The document discusses diagnostic approaches for liver disease. It outlines three common diagnostic scenarios: 1) a patient referred for clinical symptoms, 2) a patient referred for signs of liver disease, and 3) a patient found to have abnormal liver enzymes incidentally. It then reviews various causes of liver disease including viruses, autoimmunity, and other etiologies. Key diagnostic tests are outlined including imaging, biopsy, virological tests, and genetic testing. Liver enzymes are discussed in depth including their origin and interpretation of abnormal values.
The patient presented with breathlessness and swelling of the face and legs. Examination revealed elevated jugular venous pressure, bilateral pitting edema, and crepitations in both lung bases. Investigations showed cardiomegaly, bilateral pleural effusion, and hypothyroidism. The patient was diagnosed with heart failure, acute left ventricular failure, and hypothyroidism and started on diuretics, antihypertensives, and thyroxine replacement.
This document presents a case study of a 12-year-old girl who presented with prolonged fever for over 20 days. Testing showed bi-cytopenia (anemia and leukopenia), hepatosplenomegaly, lymphadenopathy, and positive EBV and parvovirus serology. A bone marrow biopsy revealed hemophagocytosis. She was ultimately diagnosed with hemophagocytic lymphohistiocytosis (HLH), a life-threatening hyperinflammatory condition. Treatment for HLH involves prompt institution of therapies like steroids, chemotherapy, to prevent irreversible organ damage from the hyperactive immune response.
This document summarizes information about hepatitis B and C co-infection with HIV. It notes that co-infection leads to faster progression of liver disease and higher rates of liver cancer and mortality. Treatment for both viruses is important, with newer regimens like tenofovir alafenamide having comparable efficacy to tenofovir disoproxil fumarate but being more tolerable with less bone and kidney toxicity. Achieving a sustained virologic response reduces complications of liver disease and improves overall health outcomes.
This document provides information about Progressive Familial Intrahepatic Cholestasis (PFIC), a rare genetic liver disease. It defines what PFIC is, describes potential symptoms, diagnostic testing and treatment options. It also outlines the three main subtypes of PFIC, defined by the gene that is mutated. Each subtype can present with different levels of itching and liver abnormalities, and may progress to complications like liver failure if left untreated. Close monitoring by medical experts and potential surgical interventions or liver transplant are important for managing PFIC.
The 41-year-old male presented with quadriplegia, muscle cramps, and hypokalemia with hypocalcemia and metabolic alkalosis. Diagnostic tests found increased urinary excretion of potassium, chloride, and calcium with normal magnesium levels. He was diagnosed with Bartter's syndrome type V, confirmed by genetic testing showing a gain of function mutation in the calcium-sensing receptor gene, which presents with hypocalcemia. Adult onset Bartter's syndrome is rare but has been reported in a few case studies of patients diagnosed between ages 28 to 52 years old.
Mitochondrial diseases are caused by defects in mitochondrial DNA or the respiratory chain. They can present with a wide variety of symptoms affecting multiple organ systems.
Fatty acid oxidation defects (FAODs) and respiratory chain defects (RCDs) are two major types of mitochondrial diseases. FAODs involve defects in breaking down fatty acids and present with hypoglycemia and liver disease in infants and children. RCDs involve defects in the mitochondrial respiratory chain and can cause liver failure in neonates or chronic liver disease.
It can be challenging to identify mitochondrial diseases due to their diverse presentations and similarities to other diseases. Biochemical testing of blood and urine can provide clues, but definitive diagnosis requires specialized testing not
The document describes a case of a 40-year-old male who presented with sudden weakness in both lower limbs for 4 hours. On examination, he had reduced tone, power and absent reflexes in both lower limbs. Investigations revealed hypokalemia of 1.3 meq/l. He was diagnosed with Bartter's syndrome type III based on hypokalemic metabolic alkalosis, hyperreninemic hyperaldosteronism and high urinary chloride and potassium levels. Intravenous potassium supplementation led to complete recovery.
Progressiv familial intrahepatic cholestasis type 1 case presentationSanjeev Kumar
This document describes the case of a 4-year-old male child presenting with itching, jaundice, and diarrhea for 3 months. He had a family history of similar cases resulting in death from liver disease. Liver tests showed elevated alkaline phosphatase. A liver biopsy showed mild degeneration and normal bile ducts. Immunostaining was positive for BSEP and MRP3. Based on the clinical features and test results, the child was diagnosed with Progressive Familial Intrahepatic Cholestasis type 1.
The patient presented with breathlessness and swelling of the face and legs. Examination revealed elevated jugular venous pressure, bilateral pitting edema, and crepitations in both lung bases. Investigations showed cardiomegaly, bilateral pleural effusion, and hypothyroidism. The patient was diagnosed with heart failure, acute left ventricular failure, and hypothyroidism and started on diuretics, antihypertensives, and thyroxine replacement.
This document presents a case study of a 12-year-old girl who presented with prolonged fever for over 20 days. Testing showed bi-cytopenia (anemia and leukopenia), hepatosplenomegaly, lymphadenopathy, and positive EBV and parvovirus serology. A bone marrow biopsy revealed hemophagocytosis. She was ultimately diagnosed with hemophagocytic lymphohistiocytosis (HLH), a life-threatening hyperinflammatory condition. Treatment for HLH involves prompt institution of therapies like steroids, chemotherapy, to prevent irreversible organ damage from the hyperactive immune response.
This document summarizes information about hepatitis B and C co-infection with HIV. It notes that co-infection leads to faster progression of liver disease and higher rates of liver cancer and mortality. Treatment for both viruses is important, with newer regimens like tenofovir alafenamide having comparable efficacy to tenofovir disoproxil fumarate but being more tolerable with less bone and kidney toxicity. Achieving a sustained virologic response reduces complications of liver disease and improves overall health outcomes.
This document provides information about Progressive Familial Intrahepatic Cholestasis (PFIC), a rare genetic liver disease. It defines what PFIC is, describes potential symptoms, diagnostic testing and treatment options. It also outlines the three main subtypes of PFIC, defined by the gene that is mutated. Each subtype can present with different levels of itching and liver abnormalities, and may progress to complications like liver failure if left untreated. Close monitoring by medical experts and potential surgical interventions or liver transplant are important for managing PFIC.
The 41-year-old male presented with quadriplegia, muscle cramps, and hypokalemia with hypocalcemia and metabolic alkalosis. Diagnostic tests found increased urinary excretion of potassium, chloride, and calcium with normal magnesium levels. He was diagnosed with Bartter's syndrome type V, confirmed by genetic testing showing a gain of function mutation in the calcium-sensing receptor gene, which presents with hypocalcemia. Adult onset Bartter's syndrome is rare but has been reported in a few case studies of patients diagnosed between ages 28 to 52 years old.
Mitochondrial diseases are caused by defects in mitochondrial DNA or the respiratory chain. They can present with a wide variety of symptoms affecting multiple organ systems.
Fatty acid oxidation defects (FAODs) and respiratory chain defects (RCDs) are two major types of mitochondrial diseases. FAODs involve defects in breaking down fatty acids and present with hypoglycemia and liver disease in infants and children. RCDs involve defects in the mitochondrial respiratory chain and can cause liver failure in neonates or chronic liver disease.
It can be challenging to identify mitochondrial diseases due to their diverse presentations and similarities to other diseases. Biochemical testing of blood and urine can provide clues, but definitive diagnosis requires specialized testing not
The document describes a case of a 40-year-old male who presented with sudden weakness in both lower limbs for 4 hours. On examination, he had reduced tone, power and absent reflexes in both lower limbs. Investigations revealed hypokalemia of 1.3 meq/l. He was diagnosed with Bartter's syndrome type III based on hypokalemic metabolic alkalosis, hyperreninemic hyperaldosteronism and high urinary chloride and potassium levels. Intravenous potassium supplementation led to complete recovery.
