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Lactic Acidosis Review

Severe Nucleoside-associated Lactic Acidosis In Human Immunodeficiency Virusinfected Patients: Report Of 12 Cases And Review Of The Literature

Severe Nucleoside-associated Lactic Acidosis In Human Immunodeficiency Virusinfected Patients: Report Of 12 Cases And Review Of The Literature

Severe Nucleoside-Associated Lactic Acidosis in Human Immunodeficiency VirusInfected Patients: Report of 12 Cases and Review of the Literature Infectious Diseases Division, Hospital Vall d'Hebron Reprints or correspondence: Dr. Vicente Falc, Infectious Diseases Division, Hospital Vall d'Hebron, Po Vall d'Hebron 119129 08035 Barcelona, Spain ( [email protected] ). Search for other works by this author on: Infectious Diseases Division, Hospital Vall d'Hebron Infectious Diseases Division, Hospital Vall d'Hebron Hospital Clnic-Institut d'Investigacions Biomdiques August Pi i Sunyer, Universitat de Barcelona Hospital Clnic-Institut d'Investigacions Biomdiques August Pi i Sunyer, Universitat de Barcelona Hospital de la Santa Creu i Sant Pau, Universitat Autnoma de Barcelona Hospital de la Santa Creu i Sant Pau, Universitat Autnoma de Barcelona Infectious Diseases Division, Hospital Vall d'Hebron Infectious Diseases Division, Hospital Vall d'Hebron Clinical Infectious Diseases, Volume 34, Issue 6, 15 March 2002, Pages 838846, Vicente Falc, Dolors Rodrguez, Esteban Ribera, Esteban Martnez, Jos Maria Mir, Pere Domingo, Ruth Diazaraque, R. Arribas Jos, Juan J. Gonzlez-Garca, Francesc Montero, Lluis Snchez, Albert Pahissa; Severe Nucleoside-Associated Lactic Acidosis in Human Immunodeficiency VirusInfected Patients: Report of 12 Cases and Review of the Literature, Clinical Infectious Diseases, Volume 34, Issue 6, 15 March 2002, Pages 838846, Lactic acidosis is a rare but often fatal complication reported in some human immunodeficiency virus (HIV)infected patients treated with nucleoside-analogue reverse-transcriptase inhibitors. We report a series of 12 patients with HIV infection treated with nucleoside analogues who developed unexplained metabolic acidosis. We have also revi Continue reading >>

Examining Clinical Similarities Between Myalgic Encephalomyelitis/chronic Fatigue Syndrome And D-lactic Acidosis: A Systematic Review

Examining Clinical Similarities Between Myalgic Encephalomyelitis/chronic Fatigue Syndrome And D-lactic Acidosis: A Systematic Review

The pursuit for clarity in diagnostic and treatment pathways for the complex, chronic condition of myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) continues. This systematic review raises a novel question to explore possible overlapping aetiology in two distinct conditions. Similar neurocognitive symptoms and evidence of d-lactate producing bacteria in ME/CFS raise questions about shared mechanisms with the acute condition of d-lactic acidosis (d-la). d-la case reports published between 1965 and March 2016 were reviewed for episodes describing both neurological symptoms and high d-lactate levels. Fifty-nine d-la episodes were included in the qualitative synthesis comparing d-la symptoms with ME/CFS diagnostic criteria. A narrative review of d-la mechanisms and relevance for ME/CFS was provided. The majority of neurological disturbances reported in d-la episodes overlapped with ME/CFS symptoms. Of these, the most frequently reported d-la symptoms were motor disturbances that appear more prominent during severe presentations of ME/CFS. Both patient groups shared a history of gastrointestinal abnormalities and evidence of bacterial dysbiosis, although only preliminary evidence supported the role of lactate-producing bacteria in ME/CFS. Interpretation of results are constrained by both the breadth of symptoms included in ME/CFS diagnostic criteria and the conservative methodology used for d-la symptom classification. Several pathophysiological mechanisms in ME/CFS were not examined. Shared symptomatology and underlying microbiotagutbrain interactions raise the possibility of a continuum of acute (d-la) versus chronic (ME/CFS) presentations related to d-lactate absorption. Measurement of d-lactate in ME/CFS is needed to effectively evaluate whether subclinical d Continue reading >>

Mortality Rate In So-called

Mortality Rate In So-called "metformin-associated Lactic Acidosis": A Review Of The Data Since The 1960s.

