Deep Vansh, Sondhi Shankerdeep, Gupta Sunita
General Medicine, Maharishi Markandeshwar Institute of Medical Sciences & Research, Mullana, IND.
Cureus. 2023 Jun 30;15(6):e41207. doi: 10.7759/cureus.41207. eCollection 2023 Jun.
Background Zinc, an essential trace element, plays a vital role in cellular metabolism, and the liver is the main organ responsible for its metabolism. Because serum zinc levels are found to be lowered in chronic liver diseases, it has been hypothesized to be a precipitating factor for the development of hepatic encephalopathy. Methodology This prospective, observational study included patients with decompensated cirrhosis of the liver who were admitted to the medical intensive care unit of a tertiary care institute in northern India between September 2021 and April 2023. The diagnosis was based on history and detailed clinical examination. The serum zinc levels of patients were estimated using atomic absorption spectrometry at admission and compared to that of healthy controls. Serum zinc levels were correlated with the severity of liver disease and hepatic encephalopathy among the cases. Results A total of 100 cases of decompensated cirrhosis of the liver and 50 healthy controls were included. The mean serum zinc level of the cases was 40.5 ± 10.0 µg/dL which was significantly lower than the mean serum zinc level (104.0±9.1 µg/dL) of controls (p < 0.0001). Serum zinc level was significantly lower in patients with higher grades of hepatic encephalopathy (p = 0.000). Similarly, serum zinc level was significantly reduced among patients with higher Child-Pugh and Model for End-stage Liver Disease scores. Conclusions Serum zinc level is significantly reduced in patients with decompensated cirrhosis of the liver, and lower serum zinc level is associated with the increased severity of the disease and higher grades of hepatic encephalopathy. In patients with decompensated cirrhosis of the liver, maintenance of adequate serum zinc levels may prevent hepatic encephalopathy.
背景 锌作为一种必需的微量元素,在细胞代谢中起着至关重要的作用,而肝脏是负责其代谢的主要器官。由于发现慢性肝病患者的血清锌水平降低,因此推测锌是肝性脑病发生的一个促发因素。
方法 这项前瞻性观察性研究纳入了2021年9月至2023年4月期间入住印度北部一家三级医疗机构内科重症监护病房的失代偿期肝硬化患者。诊断基于病史和详细的临床检查。患者入院时采用原子吸收光谱法测定血清锌水平,并与健康对照组进行比较。对病例组中血清锌水平与肝病严重程度及肝性脑病进行相关性分析。
结果 共纳入100例失代偿期肝硬化患者和50例健康对照。病例组的平均血清锌水平为40.5±10.0μg/dL,显著低于对照组的平均血清锌水平(104.0±9.1μg/dL)(p<0.0001)。肝性脑病分级较高的患者血清锌水平显著降低(p = 0.000)。同样,Child-Pugh评分和终末期肝病模型评分较高的患者血清锌水平也显著降低。
结论 失代偿期肝硬化患者的血清锌水平显著降低,较低的血清锌水平与疾病严重程度增加和肝性脑病分级较高相关。对于失代偿期肝硬化患者,维持足够的血清锌水平可能预防肝性脑病。