Progressiv familial intrahepatic cholestasis type 1 case presentationSanjeev Kumar
This document describes the case of a 4-year-old male child presenting with itching, jaundice, and diarrhea for 3 months. He had a family history of similar cases resulting in death from liver disease. Liver tests showed elevated alkaline phosphatase. A liver biopsy showed mild degeneration and normal bile ducts. Immunostaining was positive for BSEP and MRP3. Based on the clinical features and test results, the child was diagnosed with Progressive Familial Intrahepatic Cholestasis type 1.
The document discusses several nephrology cases and questions. It includes a case of a 64-year-old man with alcoholic cirrhosis and hyponatremia admitted for confusion and lethargy. Labs show hyponatremia and the cause is determined to be hepatorenal syndrome. Another case discusses a 72-year-old man who developed acute renal failure after cardiac catheterization, with findings suggesting cholesterol embolization. The document also reviews acid-base disorders and provides mnemonics for differential diagnoses of anion gap and non-gap acidosis.
Metabolic Liver Disease definitions by Dr. Ashish BavdekarSanjeev Kumar
This document discusses metabolic liver disease (MLD), including:
1. MLDs can be classified based on their effects, ranging from no harm to the liver to significant liver injury.
2. Data from Indian hospitals shows MLD cases are increasing and now represent a significant portion of liver diseases seen.
3. MLDs can present early in infancy with features like galactosemia, tyrosinemia, or cystic fibrosis or later with glycogen storage disease, Wilson's disease, or lipid storage disorders.
4. Diagnosing MLD can be challenging due to non-specific signs, genetic heterogeneity, and lack of diagnostic facilities in some areas.
Renal diseases; CK lecture notes & step up to medicineMays Yousuf
- The document discusses various types of renal diseases including definitions of renal failure, insufficiency, and end-stage renal disease. It covers causes, presentations, and treatments of different types of acute and chronic kidney injuries.
- Metabolic complications of AKI include increased potassium, phosphate, and uric acid levels and decreased sodium and calcium levels. The only effective prevention of contrast-induced renal failure is hydration.
- Allergic reactions to medications can cause rash, hemolysis, acute interstitial nephritis, and Steven-Johnson syndrome. Acute interstitial nephritis has causes including medications, infections, and connective tissue diseases.
Disease State Plasma Newsflash - January 2014 - BBI SolutionsBBISolutions
The BBI Solutions Disease State Plasma Newsflash gives details about our current inventory of disease state plasma, clinical samples and speciality blood products. This months features include our new autoimmune products and our rare infectious disease products.
The document discusses liver dysfunction in acute heart failure (AHF) and its clinical implications. Some key points:
- Liver dysfunction is common in AHF, with elevated levels of enzymes like AST, ALT and ALP seen in many patients.
- The liver dysfunction is thought to be due to congestion from elevated pressures in the liver vasculature in AHF.
- Abnormal liver enzymes in AHF are associated with worse disease severity and prognosis. Levosimendan may help reduce liver congestion compared to dobutamine, as seen by greater decreases in AST, ALT and ALP levels.
- There are complex interactions between heart and liver function, with each organ able to impact
The document discusses two cases of female patients presenting with jaundice and abdominal pain. Clinical investigations found elevated liver enzymes and antibodies associated with autoimmune hepatitis. Autoimmune hepatitis is a chronic liver disease of unknown cause characterized by ongoing liver inflammation and necrosis. It can progress to cirrhosis if left untreated. The standard treatment is immunosuppressive therapy with prednisone and azathioprine to induce and maintain remission.
A 35-year-old female presented with diminished consciousness and loss of speech for 1 day. Imaging and labs revealed she had a stroke and features of systemic lupus erythematosus (SLE), an autoimmune disease where the immune system attacks organs and tissues. She was diagnosed with rheumatoid heart disease, mitral stenosis, atrial fibrillation, cerebrovascular accident, and SLE based on her presentation of stroke, neurological deficits, immunological markers, oral ulcers, and involvement of multiple organ systems.
This document discusses drug-induced liver injury (DILI), which has been a major cause of drug withdrawals. It notes that while severe DILI is rare in phase 3 trials, mild hepatotoxicity could indicate potential for more serious cases. Close examination of individual cases is essential to determine the cause of injury and rule out other potential causes. The document also summarizes factors like inter-individual variability in drug metabolism and susceptibility that make predicting DILI challenging. Key signals of potential DILI are discussed, along with challenges in interpretation given the low prevalence of severe cases.
This document summarizes recent literature on acute renal failure (ARF). It discusses increasing incidence and mortality of ARF, as well as staging criteria like RIFLE and AKIN. Common causes of ARF include prerenal azotemia, acute tubular necrosis, interstitial nephritis, contrast-induced nephropathy. Treatment focuses on IV fluids, removing triggers, adjusting medications, and initiating dialysis for refractory complications. Prognosis depends on need for dialysis and presence of other organ failures.
This document provides an overview of acute liver failure (ALF), including definitions, causes, prognosis, management, and treatment considerations. Some key points:
- ALF is defined as coagulation abnormality with any degree of encephalopathy and illness duration under 26 weeks without preexisting cirrhosis. Prior to transplantation, survival was under 15%; it is now over 65% including those who receive transplants.
- Prognostic factors for outcomes include stage of encephalopathy, laboratory markers, etiology, INR, bilirubin, encephalopathy, and multiorgan failure. Scoring systems like MELD and King's College criteria are used but do not perfectly predict survival.
- Liver
The document discusses autoimmune hepatitis (AIH), including:
1. Natural history of AIH shows 50% 5-year survival without treatment, improving to 80-90% with steroids or transplant.
2. Treatment aims for complete histological remission or minimal inflammation to prevent fibrosis and cirrhosis progression.
3. Standard first-line treatment is prednisone and azathioprine combination to induce remission, then prednisone taper with azathioprine maintenance to control side effects from long-term steroids.
This document contains summaries of liver biopsy results from multiple patients. It describes cases of autoimmune hepatitis, primary biliary cirrhosis, primary sclerosing cholangitis, and overlapping autoimmune syndromes. The biopsies showed features ranging from mild disease to cirrhosis. Diagnoses included autoimmune hepatitis, primary biliary cirrhosis, primary sclerosing cholangitis, and possible overlapping conditions.
Amelioration of Metabolic Acidosis and Progression of CKD (Journal Club)Raj Kiran Medapalli
This document summarizes several studies on the effects of metabolic acidosis and alkali therapy in chronic kidney disease (CKD). Animal studies found that alkali therapy slowed CKD progression by reducing kidney endothelin-1 levels and tubulointerstitial injury. A human study of 134 CKD patients found that oral bicarbonate slowed decline in kidney function and reduced risks of rapid progression and end-stage renal disease over 2 years. The mechanisms of renal protection with alkali therapy involve reducing kidney endothelin-1 production and tubular injury.
This document presents a case study of a 63-year-old male who developed fatal cholestatic liver failure. He had undergone surgery for bladder cancer and cholecystectomy. His liver function tests continued rising after surgery. Extensive testing found no clear cause of cholestasis. Liver biopsies showed features of obstruction or drug effect. He was exposed to imipramine and amoxicillin-clavulanic acid, both known to cause cholestasis. Literature review found rare cases of progressive cholestasis and liver failure from these drugs. The patient's declining condition was treated supportively but he ultimately died of sepsis.
