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Metabolic Abnormalities In Alcoholic Patients: Focus On Acid Base And Electrolyte Disorders

Metabolic Abnormalities In Alcoholic Patients: Focus On Acid Base And Electrolyte Disorders

1Department of Nephrology, University Hospital of Ioannina, Ioannina, Greece 2Department of Internal Medicine, Medical School, University of Ioannina, 451 10, Ioannina, Greece *Corresponding Author: Moses Elisaf Professor of Internal Medicine Department of Medicine, Medical School University of Ioannina 451 10 Ioannina, Greece Tel: +302651007509 Fax: +302651007016 E-mail: [email protected], [email protected] Citation: Moses Elisaf MD, Rigas Kalaitzidis MD (2015) Metabolic Abnormalities in Alcoholic Patients: Focus on Acid Base and Electrolyte Disorders. J Alcohol Drug Depend 3:185. doi:10.4172/2329-6488.1000185 Copyright: ©2015 Moses Elisaf MD, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Visit for more related articles at Journal of Alcoholism & Drug Dependence Abstract Alcoholic patients commonly develop a variety of acid-base and electrolyte disturbances. The aim of this review is to describe the most commonly encountered abnormalities and their significant role in the patients’ morbidity and mortality. Physicians should be aware of these clinically important disturbances caused by alcohol abuse and their underlying pathophysiological mechanisms involved for their appropriate management. Alcoholic Keto Acidosis (AKA) is a medical emergency is more common than previously thought and is characterized by an increased anion gap metabolic acidosis. However, in AKA mixed acid-base disorders are commonly observed. Alcoholic patients also exhibit severe electrolyte derangements. Multifactorial origin hypomagnesaemia is the most common electrolyte abnormality observed. Hypocalca Continue reading >>

Alcoholic Ketoacidosis

Alcoholic Ketoacidosis

What is alcoholic ketoacidosis? Cells need glucose (sugar) and insulin to function properly. Glucose comes from the food you eat, and insulin is produced by the pancreas. When you drink alcohol, your pancreas may stop producing insulin for a short time. Without insulin, your cells won’t be able to use the glucose you consume for energy. To get the energy you need, your body will start to burn fat. When your body burns fat for energy, byproducts known as ketone bodies are produced. If your body is not producing insulin, ketone bodies will begin to build up in your bloodstream. This buildup of ketones can produce a life-threatening condition known as ketoacidosis. Ketoacidosis, or metabolic acidosis, occurs when you ingest something that is metabolized or turned into an acid. This condition has a number of causes, including: shock kidney disease abnormal metabolism In addition to general ketoacidosis, there are several specific types. These types include: alcoholic ketoacidosis, which is caused by excessive consumption of alcohol diabetic ketoacidosis (DKA), which mostly develops in people with type 1 diabetes starvation ketoacidosis, which occurs most often in women who are pregnant, in their third trimester, and experiencing excessive vomiting Each of these situations increases the amount of acid in the system. They can also reduce the amount of insulin your body produces, leading to the breakdown of fat cells and the production of ketones. Alcoholic ketoacidosis can develop when you drink excessive amounts of alcohol for a long period of time. Excessive alcohol consumption often causes malnourishment (not enough nutrients for the body to function well). People who drink large quantities of alcohol may not eat regularly. They may also vomit as a result of drinking too Continue reading >>

Severe Metabolic Acidosis In The Alcoholic: Differential Diagnosis And Management

Severe Metabolic Acidosis In The Alcoholic: Differential Diagnosis And Management

1 A chronic alcoholic with severe metabolic acidosis presents a difficult diagnostic problem. The most common cause is alcoholic ketoacidosis, a syndrome with a typical history but often misleading laboratory findings. This paper will focus on this important and probably underdiagnosed syndrome. 2 The disorder occurs in alcoholics who have had a heavy drinking-bout culminating in severe vomiting, with resulting dehydration, starvation, and then a β- hydroxybutyrate dominated ketoacidosis. 3 Awareness of this syndrome, thorough history-taking, physical examination and routine laboratory analyses will usually lead to a correct diagnosis. 4 The treatment is simply replacement of fluid, glucose, electrolytes and thiamine. Insulin or alkali should be avoided. 5 The most important differential diagnoses are diabetic ketoacidosis, lactic acidosis and salicylate, methanol or ethylene glycol poisoning, conditions which require quite different treatment. 6 The diagnostic management of unclear cases should always include toxicological tests, urine microscopy for calcium oxalate crystals and calculation of the serum anion and osmolal gaps. 7 It is suggested here, however, that the value of the osmolal gap should be considered against a higher reference limit than has previously been recom mended. An osmolal gap above 25 mosm/kg, in a patient with an increased anion gap acidosis, is a strong indicator of methanol or ethylene glycol intoxication. Continue reading >>

