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Lactic Acidosis And Insulin Resistance Associated With Epinephrine Administration In A Patient With Noninsulin-dependent Diabetes Mellitus

Lactic Acidosis And Insulin Resistance Associated With Epinephrine Administration In A Patient With Noninsulin-dependent Diabetes Mellitus

Lactic Acidosis and Insulin Resistance Associated With Epinephrine Administration in a Patient With NonInsulin-Dependent Diabetes Mellitus Epinephrine raises plasma lactate concentrations when infused intravenously in normal subjects. We studied a patient with noninsulin-dependent diabetes mellitus who developed lactic acidosis and marked insulin resistance when treated with epinephrine after open heart surgery. Caruso M, Orszulak TA, Miles JM. Lactic Acidosis and Insulin Resistance Associated With Epinephrine Administration in a Patient With NonInsulin-Dependent Diabetes Mellitus. Arch Intern Med. 1987;147(8):14221424. doi:10.1001/archinte.1987.00370080058013 New! JAMA Network Open is now accepting submissions. Learn more. Customize your JAMA Network experience by selecting one or more topics from the list below. Challenges in Clinical Electrocardiography Clinical Implications of Basic Neuroscience Health Care Economics, Insurance, Payment Scientific Discovery and the Future of Medicine United States Preventive Services Task Force JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Facial Plastic Surgery JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA OtolaryngologyHead & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry (1919-1959) AMA Manual of Style Art and Images in Psychiatry Breast Cancer Screening Guidelines Colorectal Screening Guidelines Declaration of Helsinki Depression Screening Guidelines Evidence-Based Medicine: An Oral History Fishbein Fellowship Genomics and Precision Health Health Disparities Hypertension Guidelines JAMA Network Audio JAMA Network Conferences Med Men Medical Education Opioid Management Guidelines Peer Review Congress Research Ethics Sepsis and Septic Shock 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 >>

Renal Tubular Acidosis

Renal Tubular Acidosis

Renal tubular acidosis (RTA) is a disorder in which a defect in secretion of protons by the proximal and/or distal nephron of the kidney results in bicarbonate wasting (proximal) or reduced acid secretion (distal). George J. Schwartz MD, in Pediatric Clinical Advisor (Second Edition) , 2007 Renal tubular acidosis (RTA) is a disorder in which a defect in secretion of protons by the proximal and/or distal nephron of the kidney results in bicarbonate wasting (proximal) or reduced acid secretion (distal). As a consequence, a persistent nonanion gap (hyperchloremic) metabolic acidosis develops. The serum anion gap, [Na] ([Cl] + [HCO3]), is normally 8 to 12mEq/L in adults and 20% to 30% higher in infants. Type 1 or classic RTA (i.e., distal renal tubular acidosis [DRTA]) Type 2 RTA (i.e., proximal renal tubular acidosis [PRTA]) Type 3 RTA (i.e., no longer considered a distinct entity) Type 4 RTA (i.e., hyperkalemic distal renal tubular acidosis) 588.89Acidosis, renal, tubular (distal or proximal) (Other specified disorders resulting from impaired renal function) Incidence of DRTA is 1 in 10,000 people; PRTA is less common. Although primary RTA is recognized to be a rare disease, referrals to exclude RTA are much more common than the incidence of the disease. As a referring diagnosis, primary RTA accounted for 6% of renal consultations in children of Venezuela. There is no sex predominance in DRTA or in Type 4 RTA. DRTA may be inherited as an autosomal dominant or recessive trait. Autosomal recessive DRTA often presents in infancy, whereas autosomal dominant DRTA may not present until adolescence or young adulthood. Mutations in the genes encoding carbonic anhydrase II, kidney anion exchanger 1 (kAE1), and subunits of the renal proton pump (H+ATPase) have been identified in p Continue reading >>

Trimethoprim/sulfamethoxazole-induced Severe Lactic Acidosis: A Case Report And Review Of The Literature

Trimethoprim/sulfamethoxazole-induced Severe Lactic Acidosis: A Case Report And Review Of The Literature

