scholarly journals Minding The Gap: Severe Anion Gap Metabolic Acidosis Associated With 5-Oxoproline Secondary To Chronic Acetaminophen Use

2019 ◽  
Vol 14 (4) ◽  
pp. e43-e49
Author(s):  
Claudia Frankfurter ◽  
Kevin Venus ◽  
David Frost
Keyword(s):  
Metabolic Acidosis ◽  
Anion Gap ◽  
Presumptive Diagnosis ◽  
Diffuse Abdominal Pain ◽  
Common Causes ◽  
Alkali Therapy ◽  
History Of ◽  
Douleur Abdominale ◽  
Osmolar Gap

AbstractAn 89-year-old man with multiple comorbidities presented to the emergency department with diffuse abdominal pain and dyspnea. He was found to have a severe anion-gap metabolic acidosis with the normal osmolar gap. An initial panel of investigations for common causes of anion-gap metabolic acidosis was unremarkable. Further history revealed long-term daily acetaminophen use. A presumptive diagnosis of 5-oxoprolinemia secondary to chronic acetaminophen use was made. Despite supportive care, the patient did not survive. There is emerging literature on elevated anion gap metabolic acidosis induced by the accumulation of 5-oxoproline, an intermediate organic acid in the gamma-glutamyl cycle. A quantitative profile of urinary organic acids to measure 5-oxoproline is valuable in confirming the diagnosis. Treatment is largely supportive, consisting of cessation of acetaminophen, alkali therapy, and N-acetylcysteine. Clinicians should consider 5-oxoprolemia in patients who present with an otherwise unexplained anion gap metabolic acidosis and a history of chronic acetaminophen use. RESUMEUn homme de 89 ans souffrant de comorbidités multiples s’est présenté à l’urgence avec douleur abdominale diffuse et dyspnée. On a découvert qu’il souffrait d’une acidose métabolique grave à anions nuls avec un écart osmolaire normal. Un premier groupe d’études sur les causes courantes d’acidose métabolique à intervalle anionique n’a pas été remarquable. D’autres antécédents ont révélé une utilisation quotidienne à long terme de l’acétaminophène. Un diagnostic présumé de 5-oxoprolinémie secondaire à l’utilisation chronique d’acétaminophène a été posé. Malgré des soins de soutien, le patient n’a pas survécu. Il existe une littérature émergente sur l’acidose métabolique à intervalle anionique élevé induite par l’accumulation de 5-oxoproline, un acide organique intermédiaire dans le cycle gamma-glutamyle. Un profil quantitatif d’acides organiques urinaires pour mesurer la 5-oxoproline est utile pour confirmer le diagnostic. Le traitement est largement favorable, consistant en l’arrêt de l’acétaminophène, un traitement alcalin et de la N-acétylcystéine. Les cliniciens devraient envisager l’administration de 5-oxoprolemia chez les patients qui présentent une acidose métabolique par gap anionique autrement inexpliquée et des antécédents d’utilisation chronique d’acétaminophène.

Euglycemic Diabetic Ketoacidosis in a Diabetic Patient Treated with SGLT2 Inhibitor

2021 ◽  
Vol 6 (1) ◽  
Author(s):  
Lavrynenko O ◽  
◽  
Santos H ◽  
Garza A ◽  
Qazi R ◽  
...  
Keyword(s):  
Metabolic Acidosis ◽  
Diabetic Ketoacidosis ◽  
Glucose Transporter ◽  
Sglt2 Inhibitor ◽  
Anion Gap ◽  
Laboratory Evaluation ◽  
Intravenous Insulin ◽  
Glucose Transporter 2 ◽  
Life Threatening ◽  
History Of

