RESUMO
Background: Heavy alcohol consumption is an inevitable cause of alcoholic liver disease with a high chance to progress to Alcoholic Liver Cirrhosis. Alcohol could damage the function of body organs and could cause cancer. Liver damage due to excessive alcohol consumption is usually presented as fatty liver [build-up of fats in the liver], steatohepatitis, fibrosis, alcoholic cirrhosis, and hepatocellular carcinoma. When liver fibrosis progresses, it will ultimately end up as alcoholic cirrhosis
Objective of the Study: This article was intended to explore and investigate the possible optimal diagnosis and management of Alcoholic liver cirrhosis
Methods: We searched the medical literatures to retrieve studies for the review till 30 November 2017. Electronic search in the scientific database from 1965 to 2017- [Medline, Embase. The Cochrane Library websites were searched for English Publications [both reprint requests and by searching the database]. Data extracted included authors, country, year of publication, characteristics of patients, pathophysiology, risk factors, clinical manifestations, different diagnostic approaches and treatment modalities
Conclusion: Absolute abstinence remains the foundation for any treatment of any acute or chronic Alcoholic Liver Disease. It's also important to understand that no treatment will cure cirrhosis or repair scarring in the liver that has already occurred and the only resort would be liver transplantation which is also debatable provided the complications it carries along. Nevertheless, timely diagnosis of alcoholic cirrhosis in people with alcoholic liver disease is the cornerstone for evaluation of prognosis or choosing treatment strategies such as nutritional and medical support and lifestyle change
RESUMO
Background: Heavy alcohol consumption is an inevitable cause of alcoholic liver disease with a high chance to progress to Alcoholic Liver Cirrhosis. Alcohol could damage the function of body organs and could cause cancer. Liver damage due to excessive alcohol consumption is usually presented as fatty liver [build-up of fats in the liver], steatohepatitis, fibrosis, alcoholic cirrhosis, and hepatocellular carcinoma. When liver fibrosis progresses, it will ultimately end up as alcoholic cirrhosis
Objective of the Study: This article was intended to explore and investigate the possible optimal diagnosis and management of Alcoholic liver cirrhosis
Methods: We searched the medical literatures to retrieve studies for the review till 30 November 2017. Electronic search in the scientific database from 1965 to 2017- [Medline, Embase. The Cochrane Library websites were searched for English Publications [both reprint requests and by searching the database] .Data extracted included authors, country, year of publication, characteristics of patients, pathophysiology, risk factors, clinical manifestations, different diagnostic approaches and treatment modalities
Conclusion: Absolute abstinence remains the foundation for any treatment of any acute or chronic Alcoholic Liver Disease. It's also important to understand that no treatment will cure cirrhosis or repair scarring in the liver that has already occurred and the only resort would be liver transplantation which is also debatable provided the complications it carries along. Nevertheless, timely diagnosis of alcoholic cirrhosis in people with alcoholic liver disease is the cornerstone for evaluation of prognosis or choosing treatment strategies such as nutritional and medical support and lifestyle change
RESUMO
Background: Non-alcoholic fatty liver disease [NAFLD] is a heterogeneous condition that contains steatosis and non-alcoholic steatohepatitis [NASH], in the nonexistence of significant alcohol consumption, reaching 30% of the populace. The most common risk features are: age, ethnicity, gender, obesity, drugs, diabetes mellitus [DM], insulin resistance [IR], predisposition, metabolic syndrome [MS], and polycystic ovary syndrome
Materials and Methods: Patients with non-alcoholic fatty liver disease were evaluated, with medical and epidemiological data collected after informed consent at King Abdulaziz Hospital
Results: Of the 124 patients evaluated, 75.8% were women, and 88 were aged between 49 and 70 years and had no symptoms. Ultrasonography results showed steatosis in 84%. NASH was diagnosed in 75 patients of the sample. 42 patients underwent liver biopsy, of which 36% had cirrhosis, 1 had liver cancer, and 1 pure steatosis [5% each]. Risk factors were found in 70% of patients with metabolic syndrome, 87% with increased waist circumference, 63% with dyslipidemia, 61% [n=76] with high blood pressure [HBP], 28% with DM, 52% physically inactive, and 44% with insulin resistance [IR] [HOMA> 3.5]. There was an association between IR and NASH [p=0.011], IR and obesity [p=0.031], IR and MS [p=0.007], and MS and steatosis on medical ultrasound [USG] [p=0.012]
Conclusion: The results indicated that the most frequent risk factors were MS and its variables: increased waist circumference, dyslipidemia and HBP. This highlights the significance of metabolic control in non-alcoholic fatty liver disease and confirms its role as the hepatic component of metabolic syndrome
RESUMO
Anticoagulation is the mainstay treatment of pulmonary embolism. Using low molecular weight heparin versus unfractionated heparin remains a matter of debate
Objectives: the aim of this review is to study the prognosis of using low molecular weight versus unfractionated heparin in treatment of pulmonary embolism
Methods: pubMed and Cochrane library were searched for articles comparing the efficacy of low molecular weight heparin and unfractionated heparin in management of pulmonary embolism. Ten related results were selected for review
Results: literatures studies indicated that low molecular weight heparin was effective in therapeutic treatment of acute sub-massive and massive pulmonary embolism. It was as effective as intravenous unfractionated heparin. It was not associated with higher risk of major, minor bleeding, or thrombocytopenia. Low molecular weight heparin was as effective as unfractionated heparin in prophylaxis of deep venous sinus thrombosis as well as pulmonary embolism
Discussion: low-molecular-weight heparin seemed to be as effective safe as intravenous unfractionated heparin for the treatment as well as prophylaxis of pulmonary embolism. It was also safe with no major bleeding risk or higher risk of thrombocytopenia
Conclusion: both low molecular weight and unfractionated heparin had similar efficacy and safety in management of PE