From CodaZero Live, Alex Rowell reviews the available advanced liver supports for patients with acute liver failure.
Artificial supports for the liver are quite complex and difficult. This is largely due to the liver's complex function.
Some of the advanced liver supports include CVVHDF, Molecular Adsorbent Recirculating System (MARS), Single Pass Albumin Dialysis (SPAD) and high volume plasma exchange.
In this podcast, Alex takes us through the research and evidence for these supports and shares some guidance on when they should be used.
CVVHDF is familiar and effective but we need to remember to use it early with acute liver failure patients.
Furthermore, Molecular Adsorbent Recirculating System (MARS) is widely studied but unfortunately not available in all places.
Single Pass Albumin Dialysis (SPAD) is easily implemented. Although there is less evidence on SPAD, it is generally agreed to be an effective support.
Unfortunately, there are no mortality benefits in any of these supports. They are however, useful tools in bridging to transplant.
From #CodaZero tune in to a quick, sharp & informative talk by Alex Rowell on Acute Liver Injury.
This document describes the case of a 55-year-old man who experienced episodes of sweating, shortness of breath, and diarrhea for 10 months. Imaging showed a mass in his jejunum, which was resected and found to be a carcinoid tumor. Carcinoid tumors are often associated with heart lesions due to secretion of vasoactive substances. The expected heart lesion in this case would be carcinoid heart disease, characterized by plaque-like lesions in the heart valves.
Chronic hepatitis is a group of chronic inflammatory diseases of the liver characterized by hepatocyte inflammation, necrosis and dystrophy while maintaining the lobular structure. More than 70% are asymptomatic. About 350-400 million people have chronic hepatitis B worldwide and around 180 million have hepatitis C. Treatment depends on the etiology and includes antiviral drugs and interferons with the goal of suppressing viral replication.
This document discusses the diagnosis and management of autoimmune hepatitis. It defines autoimmune hepatitis as unresolving liver inflammation of unknown cause that results from a complex interaction of triggers, autoantigens, genetics, and the immune system. The diagnosis requires the presence of interface hepatitis and portal plasma cell infiltration on histological examination, along with hypergammaglobulinemia and autoantibodies. Treatment involves the use of steroids such as prednisolone, either alone or in combination with azathioprine, to improve clinical outcomes and survival in severe cases of autoimmune hepatitis.
How to turn #400 over #5000000 sylvac.pdfSylvester1990
you can make real cash every day with your one time investment of 400 Naira, you can contact me on +2347063076507 for more information. just follow the guide lines at this eBook.
The document discusses several nephrology cases and questions. It includes a case of a 64-year-old man with alcoholic cirrhosis and hyponatremia admitted for confusion and lethargy. Labs show hyponatremia and the cause is determined to be hepatorenal syndrome. Another case discusses a 72-year-old man who developed acute renal failure after cardiac catheterization, with findings suggesting cholesterol embolization. The document also reviews acid-base disorders and provides mnemonics for differential diagnoses of anion gap and non-gap acidosis.
Metabolic Liver Disease definitions by Dr. Ashish BavdekarSanjeev Kumar
This document discusses metabolic liver disease (MLD), including:
1. MLDs can be classified based on their effects, ranging from no harm to the liver to significant liver injury.
2. Data from Indian hospitals shows MLD cases are increasing and now represent a significant portion of liver diseases seen.
3. MLDs can present early in infancy with features like galactosemia, tyrosinemia, or cystic fibrosis or later with glycogen storage disease, Wilson's disease, or lipid storage disorders.
4. Diagnosing MLD can be challenging due to non-specific signs, genetic heterogeneity, and lack of diagnostic facilities in some areas.
Renal diseases; CK lecture notes & step up to medicineMays Yousuf
- The document discusses various types of renal diseases including definitions of renal failure, insufficiency, and end-stage renal disease. It covers causes, presentations, and treatments of different types of acute and chronic kidney injuries.
- Metabolic complications of AKI include increased potassium, phosphate, and uric acid levels and decreased sodium and calcium levels. The only effective prevention of contrast-induced renal failure is hydration.
- Allergic reactions to medications can cause rash, hemolysis, acute interstitial nephritis, and Steven-Johnson syndrome. Acute interstitial nephritis has causes including medications, infections, and connective tissue diseases.
Disease State Plasma Newsflash - January 2014 - BBI SolutionsBBISolutions
The BBI Solutions Disease State Plasma Newsflash gives details about our current inventory of disease state plasma, clinical samples and speciality blood products. This months features include our new autoimmune products and our rare infectious disease products.
The document discusses liver dysfunction in acute heart failure (AHF) and its clinical implications. Some key points:
- Liver dysfunction is common in AHF, with elevated levels of enzymes like AST, ALT and ALP seen in many patients.
- The liver dysfunction is thought to be due to congestion from elevated pressures in the liver vasculature in AHF.
- Abnormal liver enzymes in AHF are associated with worse disease severity and prognosis. Levosimendan may help reduce liver congestion compared to dobutamine, as seen by greater decreases in AST, ALT and ALP levels.
- There are complex interactions between heart and liver function, with each organ able to impact
The document discusses two cases of female patients presenting with jaundice and abdominal pain. Clinical investigations found elevated liver enzymes and antibodies associated with autoimmune hepatitis. Autoimmune hepatitis is a chronic liver disease of unknown cause characterized by ongoing liver inflammation and necrosis. It can progress to cirrhosis if left untreated. The standard treatment is immunosuppressive therapy with prednisone and azathioprine to induce and maintain remission.
A 35-year-old female presented with diminished consciousness and loss of speech for 1 day. Imaging and labs revealed she had a stroke and features of systemic lupus erythematosus (SLE), an autoimmune disease where the immune system attacks organs and tissues. She was diagnosed with rheumatoid heart disease, mitral stenosis, atrial fibrillation, cerebrovascular accident, and SLE based on her presentation of stroke, neurological deficits, immunological markers, oral ulcers, and involvement of multiple organ systems.
This document discusses drug-induced liver injury (DILI), which has been a major cause of drug withdrawals. It notes that while severe DILI is rare in phase 3 trials, mild hepatotoxicity could indicate potential for more serious cases. Close examination of individual cases is essential to determine the cause of injury and rule out other potential causes. The document also summarizes factors like inter-individual variability in drug metabolism and susceptibility that make predicting DILI challenging. Key signals of potential DILI are discussed, along with challenges in interpretation given the low prevalence of severe cases.
This document summarizes recent literature on acute renal failure (ARF). It discusses increasing incidence and mortality of ARF, as well as staging criteria like RIFLE and AKIN. Common causes of ARF include prerenal azotemia, acute tubular necrosis, interstitial nephritis, contrast-induced nephropathy. Treatment focuses on IV fluids, removing triggers, adjusting medications, and initiating dialysis for refractory complications. Prognosis depends on need for dialysis and presence of other organ failures.
This document provides an overview of acute liver failure (ALF), including definitions, causes, prognosis, management, and treatment considerations. Some key points:
- ALF is defined as coagulation abnormality with any degree of encephalopathy and illness duration under 26 weeks without preexisting cirrhosis. Prior to transplantation, survival was under 15%; it is now over 65% including those who receive transplants.
- Prognostic factors for outcomes include stage of encephalopathy, laboratory markers, etiology, INR, bilirubin, encephalopathy, and multiorgan failure. Scoring systems like MELD and King's College criteria are used but do not perfectly predict survival.
- Liver
The document discusses autoimmune hepatitis (AIH), including:
1. Natural history of AIH shows 50% 5-year survival without treatment, improving to 80-90% with steroids or transplant.
2. Treatment aims for complete histological remission or minimal inflammation to prevent fibrosis and cirrhosis progression.
