Bossen Lars, Dam Gitte A, Vilstrup Hendrik, Watson Hugh, Jepsen Peter
Department of Hepatology and Gastroenterology, Aarhus University Hospital, Aarhus, Denmark.
Evotec ID, Lyon, France.
JHEP Rep. 2019 Aug 8;1(4):265-269. doi: 10.1016/j.jhepr.2019.07.008. eCollection 2019 Oct.
Both cirrhosis and diabetes are established risk factors for infections. However, it remains uncertain whether diabetes adds to the risk of infections in patients with cirrhosis who are already at high risk of infections, or increases the mortality following an infection. To answer these questions, we followed a cohort of trial participants with cirrhosis and ascites for 1 year to compare the incidence of infections and post-infection mortality between those with or without diabetes.
We used Cox regression to estimate the hazard ratio (HR) of any infection, adjusting for confounding by patient age, gender, MELD score, albumin, use of proton pump inhibitors and lactulose, cirrhosis aetiology, and severity of ascites. Further, we analysed the mortality after infection.
Among 1,198 patients with cirrhosis and ascites, diabetics (n = 289, 24%) were more likely than non-diabetics (n = 909, 76%) to be old and male, to have low platelets, and to use lactulose. At inclusion, similar proportions of diabetic and non-diabetic patients were taking a quinolone antibiotic (13% 12%) and they had similar median MELD scores (14 15). During the follow-up, 446 patients had an infection. Diabetes did not increase the HR of infections (adjusted HR 1.08; 95% CI 0.87-1.35). Further, diabetes did not increase the mortality following an infection (adjusted HR 0.93; 95% CI 0.64-1.35).
In patients with cirrhosis and ascites, diabetes did not increase infection risk or mortality after infection. The immune incompetence of each disease did not appear to be additive. In clinical terms, this means that particular attention to infections is not indicated in patients with cirrhosis and diabetes.
Cirrhosis and diabetes are chronic diseases that weaken the immune system and increase the risk of infections, but it is unknown whether their combined effects exceed the effect of cirrhosis alone. We showed that the risk of infections was the same in patients with cirrhosis, ascites and diabetes as in patients with cirrhosis and ascites alone. Thus, their combined effects do not exceed the effect of cirrhosis alone.
肝硬化和糖尿病都是已确定的感染风险因素。然而,糖尿病是否会增加已经处于高感染风险的肝硬化患者的感染风险,或者增加感染后的死亡率,仍不确定。为了回答这些问题,我们对一组患有肝硬化和腹水的试验参与者进行了为期1年的随访,以比较有或没有糖尿病的患者之间的感染发生率和感染后死亡率。
我们使用Cox回归来估计任何感染的风险比(HR),并对患者年龄、性别、终末期肝病模型(MELD)评分、白蛋白、质子泵抑制剂和乳果糖的使用、肝硬化病因以及腹水严重程度等混杂因素进行调整。此外,我们分析了感染后的死亡率。
在1198例肝硬化和腹水患者中,糖尿病患者(n = 289,24%)比非糖尿病患者(n = 909,76%)更有可能年龄较大、为男性、血小板低且使用乳果糖。纳入时,糖尿病患者和非糖尿病患者服用喹诺酮类抗生素的比例相似(13%对12%),且他们的MELD评分中位数相似(14对15)。在随访期间,446例患者发生了感染。糖尿病并未增加感染的HR(调整后的HR为1.08;95%置信区间为0.87 - 1.35)。此外,糖尿病并未增加感染后的死亡率(调整后的HR为0.93;95%置信区间为0.64 - 1.35)。
在肝硬化和腹水患者中,糖尿病并未增加感染风险或感染后的死亡率。两种疾病的免疫功能不全似乎并非相加的。从临床角度来看,这意味着对于肝硬化和糖尿病患者,无需特别关注感染问题。
肝硬化和糖尿病是削弱免疫系统并增加感染风险的慢性疾病,但它们的联合作用是否超过单独肝硬化的作用尚不清楚。我们表明,肝硬化、腹水和糖尿病患者的感染风险与仅患有肝硬化和腹水的患者相同。因此,它们的联合作用并未超过单独肝硬化的作用。