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Lactic Acidosis In Cirrhosis

Chronic Hepatitis B Patients With Liver Cirrhosis Are At Risk For Lactic Acidosis After Starting Entecavir (baraclude)

Chronic Hepatitis B Patients With Liver Cirrhosis Are At Risk For Lactic Acidosis After Starting Entecavir (baraclude)

Lactic acidosis occurs when lactate acid builds ups in the bloodstream faster than it can be removed. Lactic acidosis result when blood cells receive too little oxygen. Entecavir is one of several oral antiviral drugs approved for treatment of chronic hepatitis B virus (HBV) infection . Nucleoside analogs -- like entecavir and one class of antiretroviral drugs for HIV -- are structurally similar to the building blocks that make up strands of genetic material (DNA and RNA). As a virus attempts to copy its genetic material, if one of these drugs is added instead of a natural nucleoside to the growing chain, the replication process is halted. Unfortunately, nucleoside analogs can interfere with the workings of human cells as well as viruses. This can lead to a variety of side effects, some of which have been linked to damage to the mitochondria, small structures in cells that produce energy. Several nucleoside analogs used for HIV -- including d4T and ddI -- have fallen out of favor for this reason. Entecavir is generally safe and well-tolerated in HBV positive people who do not have advanced liver disease. Less is known however, about its safety in patients with liver cirrhosis -- a group that could potentially benefit greatly from treatment. Christian Lange from J.W. Goethe University in Frankfurt and colleagues described outcomes of 16 chronic hepatitis B patients with liver cirrhosis who were treated with entecavir. The researchers reported that 5 of these patients developed lactic acidosis -- that is, a blood lactate level of 26-200 mg/dL, pH of 7.02-7.40, base excess -5 mmol/L to -18 mmol/L -- during entecavir therapy. Lactic acidosis occurred between 4 and 240 days after entecavir initiation. Of the 5 affected individuals, 4 experienced a resolution of lactic acido Continue reading >>

Acid-base And Potassium Disorders In Liver Disease

Acid-base And Potassium Disorders In Liver Disease

Northwestern University, Feinberg school of Medicine, Chicago Acid-base and potassium disorders occur frequently in the setting of liver disease. As the liver's metabolic function worsens, particularly in the setting of renal dysfunction, hemodynamic compromise, and hepatic encephalopathy, acid-base disorders ensue. The most common acid-base disorder is respiratory alkalosis. Metabolic acidosis alone or in combination with respiratory alkalosis also is common. Acid-base disorders in patients with liver disease are complex. The urine anion gap may help to distinguish between chronic respiratory alkalosis and hyperchloremic metabolic acidosis when a blood gas is not available. A negative urine anion gap helps to rule out chronic respiratory alkalosis. In this disorder a positive urine anion gap is expected owing to suppressed urinary acidification. Distal renal tubular acidosis occurs in autoimmune liver disease such as primary biliary cirrhosis, but often is a functional defect from impaired distal sodium delivery. Potassium disorders are often the result of the therapies used to treat advanced liver disease. Do you want to read the rest of this article? ... Patients with decompensated liver disease, in the setting of sepsis or hemorrhage, may have increased serum lactate levels due to poor utilization and metabolism. [29] Lactic acidosis may be precipitated by biguanides as they inhibit mitochondrial respiration predominantly in the liver. ... Continue reading >>

Acid-base Disorders In Liver Disease.

Acid-base Disorders In Liver Disease.