3. Standard first-line treatment is prednisone and azathioprine combination to induce remission, then prednisone taper with azathioprine maintenance to control side effects from long-term steroids.
This document contains summaries of liver biopsy results from multiple patients. It describes cases of autoimmune hepatitis, primary biliary cirrhosis, primary sclerosing cholangitis, and overlapping autoimmune syndromes. The biopsies showed features ranging from mild disease to cirrhosis. Diagnoses included autoimmune hepatitis, primary biliary cirrhosis, primary sclerosing cholangitis, and possible overlapping conditions.
Amelioration of Metabolic Acidosis and Progression of CKD (Journal Club)Raj Kiran Medapalli
This document summarizes several studies on the effects of metabolic acidosis and alkali therapy in chronic kidney disease (CKD). Animal studies found that alkali therapy slowed CKD progression by reducing kidney endothelin-1 levels and tubulointerstitial injury. A human study of 134 CKD patients found that oral bicarbonate slowed decline in kidney function and reduced risks of rapid progression and end-stage renal disease over 2 years. The mechanisms of renal protection with alkali therapy involve reducing kidney endothelin-1 production and tubular injury.
This document presents a case study of a 63-year-old male who developed fatal cholestatic liver failure. He had undergone surgery for bladder cancer and cholecystectomy. His liver function tests continued rising after surgery. Extensive testing found no clear cause of cholestasis. Liver biopsies showed features of obstruction or drug effect. He was exposed to imipramine and amoxicillin-clavulanic acid, both known to cause cholestasis. Literature review found rare cases of progressive cholestasis and liver failure from these drugs. The patient's declining condition was treated supportively but he ultimately died of sepsis.
From CodaZero Live, Alex Rowell reviews the available advanced liver supports for patients with acute liver failure.
Artificial supports for the liver are quite complex and difficult. This is largely due to the liver's complex function.
Some of the advanced liver supports include CVVHDF, Molecular Adsorbent Recirculating System (MARS), Single Pass Albumin Dialysis (SPAD) and high volume plasma exchange.
In this podcast, Alex takes us through the research and evidence for these supports and shares some guidance on when they should be used.
CVVHDF is familiar and effective but we need to remember to use it early with acute liver failure patients.
Furthermore, Molecular Adsorbent Recirculating System (MARS) is widely studied but unfortunately not available in all places.
Single Pass Albumin Dialysis (SPAD) is easily implemented. Although there is less evidence on SPAD, it is generally agreed to be an effective support.
Unfortunately, there are no mortality benefits in any of these supports. They are however, useful tools in bridging to transplant.
From #CodaZero tune in to a quick, sharp & informative talk by Alex Rowell on Acute Liver Injury.
This document describes the case of a 55-year-old man who experienced episodes of sweating, shortness of breath, and diarrhea for 10 months. Imaging showed a mass in his jejunum, which was resected and found to be a carcinoid tumor. Carcinoid tumors are often associated with heart lesions due to secretion of vasoactive substances. The expected heart lesion in this case would be carcinoid heart disease, characterized by plaque-like lesions in the heart valves.
Chronic hepatitis is a group of chronic inflammatory diseases of the liver characterized by hepatocyte inflammation, necrosis and dystrophy while maintaining the lobular structure. More than 70% are asymptomatic. About 350-400 million people have chronic hepatitis B worldwide and around 180 million have hepatitis C. Treatment depends on the etiology and includes antiviral drugs and interferons with the goal of suppressing viral replication.
This document discusses the diagnosis and management of autoimmune hepatitis. It defines autoimmune hepatitis as unresolving liver inflammation of unknown cause that results from a complex interaction of triggers, autoantigens, genetics, and the immune system. The diagnosis requires the presence of interface hepatitis and portal plasma cell infiltration on histological examination, along with hypergammaglobulinemia and autoantibodies. Treatment involves the use of steroids such as prednisolone, either alone or in combination with azathioprine, to improve clinical outcomes and survival in severe cases of autoimmune hepatitis.
How to turn #400 over #5000000 sylvac.pdfSylvester1990
you can make real cash every day with your one time investment of 400 Naira, you can contact me on +2347063076507 for more information. just follow the guide lines at this eBook.
El avión Metro 3 de la línea aérea AEROCON se estrelló al aterrizar en el aeropuerto de Riberalta el 3 de noviembre de 2013, dejando 7 personas fallecidas y 10 heridas, incluidos el piloto y copiloto. La Dirección General de Aeronáutica Civil formó una comisión para investigar las causas del accidente e informó la lista de víctimas.
El documento describe las oportunidades de inversión en la industria alimentaria de Chile. Chile es una economía estable y competitiva con ventajas climáticas y geográficas para la agricultura. La industria alimentaria chilena tiene una fuerte presencia en los mercados internacionales, especialmente en frutas como uvas, manzanas y kiwis. El documento identifica oportunidades de inversión en el aprovechamiento de residuos de la industria olivícola y en la producción primaria de nueces, cerezas y fr
Estudio sobre la privacidad de los datos personales y la seguridad de la info...Abanlex
El objetivo general del estudio es la elaboración de un análisis del estado de la seguridad en redes sociales y plataformas análogas, con especial atención a los usuarios menores e incapaces, mediante una evaluación y diagnóstico de carácter jurídico, tecnológico, sociológico y de seguridad de los contenidos, los agentes participantes, así como de la privacidad y la protección de datos de los usuarios que se relacionan a través de estos sitios web.
Este documento presenta el cronograma electoral para las Elecciones Primarias Abiertas, Obligatorias y Simultáneas de 2015 en la provincia de Buenos Aires. Establece fechas límite para el reconocimiento de partidos políticos, la formación de alianzas, la presentación de listas de candidatos ante las juntas electorales partidarias y provincial, la impresión de boletas, la designación de autoridades de mesa, la campaña electoral, el escrutinio y la comunicación de resultados. Las elecciones primarias tendrán lugar el 9 de ag
Energy Management Systems: Recommendations for decision makersGimélec
The document discusses implementing an Energy Management System (EMS) to improve energy efficiency in buildings. An EMS allows continuous tracking of energy consumption and costs. It collects and analyzes consumption data to monitor performance, identify savings opportunities, and support decision making. The EMS helps reduce energy expenditures by 5-15% by raising stakeholder awareness and uniting teams around continual improvement. Implementing an EMS is an important part of an energy management program and improves management at all stages from diagnosis to operations.
Este documento anuncia el próximo Encuentro Nacional de Laicos Dehonianos que tendrá lugar del 25 al 27 de junio de 2010 en Venta de Baños, Palencia. El encuentro girará en torno al tema de la reconciliación y contará con oraciones, adoraciones, eucaristías, formaciones y actividades lúdicas organizadas por diferentes grupos de laicos. El horario incluye conferencias sobre la reconciliación desde perspectivas psicológica, espiritual y artística, así como momentos de oración, comidas y despedida
Group Comunicaciones es una agencia de publicidad con 6 áreas especializadas que trabajan de forma integrada para ofrecer todos los tipos de publicidad. La agencia desarrolla campañas 360° innovadoras con un enfoque de generar economías de escala utilizando todos los servicios internamente y un equipo de más de 90 profesionales. Actualmente la empresa se encuentra en un proceso de cambio de nombre y ubicación.
Este documento describe las tres etapas principales del método de investigación cualitativa: formulación, diseño y cierre. Explica que la formulación implica definir el objeto de estudio y la pregunta de investigación. El diseño se refiere a cómo se llevará a cabo la investigación y en qué contexto. El cierre busca sistematizar los resultados de manera progresiva a medida que avanza la investigación.