Trimethoprim/Sulfamethoxazole-Induced Severe Lactic Acidosis: A Case Report and Review of the Literature Marie Bulathsinghala; Kimberly Keefer; Andry Van de Louw Propylene glycol (PG) is used as a solvent in numerous medications, including trimethoprim/sulfamethoxazole (TMP/SMX) and lorazepam, and is metabolized in the liver to lactic acid. Cases of lactic acidosis related to PG toxicity have been described and always involved large doses of benzodiazepines and PG. We present the first case of severe lactic acidosis after a 3-day course of TMP/SMX alone, involving allegedly safe amounts of PG. A 31-year-old female with neurofibromatosis and pilocytic astrocytoma, receiving temozolomide and steroids, was admitted to the intensive care unit for pneumonia and acute respiratory failure requiring intubation. Her initial hemodynamic and acidbase statuses were normal. She was treated with intravenous TMP/SMX for possible Pneumocystis jirovecii pneumonia and was successfully extubated on day 2. On day 3, she developed tachypnea and arterial blood gas analysis revealed a severe metabolic acidosis (pH 7.2, PCO2 19 mm Hg, bicarbonates 8 mEq/L) with anion gap of 25 mEq/L and lactate of 12.1 mmol/L. TMP/SMX was discontinued and the lactate decreased to 2.9 mmol/L within 24 hours while her plasma bicarbonates normalized, without additional intervention. The patient never developed hypotension or severe hypoxia, and her renal and liver functions were normal. No other cause for lactic acidosis was identified and it resolved after TMP/SMX cessation alone, suggesting PG toxicity. Although PG-related lactic acidosis is well recognized after large doses of lorazepam, clinicians should bear in mind that TMP/SMX contains PG as well and should suspect PG toxicity in patients developing unexp Continue reading >>

Lactic Acidosis And Beta Agonist Therapy In Asthma

Lactic Acidosis And Beta Agonist Therapy In Asthma

Lactic Acidosis and Beta Agonist Therapy in Asthma A 45 y/o male with moderate persistent asthma presents with wheezing and cough following a viral URI. He is tachypneic and has diffuse wheezing. PEFR is 250 (>50% below his normal). Initial ABG is 7.46/33/70 on room air with a lactate of 2.0 mmol/L. He receives IV steroids and 4 rounds of albuterol nebulizers. On repeat evaluation, his work of breathing and wheezing have improved and his PEFR is now >300. He is completed alert and oriented with a BP of 118/70 and a HR of 110. Repeat ABG shows 7.35/35/100 on room air; however, his lactate is now 7 mmol/L. QUESTION: Is the rise in his lactate expected following beta-agonist therapy? A simple respiratory alkalosis is the most common acid-base disorder in acute asthma.[1]However, lactic acidosis is frequently identified especially in cases of severe asthma.[2-4]Possible causes of lactic acidosis in asthma include: Tissue hypoxia due to hypoxemia and the decrease in venous return caused by elevated intrinsic PEEP Relative hepatic ischemia and impaired lactate clearance due to venous congestion Increased respiratory muscle work against constricted upper airways Wait, -agonist therapy can cause an elevated lactate? How? Causes of lactic acidosis can be organized into two categories: [5-6] Type A: Secondary to tissue hypoxia (shock, cardiac arrest) Type B: Lactic acidosis without hypoxia.This can occur through several mechanisms including: Impaired pyruvate dehydrogenase activity (thiamine deficiency) Medication-induced mitochondrial dysfunction (antiretroviral therapy, linezolid, propofol, etc) Impaired conversion of lactate to glucose (hepatic dysfunction) Lactic acidosis caused by -agonist therapy is a type B lactic acidosis. The exact mechanism for the rise in lactate leve Continue reading >>

An Unusual Case Of Lactic Acidosis

An Unusual Case Of Lactic Acidosis

Keywords: Lactic Acidosis, Metabolic Acidosis, Severe Asthma, Salbutamol, Albuterol Lactic acidosis is an important cause of metabolic acidosis in hospitalised patients. This usually occurs either due to over production or under utilisation of lactate1 . Most cases of lactic acidosis are due to marked tissue hypoperfusion or hypoxia in systemic shock. Asymptomatic lactic acidosis has been reported previously during acute severe asthma and attributed to fatiguing respiratory muscles, hypoxaemia and liver ischaemia. It has also been linked to 2 agonist therapy in asthma, although lactic acidosis causing increasing dyspnoea in the asthmatic patient has only been recorded rarely. We present a case of lactic acidosis in a patient with acute severe asthma who did not have any overt signs of sepsis or tissue hypoperfusion. Mr IL was a 49 years old male who was known to have moderate asthma. He had multiple previous admissions to hospital with exacerbation of asthma but had never required an intensive care admission and had never been intubated. His other comorbidities included atrial fibrillation, ischaemic heart disease and depression. His usual medications included salbutamol, budesonide and salmeterol inhalers, aspirin, atorvastatin and digoxin. He was a mechanic by trade with no obvious occupational sensitisation. He had no pets at home. He was a smoker with a 20 pack year history. Recent lung function tests showed an FEV1/FVC of 0.68 with a post bronchodilator FEV1 of 4.17 L (95% predicted). He was admitted with a 1 week history of worsening shortness of breath, dry cough and wheeze. His baseline blood tests including full blood count, C reactive protein, liver and renal function were normal. Chest radiograph was unremarkable. Arterial blood gas showed no evidence of hyp Continue reading >>

