RESUMO
OBJECTIVES: Obesity and non-alcoholic fatty liver disease (NAFLD) are rampant in South East Asia. There is paucity of data exploring its' impact on donor suitability for living donor liver transplantation (LDLT). We aimed to describe and examine the factors related to non-utilization of potential donors in our LDLT programme. METHODS: This is an analysis of prospectively collected data on potential donors for an adult LDLT programme, between January 2017 and December 2019. RESULTS: Fifty-five donors for 33 potential recipients were evaluated. The mean age was 31.6 ± 8.5 years, 52.7% were female and the ethnic divisions were: Chinese (50.9%), Indian (25.5%) and Malay (23.6%). The mean body mass index (BMI) among potential donors was 25.1 ± 4.0 kg/m2; 25.5% of donors had normal BMI, 23.6% were overweight and 50.9% were obese. Using the CAP modality of Fibroscan®, we identified the following grades of hepatic steatosis: 36.6% S0, 19.5% S1, 2.4% S2 and 41.5% S3. The non-utilization rate of our donors was 74.5% (41/55) and the main reasons were significant hepatic steatosis and/or obesity. Compared to suitable donors, unsuitable donors had significantly greater mean BMI, mean CAP scores, higher rates of dyslipidaemia and NAFLD. CONCLUSION: NAFLD and obesity represent major challenges to an emerging LDLT programme in Malaysia.
Assuntos
Transplante de Fígado , Hepatopatia Gordurosa não Alcoólica , Adulto , Biópsia , Feminino , Humanos , Fígado , Doadores Vivos , Hepatopatia Gordurosa não Alcoólica/epidemiologia , Obesidade/complicações , Obesidade/epidemiologia , Adulto JovemRESUMO
Tumour necrosis factor alpha (TNF-alpha) is an inflammatory cytokine primarily produced by macrophages. It is a unique protein with contradictive properties; it has the ability to induce cellular death by apoptosis and oncosis, but can also induce cellular regeneration and growth. Genetic polymorphisms in TNFA have been associated with poor outcome in some surgical patients and this may provide a useful tool to screen for high-risk patients. Manipulating TNF-alpha levels in vivo may influence the progression of several pathological conditions. TNF-alpha has anti-cancer properties and has been used to treat cancer patients. Treatment with anti-TNF-alpha drugs and antibodies has been successful in rheumatoid arthritis and other autoimmune diseases, but disappointing in the management of patients with sepsis. This review article focuses on the biological activities, genetic polymorphism of TNFA and the role of TNF-alpha and anti-TNF-alpha treatments, based on animal experiments and clinical trials.
Assuntos
Inflamação/metabolismo , Inflamação/cirurgia , Fator de Necrose Tumoral alfa/metabolismo , Animais , Biomarcadores/metabolismo , DNA/genética , Humanos , Macrófagos/metabolismo , Polimorfismo Genético , Fator de Necrose Tumoral alfa/genéticaRESUMO
The restoration of blood flow to ischemic tissues causes additional damage, which is termed reperfusion injury. All tissues are susceptible to reperfusion injury, but this susceptibility varies between tissues. Reperfusion has wide clinical relevance. It influences the outcome of patients after myocardial infarction, stroke, organ transplantation, and cardiovascular surgery. Advances in the treatment of reperfusion injury have created an opportunity for plastic surgeons to apply these treatments to flaps and reimplanted tissues. The main putative mechanisms identified in animal models involve leukocyte-endothelium interactions, reactive oxygen species, and the complement system. However, it has become evident that these fundamental biological systems are controlled by many interrelated pathways. Attempts to bypass this complexity have led to a search for the early "upstream" initiating events, rather than the "downstream" cascading events. This contrasts with current clinical efforts that are directed toward hypothermia, intraarterial flushing, and preconditioning. This article outlines the molecular and cellular events that occur during reperfusion injury and then reviews the efforts that have been made to exploit this knowledge for clinical advantage.