Diabetic Ketoacidosis (DKA) is a life - threatening complication and must be diagnosed and treated promptly and aggressively. The classic triad of DKA is hyperglycemia (Blood Glucose (BG) >250mg/dl; anion gap metabolic acidosis (pH <7.30 and bicarbonate <18mEq/L); and ketonemia. With Food and Drug Administration (FDA) approval of the sodium - glucose transporter 2 inhibitors (SGLT2i), DKA can occur with BG levels below 200mg/dl and has been defined as Euglycemic DKA (EuDKA). Due to the absence of hyperglycemia, the diagnosis of EuDKA is challenging and often delayed. This 60-year-old diabetic male, treated with Empagliflozin and pioglitazone, presented with diarrhea and abdominal pain, which started 20 days ago. He was admitted with dehydration and diagnosis of colitis. On admission laboratory evaluation revealed metabolic acidosis with elevated anion gap of 18mEq/L, bicarbonate of 19mEq/L, and BG of 146mg/dL. There was no history of ingestion of alcohol, salicylates, methanol, ethylene glycol and nothing to suggest lactic acidosis. The plasma creatinine was 0.79mg/dl. On the following day, he developed an increase in the anion gap to 22mEq/L and further decrease in bicarbonate to 13mEq/L, and serum ketones were detected. The patient was treated for EuDKA in ICU with intravenous insulin, dextrose (to prevent hypoglycemia), and normal saline with resolution of his symptoms and EuDKA in 3 days. With the widespread use of SGLT2i, physicians need to have a high suspicion of EuDKA in patients who present with an unexplained anion gap acidosis without or only modest elevation in BG concentration.

Presentation of mixed diabetic ketoacidosis and metabolic acidosis due to ileal neobladder reconstruction

2021 ◽  
Vol 14 (2) ◽  
pp. e223668
Author(s):  
Dileep Kumar ◽  
Muhammad Zubair Nasim ◽  
Bilal Ahmad Shoukat ◽  
Syed Shabahat Ali Shah
Keyword(s):  
Diabetes Mellitus ◽  
Metabolic Acidosis ◽  
Diabetic Ketoacidosis ◽  
Plasma Glucose ◽  
Blood Gas Analysis ◽  
Gas Analysis ◽  
Anion Gap ◽  
Metabolic Complications ◽  
Ileal Neobladder ◽  
History Of

Diabetic ketoacidosis (DKA) is one of the most serious acute metabolic complications of diabetes mellitus. It is characterised by the biochemical triad of hyperglycaemia, ketonemia/ketonuria, and an increased anion gap metabolic acidosis. In this case, a 40-year-old male patient presented to the emergency department, with vomiting, nausea, polydipsia, polyuria and weight loss. He was found to have an elevated plasma glucose, despite having no known history of diabetes mellitus. His medical history was significant for spina bifida and ileal neobladder reconstruction. The plasma glucose level was 38 mmol/L. Blood gas analysis showed normal anion gap metabolic acidosis with high chloride and low bicarbonate. His plasma ketone level was 4.5 mmol/L. No significant reason for hyperchloraemia was identified. On initiation of DKA regimen, his condition improved and serum ketones normalised. Due to persistent hyperchloraemic metabolic acidosis, bicarbonate infusion was administered and his metabolic acidosis resolved.

Metabolic Acidosis

2017 ◽  
Author(s):  
Lisa Cohen ◽  
Dipal Savla ◽  
Shuchi Anand
Keyword(s):  
Metabolic Acidosis ◽  
Lactic Acidosis ◽  
The Body ◽  
Anion Gap ◽  
Plasma Sodium ◽  
Toxic Substances ◽  
Disease States ◽  
Common Causes ◽  
Total Body ◽  
Renal Tubular

Metabolic acidosis is a common clinical entity that can arise from a variety of disease states, medications, and toxic ingestions. This review covers the pathophysiology, diagnosis, and management of common presentations of metabolic acidosis. We have differentiated various causes of metabolic acidosis based on the presence of a normal or elevated anion gap (AG), the sum of serum anions unaccounted for by the measurement of plasma sodium, bicarbonate, and chloride levels. Normal AG metabolic acidosis, or non-AG metabolic acidosis, arises when there is excessive loss of bicarbonate from the gastrointestinal tract or in the urine. This review covers the development and diagnosis of non-AG metabolic acidosis, including a discussion of the spectrum of renal tubular acidosis subtypes. The treatment of non-AG metabolic acidosis is reviewed. Metabolic acidosis with an elevated AG, also called AG metabolic acidosis, develops when exogenous or endogenous nonchloride acid accumulates in the body. The most common causes of AG metabolic acidosis are lactic acidosis and ketoacidosis from starvation, heavy alcohol intake, or diabetes with total body insulin depletion. Medications, toxic substances, and uremia can also lead to AG acidosis. The mechanisms and management of these causes of metabolic acidosis with high AG are covered in detail. Key words: anion-gap acidosis, diabetic ketoacidosis, lactic acidosis, non–anion gap acidosis

scholarly journals SUN-003 Very Restricted Carbohydrate (Ketogenic) Diet: A Rare Cause of a Recurrent Hypoglycemic-Euglycemic Diabetic Ketoacidosis in the Pregnancy