Mortality rate in so-called "metformin-associated lactic acidosis": a review of the data since the 1960s. This study shows that, in general, mortality from metformin-associated lactic acidosis (MALA) decreased from 50% to 25% from 1960s to the present.This Recommendation is of an article referenced in an F1000 Faculty Review also written by Orson W. Moe, Amy Quynh Trang Pham and Li Hao Richie Xu. To read the rest of this recommendation and access over 145,000 article recommendations from 3,700+ journals across biomedicine, register Send a recommendation to your institution's librarian or information manager to request an extended free trial for articles in biology and medicine, contributed inclusion in F1000Prime to help you filter recommendations, plus relevant articles as engine clusters of related articles and be alerted as soon as similar articles appear in If you think you should be able to access this content, please contact us . If you've forgotten your password, please enter your email address below and we'll send you instructions on how to reset your password. The email address should be the one you originally registered with F1000. Email address not recognised, please try again We are unable to reset your password, please contact [email protected] to reactivate your account, quoting error code UACC/DEL You registered with F1000 via Google, so we cannot reset your password. If you still need help with your Google account password, please click here . You registered with F1000 via Facebook, so we cannot reset your password. If you still need help with your Facebook account password, please click here . You registered with F1000 via ORCID, so we cannot reset your password. If you still need help with your ORCID account password, please click here . Email [email protected] 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 >>

Review Metformin-associated Lactic Acidosis: Current Perspectives On Causes And Risk

Review Metformin-associated Lactic Acidosis: Current Perspectives On Causes And Risk

Abstract Although metformin has become a drug of choice for the treatment of type 2 diabetes mellitus, some patients may not receive it owing to the risk of lactic acidosis. Metformin, along with other drugs in the biguanide class, increases plasma lactate levels in a plasma concentration-dependent manner by inhibiting mitochondrial respiration predominantly in the liver. Elevated plasma metformin concentrations (as occur in individuals with renal impairment) and a secondary event or condition that further disrupts lactate production or clearance (e.g., cirrhosis, sepsis, or hypoperfusion), are typically necessary to cause metformin-associated lactic acidosis (MALA). As these secondary events may be unpredictable and the mortality rate for MALA approaches 50%, metformin has been contraindicated in moderate and severe renal impairment since its FDA approval in patients with normal renal function or mild renal insufficiency to minimize the potential for toxic metformin levels and MALA. However, the reported incidence of lactic acidosis in clinical practice has proved to be very low (< 10 cases per 100,000 patient-years). Several groups have suggested that current renal function cutoffs for metformin are too conservative, thus depriving a substantial number of type 2 diabetes patients from the potential benefit of metformin therapy. On the other hand, the success of metformin as the first-line diabetes therapy may be a direct consequence of conservative labeling, the absence of which could have led to excess patient risk and eventual withdrawal from the market, as happened with earlier biguanide therapies. An investigational delayed-release metformin currently under development could potentially provide a treatment option for patients with renal impairment pending the resu Continue reading >>