Division of Gastroenterology and Hepatology, Department of Internal Medicine III, Medical University of Vienna, Vienna, Austria; Department of Respiratory and Critical Care Medicine, Otto Wagner Spital, Vienna, Austria. Department of General Internal Medicine & Emergency Medicine, Hirslanden Klinik Im Park, Zurich, Switzerland. Division of Gastroenterology and Hepatology, Department of Internal Medicine III, Medical University of Vienna, Vienna, Austria. Division of Oncology and Hematology, Department of Internal Medicine I, Medical University of Vienna, Vienna, Austria. Department of Respiratory and Critical Care Medicine, Otto Wagner Spital, Vienna, Austria. Electronic address: [email protected] J Hepatol. 2017 Nov;67(5):1062-1073. doi: 10.1016/j.jhep.2017.06.023. Epub 2017 Jul 3. Alongside the kidneys and lungs, the liver has been recognised as an important regulator of acid-base homeostasis. While respiratory alkalosis is the most common acid-base disorder in chronic liver disease, various complex metabolic acid-base disorders may occur with liver dysfunction. While the standard variables of acid-base equilibrium, such as pH and overall base excess, often fail to unmask the underlying cause of acid-base disorders, the physical-chemical acid-base model provides a more in-depth pathophysiological assessment for clinical judgement of acid-base disorders, in patients with liver diseases. Patients with stable chronic liver disease have several offsetting acidifying and alkalinising metabolic acid-base disorders. Hypoalbuminaemic alkalosis is counteracted by hyperchloraemic and dilutional acidosis, resulting in a normal overall base excess. When patients with liver cirrhosis become critically ill (e.g., because of sepsis or bleeding), this fragile eq Continue reading >>

Renal Fellow Network: Differential Diagnosis: Lactic Acidosis

Renal Fellow Network: Differential Diagnosis: Lactic Acidosis

As discussed in a recent post describing the success of early goal-directed therapy for sepsis, the test for serum lactate has enjoyed a rise in prominence in recent years. However, all that is lactic acid is not necessarily sepsis! Here's a differential diagnosis for lactic acidosis: 1. Shock--especially cardiogenic and septic shock, which is indicative of an inability of the circulatory system to match the metabolic demands of tissue. 2. Bowel Ischemia--mesenteric ischemia, necrotic bowel, etc.--the necrosis of cells in the intestine will release free lactate into the bloodstream. 3. Cirrhosis/Liver Failure--since lactate is metabolized to bicarbonate by the liver, patients with end-stage liver disease often have elevated lactate levels, which is NOT necessarily indicative of shock/hypoperfusion (although this group of patients often represents a conundrum in that they are precisely the type of patient who can get septic & die rapidly.) 4. Grand-mal Seizures: can lead to a transient increase in serum lactate which typically reverses on its own pretty quickly. 5. Thiamine Deficiency: thiamine is a cofactor for enzymes in the glycolytic pathway; its absence prevents adequate cellular metabolism and lactate can build up. 6. Citrate Toxicity in patients on CVVH given citrate-based replacement solution--this is heralded by an increased total calcium concentration along with a decreased ionized calcium concentration. 7. D-lactic acidosis: this atypical form of lactic acidosis occurs when bacterial overgrowth (as might occur in patients with GI bypass surgery) results in the metabolic synthesis of the D-isoform of lactic acidosis, which is not metabolizable to bicarbonate endogenously as is the naturally-occurring L-isoform of lactate. 8. Severe alkalosis: an increase in la Continue reading >>

Lactic Acidosis In Patients With Hepatitis C Virus Cirrhosis And Combined Ribavirin/sofosbuvir Treatment | Snfge.org - Socit Savante Mdicale Franaise D'hpato-gastroentrologie Et Doncologie Digestive

Lactic Acidosis In Patients With Hepatitis C Virus Cirrhosis And Combined Ribavirin/sofosbuvir Treatment | Snfge.org - Socit Savante Mdicale Franaise D'hpato-gastroentrologie Et Doncologie Digestive