- Willem van Valkenburg is the director of TU Delft OpenCourseWare and manages the university's learning management system. He discusses the goals and usage of OpenCourseWare.
- OpenCourseWare makes high-quality educational course materials freely available online to educators and learners worldwide. While not a distance learning program, it allows open access to and sharing of course content.
- Analysis of MIT OpenCourseWare usage shows that educators use it to improve knowledge and teaching methods while students use it to supplement courses or plan studies. Self-learners explore new topics or review professional fields.
The document is the version 1.21 of the SIM5218 AT Command Manual, released on January 13, 2011. It provides documentation on the AT commands for the SIM5218 module to support application and engineering efforts. The manual includes notes on general information, copyright, version history and 22 chapters describing various AT commands.
El punto de partida de un proyecto (web o de otra índole) consiste en definir los límites del propio proyecto. Cuanto más definido esté el proyecto y contrastado con el cliente más cerca estaremos de dimensionar correctamente el alcance del mismo y lograr los objetivos.
El documento proporciona información sobre las bases de datos que ofrece la biblioteca virtual ITM. Explica que la biblioteca tiene una misión de divulgar el conocimiento científico y apoyar procesos como la enseñanza y la investigación. Luego describe algunas de las bases de datos más importantes que la biblioteca ofrece, como Science Direct, Scopus, E-libro y Embase. También menciona algunas bases de datos apropiadas para la gestión administrativa como Redalyc y SciELO.
This document provides information on laboratory diagnostic approaches to liver biochemistry and function. It discusses liver anatomy and function, key biochemical parameters and their relation to liver disorders, bilirubin metabolism, diagnostic principles and indices, clinical causes of jaundice, and case studies. The goal is for clinical laboratory staff to understand liver biochemistry parameters and how to make appropriate diagnoses and deduce the underlying liver pathology.
The document provides an overview of approach to evaluating abnormal liver function tests (LFTs). It defines relevant liver enzymes and tests. Epidemiology studies show most abnormal LFT cases can be diagnosed noninvasively, and the most common findings are non-alcoholic fatty liver disease and steatohepatitis. A thorough history and physical exam is important to identify potential causes like medications, viruses, autoimmune conditions, or metabolic disorders. Common patterns on lab testing can help indicate hepatocellular injury, cholestasis or other chronic processes. A methodical evaluation and testing approach is outlined.
Metabolic liver disease presenting with cholestasis talk anshu srivastavaSanjeev Kumar
This document discusses metabolic liver disease presenting with cholestasis. It begins by defining cholestasis and describing the differences between intrahepatic and extrahepatic cholestasis. In neonates, a metabolic etiology is often the cause of cholestasis and can include conditions like galactosemia or tyrosinemia. The document then examines various etiologies of cholestasis across different age groups. It provides details on progressive familial intrahepatic cholestasis (PFIC), benign recurrent intrahepatic cholestasis (BRIC), and intrahepatic cholestasis of pregnancy. The document emphasizes the importance of early identification of treatable metabolic causes of chole
This document discusses various enzymes used as diagnostic and therapeutic markers. It defines enzymes and their role in biological systems. It describes enzymes like ALT, AST, GGT, LDH, CK, ALP that are used to diagnose conditions like liver disease, myocardial infarction, muscle diseases. It explains how increased or decreased levels of these enzymes can indicate different pathological conditions. It also discusses enzymes like amylase and lipase that are markers for pancreatic disorders. Therapeutic enzymes mentioned include streptokinase, trypsin, asparaginase.
This document provides an overview of jaundice and its causes. It defines jaundice as a yellowish discoloration of the skin and eyes. Jaundice can be classified as pre-hepatic (haemolytic), hepatocellular, or obstructive based on its underlying mechanism. Common causes discussed include viral hepatitis, alcoholic liver disease, gallstones, and tumors. The document outlines approaches to evaluating a jaundiced patient through history, examination, and laboratory and imaging tests. It also describes treatment principles and specific therapies for acute viral hepatitis and liver failure.
Abnormal liver function tests can indicate underlying liver disease but may also be caused by extrahepatic factors. A thorough evaluation is needed and includes considering the pattern of test abnormalities, severity of changes, and potential etiologies. For hepatocellular predominant abnormalities, further workup may include tests for viral hepatitis, autoimmune disease, and iron overload. Liver biopsy may be needed if initial testing is unrevealing. Proper diagnosis guides management and treatment of underlying liver conditions.
Interpret tests for metabolic diseases talk sk yachhaSanjeev Kumar
Clinical suspicion of inborn errors of metabolism should arise with parental consanguinity, positive family history, unexplained sibling deaths, or recurrent issues like hypoglycemia, acidosis, or encephalopathy. Initial screening tests available in India can help identify aminoaciduria, organic acidemias, or fatty acid oxidation defects while definitive testing requires samples not readily available, like fresh tissue, to analyze specific enzyme activities. Managing treatable conditions like hereditary fructose intolerance or some organic acidemias can improve outcomes.
This document discusses investigations for jaundice, including liver function tests (LFTs), CT scan, MRI scan, ERCP, and EUS. It provides detailed information on various LFTs such as aminotransferases, alkaline phosphatase, bilirubin, and GGT. It describes characteristic patterns seen in different liver diseases and notes that additional tests may include hepatitis markers, iron studies, tumor markers, and endoscopic ultrasound. Reference sources include medical textbooks and Wikipedia.
1.Detect presence of liver disease.
2.Distinguish among different types of liver diseases.
3.Estimate the extent of known liver damage.
4.Follow the response of treatment
Approach to the Patient with Liver Disease.pptxRaj Kumar
This document provides information on evaluating and diagnosing patients with liver disease. It discusses taking a history, performing a physical exam, and ordering lab tests and imaging to classify the type of jaundice a patient may be experiencing as pre-hepatic, hepatic, or post-hepatic. Pre-hepatic jaundice is caused by hemolysis, hepatic jaundice by liver disease, and post-hepatic jaundice by biliary obstruction. Common liver enzymes, bilirubin levels, and urine and stool characteristics are outlined to distinguish the three types of jaundice. Three case examples are presented and the document describes diagnosing the likely cause based on the patient's reported symptoms and lab results.
Liver Function Tests - An Approach for Primary CareJarrod Lee
This presentation is aimed at primary care physicians. It covers the fundamentals of liver function tests, including the basic principles of interpretation, and the key patterns of abnormalities. The focus is on how to approach liver function tests in a primary care setting.
Thank you for explaining the process. I will be sure to follow the mark scheme closely when consenting patients. Effective communication is so important to ensure informed consent.
This document discusses a case of alcoholic liver disease being investigated by Dr. N. Gautam. It provides background information on liver anatomy, alcohol metabolism, and the pathophysiology and clinical presentations of alcoholic liver disease. It describes the typical laboratory investigations performed for ALD including liver enzymes, bilirubin, proteins, and coagulation factors. The document then presents findings from a 45-year-old chronic alcoholic male patient presenting with abdominal pain, jaundice and altered sensorium, with laboratory results consistent with severe alcoholic hepatitis.
The document discusses various laboratory tests used to evaluate liver function and disease. It describes tests for hepatocellular damage like ALT and AST, tests for cholestasis like alkaline phosphatase, and tests for liver synthetic function like albumin. Common causes of abnormal liver enzymes are also summarized, along with risk factors for liver disease.