132 Steroid-induced Lactic Acidosis In Lymphoma. | Journal Of Investigative Medicine

132 Steroid-induced Lactic Acidosis In Lymphoma. | Journal Of Investigative Medicine

132 STEROID-INDUCED LACTIC ACIDOSIS IN LYMPHOMA. SOUTHERN ABSTRACTS: Hematology and Oncology Joint Poster Session 5:00 PM: Thursday, February 8, 2007 132 STEROID-INDUCED LACTIC ACIDOSIS IN LYMPHOMA. 1Louisiana State University Health Sciences Center, Shreveport, LA. Introduction Lactic acidosis may occur in lymphoma from various mechanisms. We describe a case of lymphoma-associated lactic acidosis that may have been precipitated by corticosteroid therapy. Case A 50-year-old woman was admitted with a 3-week history of fatigue, anorexia, headaches, and fever. Physical examination was remarkable for a blood pressure of 90/70 mm Hg, pulse 120/min, and dry mucus membranes. No lymphadenopathy or hepatosplenomegaly were noted. Pertinent laboratory data: Hgb 13.6 g/dL, WBC 4,500/mm3, Na+ 132 mEq/L, K+ 3.4 mEq/L, BUN 31 mg/dL, and creatinine 2.1 mg/dL. She was hydrated aggressively, with marked improvement in blood pressure and creatinine (1.3 mg/dL). Bilateral suprarenal masses on ultrasonography led to CT of the chest, abdomen, and pelvis. Multiple pulmonary nodules, mediastinal lymphadenopathy, and nonenhancing bilateral adrenal masses (right 10 7.3 cm; left 9 7.9 cm) were found. Subsequent evaluation revealed adrenal insufficiency. MRI of the brain revealed a 19 mm pituitary mass compressing the optic chiasm. Visual fields were intact. Hydrocortisone 30 mg po bid was initiated. Prior to percutaneous mediastinal lymph node biopsy, she received hydrocortisone 100 mg IV for 2 days. Four days later, she developed worsening renal failure, lactic acidosis (10 mmol/L), and drowsiness. Hydrocortisone was increased to 100 mg IV q8h. Because of a nondiagnostic mediastinal biopsy, mediastinoscopy was performed, which revealed malignant lymphoma. Bone marrow biopsy and immunophenotypin Continue reading >>

Metformin And Fatal Lactic Acidosis

Metformin And Fatal Lactic Acidosis

Publications Published: July 1998 Information on this subject has been updated. Read the most recent information. Dr P Pillans,former Medical Assessor, Centre for Adverse Reactions Monitoring (CARM), Dunedin Metformin is a useful anti-hyperglycaemic agent but significant mortality is associated with drug-induced lactic acidosis. Significant renal and hepatic disease, alcoholism and conditions associated with hypoxia (eg. cardiac and pulmonary disease, surgery) are contraindications to the use of metformin. Other risk factors for metformin-induced lactic acidosis are sepsis, dehydration, high dosages and increasing age. Metformin remains a major reported cause of drug-associated mortality in New Zealand. Of the 12 cases of lactic acidosis associated with metformin reported to CARM since 1977, 2 occurred in the last year and 8 cases had a fatal outcome. Metformin useful but small risk of potentially fatal lactic acidosis Metformin is a useful therapeutic agent for obese non-insulin dependent diabetics and those whose glycaemia cannot be controlled by sulphonylurea monotherapy. Lactic acidosis is an uncommon but potentially fatal adverse effect. The reported frequency of lactic acidosis is 0.06 per 1000 patient-years, mostly in patients with predisposing factors.1 Examples of metformin-induced lactic acidosis cases reported to CARM include: A 69-year-old man, with renal and cardiac disease, was prescribed metformin due to failing glycaemic control on glibenclamide monotherapy. He was well for six weeks, then developed lactic acidosis and died within 3 days. Post-surgical lactic acidosis caused the death of a 70-year-old man whose metformin was not withdrawn at the time of surgery. A 56-year-old woman, with no predisposing disease, died from lactic acidosis following major Continue reading >>

