Risk stratification for postoperative pancreatic fistula using the pancreatic surgery registry StuDoQ|Pancreas of the German Society for General and Visceral Surgery

Background

Postoperative pancreatic fistula (POPF) is a major factor for morbidity and mortality after pancreatic resection. Risk stratification for POPF is important for adjustment of treatment, selection of target groups in trials and quality assessment in pancreatic surgery. In this study, we built a risk-prediction model for POPF based on a large number of predictor variables from the German pancreatic surgery registry StuDoQ|Pancreas.

Increased blood lactate is prevalent and identifies poor prognosis in patients with acute heart failure without overt peripheral hypoperfusion

Aims

Lactate is produced by anaerobic metabolism and may reflect inadequate tissue perfusion in conditions such as acute heart failure (AHF). We evaluated the prevalence and clinical significance of elevated blood lactate on admission in patients with AHF.

Methods and results

We enrolled 237 patients with AHF (mean age 67 ± 12 years; 70% men) presenting without overt clinical evidence of peripheral hypoperfusion (‘warm haemodynamic profile’). Median (upper and lower quartiles) blood lactate on admission was 1.8 (1.5; 2.4) mmol/L; 103 (43%) patients had an elevated blood lactate (≥2 mmol/L). Patients with an elevated lactate had higher blood high‐sensitivity troponin I [15.4 (8.5; 26.1) vs. 9.9 (4.3; 19.6) pg/mL], aspartate aminotransferase [28 (20; 44) vs 24 (19; 36) IU/L] and endothelin‐1 (12.1 ± 6.2 vs. 9.3 ± 3.9 pg/mL) (all P < 0.05). In this group plasma concentration of neutrophil gelatinase‐associated lipocalin increased during the first 48 h, whereas values fell for those with normal baseline lactate [1.9 (–3.2; 9.7) vs. –1.3 (–13.9; 5.6) μg/dL; P < 0.05). One‐year mortality was higher amongst patients with an elevated blood lactate (36% vs. 21%; P < 0.05). After adjustment for other well‐established prognostic variables, blood lactate on admission predicted poor outcome (hazard ratio 1.24, 95% confidence interval 1.08–1.41; P < 0.05).

Conclusions

An elevated blood lactate on admission is common in AHF patients without overt clinical evidence of peripheral hypoperfusion and is associated with markers of organ dysfunction/damage and a worse prognosis.

     

The association of lower testosterone level with coronary artery disease in postmenopausal women

OBJECTIVE: Testosterone (T) is assumed to be a risk factor for coronary artery disease (CAD). However, recent studies have demonstrated a beneficial effect of T on myocardial ischaemia in men with CAD. To assess the potential role of T in CAD in postmenopausal women we investigated the association between T level and CAD and relationship between T and other CAD metabolic risk factors. RESULTS: Within the 12-month study period, 108 consecutive, postmenopausal women (age 62+/-7 years) referred for diagnostic coronary angiography were prospectively included in the study. In all patients serum level of T, sex hormone-binding globulin (SHBG), total cholesterol (T-chol), LDL-chol, HDL-chol, triglycerides (TG), apolipoproteins A(1) and B (apo A(1), apo B), lipoprotein a [Lp(a)], and C reactive protein were measured. Testosterone free index (TFI) was calculated as Tx100/SHBG. CAD was documented in 51 (47%) patients (CAD+). Women with CAD had decreased T level and lower TFI (T: 0.99+/-0.4 vs. 1.41+/-0.7 nmol/l, P=0.005; TFI: 3.2+/-1.4 vs. 4.2+/-2.2, P=0.04, CAD+ vs. CAD-, respectively). No difference in SHBG was found between the two groups. In 16 women (six CAD+, 10 CAD-) who were on hormonal replacement therapy (HRT+) we observed significantly elevated T level and TFI (T: 1.62+/-0.5 vs. 1.15+/-0.7 nmol/l; TFI: 5.0+/-2.2 vs. 3.5+/-1.8, HRT+ vs. HRT-, respectively, P<0.05). When these women were excluded from the analysis, T level remained decreased in CAD+ group (0.96+/-0.4 vs. 1.22+/-0.5 nmol/l, CAD+ vs. CAD- respectively, P<0.02). CAD+ group had an unfavourable profile of metabolic CAD risk factors as evidenced by elevated T-chol, LDL-chol, Lp(a), apoB, and decreased apoA(1) (P<0.05 vs. CAD- in all comparisons). Neither T nor TFI correlated with CAD metabolic risk factors (r<0.2, P>0.1 for all correlations), apart from an inverse correlation between T and Lp(a) (r=-0.24, P=0.04). CONCLUSION: In postmenopausal women decreased T level is associated with CAD independently of the other CAD metabolic risk factors. Hormonal replacement therapy tends to increase T level which may further support the beneficial role of HRT in postmenopausal women.     