This document provides an overview of dyslipidemia. It defines dyslipidemia as abnormal levels of lipids in the blood such as total cholesterol, LDL cholesterol, triglycerides, and others. The document then discusses the epidemiology of dyslipidemia, noting that over half of US adults over age 20 have total cholesterol levels at or above 200 mg/dL. It also summarizes the Fredrickson classification system for different types of hyperlipidemias based on abnormal lipid levels and lipoproteins. The document concludes by listing some of the primary genetic causes of hypercholesterolemia and hypertriglyceridemia.
This document provides an overview of common liver problems, including identifying causes of abnormal liver function tests, approaches to acute hepatic injury and chronic hepatitis, viral marker interpretation, and treatment of ascites and hepatic encephalopathy. It discusses evaluation and treatment of acute viral hepatitis and asymptomatic abnormal liver function tests. It also covers chronic hepatitis B and C, including serological markers, natural history, and diagnosis. Treatment of spontaneous bacterial peritonitis with antibiotics is emphasized.
An inherited enzyme deficiency leading to the disruption of normal bodily metabolism.
Accumulation of a toxic substrate.
Impaired formation of a product normally produced by the deficient enzyme.
The document discusses liver function tests and the clinical significance of various enzymes and biomarkers. It is divided into several sections that cover: the functions of the liver; classification of liver function tests into groups that indicate hepatocellular damage or cholestasis; specific enzymes such as ALT, AST, ALP, GGT and their levels in different liver conditions or diseases; clinical cases and how to interpret abnormal enzyme profiles and biomarkers.
The document discusses liver function tests and the clinical significance of various enzymes and biomarkers. It is divided into several sections that cover: the functions of the liver; classification of liver function tests into groups that indicate hepatocellular damage or cholestasis; specific enzymes such as ALT, AST, ALP, GGT and their levels in different liver conditions or diseases; clinical cases and how to interpret abnormal enzyme profiles and biomarkers.
This document provides guidance for general practitioners on interpreting common routine laboratory investigations. It discusses the importance of laboratory tests in confirming clinical diagnoses and guidelines treatment while supplementing, not replacing, clinical examination. The key laboratory tests a general practitioner should be familiar with interpreting are described in detail, including complete blood count, blood sugars, urine analysis, renal and liver function tests. Normal ranges are provided and abnormal results are interpreted for each test to guide practitioners in reaching the right diagnosis.
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SANDRI G. La Nutrizione Clinica al S.Eugenio. ASMaD 2017Gianfranco Tammaro
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2) Quality indicators like adequate bowel preparation, adenoma detection rates, and cecal intubation rates are important for colonoscopy effectiveness.
3) New technologies like HD imaging, water jets, and wide-angle endoscopes aim to improve polyp detection rates and make the procedure more comfortable and effective.
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GASTROINTESTINAL INFECTIONS AND GASTRITIS
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Gastrointestinal Infections
GASTROINTESTINAL INFECTIONS result from the ingestion of pathogens that cause infections at the level of this tract, generally being transmitted by food, water and hands contaminated by microorganisms such as E. coli, Salmonella, Shigella, Vibrio cholerae, Campylobacter, Staphylococcus, Rotavirus among others that are generally contained in feces, thus configuring a FECAL-ORAL type of transmission.
Among the factors that lead to the occurrence of gastrointestinal infections are the hygienic and sanitary deficiencies that characterize our markets and other places where raw or cooked food is sold, poor environmental sanitation in communities, deficiencies in water treatment (or in the process of its plumbing), risky hygienic-sanitary habits (not washing hands after major and/or minor needs), among others.
These are generally consequences (signs and symptoms) resulting from gastrointestinal infections: diarrhea, vomiting, fever and malaise, among others.
The treatment consists of replacing lost liquids and electrolytes (drinking drinking water and other recommended liquids, including consumption of juicy fruits such as papayas, apples, pears, among others that contain water in their composition).
To prevent this, it is necessary to promote health education, improve the hygienic-sanitary conditions of markets and communities in general as a way of promoting, preserving and prolonging PUBLIC HEALTH.
Gastritis and Gastric Health
Gastric Health is one of the most relevant concerns in human health, with gastrointestinal infections being among the main illnesses that affect humans.
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Breast cancer in postmenopausal women with hormone receptor-positive (HR+) status is a common and complex condition that necessitates a multifaceted approach to management. HR+ breast cancer means that the cancer cells grow in response to hormones such as estrogen and progesterone. This subtype is prevalent among postmenopausal women and typically exhibits a more indolent course compared to other forms of breast cancer, which allows for a variety of treatment options.
Diagnosis and Staging
The diagnosis of HR+ breast cancer begins with clinical evaluation, imaging, and biopsy. Imaging modalities such as mammography, ultrasound, and MRI help in assessing the extent of the disease. Histopathological examination and immunohistochemical staining of the biopsy sample confirm the diagnosis and hormone receptor status by identifying the presence of estrogen receptors (ER) and progesterone receptors (PR) on the tumor cells.
Staging involves determining the size of the tumor (T), the involvement of regional lymph nodes (N), and the presence of distant metastasis (M). The American Joint Committee on Cancer (AJCC) staging system is commonly used. Accurate staging is critical as it guides treatment decisions.
Treatment Options
Endocrine Therapy
Endocrine therapy is the cornerstone of treatment for HR+ breast cancer in postmenopausal women. The primary goal is to reduce the levels of estrogen or block its effects on cancer cells. Commonly used agents include:
Selective Estrogen Receptor Modulators (SERMs): Tamoxifen is a SERM that binds to estrogen receptors, blocking estrogen from stimulating breast cancer cells. It is effective but may have side effects such as increased risk of endometrial cancer and thromboembolic events.
Aromatase Inhibitors (AIs): These drugs, including anastrozole, letrozole, and exemestane, lower estrogen levels by inhibiting the aromatase enzyme, which converts androgens to estrogen in peripheral tissues. AIs are generally preferred in postmenopausal women due to their efficacy and safety profile compared to tamoxifen.
Selective Estrogen Receptor Downregulators (SERDs): Fulvestrant is a SERD that degrades estrogen receptors and is used in cases where resistance to other endocrine therapies develops.
Combination Therapies
Combining endocrine therapy with other treatments enhances efficacy. Examples include:
Endocrine Therapy with CDK4/6 Inhibitors: Palbociclib, ribociclib, and abemaciclib are CDK4/6 inhibitors that, when combined with endocrine therapy, significantly improve progression-free survival in advanced HR+ breast cancer.
Endocrine Therapy with mTOR Inhibitors: Everolimus, an mTOR inhibitor, can be added to endocrine therapy for patients who have developed resistance to aromatase inhibitors.
Chemotherapy
Chemotherapy is generally reserved for patients with high-risk features, such as large tumor size, high-grade histology, or extensive lymph node involvement. Regimens often include anthracyclines and taxanes.
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Puoti Claudio. FAD HT 2012. Come interpretare alterazioni lievi di laboratorio della Funzionalità Epatica. ASMaD 2012
1. MGH
Claudio Puoti
S.C. di Medicina Epato-Gastroenterologica,
Emodinamica Epatica ed Endoscopia Digestiva
Marino, Roma
2. Three diagnostic scenarios
1. A patient who has been referred because of clinical
symptoms (asthenia, fatigue, itching, vomiting…)
2. A patient who has been referred because of signs
(hepatomegaly, jaundice, bruises, bleeding, ascites)
3. A patient who has just been found by chance to have
slight liver enzymes abnormalities (sporadic
determinations).