Lactic Acidosis

Lactic Acidosis

Background In basic terms, lactic acid is the normal endpoint of the anaerobic breakdown of glucose in the tissues. The lactate exits the cells and is transported to the liver, where it is oxidized back to pyruvate and ultimately converted to glucose via the Cori cycle. In the setting of decreased tissue oxygenation, lactic acid is produced as the anaerobic cycle is utilized for energy production. With a persistent oxygen debt and overwhelming of the body's buffering abilities (whether from chronic dysfunction or excessive production), lactic acidosis ensues. [1, 2] (See Etiology.) Lactic acid exists in 2 optical isomeric forms, L-lactate and D-lactate. L-lactate is the most commonly measured level, as it is the only form produced in human metabolism. Its excess represents increased anaerobic metabolism due to tissue hypoperfusion. (See Workup.) D-lactate is a byproduct of bacterial metabolism and may accumulate in patients with short-gut syndrome or in those with a history of gastric bypass or small-bowel resection. [3] By the turn of the 20th century, many physicians recognized that patients who are critically ill could exhibit metabolic acidosis unaccompanied by elevation of ketones or other measurable anions. In 1925, Clausen identified the accumulation of lactic acid in blood as a cause of acid-base disorder. Several decades later, Huckabee's seminal work firmly established that lactic acidosis frequently accompanies severe illnesses and that tissue hypoperfusion underlies the pathogenesis. In their classic 1976 monograph, Cohen and Woods classified the causes of lactic acidosis according to the presence or absence of adequate tissue oxygenation. (See Presentation and Differentials.) The causes of lactic acidosis are listed in the chart below. Go to Acute Lactic Ac Continue reading >>

Lactic Acidosis: Symptoms, Causes, And Treatment

Lactic Acidosis: Symptoms, Causes, And Treatment

Lactic acidosis occurs when the body produces too much lactic acid and cannot metabolize it quickly enough. The condition can be a medical emergency. The onset of lactic acidosis might be rapid and occur within minutes or hours, or gradual, happening over a period of days. The best way to treat lactic acidosis is to find out what has caused it. Untreated lactic acidosis can result in severe and life-threatening complications. In some instances, these can escalate rapidly. It is not necessarily a medical emergency when caused by over-exercising. The prognosis for lactic acidosis will depend on its underlying cause. A blood test is used to diagnose the condition. Lactic acidosis symptoms that may indicate a medical emergency include a rapid heart rate and disorientaiton. Typically, symptoms of lactic acidosis do not stand out as distinct on their own but can be indicative of a variety of health issues. However, some symptoms known to occur in lactic acidosis indicate a medical emergency. Lactic acidosis can occur in people whose kidneys are unable to get rid of excess acid. Even when not related to just a kidney condition, some people's bodies make too much lactic acid and are unable to balance it out. Diabetes increases the risk of developing lactic acidosis. Lactic acidosis may develop in people with type 1 and 2 diabetes mellitus , especially if their diabetes is not well controlled. There have been reports of lactic acidosis in people who take metformin, which is a standard non-insulin medication for treating type 2 diabetes mellitus. However, the incidence is low, with equal to or less than 10 cases per 100,000 patient-years of using the drug, according to a 2014 report in the journal Metabolism. The incidence of lactic acidosis is higher in people with diabetes who Continue reading >>

Lactic Acidosis: An Update

Lactic Acidosis: An Update

Clinical Chemistry and Laboratory Medicine (CCLM) Published in Association with the European Federation of Clinical Chemistry and Laboratory Medicine (EFLM) Ed. by Gillery, Philippe / Lackner, Karl J. / Lippi, Giuseppe / Melichar, Bohuslav / Payne, Deborah A. / Schlattmann, Peter / Tate, Jillian R. Source Normalized Impact per Paper (SNIP) 2016: 1.112 [D] 1975.00 / US$ 2960.00 / GBP 1619.00 * [D] 1975.00 / US$ 2960.00 / GBP 1619.00 * [D] 2370.00 / US$ 3551.00 / GBP 1943.00 * [D] 2370.00 / US$ 3551.00 / GBP 1943.00 * *Prices in US$ apply to orders placed in the Americas only. Prices in GBP apply to orders placed in Great Britain only. Prices in represent the retail prices valid in Germany (unless otherwise indicated). Prices are subject to change without notice. Prices do not include postage and handling if applicable. RRP: Recommended Retail Price. Department of Anaesthesia and Critical Care, Adelaide and Meath Hospital, Tallaght, Dublin, Ireland Department of Clinical Chemistry, Adelaide and Meath Hospital, Tallaght, Dublin, Ireland Published Online: 2016-08-15 | DOI: Lactate is one of the most crucial intermediates in carbohydrate and nonessential amino acid metabolism. The complexity of cellular interactions and metabolism means that lactate can be considered a waste product for one cell but a useful substrate for another. The presence of elevated lactate levels in critically ill patients has important implications for morbidity and mortality. In this review, we provide a brief outline of the metabolism of lactate, the pathophysiology of lactic acidosis, the clinical significance of D-lactate, the role of lactate measurement in acutely ill patients, the methods used to measure lactate in blood or plasma and some of the methodological issues related to interferences Continue reading >>

