Background: Although lactate is a well-established marker in intensive care, our understanding of its utility in acute heart failure (AHF) is modest and based on studies with a single measurement of this marker. Aim: We aimed to investigate whether persistent elevation of lactate during hospitalisation is related to a higher risk of adverse events. Methods: We conducted a prospective study to assess AHF patients hospitalised in one cardiac centre. The diagnosis of persistent hyperlactataemia was based on two measurements of the marker (on admission and at 24 h of hospitalisation) and it was defined as lactate elevation (≥ 2 mmol/L) at both time points. Results: The population consisted of 222 patients at a mean age of 70 ± 13 years. Mean ejection fraction and creatinine level on admission were 37% ± 16% and 1.36 ± 0.51 mg/dL, respectively. The percentage of patients with elevated lactates on admission, at 24 h of hospitalisation, and persistent hyperlactataemia were 47%, 35%, and 24%, respectively. The group with persistent hyperlactataemia did not differ in most clinical and laboratory variables from the rest of the population. Patients with persistent hyperlactataemia had higher rate of adverse events during hospitalisation: worsening of heart failure (22.6% vs. 6.5%, p < 0.05), inotrope use (22.6% vs. 5.3%, p < 0.05), and increase of N-terminal pro-B-type natriuretic peptide at 48 h of hospitalisation (30% vs. 18%, p < 0.05). Persistent hyperlactataemia was an independent predictor of one-year mortality (hazard ratio 2.5, 95% confidence interval 1.5-4.3, p < 0.001). Conclusions: Persistent hyperlactataemia within the first 24 h of hospitalisation is a predictor of a worse outcome in AHF and is related to higher rates of in-hospital adverse events and one-year mortality.
Summary Diarrhea is a frequent complication in patients after solid organ transplantation. We describe two cases of severe new onset colitis in kidney transplant recipients that developed shortly after the introduction of the therapy with prolonged‐release formulation of tacrolimus replacing standard twice daily formulation of tacrolimus in one case and cyclosporine A in the second case. Both patients developed severe, intermittent bloody diarrhea with abdominal pain, weight loss, dehydration and worsening graft function that required immediate hospitalization. The symptoms did not diminish after dose reduction or withdrawal of mycophenolic acid derivatives. After excluding bacterial, viral, fungal, and parasite infections, colonoscopy with colonic biopsy was performed in both patients, which revealed features typical of colitis. Both patients received mesalazine until the symptoms stopped. In one of the patients, standard formulation of tacrolimus was immediately reintroduced. The second patient was given everolimus in an acute phase of diarrhea. Although the two cases presented in this report cannot fully support a causal relationship between the prolonged‐release tacrolimus and colitis, they should increase awareness among transplant physicians and prompt more close monitoring of such potential side effects as a part of the pharmacovigilance plan for a new formulation of the well‐established immunosuppressive drug.
Cyclooxygenase two (COX-2) is an important enzyme metabolizing arachidonic acid. In contrast to constitutive cyclooxygenase one (COX-1), COX-2 is induced by proinflammatory factors. Polymorphism -765 G/C in COX-2-encoding gene promoter is associated with development of Alzheimer's disease, depression, carcinoma of the pancreas in smokers, breast cancer and rheumatoid arthritis. It is interesting whether the -765 G/C polymorphism in COX-2-encoding gene promoter can be associated with COPD, a disease which is inflammatory in character. It is highly probable as the breast and pancreas cancers, whose associations with the analyzed polymorphism have been studied, are smoking-dependent tumors. Additionally, tobacco smoke has been demonstrated to induce COX-2 in the lungs. The study group consisted of 122 COPD patients (48 females, 74 males). The control group consisted of 149 healthy nonsmoking subjects (83 females, 66 males). Polymerase chain reaction/restriction fragment length polymorphism was used for genotyping. A statistically significant difference in genotype distribution was observed as a result of the comparison between healthy subjects and patients with COPD. The distribution of alleles in both groups conformed with Hardy-Weinberg equilibrium. In the group of COPD patients, GG allele was found in 79 subjects, GC in 36, and CC in 7 subjects (F = 0.094, P = 0.296927); in the control group, 73 subjects had GG allele, 68--GC and 8--CC (F = 0.12728, P = 0.120265). The allele frequency revealed differences between those groups, attaining the level of statistical significance (χ(2) = 29.043, df = 2, P = 0.0000. The carriers of -765 G allele are at 1.53-fold higher risk of developing COPD. The presence of GG genotype does not increase significantly the risk of the disease. It is also noteworthy that the carriers of CC or GC genotypes are at significantly lower risk of developing COPD than the group of subjects with GG genotype.
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