The contribution of ulcer surgery to modern sleeve gastrectomy is highlighted. Furthermore, the current value of sleeve gastrectomy within the spectrum of bariatric surgical procedures will be discussed. Relevant medical literature from PubMed to April 2010 was reviewed.     

Vasculitic complications of interferon-α treatment for chronic hepatitis C virus infection: case report and review of the literature

Chronic infection with hepatitis C virus (HCV) may be complicated by the development of systemic vasculitis. Vasculitis is either caused by mixed cryoglobulinemia or a non-cryoglobulinemic vasculitis resembling polyarteritis nodosa (PAN). Antiviral treatment with interferon- (IFN) and subsequent clearing of HCV mostly leads to improvement of vasculitic symptoms, but vasculitis may also be exacerbated and even cases of new onset of vasculitis may occur. Exacerbations of both cryoglobulinemic and PAN-type vasculitis in chronic HCV infection have been described under treatment with IFN. The most common symptom is vasculitic neuropathy. However, peripheral neuropathy in a HCV-infected patient treated with IFN may also be caused by direct neurotoxic or antiangiogenic effects of IFN itself, often requiring a nerve biopsy to establish the exact diagnosis. The clinical course of vasculitic complications of IFN treatment is variable and ranges from regression of symptoms despite continuation of IFN treatment to fatal exacerbations despite termination of IFN treatment and additional immunosuppressive therapy. In most cases of IFN-induced vasculitis, immunosuppressive therapy with corticosteroids has been employed, leading to improvement of symptoms. We report the case of a patient with chronic HCV infection who first developed cryoglobulinemic vasculitis after initiation of therapy with the polyethylene glycol (PEG)-conjugated form of IFN (PEG-IFN) and discuss it in the context of the relevant literature. First onset of cryoglobulinemic vasculitis after initiation of IFN therapy has not been described so far.     

Nicotine and methyl methane sulfonate in mini organ cultures of human parotid gland tissue

The aim was to demonstrate the applicability of using mini organ cultures (MOC) of the human parotid gland for indicating DNA damage by nicotine.