Sofosbuvir (SOF) based interferon-alfa free antiviral therapy has become the treatment of choice for patients with chronic hepatitis C virus (HCV) infection. Little is known about safety of drug combinations using two nucleos(t)ide polymerase inhibitors in patients with HCV associated advanced cirrhosis. Here, we report frequent occurrence of lactic acidosis associated with acute-on-chronic hepatic decompensation during ribavirin (RBV) plus SOF based antiviral therapy. Thirty-five patients with chronic hepatitis C and advanced fibrosis, compensated cirrhosis, and decompensated cirrhosis without and after liver transplantation were treated with SOF based antiviral therapy with and without RBV. Adverse events including lactic acidosis (pH <7.35, lactate >20mg/dl) were recorded 24weeks before and during (meanSD, 1811weeks) antiviral therapy. Efficacy was determined by assessment of serum HCV RNA. We observed severe adverse events in 15/35 (43%) patients before (24weeks) and in 12/35 (34%) patients during antiviral therapy, the majority in association with acute-on-chronic hepatic decompensation. Lactic acidosis occurred in 5/35 (14%) patients during therapy, while no event of lactic acidosis was observed prior to therapy. Lactic acidosis was associated with hepatic decompensation including renal failure and infection, and was severe (pH <7.3) in two patients. RBV in combination with SOF based antiviral therapy in patients with HCV associated advanced cirrhosis may be associated with the development of lactic acidosis. Impaired renal function, and higher MELD/Child-Pugh scores were identified as potential risk factors. Il sagit de lobservation dune association entre acidose lactique et traitement par sofosbuvir et ribavirine chez les malades cirrhotiques. Continue reading >>

Metformin‐associated Lactic Acidosis In A Patient With Liver Disease

Metformin‐associated Lactic Acidosis In A Patient With Liver Disease

Sir, Metformin is an orally active biguanide, and was found to reduce mortality and complications in obese diabetic patients in the UK Prospective Diabetes Study.1 As a result, the drug is widely used as first‐line therapy for patients with obesity and type 2 diabetes. We would like to remind prescribers of a rare, but commonly fatal complication of metformin therapy in patients with liver or renal disease. A 40‐year‐old Gujerati man was admitted through accident and emergency. On admission, little history was available from the patient, and no corroborative history was available, apart from the fact that he was diabetic and on metformin. He was short of breath at rest, with oxygen saturation of 84% on air, and had a Glasgow Coma Score of 13/15. Capillary blood glucose was 1.7 mmol/l. Arterial blood gas analysis on 60% oxygen revealed severe metabolic acidosis: pH 6.62, pCO2 8.3 kPa, pO2 47.8 kPa, base excess −31.2, bicarbonate 6.4 mmol/l, anion gap 37 mmol/l. Serum lactate was extremely high at >20 mmol/l. He had a low urea of 2.4 mmol/l, normal creatinine of 63 µmol/l, a raised aspartate transaminase (110 IU/l, NR 10–50), bilirubin (64 µmol/l, NR 2–17) and alkaline phosphatase (323 IU/l, NR 40–135). He had a macrocytic anaemia (haemoglobin 9.7 g/dl, NR 13.0–17.0; MCV 99.0 fl, NR 76.0–96.0), and deranged clotting (PT 30 s, control 12 s; KPTT 65 s, control 35 s), but normal platelet count (152×109/l, NR 135–450). Hypoglycaemia was confirmed by a venous plasma glucose of 1.9 mmol/l. On review of his medical notes, he had been diagnosed with type 2 diabetes 3 years prior to admission. He had not been seen at diabetic clinic for over 2 years, when his diabetes was well controlled with metformin 850 mg twice daily. Eighteen months previously, he was a Continue reading >>