Metformin And Lactic Acidosis: Cause Or Coincidence? A Review Of Case Reports

Metformin And Lactic Acidosis: Cause Or Coincidence? A Review Of Case Reports

Metformin has been associated with the serious side-effect lactic acidosis. However, it remains unclear whether the use of metformin was a cause or a coincidence in lactic acidosis.A literature search of the Index Medicus (1959-66) and of the databases Embase, Medline, Medline Express (1966-99) was performed using the keywords metformin, biguanides and lactic acidosis. All articles of cases with metformin-induced lactic acidosis (MILA) were cross-referenced.Cases were included for analysis if they met the following criteria: serum pH < or =7.35, lactate concentration > or =5 mmol L(-1).A forum of six experts in intensive care medicine independently categorized the cases in MILA unlikely (score 0), possible MILA (score 1) or probable MILA (score 2).Statistical analysis included the paired interobserver agreement (kappa) and multivariate regression analysis.Of 80 reported cases, 33 were excluded because of insufficient quality. The forum scores of the remaining 47 cases were distributed normally with a mean score of 7 (range 2-10). The kappa-value was 0.041 (SD = 0.24, range -0.514, 0.427). Neither lactate concentration nor mortality correlated with serum metformin concentrations.Given the low interobserver agreement and the lack of any relationship between metformin levels and outcome parameters, the concept that there is a simple, causal relationship between metformin use and lactic acidosis in diabetic patients has to be reconsidered. Do you want to read the rest of this article? ... Con- versely, several types of B-Raf-mutant melanoma cells are resistant to metformin through increased angiogenesis [46]. This discrepancy could be caused by high concentrations of serum metformin in nude mice in the study by Martin et al [53], and the side effects of high serum metformi Continue reading >>

Lactic Acidosis: Background, Etiology, Epidemiology

Lactic Acidosis: Background, Etiology, Epidemiology

Author: Kyle J Gunnerson, MD; Chief Editor: Michael R Pinsky, MD, CM, Dr(HC), FCCP, MCCM more... In basic terms, lactic acid is the normal endpoint of the anaerobic breakdown of glucose in the tissues. The lactate exits the cells and is transported to the liver, where it is oxidized back to pyruvate and ultimately converted to glucose via the Cori cycle. In the setting of decreased tissue oxygenation, lactic acid is produced as the anaerobic cycle is utilized for energy production. With a persistent oxygen debt and overwhelming of the body's buffering abilities (whether from chronic dysfunction or excessive production), lactic acidosis ensues. [ 1 , 2 ] (See Etiology.) Lactic acid exists in 2 optical isomeric forms, L-lactate and D-lactate. L-lactate is the most commonly measured level, as it is the only form produced in human metabolism. Its excess represents increased anaerobic metabolism due to tissue hypoperfusion. (See Workup.) D-lactate is a byproduct of bacterial metabolism and may accumulate in patients with short-gut syndrome or in those with a history of gastric bypass or small-bowel resection. [ 3 ] By the turn of the 20th century, many physicians recognized that patients who are critically ill could exhibit metabolic acidosis unaccompanied by elevation of ketones or other measurable anions. In 1925, Clausen identified the accumulation of lactic acid in blood as a cause of acid-base disorder. Several decades later, Huckabee's seminal work firmly established that lactic acidosis frequently accompanies severe illnesses and that tissue hypoperfusion underlies the pathogenesis. In their classic 1976 monograph, Cohen and Woods classified the causes of lactic acidosis according to the presence or absence of adequate tissue oxygenation. (See Presentationand Differe 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 >>