2020 ◽  
Vol 4 (Supplement_1) ◽  
Author(s):  
Marianna Yaron ◽  
Roy Shalit ◽  
Doron Kreiser ◽  
Tali Cukierman-Yaffe ◽  
Eduardo Israel ◽  
...  
Keyword(s):  
Metabolic Acidosis ◽  
Bulimia Nervosa ◽  
Ketogenic Diet ◽  
Dietary Habits ◽  
Brain Mri ◽  
Daily Intake ◽  
Fetal Brain ◽  
Carbohydrate Restriction ◽  
Diffuse Abdominal Pain ◽  
History Of

Abstract Introduction: Although potential risk of DKA, ketogenic diet became popular among T1DM patients as proven to reduce the incidence of hypoglycemia, glycemic variability, and HbA1c (1). Severe carbohydrate restriction had not been included among DKA precipitating factors in pregnancy since a minimum consumption of 175 g of carbohydrates a day is recommended for pregnant women by the IOM and ADA. Proband: A 35-year-old pregnant woman (G2P1 at 29 weeks’ gestation) was admitted to the ICU because of a 12-hour history of severe nausea, 4 vomiting episodes (stomach contain), weakness, and metabolic acidosis accompanied by low normal BG values for pregnancy. She had a history of bulimia nervosa since 15 years of age that was well-controlled by severe carbohydrate restriction prior to pregnancy, and T1DM since 19 years of age. Her pre-pregnancy carbohydrate daily intake was ~ 20–30 g and BMI 24.1 kg/m2. Good glycemic control was established before conception and continued until delivery. Upon admission, she was tachypneic and suffering from diffuse abdominal pain. Fetal monitoring and abdominal ultrasonography showed no significant changes, and the sonographic fetal weight was appropriate for gestational age. The laboratory results revealed metabolic acidosis pH 7.23, bicarbonate 11.7 mmol/L, anion gap 22.5, and BG 78 mg/dL. Lactate and salicylate blood levels were normal. The blood β-hydroxybutyrate was highly positive and the patient was diagnosed with euglycemic DKA. She was managed with a continuous intravenous insulin infusion and fluid and electrolytes repletion. The patient was discharged after three days of hospitalization only to return four days later because of the similar complaints with findings of blood β-hydroxybutyrate 7.7 mmol/L and BG levels of 61–65 mg/dL. Because of persistent ketonemia with low normal BG levels, patient was questioning about her dietary habits and revealed to maintain severe carbohydrate-restricted pre-conception eating manners. After repeated consultations by specialists for eating disorder, patient agreed to increase her carbohydrate intake to 120 gr per day. Fetal brain MRI, fetal heart and brain ultrasound were performed to evaluate potential negative effects of ketones, and all were found normal. No major malformations were observed in the newborn, and a normal growth pattern was observed at 5 months of age. Conclusion: This is the first report of a pregnant T1DM patient with long lasting bulimia nervosa excellently controlled by severe carbohydrate restriction prior pregnancy and occultly continued against medical advice through the pregnancy, causing repeatedly hypoglycemic-euglycemic DKA. References: 1. Schmidt S, Christensen MB, Serifovski N, et al. Low versus high carbohydrate diet in type 1 diabetes: A 12-week randomized open-label crossover study. Diabetes Obes Metab 2019; 21:1680- 1688

scholarly journals A Rare Case of Metformin Associated Lactic Acidosis in a Type 2 Diabetic Patient With No Known Contraindications for Metformin Prescription - a Diagnostic Conundrum!