Lactic Acidosis

Lactic Acidosis

Lactic acidosis is a medical condition characterized by the buildup of lactate (especially L-lactate) in the body, which results in an excessively low pH in the bloodstream. It is a form of metabolic acidosis, in which excessive acid accumulates due to a problem with the body's metabolism of lactic acid. Lactic acidosis is typically the result of an underlying acute or chronic medical condition, medication, or poisoning. The symptoms are generally attributable to these underlying causes, but may include nausea, vomiting, rapid deep breathing, and generalised weakness. The diagnosis is made on biochemical analysis of blood (often initially on arterial blood gas samples), and once confirmed, generally prompts an investigation to establish the underlying cause to treat the acidosis. In some situations, hemofiltration (purification of the blood) is temporarily required. In rare chronic forms of lactic acidosis caused by mitochondrial disease, a specific diet or dichloroacetate may be used. The prognosis of lactic acidosis depends largely on the underlying cause; in some situations (such as severe infections), it indicates an increased risk of death. Classification[edit] The Cohen-Woods classification categorizes causes of lactic acidosis as:[1] Type A: Decreased tissue oxygenation (e.g., from decreased blood flow) Type B B1: Underlying diseases (sometimes causing type A) B2: Medication or intoxication B3: Inborn error of metabolism Signs and symptoms[edit] Lactic acidosis is commonly found in people who are unwell, such as those with severe heart and/or lung disease, a severe infection with sepsis, the systemic inflammatory response syndrome due to another cause, severe physical trauma, or severe depletion of body fluids.[2] Symptoms in humans include all those of typical m Continue reading >>

Effect Of Liver Disease On The Kinetics Of Lactate Removal After Heavy Exercise

Effect Of Liver Disease On The Kinetics Of Lactate Removal After Heavy Exercise

, Volume 59, Issue12 , pp 8997 | Cite as Effect of liver disease on the kinetics of lactate removal after heavy exercise Recovery from heavy exercise requires clearance of lactic acid from the blood and body tissues. Although it has long been felt that the liver plays the major role in lactate removal, it has more recently been asserted that skeletal muscle plays the dominant role. We felt it relevant to this controversy to determine whether patients with liver dysfunction have slowed lactate removal following heavy exercise. Eight patients with alcoholic liver disease and 5 normal subjects were studied. Liver function was measured by the14C-aminopyrine breath test; the results were expressed as the rate of appearance of14CO2 in the breath two hours after ingestion, as a fraction of the ingested14C dose (%h1). Each participant exercised on a cycle ergometer for 7 min at a work rate which was moderately heavy for that subject (mean peak lactate=5.3 mmolL1). During, and for 45 minutes after exercise, blood was drawn from a hand vein catheter. The time required for blood lactate to decrease halfway toward resting levels (t1/2LA) was determined. Compared to the normal subjects and historical controls, seven of the patients had distinctly slowed lactate removal. The t1/2LA was as long as 46 min (as compared to approximately 15 min seen normally). Further, among the patients the 2 h breath excretion of14C was well correlated with the rate constant of lactate removal (r=0.82,P<0.01). Four of the patients with severe liver dysfunction performed a second exercise test in which, instead of resting after heavy exercise, low level exercise was continued. The t1/2LA of the averaged responses decreased by 29%. We conclude that liver disease slows lactate removal at rest. Lactate rem Continue reading >>

American Thoracic Society - Liver Dysfunction And Severe Lactic Acidosis In A Previously Healthy Man

American Thoracic Society - Liver Dysfunction And Severe Lactic Acidosis In A Previously Healthy Man

Liver dysfunction and severe lactic acidosis in a previously healthy man A man in his eighth decade presented to his primary doctor three weeks prior to admission with easy bruising. A complete blood count revealed low counts in all three major cell lines and a subsequent bone marrow biopsy demonstrated B-cell follicular lymphoma. Other biochemical parameters, including tests of liver transaminases and bilirubin, were normal. Two weeks later he developed a cough and shortness of breath and he received a diagnosis of acute bronchitis, for which he was prescribed azithromycin along with an inhaler of salmeterol and fluticasone. His cough and dyspnea did not improve and he was admitted to another hospital for further evaluation. A diagnosis of liver failure was made based on elevated liver function tests (aspartate aminotransferase=995 U/L, alanine aminotransferase=552 U/L, total bilirubin=7.2 mg/dL, direct bilirubin=5.5 mg/dL); worsening pancytopenia was noted. Evaluation of the acute liver failure did not reveal an etiology, and he was transferred to a tertiary care hospital for further evaluation and care. Thyroid cancer, s/p partial thyroidectomy Denies excessive alcohol and illicit drug use 40 pack-year cigarette smoking history, stopped in 2004 Laboratory investigation did not reveal occult infectious hepatitis or autoimmune disease. Diagnostic imaging of the liver revealed a large intra-hepatic mass and trans-jugular liver biopsy showed extensive hepatic infiltration by lymphoma. His respiratory status became increasingly tenuous and his trachea was intubated and positive-pressure mechanical ventilation was initiated. He was transferred to the ICU but suffered the rapid onset of shock despite infusions of sodium bicarbonate and norepinephrine. After a conversation Continue reading >>