Tumor Lysis Syndrome Induced By Dexamethasone | Anesthesiology | Asa Publications

Tumor Lysis Syndrome Induced By Dexamethasone | Anesthesiology | Asa Publications

Tumor Lysis Syndrome Induced by Dexamethasone *Assaf Harofeh Medical Center, Zerifin, Israel. Tumor Lysis Syndrome Induced by Dexamethasone Anesthesiology 9 2006, Vol.105, 633-634. doi: Anesthesiology 9 2006, Vol.105, 633-634. doi: Michael Chanimov, Maya Koren-Michowitz, MathiasL. Cohen, Semion Pilipodi, Murat Bahar; Tumor Lysis Syndrome Induced by Dexamethasone. Anesthesiology 2006;105(3):633-634. 2018 American Society of Anesthesiologists Tumor Lysis Syndrome Induced by Dexamethasone You will receive an email whenever this article is corrected, updated, or cited in the literature. You can manage this and all other alerts in My Account Acute tumor lysis syndrome is being reported with increasing frequency by many hematologic units worldwide, and it deserves greater familiarity and awareness on the part of anesthesiologists and critical caregivers. It occurs when rapidly dividing large volume tumors, such as highly aggressive lymphomas and acute leukemias, are treated with cytotoxic agents. It is characterized by the rapid development of hyperkalemia, hyperuricemia, hyperphosphatemia, hypocalcemia, and lactic acidosis and may terminate in renal failure if not considered early enough in the differential diagnosis. A 42-yr-old female patient with no previously known malady was admitted to our Ear Nose and Throat Department for investigation of bilateral parotid gland enlargement accompanied by multiple enlarged cervical lymph nodes. Initial laboratory investigations revealed a normal complete blood count and normal blood coagulation and biochemistry profiles, apart from an increased lactate dehydrogenase value of 937 U/l. On the prebiopsy day, she underwent an excisional biopsy of a cervical lymph node under a short general anesthesia. At the end of this procedure, she w Continue reading >>

A Case Report Of Severe Type B Lactic Acidosis Following First Dose Of Nivolumab In A Vhl-mutated Metastatic Renal Cell Carcinoma

A Case Report Of Severe Type B Lactic Acidosis Following First Dose Of Nivolumab In A Vhl-mutated Metastatic Renal Cell Carcinoma

A Case Report of Severe Type B Lactic Acidosis Following First Dose of Nivolumab in a VHL-Mutated Metastatic Renal Cell Carcinoma Authors: Nakajima, Erica a | Leger, Paul a | Mayer, Ingrid A. b | Neuss, Michael N. b | Chism, David D. b | Rathmell, W. Kimryn b ; * Affiliations: [a] Department of Medicine, Vanderbilt University Medical Center, Nashville, TN, USA | [b] Division of Hematology and Oncology, Vanderbilt-Ingram Cancer Center, Vanderbilt University Medical Center, Nashville, TN, USA Correspondence: [*] Correspondence to: W. Kimryn Rathmell, 2220 Pierce Avenue, 777 Preston Research Building, Vanderbilt University Medical Center, Nashville, TN 37232, USA. Tel.: +1 615 875 9731; Fax: +1 615 343 7602; E-mail: [email protected] . Keywords: Renal cell carcinoma, acidosis, everolimus Journal: Kidney Cancer , vol. 1, no. 1, pp. 83-88, 2017 We report a case of severe type B lactic acidosis (LA) in a 51-year-old male, 12 days after he received his first dose of nivolumab for metastatic Von Hippel Lindau (VHL)-mutated, clear cell renal cell carcinoma. Throughout his hospital course, infection, hypoperfusion, and tissue necrosis were not identified. We propose that his LA may have resulted from either inherent tumor glycolysis or immune activation and enhanced metabolism. The patients course was complicated by acute renal failure, and his LA rose progressively, eventually necessitating daily hemodialysis (HD). After receiving five consecutive days of HD, the patient started everolimus daily with the intent of reducing glycolytic metabolism. Subsequently, the rate of lactic acid production slowed, and HD was no longer required after two doses of everolimus. To our knowledge, this is the first reported case of type B LA following nivolumab administration, and th Continue reading >>