Toxic Alcohol Ingestions: Clinical Features, Diagnosis, And Management

Toxic Alcohol Ingestions: Clinical Features, Diagnosis, And Management

Abstract Alcohol-related intoxications, including methanol, ethylene glycol, diethylene glycol, and propylene glycol, and alcoholic ketoacidosis can present with a high anion gap metabolic acidosis and increased serum osmolal gap, whereas isopropanol intoxication presents with hyperosmolality alone. The effects of these substances, except for isopropanol and possibly alcoholic ketoacidosis, are due to their metabolites, which can cause metabolic acidosis and cellular dysfunction. Accumulation of the alcohols in the blood can cause an increment in the osmolality, and accumulation of their metabolites can cause an increase in the anion gap and a decrease in serum bicarbonate concentration. The presence of both laboratory abnormalities concurrently is an important diagnostic clue, although either can be absent, depending on the time after exposure when blood is sampled. In addition to metabolic acidosis, acute renal failure and neurologic disease can occur in some of the intoxications. Dialysis to remove the unmetabolized alcohol and possibly the organic acid anion can be helpful in treatment of several of the alcohol-related intoxications. Administration of fomepizole or ethanol to inhibit alcohol dehydrogenase, a critical enzyme in metabolism of the alcohols, is beneficial in treatment of ethylene glycol and methanol intoxication and possibly diethylene glycol and propylene glycol intoxication. Given the potentially high morbidity and mortality of these intoxications, it is important for the clinician to have a high degree of suspicion for these disorders in cases of high anion gap metabolic acidosis, acute renal failure, or unexplained neurologic disease so that treatment can be initiated early. Effect of Alcohols on Serum Osmolality and the Osmolal Gap The normal serum Continue reading >>

Metabolic Acidosis In A Patient With Isopropyl Alcohol Intoxication: A Case Report

Metabolic Acidosis In A Patient With Isopropyl Alcohol Intoxication: A Case Report

Metabolic Acidosis in a Patient With Isopropyl Alcohol Intoxication: A Case Report Xiaomei Meng, MD, PhD; Suman Paul, MBBS, PhD; Douglas J. Federman, MD From University of Toledo Medical Center, Toledo, Ohio; and University of Toledo College of Medicine, Toledo, Ohio. From University of Toledo Medical Center, Toledo, Ohio; and University of Toledo College of Medicine, Toledo, Ohio. From University of Toledo Medical Center, Toledo, Ohio; and University of Toledo College of Medicine, Toledo, Ohio. Author, Article, and Disclosure Information From University of Toledo Medical Center, Toledo, Ohio; and University of Toledo College of Medicine, Toledo, Ohio. Disclosures: Authors have disclosed no conflicts of interest. Forms can be viewed at www.acponline.org/authors/icmje/ConflictOfInterest Forms.do?msNum=L14-0336 . Background: An elevated plasma osmolal gap is common in all forms of alcohol intoxication. Methyl alcohol and ethylene glycol are metabolized to compounds that produce metabolic acidosis. Isopropyl alcohol, however, is metabolized to acetone, which does not cause metabolic acidosis and cannot be metabolized to compounds that do ( 1 ). Therefore, the presence of metabolic acidosis is used to rule out isopropyl alcohol intoxication. This distinction is important because fomepizole is used to treat methyl alcohol and ethylene glycol intoxication but is contraindicated in isopropyl alcohol intoxication because it reduces the clearance of isopropyl alcohol and thus prolongs its effects ( 2 ). Continue reading >>