Ribavirin May Increase Lactic Acidosis Occurrence For Hcv-related Cirrhosis

Ribavirin May Increase Lactic Acidosis Occurrence For Hcv-related Cirrhosis

Ribavirin may increase lactic acidosis occurrence for HCV-related cirrhosis Welker M-W, et al. J Hepatol. 2015;doi:10.1016/j.jhep.2015.11.034. New findings published in the Journal of Hepatology show that patients with hepatitis C virus infection-related cirrhosis undergoing antiviral therapy with ribavirin may have increased risk for developing lactic acidosis. In a retrospective analysis, researchers collected data of 35 patients with chronic HCV with advanced fibrosis, compensated cirrhosis and decompensated cirrhosis before and after liver transplantation treated with Sovaldi (sofosbuvir, Gilead Sciences)-based antiviral therapy with and without ribavirin. Adverse events were measured over a period of 24 weeks before and during therapy. Overall, 43% of patients experienced a serious adverse event (n = 15) before 24 weeks and 34% (n = 12) during antiviral therapy. A majority of the adverse events were associated with acute-on-chronic hepatic decompensation. Lactic acidosis was observed in 14% of patients during therapy (n = 5). No evidence of lactic acidosis was seen prior to the start of antiviral therapy . Severe lactic acidosis, meaning an arterial lactate concentration greater than 20 mg/dL, was found in two patients (pH < 7.3). Ribavirin doses of 200 mg to 1,200 mg per day were being given at the time of diagnosis. Lactic acidosis was found in patients with more advanced cirrhosis and impaired kidney function compared with patients who did not development lactic acidosis. The researchers concluded: Our data indicate a risk for the development of lactic acidosis complicating acute-on-chronic hepatic decompensation during [ribavirin/sofosbuvir]-based antiviral therapy in patients with HCV-associated cirrhosis. Impaired renal function and higher MELD/Child-Pugh sc Continue reading >>

A Man With Severe Cirrhosis And Profound Acid-base Disturbance

A Man With Severe Cirrhosis And Profound Acid-base Disturbance

A Man With Severe Cirrhosis and Profound Acid-Base Disturbance A 66-year-old man was brought from home by his family out of concern for his altered mental status and abnormal breathing. He had a past medical history significant for severe and advanced cirrhosis of the liver as a result of alcohol abuse and hepatitis C. He had had many complications, including variceal bleeding, numerous episodes of hepatic encephalopathy, and ascites requiring frequent paracentesis. He had been evaluated for transplantation but had never been able to achieve the required period of abstinence from alcohol. His family noted a progressive lethargy and obtundation beginning 2 to 3 days ago, and now he was very difficult to arouse. In addition, the family noted very deep and heavy respirations. The mans only regularly used medications were lactulose and diuretics. Physical examination revealed an obtunded man who was difficult to arouse and was disoriented to time, place, and person. Temperature was 37.8C, pulse was 100 beats/min, blood pressure was 90/60 mm Hg, and Kussmaul respirations were at 18/min. There was slight scleral icterus. His chest was clear, and his heart was in regular rhythm, without murmurs or gallop. Gross ascites was present. His skin had multiple spider angiomas, and he had bilateral leg edema. Neurologic examination revealed altered mentation without focal findings. Beats of asterixis of the wrists were elicited. Laboratory test results were diffusely abnormal. Highlights included the following values: hemoglobin, 9 g/dL; white blood cell count, 14,100/L with a left-shifted differential; platelet count, 59 103/L; serum sodium, 121 mEq/L; serum potassium, 2.9 mEq/L; serum chloride, 90 mEq/L; and bicarbonate, 15 mEq/L with an anion gap of 29 mEq/L. Random blood glucose Continue reading >>