3. Virus Alcohol
Autoimmunity
The galaxy
of liver diseases
Other
HCC Steatosis
Metastases
Vascular Haemochromatosis
4. Genetic testing
Fibroscan
C282Y
Hemodynamic
Liver Biopsy
Virological tests
Antibody detection Biochemistry
EIA, RIBA Liver biochemistry
Genome detection PLT count
PCR, TMA History, Prothrombin time
Genotyping Clinical A/G ratio
examination Fibrosis serum markers
Imaging
US Endoscopy
CT, NMR
8. De Ritis F, Coltorti M, Giusti G.Clin Chim Acta 1957; 2:70-4
9. Where do they come from?
AST ALT
• Cytosol and
mitochondria • Cytosol
• Liver • Liver
• Kidney • Skeletal muscle
• Heart
• Kidney
• Skeletal muscle
• Spleen
• Lung
• Erythrocytes
10. Interpretation of Abnormal
Liver Biochemistry Values
2.5% below Normal people 2.5% above
2 SD 2 SD
Age
Age
Gender
Gender
Blood group
Blood group
Post-prandial state
Post-prandial state
BMI
BMI
Alcohol
Alcohol
Lipid metabolism
Lipid metabolism
Carbohydrate metabolism
Carbohydrate metabolism
Smoke
Smoke
AGA technical Review, Gastro 2002
Ruhl et al, Gastro 2003
17. 354 patients with abnormal ALT and negative
serological/virological markers
AIH PBC OTHER
ALCOHOL
NORMAL
DRUGS NASH
CRYPTOGENIC
HEPATITIS
STEATOSIS Skelly MM, J Hepatol 2001
18. OTHER ABNORMALITIES
MAGNITUDE
(GGT, bilirubin, ALP, PLT,
cholesterol…)
ELEVATED
AMINOTRANSFERASE AST/ALT
RATIO
LEVELS
SYMPTOMS SIGNS
DURATION
AGA technical Review, Gastro 2002
19. RISK EXTRA-HEPATIC
FACTORS DISEASES
ELEVATED
AMINOTRANSFERASE
LEVELS
HISTORY AGE
AGA technical Review, Gastro 2002
20. Diagnosis of symptomless ALT elevation :
role of clinical parameters
History Signs Blood tests
• Alcohol abuse • Abdominal wall veins • Albumin
• Blood exposure • Ascites • AST/ALT ratio
• Drugs • Jaundice • Bilirubin
• Family history
• Liver failure signs • GGT, ALP
• • Obesity •
IVDA Lipids
• Spider naevi
• Occupational exposure • PLT count
• Splenomegaly
• Previous diseases • PT
• WBC
21. Male
Female
Middle-aged GGT ALT < 2-5 ULN
ALT > 5-10 ULN ALP, GGT, Glucose, lipidsHigh GGT
NASH/
Obesity
gallstones
abnormal GGT, ALPBILIRUBIN ASH
Diabetes
Jaundice
?
Alcohol abuse
RUQ pain
IVDA Young
Chronic
ALT 2-10 ULN HBsAg,
WBC count ALT x 5-10
EBV serologyleukocytosis
HCV/
Normal ALP
a-HCV IMN
Normal bilirubin fever, chills
HBV
Asymptomatic limphadenopathy
sore throat
22. Exclude:
ALT > 10 ULN drugs
no history or physical evidence of CLD alcohol
CBD disease
Vascular disease
HAV-IgM
HBsAg identify > 90% of cases
anti-HCV
positive:
acute viral hepatitis
AGA Gastro 2002
23. Exclude:
ALT > 10 ULN drugs
no history or physical evidence of CLD alcohol
CBD disease
Vascular disease
HAV-IgM
HBsAg identify > 90% of cases
anti-HCV
negative:
Autoimmunity
positive: HCV RNA
acute viral hepatitis HBcAb IgM each cause
anti-HEV has a very
ceruloplasmin low frequency
others (<1%)
AGA Gastro 2002
24. Exclude:
ALT > 10 ULN drugs (DILI)
no history or physical evidence of CLD alcohol
CBD disease
Vascular disease
HAV-IgM
HBsAg identify > 90% of cases
anti-HCV re-evaluate
negative: negative
Autoimmunity
positive: HCV RNA
acute viral hepatitis HBcAb IgM each cause
anti-HEV has a very
ceruloplasmin low frequency
others (<1%)
AGA Gastro 2002
25. GGT ? HCV
Alcohol PLT? +++
abuse other liver chemistry ?
++ HBV
+
Chronically raised ALT HBV/HDV
Drug < 10 ULN +/-
toxicity
+/-
Wilson disease
NASH
Haemochromatosis
+++
α-1-AT deficiency
others
+/- vs +
AGA Gastro 2002
26.
27.
28. Other liver enzyme abnormalities
Gamma GT
Liver cells and biliary enzyme activity
Cholestasis
Steatosis
Drugs injury
Heavy alcohol abuse
GGT levels migth increase also during the course of:
uraemia, renal tumours, myocardial infartion, COPD ,
diabetes, intestinal infacrtion or ischemia
High sensitivity, low specificity
29. Other liver enzyme abnormalities
Alkaline phosphatase
Biliary cells enzyme activity
It means cholestasis
Intra-hepatic : PBC, PSC
Extra-hepatic: CBD obstruction (gallstones, malignancy)
Several isoenzymes (bone, kidney, gut, leucocytes…)
High specificity, low sensitiviy
30. Messaggio conclusivo I
• Lievi alterazioni di laboratorio della funzionalità epatica
non sono rare in soggetti apparentemente sani.
• Quasi sempre queste alterazioni vengono rilevate a
seguito di controlli biochimici casuali ed in assenza di
qualunque sintomo o segno obiettivo.
• Le alterazioni più frequenti riguardano le transaminasi e
sono in genere inferiori a 2 volte i valori normali.
31. Messaggio conclusivo II
• Nel nostro Paese, le cause più frequenti di modeste
elevazioni degli enzimi epatici sono rappresentate dalla
steatosi non alcolica, dalla epatite cronica da HCV, da cause
iatrogene (farmaci, erbe) e dall’ abuso di alcol.
• Molto più raramente sono riscontrabili altre cause (HBV,
emocromatosi, autoimmunità, celiachia, ecc).
• La corretta interpretazione del dato di laboratorio non può
prescindere dalla valutazione integrata di tutti i parametri di
funzione epatica, dell’ emocromo, dell’assetto metabolico
(glicemia, lipidi) e dal dato ecografico.
32. Messaggio conclusivo III
• Una corretta anamnesi personale, patologica e farmacologica
consente la diagnosi clinica nella maggior parte dei casi.
• L’assunzione di sostanze medicamentose “alternative”
(“herbal medicine”) deve essere sempre indagata perché
sovente il paziente tende a tacerne l’ uso, considerandole del
tutto innocue.
• Non si deve infine dimenticare che diverse patologie extra-
epatiche sia gastroenteriche (celiachia, MICI) che sistemiche
(neoplasie, patologie scheletriche, ecc) possono determinare
alterazioni enzimatiche.
Editor's Notes
L’alterazione degli enzimi epatici può essere rilevata a seguito di sintomi soggettivi (astenia, nausea, ecc), di segni oggettivi (epatomegalia, ittero, ecc), o essere identificata del tutto casualmente a seguito di controlli ematochimici di routine.
Numerose sono le patologie del fegato in grado di determinare alterazioni persistenti, anche lievi, della biochimica epatica : virali (infezioni croniche da virus HBV e HCV), metaboliche (steatosi alcolica, steatoepatite non alcolica), da accumulo (emocromatos, morbo di Wilson), vascolari (sindrome di Budd Chiari), neoplastiche (epatocarcinoma, metastasi), autoimmuni.