Alcoholic Ketoacidosis

Alcoholic Ketoacidosis

Go to: CHARACTERISATION In 1940, Dillon et al1 described a series of nine patients who had episodes of severe ketoacidosis in the absence of diabetes mellitus, all of whom had evidence of prolonged excessive alcohol consumption. It was not until 1970 that Jenkins et al2 described a further three non‐diabetic patients with a history of chronic heavy alcohol misuse and recurrent episodes of ketoacidosis. This group also proposed a possible underlying mechanism for this metabolic disturbance, naming it alcoholic ketoacidosis. Further case series by Levy et al, Cooperman et al, and Fulop et al were subsequently reported, with remarkably consistent features.3,4,5 All patients presented with a history of prolonged heavy alcohol misuse, preceding a bout of particularly excessive intake, which had been terminated several days earlier by nausea, severe vomiting, and abdominal pain. Clinical signs included tachypnoea, tachycardia, and hypotension. In 1974, Cooperman's series of seven ketoacidotic alcoholic patients all displayed diffuse epigastric tenderness on palpation.4 In contrast to patients with diabetic ketoacidosis, the patients were usually alert and lucid despite the severity of the acidosis and marked ketonaemia. When altered mental status occurred, this was clearly attributable to other causes. Laboratory results included absent blood alcohol with normal or low blood glucose level, no glycosuria, and a variably severe metabolic acidosis with a raised anion gap. This acidosis appeared to result from the accumulation in plasma of lactate and ketone bodies including beta‐hydroxybutyrate (BOHB) and acetoacetate (AcAc).3 Cooperman et al found that near patient testing for ketone bodies using nitroprusside test (Acetest, Ketostix) produced a low to moderate result in th Continue reading >>

Alcoholic Ketoacidosis

Alcoholic Ketoacidosis

Alcoholic ketoacidosis is a metabolic complication of alcohol use and starvation characterized by hyperketonemia and anion gap metabolic acidosis without significant hyperglycemia. Alcoholic ketoacidosis causes nausea, vomiting, and abdominal pain. Diagnosis is by history and findings of ketoacidosis without hyperglycemia. Treatment is IV saline solution and dextrose infusion. Alcoholic ketoacidosis is attributed to the combined effects of alcohol and starvation on glucose metabolism. Alcohol diminishes hepatic gluconeogenesis and leads to decreased insulin secretion, increased lipolysis, impaired fatty acid oxidation, and subsequent ketogenesis, causing an elevated anion gap metabolic acidosis. Counter-regulatory hormones are increased and may further inhibit insulin secretion. Plasma glucose levels are usually low or normal, but mild hyperglycemia sometimes occurs. Diagnosis requires a high index of suspicion; similar symptoms in an alcoholic patient may result from acute pancreatitis, methanol or ethylene glycol poisoning, or diabetic ketoacidosis (DKA). In patients suspected of having alcoholic ketoacidosis, serum electrolytes (including magnesium), BUN and creatinine, glucose, ketones, amylase, lipase, and plasma osmolality should be measured. Urine should be tested for ketones. Patients who appear significantly ill and those with positive ketones should have arterial blood gas and serum lactate measurement. The absence of hyperglycemia makes DKA improbable. Those with mild hyperglycemia may have underlying diabetes mellitus, which may be recognized by elevated levels of glycosylated Hb (HbA1c). Typical laboratory findings include a high anion gap metabolic acidosis, ketonemia, and low levels of potassium, magnesium, and phosphorus. Detection of acidosis may be com Continue reading >>

Lactic Acidosis And Acute Ethanol Intoxication - Sciencedirect

Lactic Acidosis And Acute Ethanol Intoxication - Sciencedirect

Volume 12, Issue 1 , January 1994, Pages 32-35 Get rights and content Ethanol intoxication has been widely reported as a cause of lactic acidosis. To determine the frequency and severity of ethanol-induced lactic acidosis, patients who presented to an emergency department with a clinical diagnosis of acute ethanol intoxication and a serum ethanol concentration of at least 100 mg/dL were studied. Arterial blood was sampled for lactate and blood gas determinations. A total of 60 patients (mean age, 41 years) were studied. Twenty-two patients sustained minor trauma. Ethanol concentrations ranged from 100 to 667 mg/dL (mean, 287 mg/dL). Lactate concentrations were abnormal (>2.4 mmol/L) in seven patients (11.7%). In all cases, blood lactate was less than 5 mmol/L. Of the patients with elevated lactate, other potential causes for lactic acidosis, including hypoxia, seizures, and hypoperfusion, were also present. Only one case with elevated blood lactate concentration had associated acidemia. Significant elevations of blood lactate are uncommon in acute ethanol intoxication. In patients with ethanol intoxication who are found to have lactic acidosis, other etiologies for the elevated lactate level should be considered. Continue reading >>

