The Experts below are selected from a list of 44805 Experts worldwide ranked by ideXlab platform
Moses Elisaf - One of the best experts on this subject based on the ideXlab platform.
-
Pharmacologically-Induced Metabolic Acidosis
Drug Safety, 2010Co-Authors: George Liamis, Haralampos J. Milionis, Moses ElisafAbstract:Metabolic Acidosis may occasionally develop in the course of treatment with drugs used in everyday clinical practice, as well as with the exposure to certain chemicals. Drug-induced Metabolic Acidosis, although usually mild, may well be life-threatening, as in cases of lactic Acidosis complicating antiretroviral therapy or treatment with biguanides. Therefore, a detailed medical history, with special attention to the recent use of culprit medications, is essential in patients with acid-base derangements. Effective clinical management can be handled through awareness of the adverse effect of certain pharmaceutical compounds on the acid-base status. In this review, we evaluate relevant literature with regard to Metabolic Acidosis associated with specific drug treatment, and discuss the clinical setting and underlying pathophysiological mechanisms. These mechanisms involve renal inability to excrete the dietaryH^+ load (including types I and IV renal tubular acidoses), Metabolic Acidosis owing to increased H^+ load (including lactic Acidosis, ketoAcidosis, ingestion of various substances, administration of hyperalimentation solutions and massive rhabdomyolysis) and Metabolic Acidosis due to HCO_3 ^− loss (including gastrointestinal loss and type II renal tubular Acidosis). Determinations of arterial blood gases, the serum anion gap and, in some circumstances, the serum osmolar gap are helpful in delineating the pathogenesis of the acid-base disorder. In all cases of drug-related Metabolic Acidosis, discontinuation of the culprit medications and avoidance of readministration is advised.
-
Pharmacologically-Induced Metabolic Acidosis
Drug Safety, 2010Co-Authors: George Liamis, Haralampos J. Milionis, Moses ElisafAbstract:Metabolic Acidosis may occasionally develop in the course of treatment with drugs used in everyday clinical practice, as well as with the exposure to certain chemicals. Drug-induced Metabolic Acidosis, although usually mild, may well be life-threatening, as in cases of lactic Acidosis complicating antiretroviral therapy or treatment with biguanides. Therefore, a detailed medical history, with special attention to the recent use of culprit medications, is essential in patients with acid-base derangements. Effective clinical management can be handled through awareness of the adverse effect of certain pharmaceutical compounds on the acid-base status. In this review, we evaluate relevant literature with regard to Metabolic Acidosis associated with specific drug treatment, and discuss the clinical setting and underlying pathophysiological mechanisms. These mechanisms involve renal inability to excrete the dietaryH^+ load (including types I and IV renal tubular acidoses), Metabolic Acidosis owing to increased H^+ load (including lactic Acidosis, ketoAcidosis, ingestion of various substances, administration of hyperalimentation solutions and massive rhabdomyolysis) and Metabolic Acidosis due to HCO_3 ^− loss (including gastrointestinal loss and type II renal tubular Acidosis). Determinations of arterial blood gases, the serum anion gap and, in some circumstances, the serum osmolar gap are helpful in delineating the pathogenesis of the acid-base disorder. In all cases of drug-related Metabolic Acidosis, discontinuation of the culprit medications and avoidance of readministration is advised.
-
Pharmacologically-Induced Metabolic Acidosis A Review
Drug safety, 2010Co-Authors: George Liamis, Haralampos J. Milionis, Moses ElisafAbstract:Metabolic Acidosis may occasionally develop in the course of treatment with drugs used in everyday clinical practice, as well as with the exposure to certain chemicals. Drug-induced Metabolic Acidosis, although usually mild, may well be life-threatening, as in cases of lactic Acidosis complicating antiretroviral therapy or treatment with biguanides. Therefore, a detailed medical history, with special attention to the recent use of culprit medications, is essential in patients with acid-base derangements. Effective clinical management can be handled through awareness of the adverse effect of certain pharmaceutical compounds on the acid-base status. In this review, we evaluate relevant literature with regard to Metabolic Acidosis associated with specific drug treatment, and discuss the clinical setting and underlying pathophysiological mechanisms. These mechanisms involve renal inability to excrete the dietary H+ load (including types I and IV renal tubular acidoses), Metabolic Acidosis owing to increased H+ load (including lactic Acidosis, ketoAcidosis, ingestion of various substances, administration of hyperalimentation solutions and massive rhabdomyolysis) and Metabolic Acidosis due to HCO3- loss (including gastrointestinal loss and type II renal tubular Acidosis). Determinations of arterial blood gases, the serum anion gap and, in some circumstances, the serum osmolar gap are helpful in delineating the pathogenesis of the acid-base disorder. In all cases of drug-related Metabolic Acidosis, discontinuation of the culprit medications and avoidance of readministration is advised.
George Liamis - One of the best experts on this subject based on the ideXlab platform.
-
Pharmacologically-Induced Metabolic Acidosis
Drug Safety, 2010Co-Authors: George Liamis, Haralampos J. Milionis, Moses ElisafAbstract:Metabolic Acidosis may occasionally develop in the course of treatment with drugs used in everyday clinical practice, as well as with the exposure to certain chemicals. Drug-induced Metabolic Acidosis, although usually mild, may well be life-threatening, as in cases of lactic Acidosis complicating antiretroviral therapy or treatment with biguanides. Therefore, a detailed medical history, with special attention to the recent use of culprit medications, is essential in patients with acid-base derangements. Effective clinical management can be handled through awareness of the adverse effect of certain pharmaceutical compounds on the acid-base status. In this review, we evaluate relevant literature with regard to Metabolic Acidosis associated with specific drug treatment, and discuss the clinical setting and underlying pathophysiological mechanisms. These mechanisms involve renal inability to excrete the dietaryH^+ load (including types I and IV renal tubular acidoses), Metabolic Acidosis owing to increased H^+ load (including lactic Acidosis, ketoAcidosis, ingestion of various substances, administration of hyperalimentation solutions and massive rhabdomyolysis) and Metabolic Acidosis due to HCO_3 ^− loss (including gastrointestinal loss and type II renal tubular Acidosis). Determinations of arterial blood gases, the serum anion gap and, in some circumstances, the serum osmolar gap are helpful in delineating the pathogenesis of the acid-base disorder. In all cases of drug-related Metabolic Acidosis, discontinuation of the culprit medications and avoidance of readministration is advised.
-
Pharmacologically-Induced Metabolic Acidosis
Drug Safety, 2010Co-Authors: George Liamis, Haralampos J. Milionis, Moses ElisafAbstract:Metabolic Acidosis may occasionally develop in the course of treatment with drugs used in everyday clinical practice, as well as with the exposure to certain chemicals. Drug-induced Metabolic Acidosis, although usually mild, may well be life-threatening, as in cases of lactic Acidosis complicating antiretroviral therapy or treatment with biguanides. Therefore, a detailed medical history, with special attention to the recent use of culprit medications, is essential in patients with acid-base derangements. Effective clinical management can be handled through awareness of the adverse effect of certain pharmaceutical compounds on the acid-base status. In this review, we evaluate relevant literature with regard to Metabolic Acidosis associated with specific drug treatment, and discuss the clinical setting and underlying pathophysiological mechanisms. These mechanisms involve renal inability to excrete the dietaryH^+ load (including types I and IV renal tubular acidoses), