STUDY OF THE ACTIVITY OF SOME RAT SERUM ENZYMES IN THE DYNAMICS OF EXTRAHEPATIC CHOLESTASIS

Extrahepatic cholestasis occurs with mechanical obstruction of the main extrahepatic or main intrahepatic ducts. The most common cause of extrahepatic cholestasis is common bile duct stones. This article describes hypertension in the bile ducts and acholysis developing in cholestasis, which cause serious functional and morphological changes in the liver and lead to the rapid growth of liver insufficiency. Thus, in the dynamics of extrahepatic cholestasis development there are significant shifts in blood serum of experimental animals, manifested by hyperfermentemia. These changes indicate the involvement of the liver in the pathological process, which naturally requires their correction.

Carnitine-Acylcarnitine Translocase Deficiency Masked by Extreme Prematurity

Carnitine-acylcarnitine translocase (CACT) deficiency is a rare disorder of long chain fatty acid oxidation with a very high mortality rate due to cardiomyopathy or multiorgan failure. We present the course of a very premature infant with early onset CACT deficiency complicated by multiple episodes of necrotizing enterocolitis, sepsis, and liver insufficiency, followed by eventual demise. The complications of prematurity, potentiated by the overlay of CACT deficiency, contributed to the difficulty of reaching the ultimate diagnosis of CACT deficiency.

The Role of Intestinal Bacteria and Gut–Brain Axis in Hepatic Encephalopathy

Hepatic encephalopathy (HE) is a neurological disorder that occurs in patients with liver insufficiency. However, its pathogenesis has not been fully elucidated. Pharmacotherapy is the main therapeutic option for HE. It targets the pathogenesis of HE by reducing ammonia levels, improving neurotransmitter signal transduction, and modulating intestinal microbiota. Compared to healthy individuals, the intestinal microbiota of patients with liver disease is significantly different and is associated with the occurrence of HE. Moreover, intestinal microbiota is closely associated with multiple links in the pathogenesis of HE, including the theory of ammonia intoxication, bile acid circulation, GABA-ergic tone hypothesis, and neuroinflammation, which contribute to cognitive and motor disorders in patients. Restoring the homeostasis of intestinal bacteria or providing specific probiotics has significant effects on neurological disorders in HE. Therefore, this review aims at elucidating the potential microbial mechanisms and metabolic effects in the progression of HE through the gut–brain axis and its potential role as a therapeutic target in HE.

Lights and Shadows in Hepatic Encephalopathy Diagnosis

Hepatic encephalopathy (HE) is a form of brain dysfunction that is caused by liver insufficiency and/or portal-systemic shunting. The exact nature of HE is debated; as such, conflicting uses of the term “HE” may cause inconsistencies in its detection and management. This review highlights the meaning of the term “HE” on the basis of its historical origins and current consensus. It also provides criteria for the diagnosis of the condition based on its phenotypes and risk factors for its occurrence. The procedure for differential diagnosis from other conditions which result in similar phenotypes is considered, together with precipitants and confounders. Finally, the current multidimensional approach for the correct clinical reporting of HE episodes is discussed.

Low Surgical Morbidity and Mortality After Fast-Track Liver Surgery for Colorectal Liver Metastases: A Study of Complications in a High-Volume Centre

BackgroundFor colorectal liver metastases, surgery is a high-risk procedure due to perioperative morbidity. The objective was to assess complications after fast-track liver surgery for colorectal liver metastases.MethodsAll patients were treated according to the same fast-track programme. Complications were graded according to the Clavien-Dindo classification for patients undergoing surgery from 2013 to 2015. Correlation between complications and length of stay was analysed by multivariate linear regression.Results564 patient cases were included of which three patients died within 3 months (0.53%, 95% CI: 0.17-1.64%). Complications were common with Grade 2 in 167 patients (30%) and ≥Grade 3a in 93 (16%). Patients without complications had a mean length of stay of 4.1 days, which increased with complications: 1.4 days (95% CI: 1.3 – 1.5) for Grade 2, 1.7 days (1.5 – 2.0) for Grade 3a, 2.3 days (1.7 – 3.0) for Grade 3b, 2.6 days (1.6 – 4.2) for Grade 4a, and 2.9 days (2.8 – 3.1) for Grade 4b. Following were associated with increased length of stay: complication severity grade, liver insufficiency, ascites, and biliary, cardiopulmonary, and infectious complications. ConclusionsComplications after liver surgery for colorectal liver metastases, in a high-volume centre, were associated with low mortality, few severe complications, and short but increased length of stay.

Lights and Shadows on Hepatic Encephalopathy Diagnosis

Hepatic encephalopathy (HE) is a form of brain dysfunction that is specifically caused by liver insufficiency and/or portal-systemic shunt. The exact nature of HE is debated, so that conflicting uses of the term HE may cause inconsistencies in its detection and, in turn, issues with its management. This review highlights the meaning of the term HE on the basis of both its historical origins and current consensus. It also provides criteria for the diagnosis of the condition, on the basis of its phenotypes and the risk factors for its occurrence. The procedure for differential diagnosis from other conditions which result in similar phenotypes is considered, together with precipitants and confounders. Finally, the current multidimensional approach for the correct clinical recording of HE episodes is discussed.

CORRECTION OF ALBENDAZOLE DOSAGE AFTER LIVER ECHINOCOCCTOMY

Purpose. To improve the quality of treatment of patients with liver echinococcosis by optimizing postoperative chemotherapy. Material and methods. 226 patients with liver echinococcosis were admitted to the surgical department of the 2nd Clinic of the Samarkand State Medical Institute in 2009-2017. Patients were divided into two groups. In 2009-2012, 112 (49.5%) patients were operated on and were included into a control group. In 2013-2017, 114 (50.5%) patients were followed -up and were included into a study group. In the control group, postoperative chemotherapy was made by the standard protocol. In the studied group, Albendazole dosage was corrected according to the initial functional state of the liver. Due to positive findings in the experimental group, Albendazole was used at the dosage 5 mg / kg / day in patients with verified chronic liver disease and if liver enzymes were elevated before surgery. Results. Adverse reactions of Albendazole chemotherapy, by clinical and laboratory parameters, could develop in 52.7% - due to the preparation toxic effect and concomitant chronic diffuse liver pathology- while under dose correction, this figure is reduced to 18.3%. Conclusion. The proposed dose correction in patients with signs of liver insufficiency normalizes biochemical parameters and reduces toxic manifestations during chemotherapy. Of these 144 patients, long-term observations revealed echinococcosis relapse in 6 (4.2%) patients.

Detection of lipoprotein X (LPX) – a challenge in patients with severe hypercholesterolaemia

Summary Background Lipoprotein X (LpX) is an abnormal lipoprotein fraction, which can be detected in patients with severe hypercholesterolaemia and cholestatic liver disease. LpX is composed largely of phospholipid and free cholesterol, with small amounts of triglyceride, cholesteryl ester and protein. There are no widely available methods for direct measurement of LpX in routine laboratory practice. We present the heterogeneity of clinical and laboratory manifestations of the presence of LpX, a phenomenon which hinders LpX detection. Methods The study was conducted on a 26-year-old female after liver transplantation (LTx) with severely elevated total cholesterol (TC) of 38 mmol/L and increased cholestatic liver enzymes. TC, free cholesterol (FC), cholesteryl esters (CE), triglycerides, phospholipids, HDL-C, LDL-C, and apolipoproteins AI and B were measured. TC/apoB and FC:CE ratios were calculated. Lipoprotein electrophoresis was performed using a commercially available kit and laboratory-prepared agarose gel. Results Commercially available electrophoresis failed to demonstrate the presence of LpX. Laboratory-prepared gel clearly revealed the presence of lipoproteins with γ mobility, characteristic of LpX. The TC/apoB ratio was elevated and the CE level was reduced, confirming the presence of LpX. Regular lipoprotein apheresis was applied as the method of choice in LpX disease and a bridge to reLTx due to chronic liver insufficiency. Conclusions The detection of LpX is crucial as it may influence the method of treatment. As routinely available biochemical laboratory tests do not always indicate the presence of LpX, in severe hypercholesterolaemia with cholestasis, any discrepancy between electrophoresis and biochemical tests should raise suspicions of LpX disease.