Drug-induced Metabolic Acidosis

Drug-induced Metabolic Acidosis

Go to: Introduction Metabolic acidosis is defined as an excessive accumulation of non-volatile acid manifested as a primary reduction in serum bicarbonate concentration in the body associated with low plasma pH. Certain conditions may exist with other acid-base disorders such as metabolic alkalosis and respiratory acidosis/alkalosis 1. Humans possess homeostatic mechanisms that maintain acid-base balance ( Figure 1). One utilizes both bicarbonate and non-bicarbonate buffers in both the intracellular and the extracellular milieu in the immediate defense against volatile (mainly CO 2) and non-volatile (organic and inorganic) acids before excretion by the lungs and kidneys, respectively. Renal excretion of non-volatile acid is the definitive solution after temporary buffering. This is an intricate and highly efficient homeostatic system. Derangements in over-production, under-excretion, or both can potentially lead to accumulation of excess acid resulting in metabolic acidosis ( Figure 1). Drug-induced metabolic acidosis is often mild, but in rare cases it can be severe or even fatal. Not only should physicians be keenly aware of this potential iatrogenic complication but they should also be fully engaged in understanding the pathophysiological mechanisms. Metabolic acidosis resulting from drugs and/or ingestion of toxic chemicals can be grouped into four general categories ( Figure 2): Some medications cannot be placed into one single category, as they possess multiple mechanisms that can cause metabolic acidosis. In suspected drug-induced metabolic acidosis, clinicians should establish the biochemical diagnosis of metabolic acidosis along with the evaluation of respiratory compensation and whether there is presence of mixed acid-based disorders 2, then convert the bioche Continue reading >>

Internet Scientific Publications

Internet Scientific Publications

S Mathur, I Khalid, G Pesola. Beta Agonist-Induced Lactic Acidosis in Asthma. The Internet Journal of Asthma, Allergy and Immunology. 2012 Volume 8 Number 1. Patients admitted to the hospital with an asthma exacerbation will on occasion develop an elevated lactate. This immediately triggers increased patient surveillance due to the possibility that the lactate may signify inadequate delivery of oxygen to the tissues that results in a lactic acidosis type A. Type A lactic acidosis may be related to septicemia or heart failure as very common factors and intensive care unit management would be a consideration. Alternatively, it may simply be due to the more benign type B2 lactic acidosis that is now commonly seen in asthma (1,2,3,4). The onus is on the clinician to make this distinction. A 32-year-old slim black female (BMI = 23) with moderate persistent asthma on fluticasone 500 ug/salmeterol 50 ug inhaler, montelukast 10 mg daily, and albuterol as needed was seen in the emergency department (ED) for worsening dyspnea unrelieved by home treatment in January of 2012. The home treatment included nebulized albuterol at 2.5 mg given three times that day, use of an albuterol inhaler at least 5 times that day with two (90 ug/puff) or more puffs each time, and an albuterol nebulization of 2.5 mg in the ambulance. In the ED she was noted to be in respiratory distress with a blood pressure of 151/80 mm Hg++, heart rate (HR) at 110 beats/min, and respiratory rate of 30 breaths/min with a pulse oximeter saturation of 100% while receiving intermittent bronchodilator nebulizations. She had bilateral diffuse wheezing. She was given nebulized albuterol 2.5 mg with ipratropium bromide three times, terbutaline 0.25 mg subcutaneously twice, magnesium sulfate 2 grams intravenously, and int Continue reading >>