Cardiac tamponade in hypothyroidism. Probability of coexisting viral pericarditis--a case report

The authors describe a case of a 50-year-old woman admitted to hospital with clinical symptoms of a cardiac tamponade. Pericardiocentesis was done and 850 ml of fluid were drained during three days. Relatively slow heart rate (82/min before, and 60/min post intervention) and initial laboratory data: marked hipercholesterolemia (8.2 mmol/l) and high CK activity (1830 IU/l) were typical of hypothyroidism. Examination of hormone levels confirmed this suspicion (TSH 162 uIU/ml, fT4 0.11 microg/dl, fT3 0.4 pmol/l). USG image and antithyroid antibodies presence (anti-TPO >3000 U/ml) helped in diagnosing of autoimmune thyroiditis. During substitution therapy with L-thyroxine her clinical status improved systematically. Additionally, an increased raised serum titre of Coxackie B virus antibodies (B3-B5 >1/256) suggested coexisting viral pericarditis. Two months before hospitalization she had symptoms of viral infection. A review of current literature on the subject is presented.     

Cardiomyocytes undergo apoptosis in human immunodeficiency virus cardiomyopathy through mitochondrion- and death receptor-controlled pathways

We investigated 18 AIDS hearts (5 with and 13 without cardiomyopathy) by using immunocytochemistry and computerized image analysis regarding the roles of HIV-1 proteins and tumor necrosis factor ligands in HIV cardiomyopathy (HIVCM). HIVCM and cardiomyocyte apoptosis were significantly related to each other and to the expression by inflammatory cells of gp120 and tumor necrosis factor-alpha. In HIVCM heart, active caspase 9, a component of the mitochondrion-controlled apoptotic pathway, and the elements of the death receptor-mediated pathway, tumor necrosis factor-alpha and Fas ligand, were expressed strongly on macrophages and weakly on cardiomyocytes. HIVCM showed significantly greater macrophage infiltration and cardiomyocyte apoptosis rate compared with non-HIVCM. HIV-1 entered cultured neonatal rat ventricular myocytes by macropinocytosis but did not replicate. HIV-1- or gp120-induced apoptosis of rat myocytes through a mitochondrion-controlled pathway, which was inhibited by heparin, AOP-RANTES, or pertussis toxin, suggesting that cardiomyocyte apoptosis is induced by signaling through chemokine receptors. In conclusion, in patients with HIVCM, cardiomyocytes die through both mitochondrion- and death receptor-controlled apoptotic pathways.     

Nutritional supplementation with l-arginine prevents pelvic radiation-induced changes in morphology, density, and regulating factors of blood vessels in the wall of rat bladder

Purpose

To determine whether l-arginine has protective effects against radiation-induced alterations in the morphology and regulatory factors of vesical blood vessels in rats.

Methods

Male rats aged 3–4 months were divided into groups of 10 animals each: (a) controls, consisting of non-treated animals; (b) radiated-only rats; and (c) radiated rats receiving l-arginine supplementation. Radiation was in one session of 10 Gy and was aimed at the pelvic-abdominal region. l-arginine was administered once a day (0.65 g/kg body weight), starting 7 days before radiation and continuing until killing on the 16th day after radiation. The density, relative area, and wall thickness of blood vessels were measured in the vesical lamina propria using histological methods, and the expression of vascular endothelial growth factor (VEGF) and fibroblast growth factors (FGF) in the bladder wall was assessed by RT-PCR.

Results

Compared with controls, radiation alone decreased the density and relative area of blood vessels by 32 % (p < 0.01) and 25 % (p < 0.05), respectively, and reduced the arterial wall thickness by 42 % (p < 0.004). VEGF and FGF mRNA levels after radiation were diminished by 67 % (p < 0.002) and 56 % (p < 0.04), respectively. The radiated animals supplemented with l-arginine were not significantly different from controls.

Conclusions

Pelvic radiation leads to significant vesical modifications, as in the morphology of blood vessels and in VEGF and FGF expression. All these changes, however, were prevented by l-arginine treatment. These results emphasize, therefore, the potential use of this amino acid as a radioprotective drug.