Alcohol Intoxication

Alcohol Intoxication

Alcohol intoxication is a significant risk factor for TBI, and TBI should be appreciated as a heterogeneous, dynamic pathophysiological process that occurs at the moment of impact and continues over time with sequelae potentially seen many years after the initial event (Currie et al., 2016). Young-chul Jung*, Kee Namkoong, in Handbook of Clinical Neurology , 2014 Alcohol intoxication refers to a clinically harmful condition induced by recent ingestion of alcohol, when alcohol and its metabolites accumulate in the blood stream faster than they can be metabolized by the liver. Due to the long history and widespread use of alcohol as a recreational beverage, the clinical manifestations of alcohol intoxication are usually not taken seriously and considered to subside spontaneously with time; however, the adverse effects of alcohol at sufficiently high levels can cause coma and respiratory depression. In addition, individuals who seek medical treatment for acute alcohol intoxication likely have additional medical problems related to chronic alcohol consumption or alcohol dependence. The aims of this chapter are to delineate and discuss: (1) the acute and chronic effects of ethanol on organ systems; (2) diagnostic criteria of alcohol intoxication; and (3) clinical conditions, which can accompany acute alcohol intoxication, especially those that are associated with chronic alcohol consumption (e.g., hepatic encephalopathy and Wernicke's encephalopathy); and (4) treatment. Rachel L. Vassar1, Jessica Rose2*, in Handbook of Clinical Neurology , 2014 Acute alcohol intoxication and chronic alcohol dependence alter the neurologic control of posture and motor function. Ethanol delays the conduction of electric signals from the central nervous system to the muscles controlling postur Continue reading >>

Alcohol Toxicity - Cancer Therapy Advisor

Alcohol Toxicity - Cancer Therapy Advisor

Alcohol toxicity or poisoning is caused by drinking large quantities of alcohol in a short period of time. According to Centers for Disease Control (CDC) data released January 2015, an average of 6 people died of alcohol poisoning each day in the US from 2010-2012. Seventy-six percent of alcohol poisoning deaths are among adults ages 35-64 years old, the majority of whom are men and non-Hispanic whites. While alcohol dependence was identified as a factor in 30% of alcohol poisoning deaths, binge drinking (defined as more than 5 drinks on an occasion for men or 4 or more drinks on an occasion for women) can also lead to death from alcohol poisoning. A standard drink in the US is considered either 12 ounces (oz) of beer (5% alcohol), 8 oz of malt liquor (7% alcohol), 5 oz of wine (12% alcohol), or 1.5 oz of distilled spirits (40% alcohol; 80 proof). The current Dietary Guidelines for Americans recommend not to exceed 1 drink a day for women or 2 drinks a day for men. Any alcohol can be toxic if ingested in large enough quantities. While alcohol toxicity most commonly results from the abuse of ethanol ("drinking alcohol") found in alcoholic beverages, it can also result from the ingestion of isopropanol (rubbing alcohol) and the toxic alcohols which include methanol (found in commercially available products such as solvents, windshield washing fluids and paint removers) and ethylene glycol (the primary ingredient in anti-freeze). Toxic alcohols share the characteristic of the parent compounds causing inebriation with little toxicity while their active metabolites have the potential to cause metabolic acidosis and significant end organ damage. Toxic alcohol poisoning is far less prevalent than ethanol abuse, with most exposures in the US resulting from unintentional ingest Continue reading >>