Di conseguenza, numerose sono le indagini biochimiche, virologiche, immunologiche, genetiche, istologiche, di imaging, ecc. che consentono di pervenire ad una corretta diagnosi della epatopatia responsabile delle alterazioni biochimmiche.
I tests biochimici di base esplorano diverse funzioni epatiche ed hanno diversi significati : citolisi (transaminasi), colestasi (fosfatasi alcalina, gamma GT), induzione enzimatica (gamma GT), sintesi proteica (albumina, protrombina, capacità di captazione e coniugazione (bilirubina).
Non è inutile ricordare che le transaminasi sono una “gloria” tutta italiana, e più specificamente napoletana, essendo state identificate nei primi anni 50 da ricercatori della Clinica delle Malattie Infettive dell’ Università di Napoli.
Alla straordinaria intuizione del prof. De Ritis e dei suoi allora giovani assistenti dr. Coltorti e dr. Giusti dobbiamo la possibilità di identificare, ancora a distanza di circa 60 anni, le alterazioni epatiche con un test semplice e poco costoso.
La diapositiva – tratta dalla rivista Cinica Chimica Acta che nel 2006 volle onorare la memoria del prof. De Ritis, riporta una delle immagini che illustravano il lavoro originale. I grafici ovviamente erano disegnati a mano.
Non bisogna peraltro dimenticare che mentre la transaminasi ALT (SGPT) si trova quasi esclusivamente nel fegato, ed in minore quantità nel muscolo striato e nel rene, la transaminasi AST (SGOT) è praticamente ubiquitaria. Inoltre la ALT si rileva in grandi quantità solo nel citosol dell’ epatocita, mentre la AST si trova anche nei mitocondri.
Infine, va ricordato che molti soggetti senza alcun danno epatico possono avere livelli di transaminasi leggermente più elevati rispetto ai valori normali, e che ciò può dipendere dall’eta, sesso, fumo, assunzione alcolica, assetto lipidico, peso corporeo, gruppo sanguigno.
Recenti ricerche inoltre tendono ad abbassare i livelli considerati storicamente normali di transaminasi: probabilmente i veri livelli massimi di normalità vanno ridotti a 30 Unità per gli uomini e 19 Unità per le donne.
Una ricerca condotta negli USA su un campione d reclute – quindi soggetti giovani di ambo i sessi – ha rilevato alterazioni delle transaminasi solo nello 0.5% dei casi, e solo nel 12% di questi si riuscì ad identificare una causa di danno epatico (HBV, HCV, epatite autoimmune, colelitiasi, ecc).
In un altro studio condotto in Scozia su popolazione generale, le alterazioni delle transaminasi erano rilevabili nel 5% della popolazione apparentemente sana. Solo il 13% dei soggetti esaminati presentava alterazione enzimatica importante.
Un altro studio condotto su popolazione generale in Oriente (Cina Popolare) invece ha identificato alterazioni degii enzimi epatici nel 14% dei casi, nella maggior parte dei casi attribuibili a steatosi epatica o sindrome metabolica.
In Italia il noto studio Dyonisos, condotto su popolazione generale in due cittadine del Nord (Emilia e Friuli) ha rilevato una prevalenza di alterazioni delle transaminasi nel 17.5% dei soggetti esaminati. Anche in questo studio la maggior parte delle alterazioni era dovuta a steatosi epatica.
In conclusione, nella maggior parte dei casi una elevazione delle transaminasi è dovuta a steatosi alcolica o non alcolica, a infezioni da virus HBV e HCV, ad assunzione di farmaci o erbe, mentre altre patologie (autoimmuni, da accumulo di metalli, cause extra epatiche) sono più rare.
In Europa, come dimostra questo studio inglese, al primo posto fra le patologie responsabili di aumento delle transaminasi troviamo sicuramente la steatosi epatica, mentre in una elevata percentuale di soggetti la causa rimane spesso indeterminata.
Di fronte al paziente con elevazione degli enzimi epatici sono indispensabili una accurata anamnesi, un attento esame obiettivo, la valutazione di eventuali anomalie degli altri enzimi e della entità della anomalia enzimatica.
Andranno quindi considerati i fattori di rischio, la storia personale del paziente, l’età, la presenza di malattie sistemiche.
La storia clinica potrà rivelare eventuale abuso alcolico, tossicodipendenza, assunzione abituale di farmaci, patologie epatiche familiari, tipo di occupazione lavorativa, eventuale esposizione a tossici professionali. L’esame obiettivo consente in molti casi di identificare la presenza di ascite, spider naevi, splenomegalia, ecc. Infine, sarà necessaria la valutazione comparata dei tutti i tests biochimici, a cominciare dall’ emocromo, dalla albuminemia e dagli indici di colestasi.
Come dimostra questa diapositiva, la alterazione degli stessi enzimi (transaminasi) può avere significati assai diversi a seconda delle entità, della alterazione o meno di altri enzimi epatici, dell’ habitus del paziente, della rapidità o meno di insorgenza, della presenza di eventuali sintomi o segni obiettivi.
In caso di alterazione delle transaminasi superiore a 10 volte il normale andranno innanzitutto escluse epatiti virali acute o riacutizzazione di epatiti croniche , abuso alcolico, patologie vascolari, assunzione di farmaci epatotossici…
… di autoimmunità, di morbo di Wilson, di emocromatosi..
… e se tutti i tests saranno negativi andrà rivalutata la situazione biochimica ed eventualmente ricercate cause internistiche. Alla fine del percorso diagnostico può essere utile la biopsia epatica.
Più facile invece il percorso in caso di elevazione ieve (inferiore a 10 volte la norma) e persistente delle transaminasi. In tal caso andranno innanzitutto escluse la steatosi alcolica e non alcolica e le epatiti croniche da HBV e HCV, nonché le patologie ben più rare da accumulo.
Non va dimenticato infine che molti farmaci anche di uso comune possono determinare danno epatico anche grave e progressivo. La diapositiva elenca alcuni dei principali farmaci noti per la loro epatotossicità.
Anche le erbe, considerate tradizionalmente innocue dai pazienti, possono indurre danno epatico acuto o cronico, anche di notevole severità. Sono qui riportati tre articoli comparsi nella letteratura scientifica epatologica internazionale che mettono in dubbio la innocuità dei ritrovati di erboristeria (“herbal medicine”).
Per quanto riguarda gli altri enzimi epatici, la gamma GT è molto sensibile ma poco specifica, in quanto può elevarsi rapidamente in caso di abuso alcolico e di assunzione di farmaci, e cronicamente nella steatosi epatica, nella colestasi, ed in molte patologie extra epatiche, qui riportate.
Al contrario, la fosfatasi alcalina è un enzima poco sensibile ma molto specifico : in assenza di patologia scheletrica, una sua elevazione indica colestasi intraepatica (cirrosi biliare primitiva, colangite sclerosante) o extra epatica (litiasi coledocica, neoplasie del pancreas, ecc).
In conclusione, si vuole ricordare che alterazioni degli enzimi epatici non implicano necessariamente patologie del fegato, potendo essere presenti anche in soggetti peraltro sani.
In Italia e in genere in tutto il mondo occidentale la prima causa di lieve alterazione delle transaminasi è sicuramente la steatosi epatica, sia alcolica che non alcolica, seguita da abuso di farmaci, epatiti virali croniche (soprattutto da HCV), mentre molto più rare sono altre cause.
Infine, nella pratica clinica non va mai dimenticato di indagare su eventuale uso di sostanze medicamentose “alternative” (erbe), che il paziente spesso tende a non raccontare; va inoltre sottolineato che diverse cause extra epatiche, sia gastroenteriche che sistemiche, possono essere alla base di incrementi enzimatici altrimenti inspiegabili.