Elevated Lactate In Asthmatics

Elevated Lactate In Asthmatics

By sinaiem | critical care , Pulm | Comments are Closed | 28 October, 2015 | 0 Youre treating an asthmatic 22-year-old. You give 5 back-to-back nebs, steroids and mag. When you reassess, shes moving air better with minimal wheezing, but more tachypneic. Additionally, her lactate has climbed from 2 to 6.8 in 2 hours. Shes not hypoxic and there are no signs of hypoperfusion. What gives? This patient has albuterol-induced hyperlactatemia. As opposed to Type A lactic acidoses, this is not caused by hypoxia or hypoperfusion. As a type B lactic acidosis, the exact etiology is not entirely understood. However, studies point to an increase in both endogenous and exogenous catecholamines. Enhanced beta 2 receptor activation leads to increased glycogenolysis, gluconeogenesis, lipolysis and conversion of pyruvate to lactic acid. Corticosteroid use may potentiate these affects. The idea that increased respiratory muscle usage leads to increased lactate production has been shown to be less likely, given that even paralyzed and ventilated patients can have similarly elevated lactate levels in the setting of albuterol usage. This phenomenon is still undergoing study. Not all patients receiving high dose albuterol develop lactic acidosis and the reasons behind this are not well understood. The dose-response curve is also being elucidated. Most reports are case studies showing elevated lactate after back-to-back dosing and/or IV dosing within a few hours. One prospective, randomized trial looked at the relationship between serum albuterol levels and lactate levels, determining that there was a 3.1 mg/dL increase in the 1.25h serum lactate concentration for each 5ng x h/mL increase in total plasma albuterol level. How this relates to dosing is not defined, but it appears that higher dos Continue reading >>

Severe Lactic Acidosis In A Patient With B-cell Lymphoma: A Case Report And Review Of The Literature

Severe Lactic Acidosis In A Patient With B-cell Lymphoma: A Case Report And Review Of The Literature

Severe Lactic Acidosis in a Patient with B-Cell Lymphoma: A Case Report and Review of the Literature 1Department of Internal Medicine, Division of Hematology, Oncology and Palliative Care, Virginia Commonwealth University, Richmond, VA 23298, USA 2Department of Internal Medicine, Division of Nephrology, Virginia Commonwealth University, Richmond, VA 23298, USA Received 4 September 2009; Accepted 20 November 2009 Copyright 2009 Farn Huei Chan et al. This is an open access article distributed under the Creative Commons Attribution License , which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Lactic acidosis is commonly observed in clinical situations such as shock and sepsis, as a result of tissue hypoperfusion and hypoxia. Lymphoma and leukemia are among other clinical situations where lactic acidosis has been reported. We present a case of a 59-year-old female with lactic acidosis who was found to have aggressive B-cell lymphoma. There have been 29 cases of lymphoma induced lactic acidosis reported thus far; however all reported cases have abnormal vital signs or concomitant medical conditions that may lead to lactic acidosis. The pathogenesis of malignancy-induced lactic acidosis is not well understood; however associated factors include increased glycolysis, increased lactate production by cancer cells, and decreased hepatic clearance of lactate. When it occurs, lactic acidosis is a poor prognostic sign in these patients. Prompt diagnosis and treatment of underlying lymphoma or leukemia remains the only way to achieve complete resolution of lactic acidosis in these patients. Lactic acidosis is a common cause of an anion gap acidosis that often carries a significant risk for mortality. Lactic acid Continue reading >>

Lactic Acidosis | Hivbook.com

Lactic Acidosis | Hivbook.com

Christiane Schieferstein-Knauer, Thomas Buhk Patients on ART commonly suffer from side effects. As a result, treatment of HIV infection has become a complicated balancing act between the benefits of durable HIV suppression and the risks of drug toxicity. Adherence problems, regimen changes or even withdrawal from therapy are often the result of drug toxicity. In former times at least 25% of patients stopped therapy within the first year on ART because of side effects (dArminio Monforte 2000, Yuan 2006). Between 2003 and 2007, the rate was still about 20% (Cicconi 2010). Only over the last three years tolerability of ART has been improved, thanks to new drugs becoming available. Treatment cessation due to side effects has become less frequent (Carr 2009). Factors for poor or non-adherence include poverty, intravenous drug abuse, young age, Afro American origin, hepatitis co-infection and regular alcohol consumption (Robison 2008, Hendershot 2009). The patient should be counseled in detail on the potential side effects, so that he or she is in a position to recognize them and to contact their physician in time. This can save lives, for example in the case of abacavir hypersensitivity reaction, or prevent the irreversible damage of some side effects, such as polyneuropathy. Being prepared for the occurrence of possible problems and providing potential solutions improves both the acceptance of treatment and adherence. This information needs to be presented by the provider to the patient in a user-friendly and accessible manner the extensive package inserts tend to frighten patients. It must be stressed that the majority of patients are able to tolerate ART well, even for years. Nevertheless, the regular monitoring of treatment by an HIV clinician, even in asymptomatic pati Continue reading >>

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