Emergent Treatment Of Alcoholic Ketoacidosis

Emergent Treatment Of Alcoholic Ketoacidosis

Emergent Treatment of Alcoholic Ketoacidosis Author: Adam Blumenberg, MD, MA; Chief Editor: Erik D Schraga, MD more... Alcoholic ketoacidosis (AKA) is an acute metabolic acidosis seen in persons with a recent history of binge drinking and little or no nutritional intake. Alcoholic ketoacidosis is characterized by high serum ketone levels and an elevated anion gap (see the Anion Gap calculator). A concomitant metabolic alkalosis is also common, resulting from vomiting and volume depletion. Although AKA most commonly occurs in adults with alcoholism, alcoholic ketoacidosis has been reported in less-experienced drinkers of all ages. [ 1 , 2 ] Go to Alcoholic Ketoacidosis , Metabolic Alkalosis , and Pediatric Metabolic Alkalosis for complete information on these topics. Assess the patient's airway and manage as clinically indicated. Administer oxygen as indicated. Obtain intravenous access and administer fluid resuscitation for volume depletion and/or hypotension. Consider and treat hypoglycemia. [ 3 ] If the patient's mental status is diminished, consider administration of naloxone and thiamine . Note information about the patient's social situation and the presence of intoxicating agents besides alcohol. Suspect alcoholic ketoacidosis in any patient with recent binge drinking and an elevated anion gap. A history of alcoholism is not necessary for the development of alcoholic ketoacidosis. One episode of heavy alcohol intake combined with inadequate carbohydrate intake is sufficient to generate this disease state. Presenting symptoms may include nausea & vomiting, malaise, abdominal pain, dizziness, tremulousness, tachypnea, tachycardia, and hypotension. [ 4 ] Urine tests for ketones may be falsely negative or only trace positive in alcoholic ketoacidosis. This is because Continue reading >>

Alcohol Intoxication

Alcohol Intoxication

"Drunk" redirects here. For other uses, see Drunk (disambiguation) . Alcohol intoxication, also known as drunkenness among other names, is a physiological condition that may result in psychological alterations of consciousness . Symptoms of alcohol intoxication include euphoria , flushed skin , and decreased social inhibition at lower doses, [1] with larger doses producing progressively severe impairments of balance, and decision-making ability as well as nausea or vomiting from alcohol's disruptive effect on the semicircular canals of the inner ear and chemical irritation of the gastric mucosa .[ citation needed ] Extreme levels of blood-borne alcohol may result in coma or death . Alcohol intoxication is the result of drinking alcohol such that it enters the bloodstream faster than it can be metabolized by the body. Metabolism results in breaking down the ethanol into non-intoxicating byproducts. Some effects of alcohol intoxication, such as euphoria and lowered social inhibition , are central to alcohol's desirability as a beverage .[ citation needed ] Throughout history it has been one of the world's most widespread recreational drugs . Despite this widespread use and alcohol's legality in most countries, many medical sources tend to describe any level of alcohol intoxication as a form of poisoning due to ethanol's damaging effects on the body in large doses. Some religions consider alcohol intoxication to be a sin . Wine is a Mocker by Dutch artist Jan Steen c. 1663 Acute alcohol poisoning is a related medical term used to indicate a dangerously high concentration of alcohol in the blood, high enough to induce coma, respiratory depression , or even death. It is considered a medical emergency . The term is mostly used by healthcare providers . Toxicologists use the Continue reading >>

How To Correct High Anion Gap Metabolic Acidosis In Acute Alcohol...| Dailyrounds

How To Correct High Anion Gap Metabolic Acidosis In Acute Alcohol...| Dailyrounds

palliative rx when ph < 7.2 bicarbonate supplementation dose= 0.3 (24 - pt's bicarb) wt (kg) 1/3 dose given as bollus remaining as infusion over 8 to 24 hr specific rx treat underline cause Dr Kieran V J Mullins Internal Medicine 11 Sep Metabolic acidosis with ethanol poisoning may be secondary to ketoanions or lactic acidosis. These are organic anion acidoses and as such treatment should centre on correction of associated abnormalities rather than administration of bicarbonate which has potential serious risks in such circumstances (intracellular acidosis, overshoot alkalosis, impaired O2 unloading due to left shift of the O2 dissociation curve, hypernatraemia, hypercapnia). Recall that in the presence of an optimised intravascular volume and normal hepatic function organic anions serve as avid bicarbonate precursors. It would have been helpful to have the PCO2 to assess the patient's degree of compensation (if any) and hence their reserve in terms of further respiratory compensation should the metabolic component evolve further. In the above patient I would optimise Intravascular filling with an isotonic crystalloid such as NaCl 0.9% and administer IV thiamine (remember that for the TCA cycle to proceed the pyruvate dehydrogenase complex requires vitamin B1 as a coenzyme and B vitamins are often deficient in alcoholics). Repeat blood gas analysis is indicated to assess response to treatment. Only a clinically deteriorating, non responsive (persistent pH<7.1) or refractorily hyperkalemic patient would I administer IV bicarbonate. Should bicarbonate be administered then a crude estimation of the requirement may be made by 0.5*BW*(24-pt's HCO3-) with half over 4 hrs and the remainder over 20 hrs. Excellent ventilation must be maintained when such a therapy is instituted Continue reading >>