Causes Of Lactic Acidosis

Causes Of Lactic Acidosis

INTRODUCTION AND DEFINITION Lactate levels greater than 2 mmol/L represent hyperlactatemia, whereas lactic acidosis is generally defined as a serum lactate concentration above 4 mmol/L. Lactic acidosis is the most common cause of metabolic acidosis in hospitalized patients. Although the acidosis is usually associated with an elevated anion gap, moderately increased lactate levels can be observed with a normal anion gap (especially if hypoalbuminemia exists and the anion gap is not appropriately corrected). When lactic acidosis exists as an isolated acid-base disturbance, the arterial pH is reduced. However, other coexisting disorders can raise the pH into the normal range or even generate an elevated pH. (See "Approach to the adult with metabolic acidosis", section on 'Assessment of the serum anion gap' and "Simple and mixed acid-base disorders".) Lactic acidosis occurs when lactic acid production exceeds lactic acid clearance. The increase in lactate production is usually caused by impaired tissue oxygenation, either from decreased oxygen delivery or a defect in mitochondrial oxygen utilization. (See "Approach to the adult with metabolic acidosis".) The pathophysiology and causes of lactic acidosis will be reviewed here. The possible role of bicarbonate therapy in such patients is discussed separately. (See "Bicarbonate therapy in lactic acidosis".) PATHOPHYSIOLOGY A review of the biochemistry of lactate generation and metabolism is important in understanding the pathogenesis of lactic acidosis [1]. Both overproduction and reduced metabolism of lactate appear to be operative in most patients. Cellular lactate generation is influenced by the "redox state" of the cell. The redox state in the cellular cytoplasm is reflected by the ratio of oxidized and reduced nicotine ad Continue reading >>

Lactic Acidosis

Lactic Acidosis

hyperlactaemia: a level from 2 to 5 mmol/L normal production is 20 mmols/kg/day, enters the circulation and undergoes hepatic and renal metabolism (Cori cycle) all tissues can produce lactate under anaerobic conditions lactic acid has a pK value of about 4 so it is fully dissociated into lactate and H+ at body pH (i.e. it is a strong ion) during heavy exercise, the skeletal muscles contribute most of the much increased circulating lactate during pregnancy, the placenta is an important producer of lactate (can pass to fetus as well) major source in sepsis and ARDS is the lung lactate is metabolised predominantly in the liver (60%) and kidney (30%) the heart can also use lactate for ATP production 50% is converted into glucose (gluconeogenesis) and 50% into CO2 and water (citric acid cycle) this results in no net acid accumulation but requires aerobic metabolism the small amount of lactate that is renally filtered (180mmol/day) is fully reabsorbed (ii) impaired hepatic metabolism of lactate (large capacity to clear) clinically there is often a combination of the above to produce a persistent lactic acidosis anaerobic muscular activity (sprinting, generalised convulsions) tissue hypoperfusion (shock, cardiac arrest, regional hypoperfusion -> mesenteric ischaemia) reduced tissue oxygen delivery (hypoxaemia, anaemia) or utilisation (CO poisoning) Type B No Evidence of Inadequate Tissue Oxygen Delivery once documented the cause must be found and treated appropriately D lactate is isomer of lactate produced by intestinal bacterial and not by humans it is not detected on standard lactate assays a bed side test may be able to be developed to help with diagnosis of mesenteric ischaemia venous samples are equivalent to arterial in clinical practice do not need to take off tourniq Continue reading >>

Lactic Acidosis In Patients With Hepatitis C Virus Cirrhosis And Combined Ribavirin/sofosbuvir Treatment - Sciencedirect