2021 ◽  
Vol 5 (Supplement_1) ◽  
pp. A361-A362
Author(s):  
Rima Gandhi ◽  
Randa Abdelmasih ◽  
Alauddin El-Hag ◽  
Elis Cruz Salcedo
Keyword(s):  
Lactic Acid ◽  
Metabolic Acidosis ◽  
Lactic Acidosis ◽  
Diabetic Patient ◽  
Side Effect ◽  
Anion Gap ◽  
Type 2 Dm ◽  
History Of ◽  
Type 2 Diabetic

Abstract Introduction: Metformin is a biguanide drug primarily inhibits hepatic gluconeogenesis and improves insulin sensitivity. Lactic acidosis is a rare complication of metformin. The incidence of Metformin-associated lactic acidosis (MALA) is 6.3 per 100,000 patient-years. Metformin raises lactate levels by inhibiting the conversion of lactate and pyruvate into glucose, shunting towards anaerobic glycolysis. Although, MALA is a reported side effect, metformin is still identified as the drug of choice for Type 2 DM. Here we present a case of MALA in a Type 2 Diabetic patient to shed light on this controversial dilemma. Case Presentation: A 56-year-old African-American male with Type 2 DM and diabetic retinopathy presented after a fall and generalized weakness. Upon arrival, his blood sugar was 22 mg/dL. Patient was vitally stable with signs of dehydration. Home medications includes Metformin 1000 mg twice daily and Glipizide. Laboratory results showed an anion gap metabolic acidosis of 18 mmol/L, Lactic acid was 6.5 mmol/L with repeat of 7.6 mmol/L. Creatinine was 6.0 mg/dL with a BUN of 89 mg/dL. Baseline creatinine from 1 year prior was 1.3–1.5 mg/dL with GFR of 52 mL/min. Hemoglobin A1c was 5.9%. Sodium bicarbonate infusion in 5% dextrose in water. The patient clinically improved with closure of the anion gap and resolution of the metabolic acidosis. Metformin level was 10 mcg/mL. He was discharged on basal insulin and discontinued Metformin and Glipizide. Discussion: Metformin is the first line treatment of Type 2 DM due to its safety. The most common adverse events of Metformin include nausea, bloating, and diarrhea. MALA is a rare, yet serious side effect with a reported mortality of 45%. Higher mortality was associated with increased age, lower arterial pH, and need for mechanical ventilation and vasopressor medicationsThe following criteria should raise concern for MALA in patients with history of Metformin use; elevated lactate level, high anion gap, severe acidosis, low serum bicarbonate level and a history of renal insufficiency. Our patient met the above criteria. The treatment approach for MALA includes adequate supportive measures and correction of acidosis with the acceleration of lactic acid metabolism. Ultimately, if there is no improvement with the aforementioned strategies, then the next step is elimination of the offending agent by renal excretion or dialysis. Fortunately our patient improved with intravenous hydration and did not require advanced intervention. This case highlights the importance of the early recognition of MALA in a patient with unexplained anion gap acidosis and history of Metformin use as even with no risk factors, an episode of gastroenteritis can be enough to impair renal function which increases the risk of MALA. More importantly, it is crucial to educate patients to withhold Metformin in the setting of acute illness and volume contraction to prevent MALA.

scholarly journals High Anion Gap Metabolic Acidosis due to Euglycemic Diabetic Ketoacidosis Caused by Sodium-Glucose Co-transporter 2 inhibitor

2019 ◽  
Author(s):  
Awad Magbri ◽  
Eusera El-Magbri ◽  
Mariam El-Magbri ◽  
Brar Balhinder ◽  
Shauket Rashid
Keyword(s):  
Metabolic Acidosis ◽  
Vital Signs ◽  
Blood Gas Analysis ◽  
Gas Analysis ◽  
Anion Gap ◽  
Urine Ph ◽  
History Of ◽  
Lactate Levels ◽  
Breathing Room ◽  
Work Up