Further Clarifying The Relationship Between Metformin, Acute Kidney Injury And Lactic Acidosis

Further Clarifying The Relationship Between Metformin, Acute Kidney Injury And Lactic Acidosis

Further clarifying the relationship between metformin, acute kidney injury and lactic acidosis Subscribe to Nature Reviews Nephrology for full access: Diabetes mellitus: complex interplay between metformin, AKI and lactic acidosis Bell, S., Soto-Pedre, E., Connelly, P., Livingstone, S. & Pearson, E. Clarifying the relationship between metformin, acute kidney injury and lactic acidosis . Nat. Rev. Nephrol. , (2017). Rhee, C. M., Kovesdy, C. P. & Kalantar-Zadeh, K. Risks of metformin in type 2 diabetes and chronic kidney disease: lessons learned from Taiwanese data Risk of acute kidney injury and survival in patients treated with metformin: an observational cohort study Acute kidney injury, plasma lactate concentrations and lactic acidosis in metformin users: a GoDarts study . Diabetes Obes. Metab. 19, 1579–1586 (2017). Inzucchi, S. E., Lipska, K. J., Mayo, H., Bailey, C. J. & McGuire, D. K. Metformin in patients with type 2 diabetes and kidney disease: a systematic review Restricting metformin in CKD: continued caution warranted . Am. J. Kidney Dis. 66, 1101–1102 (2015). Should restrictions be relaxed for metformin use in chronic kidney disease? Yes, they should be relaxed! What's the fuss? Should restrictions be relaxed for metformin use in chronic kidney disease? No, we should never again compromise safety! Metformin in chronic kidney disease: more harm than help? Lancet Diabetes Endocrinol. 3, 579–581 (2015). Metformin use in type 2 diabetes mellitus With CKD: is it time to liberalize dosing recommendations? Kalantar-Zadeh, K., Uppot, R. N. & Lewandrowski, K. B. Case records of the Massachusetts General Hospital. Case 23–2013. A 54-year-old woman with abdominal pain, vomiting, and confusion United States Renal Data System. USRDS 2017 Annual Data Report: Atlas Continue reading >>

D-lactic Acidosis A Very Rare Form Of Metabolic Acidosis Explained

D-lactic Acidosis A Very Rare Form Of Metabolic Acidosis Explained

D-lactic acidosis a very rare form of metabolic acidosis explained Summarized from Kowgli N, Chhabra L. D-lactic acidosis: an underrecognized complication of short bowel syndrome. Gastroenterology Research and Practice 2015. Available on line at: Health demands that the pH of blood is maintained within a narrow range (7.35-7.45). Monitoring this physiological imperative and detection of so-called acid-base disturbance, in which blood pH is either increased or decreased, is one of the principal clinical utilities of blood gas analysis. Metabolic acidosis one of the four classes of acid-base disturbance identified by blood gas analysis is most commonly the result of abnormal accumulation of lactic acid, either due to increased metabolic production, reduced elimination or a combination of the two.This most common form of metabolic acidosis should, strictly speaking, be called L-lactic acidosis rather than simply lactic acidosis, as is usually the case. The nomenclature, L-lactic acidosis recognizes that in nature lactic acid can exist in two stereoisomeric forms: L-lactic acid and D-lactic acid. In humans (and indeed all mammals) lactic acid exists almost exclusively as the L-isoform, and it is accumulation of this isoform that accounts for almost all cases of lactic acidosis. A recently published article focuses on the very rare instance in which lactic acidosis is caused not by accumulation of L-lactic acid, but rather accumulation of D-lactic acid. The authors provide the detail of D-lactic acidosis under five headings: pathophysiology, clinical features, diagnosis and treatment. Central to an understanding of the pathophysiology of D-lactic acidosis is the recognition that many bacterial species normally present in the colon produce D-lactic acid. An overgrowth of the Continue reading >>

Does Metformin Increase The Risk Of Fatal Or Nonfatal Lactic Acidosis?