Lactic Acidosis In Patients With Hepatitis C Virus Cirrhosis And Combined Ribavirin/sofosbuvir Treatment - Sciencedirect

Volume 64, Issue 4 , April 2016, Pages 790-799 Lactic acidosis in patients with hepatitis C virus cirrhosis and combined ribavirin/sofosbuvir treatment Author links open overlay panel Martin-WalterWelker1 Get rights and content Sofosbuvir (SOF) based interferon-alfa free antiviral therapy has become the treatment of choice for patients with chronic hepatitis C virus (HCV) infection. Little is known about safety of drug combinations using two nucleos(t)ide polymerase inhibitors in patients with HCV associated advanced cirrhosis. Here, we report frequent occurrence of lactic acidosis associated with acute-on-chronic hepatic decompensation during ribavirin (RBV) plus SOF based antiviral therapy. Thirty-five patients with chronic hepatitis C and advanced fibrosis, compensated cirrhosis, and decompensated cirrhosis without and after liver transplantation were treated with SOF based antiviral therapy with and without RBV. Adverse events including lactic acidosis (pH <7.35, lactate >20mg/dl) were recorded 24weeks before and during (meanSD, 1811weeks) antiviral therapy. Efficacy was determined by assessment of serum HCV RNA. We observed severe adverse events in 15/35 (43%) patients before (24weeks) and in 12/35 (34%) patients during antiviral therapy, the majority in association with acute-on-chronic hepatic decompensation. Lactic acidosis occurred in 5/35 (14%) patients during therapy, while no event of lactic acidosis was observed prior to therapy. Lactic acidosis was associated with hepatic decompensation including renal failure and infection, and was severe (pH <7.3) in two patients. RBV in combination with SOF based antiviral therapy in patients with HCV associated advanced cirrhosis may be associated with the development of lactic acidosis. Impaired renal function, and h Continue reading >>

Fatal Lactic Acidosis In Hepatitis B Virus-associated Decompensated Cirrhosis Treated With Tenofovir: A Case Report

Fatal Lactic Acidosis In Hepatitis B Virus-associated Decompensated Cirrhosis Treated With Tenofovir: A Case Report

All nucleot(s)ide analogs treatment can induce lactic acidosis by inhibiting mitochondrial polymerase inside the liver and muscle. [1] There are reports that lamivudine administration led to lactic acidosis in chronic hepatitis B (CHB) patients. However, most previous cases comprised decompensated cirrhotic patients or patients who had taken several antiviral agents to control human immunodeficiency virus (HIV) coinfection. [2] Moreover, there are also reports that entecavir treatment in patients with high model for end stage liver disease (MELD) score (>20 points) can cause lactic acidosis. [3] The previous tenofovir disoproxil fumarate (TDF) studies believed that the incidence of lactic acidosis is low as compared to other nucleotide analog-type antiviral agents. [4] A total of 4 previously known fatal lactic acidosis cases caused by TDF were all taking several antiviral agents at that time. [58] This is the first case of TDF-treatment-induced fatal lactic acidosis in CHB patient without HIV coinfection. A 59-year-old male patient (56 kg) presented with abdominal distention for 15 days before visiting hospital. The patient was taking a calcium channel blocker for hypertension. His viral markers indicated CHB hepatitis B virus surface antigen (+), hepatitis B core antibody Immunoglobulin G (+), and hepatitis C virus Antibody (). The blood biochemistry showed serum creatinine of 0.96 mg/dL, blood urea nitrogen (BUN) of 16.1 mg/dL, total bilirubin of 1.26 mg/dL, aspartate aminotransferase (AST) of 39 U/L, and alanine aminotransferase (ALT) of 20 U/L. Liver cirrhosis and moderate ascites were observed on abdominal computed tomography. The patient was diagnosed as e antigen-positive CHB with cirrhosis and a MELD score of 13 and a ChildPugh score of 8 points. The patient w Continue reading >>

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