The case is that of 58 year-male with type 2 diabetes mellitusfor 7 years, hypertension, hypercholesterolemia, who was admittedto the hospital with left lower limb cellulitis over the past 8 days.On work-up he was found to have high anion-gap metabolic acidosis(AGMA) with anion gap of 25, his lactate levels were normal (Dand L-lactate). He denies overdosing with any medications and histoxicology screen for methanol, ethanol, aspirin, and ethylene glycolwere negative. He has no psychiatric history of note. He denies usingover the counter medications like acetaminophen. No bowel surgerycould be elicited. He felt dehydrated and nauseous but otherwisefine.His medications includes; carvedalol 25mg twice daily,hydrochlothiazide 25 mg daily, Lipitor 20 mg daily, insulin, aspirin81 mg daily, and was started on canagliflozoin 300 mg daily 4 weeksago to control his blood sugar level and A1C.Physical examination of the patient revealed, slightly dehydratedbut well-nourished man, his vital signs; heart rate of 78 BPM andregular, BP 143/85 mmHg, temperature 98.7 F, and his oxygensaturation while breathing room air was 92%. Examination of theheart, abdomen, and chest were unremarkable. He had left lower legcellulitis but no edema or tenderness.His work-up including chemistry-7 which showed sodium of142 mmol/L, potassium of 4.3 mmol/L, chloride of 102 mmol/L,bicarbonate of 13 mmol/L, BUN and creatinine of 18 mg/L and 0.78mg/L respectively. His blood glucose level was 178 mg/L with A1Cof 8.2. His serum osmolality was 312 mosm/L, and his arterial bloodpH was 7.2 with a carbon dioxide in blood gas analysis (Pco2) of32mmHg. His calculated anion gap was 25 given his normal albuminlevel. His investigation also showed positive ketones in the serumand urine. His urine PH was 5.5 and the urine contain &gt;800 mg ofglucose

scholarly journals Recurrent Encephalopathy and Severe Anion Gap Metabolic Acidosis in a Patient with Short Bowel: It Is D-Lactic Acidosis

2021 ◽  
pp. 92-96
Author(s):  
Avni Jain ◽  
Kiran Jhinger ◽  
Jonathon Bellas
Keyword(s):  
Metabolic Acidosis ◽  
Lactic Acidosis ◽  
Short Bowel Syndrome ◽  
Rare Condition ◽  
Acute Onset ◽  
Anion Gap ◽  
Short Bowel ◽  
Common Clinical Presentation ◽  
History Of ◽  
Carbohydrate Load

D-lactic acidosis is a rare and potentially underrecognized condition in patients with short bowel syndrome. We present the case of a 61-year-old female with a history of an ileojejunal bypass at age 18 who presented to hospital with acute-onset encephalopathy, ataxia, and severe anion gap metabolic acidosis (AGMA). On initial investigations there were no identifiable etiologies for the AGMA. Further history revealed that she had been experiencing these symptoms on a recurrent basis for the past 40 years. An oral carbohydrate load was given to the patient in hospital which reproduced her symptoms and the AGMA. A serum D-lactate level returned elevated several weeks later. A 2-month follow-up revealed that all her symptoms had ceased with limitation of carbohydrates to 150 g per day. Patients with short bowel syndrome are susceptible to developing D-lactic acidosis due to the large carbohydrate loads that are delivered to the colon, where they are then metabolized. Due to its rarity, it is likely that there is a delay in recognition of this condition. This case report describes a common clinical presentation of this rare condition and describes the pathophysiology, diagnosis, and management of D-lactic acidosis in small bowel syndrome.

Metabolic Acidosis

2017 ◽  
Author(s):  
Lisa Cohen ◽  
Dipal Savla ◽  
Shuchi Anand
Keyword(s):  
Metabolic Acidosis ◽  
Lactic Acidosis ◽  
The Body ◽  
Anion Gap ◽  
Plasma Sodium ◽  
Toxic Substances ◽  
Disease States ◽  
Common Causes ◽  
Total Body ◽  
Renal Tubular

Metabolic acidosis is a common clinical entity that can arise from a variety of disease states, medications, and toxic ingestions. This review covers the pathophysiology, diagnosis, and management of common presentations of metabolic acidosis. We have differentiated various causes of metabolic acidosis based on the presence of a normal or elevated anion gap (AG), the sum of serum anions unaccounted for by the measurement of plasma sodium, bicarbonate, and chloride levels. Normal AG metabolic acidosis, or non-AG metabolic acidosis, arises when there is excessive loss of bicarbonate from the gastrointestinal tract or in the urine. This review covers the development and diagnosis of non-AG metabolic acidosis, including a discussion of the spectrum of renal tubular acidosis subtypes. The treatment of non-AG metabolic acidosis is reviewed. Metabolic acidosis with an elevated AG, also called AG metabolic acidosis, develops when exogenous or endogenous nonchloride acid accumulates in the body. The most common causes of AG metabolic acidosis are lactic acidosis and ketoacidosis from starvation, heavy alcohol intake, or diabetes with total body insulin depletion. Medications, toxic substances, and uremia can also lead to AG acidosis. The mechanisms and management of these causes of metabolic acidosis with high AG are covered in detail. Key words: anion-gap acidosis, diabetic ketoacidosis, lactic acidosis, non–anion gap acidosis

scholarly journals Hipopara-Red, Real Life Experience in 322 Patients With Hypoparathyroidism