Does Metformin Increase The Risk Of Fatal Or Nonfatal Lactic Acidosis?

WILLIAM E. CAYLEY, JR., MD, MDiv, University of Wisconsin Department of Family Medicine, Eau Claire, Wisconsin Am Fam Physician. 2010 Nov 1;82(9):1068-1070. Clinical Scenario A 70-year-old woman with type 2 diabetes mellitus who is in otherwise good health is experiencing gradually increasing glucose levels. Her physician considers starting her on an oral diabetes agent, but is concerned that her age may put her at risk for adverse effects if she is treated with metformin (Glucophage). Clinical Question Does metformin increase the risk of fatal or nonfatal lactic acidosis? Evidence-Based Answer In patients without standard contraindications to metformin therapy, metformin does not increase the risk of lactic acidosis.1 (Strength of Recommendation = B, based on inconsistent or limited-quality patient-oriented evidence) Practice Pointers The first-line treatments recommended for type 2 diabetes are lifestyle changes and metformin, which is a biguanide antihyperglycemic agent.2 Demonstrated benefits of metformin include lower cardiovascular mortality than other oral diabetes medications3 and a reduced risk of death or myocardial infarction in overweight patients with type 2 diabetes.4 However, because an earlier biguanide, phenformin, was removed from the market after being linked to several cases of lactic acidosis, there have been concerns that metformin may predispose patients to lactic acidosis as well. In light of this, metformin is considered contraindicated in patients with chronic renal insufficiency, pulmonary disease, or hypoxic conditions; abnormal hepatic function; peripheral vascular disease; and in those older than 65 years. The use of metformin in patients with heart failure continues to be controversial.1 The authors of this Cochrane review found no cases o Continue reading >>

Fatal Type-b Lactic Acidosis In Association With Hiv Associated Lymphoma - A Case Report With Review Of Literature

Fatal Type-b Lactic Acidosis In Association With Hiv Associated Lymphoma - A Case Report With Review Of Literature

Fatal Type-B Lactic Acidosis in Association with HIV Associated Lymphoma - A Case Report with Review of Literature Asif Salim, Sara Chinthu, Shobhana Nayak Rao * and Pradeep Shenoy M Department of Nephrology, K.S. Hegde Medical Academy, Medical Sciences Complex, Derlakatte, Mangalore 575013, Karnataka, India Associate Professor and Head, Department of Nephrology, K.S. Hegde Medical Academy, Derlakatte, Mangalore 575013, Karnataka, India Received date: June 27, 2017; Accepted date: June 27, 2017; Published date: July 24, 2017 Citation: Salim A, Chinthu S, Rao SN, Shenoy PM (2017) Fatal Type-B Lactic Acidosis in Association with HIV Associated Lymphoma- A Case Report with Review of Literature. Jour Ren Med Vol.1. No.2: 8. Visit for more related articles at Journal of Renal Medicine Hyperlactemia is defined as whole blood lactate levels > 2 mmol/L. Type-B lactic acidosis refers to conditions wherein overproduction of lactate is not related to reduction in tissue oxygen. The occurrence of severe lactic acidosis in malignancies is a rare and often pre-terminal complication. We present two HIV positive patients with type-B lactic acidosis as a pre-terminal event after being diagnosed with non Hodgkins lymphoma. The first patient, a 45-year-old male, HIV positive since 2012 on therapy admitted with h/o of pedal edema, generalized weakness and decreased appetite 1 week duration. Abdominal ultrasound scan revealed bilateral moderate hydro-ureteronephrosis with large left pleural effusion, cytology revealed malignant serous lymphoma confirmed by supraclavicular lymph node biopsy. Before initiation of chemotherapy, his general condition rapidly worsened with onset of lactic acidosis (10 mmol/L) and he expired. The second patient, a 59-year-old male presented with acute hematemesi Continue reading >>

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