Alcoholic Ketoacidosis

Alcoholic Ketoacidosis

Increased production of ketone bodies due to: Dehydration (nausea/vomiting, ADH inhibition) leads to increased stress hormone production leading to ketone formation Depleted glycogen stores in the liver (malnutrition/decrease carbohydrate intake) Elevated ratio of NADH/NAD due to ethanol metabolism Increased free fatty acid production Elevated NADH/NAD ratio leads to the predominate production of β–hydroxybutyrate (BHB) over acetoacetate (AcAc) Dehydration Fever absent unless there is an underlying infection Tachycardia (common) due to: Dehydration with associated orthostatic changes Concurrent alcohol withdrawal Tachypnea: Common Deep, rapid, Kussmaul respirations frequently present Nausea and vomiting Abdominal pain (nausea, vomiting, and abdominal pain are the most common symptoms): Usually diffuse with nonspecific tenderness Epigastric pain common Rebound tenderness, abdominal distension, hypoactive bowel sounds uncommon Mandates a search for an alternative, coexistent illness Decreased urinary output from hypovolemia Mental status: Minimally altered as a result of hypovolemia and possibly intoxication Altered mental status mandates a search for other associated conditions such as: Head injury, cerebrovascular accident (CVA), or intracranial hemorrhage Hypoglycemia Alcohol withdrawal Encephalopathy Toxins Visual disturbances: Reports of isolated visual disturbances with AKA common History Chronic alcohol use: Recent binge Abrupt cessation Physical Exam Findings of dehydration most common May have ketotic odor Kussmaul respirations Palmar erythema (alcoholism) Lab Acid–base disturbance: Increased anion gap metabolic acidosis hallmark Mixed acid–base disturbance common: Respiratory alkalosis Metabolic alkalosis secondary to vomiting and dehydration Hyperchlorem Continue reading >>

Toxic Alcohol Ingestion

Toxic Alcohol Ingestion

This month, EBMedicines Emergency Medicine Practice series tackles toxic alchol ingestion: Patil N, Becker MWL, Ganetsky M (2010). Toxic Alcohols: Not Always A Clear-Cut Diagnosis. Emergency Medicine Practice, 12 (11). [ Abstract and subscription link ] The article begins with a clinical scenario and then moves rapidly into an in-depth discussion of the relevant aetiology, pathophysiology and clinical features of toxic alcohol poisoning, focusing on the three most common toxic alcohol ingestions: methanol , ethylene glycol and isopropanol . This is followed by detailed sections on diagnosis, treatment and disposition including evidence-based treatment algorithms for toxic alcohol ingestion (these are gold!) and a step-by-step approach to calculating the osmolar gap, anion gap and estimating toxic alcohol concentrations. The review concludes with a discussion of toxic alcohol poisoning in special circumstances (paediatric patients and pregnancy), recent controversies/new developments, some common pitfalls in risk management and finally a CME quiz to assess your learning. It is a huge review, so I have chosen to focus on the following topics: Aetiology, pathophysiology and clinical features Aetiology, Pathophysiology and Clinical Features Methanol is commonly found in windshield-wiper fluid and de-icing products, and may also be found in gas-line antifreeze, paint removers, shoe dyes and embalming fluid. Methanol is metabolised by alcohol dehydrogenase (ADH) to formaldehyde, which is further metabolised by aldehyde dehydrogenase (ALDH) to formic acid. Formic acid is the main toxic metabolite responsible for the retinal, ophthalmic and neural toxicity seen with methanol ingestion. Ocular effects include blurry vision, reduced visual acuity, photophobia and the classic sno Continue reading >>

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