2020 ◽  
Vol 5 (2) ◽  
Author(s):  
María Belén Zanchetta ◽  
Damián Robbiani ◽  
Beatriz Oliveri ◽  
Evangelina Giacoia ◽  
Adriana Frigeri ◽  
...  
Keyword(s):  
Natural History ◽  
Clinical Management ◽  
Life Experience ◽  
Real Life ◽  
Clinical Complications ◽  
Common Causes ◽  
History Of ◽  
The Mean ◽  
Nonsurgical Patients

Abstract Context Hypoparathyroidism is a rare disease and, as such, its natural history, long-term complications, and correct clinical management remain unclear. Objective To describe the natural history and clinical characteristics of the disease. Design and Setting To present a retrospective observational analysis from 7 specialized centers in Buenos Aires, Argentina. Patients Chronic hypoparathyroid patients followed-up between 1985 and December 2018. Main Outcome Measures Data on demographics, etiology, clinical complications, biochemical parameters, dual-energy x-ray absorptiometry (DXA) values, and treatment doses were collected. Results A total of 322 subjects with chronic hypoparathyroidism were included; 85.7% were female, the mean age was 55.2 ± 16.8 years, and the mean age at diagnosis was 43.8 ± 16.8 years. Prevalence of surgical hypoparathyroidism was 90.7%, with the most common causes being thyroid carcinoma and benign thyroid disease. A history of hypocalcemia requiring hospitalization was present in 25.7% of the whole group and in 4.3% of patients who had a history of seizures. Overall, 40.9% of our patients had reported at least 1 neuromuscular symptom. Renal insufficiency was present in 22.4% of our patients and was significantly associated with age (P &lt; 0.0001). Hyperphosphatemia was present in 42% of patients. A history of severe hypocalcemia, paresthesias, tetany, ganglia calcifications, seizures, and cataracts was significantly higher in nonsurgical patients. Conclusion Although these patients were followed-up by experienced physicians, clinical management was heterogeneous and probably insufficient to assess all the potential complications of this chronic disease. Almost 70% of the study’s group of patients met the experts’ indications for considering the use of rhPTH 1–84. Being aware of this fact is the 1st step in improving our medical management of this disease in the future.

scholarly journals Transient 5-oxoprolinuria and high anion gap metabolic acidosis: clinical and biochemical findings in eleven subjects

1998 ◽  
Vol 44 (7) ◽  
pp. 1497-1503 ◽  
Author(s):  
James J Pitt ◽  
Simon Hauser
Keyword(s):  
Metabolic Acidosis ◽  
Organic Acids ◽  
Organic Acid ◽  
Clinical Features ◽  
Reference Range ◽  
Anion Gap ◽  
Urinary Organic Acid ◽  
Liver Glutathione ◽  
Liver Functions

Abstract We describe biochemical and clinical features of 11 subjects (ages, 1.2–84 years, nine females and two males) with transient 5-oxoprolinuria (0.6–23.6 mol/mol of creatinine, reference range &lt;0.07). A variety of conditions preceded the onset of acidosis, and all had taken acetaminophen (paracetamol), although in therapeutic amounts in most subjects. Metabolic acidosis was documented in nine subjects, and all had an increased anion gap and abnormal liver functions. 5-Oxoproline was the major urinary organic acid in five subjects, whereas the rest had more complex profiles comprising 5-oxoproline and other organic acids, such as lactate, 3-hydroxybutyrate, and 4-hydroxyphenyl lactate. The 5-oxoproline was predominantly of the l-configuration. One subject died during an acidotic episode, and the rest recovered with no apparent long-term ill effects. Urinary 5-oxoproline was within the reference range in six subjects that were re-tested after the anion gap normalized. These findings suggest that acetaminophen, in association with other unidentified factors, is involved in the development of this condition through a mechanism of depletion of liver glutathione stores.

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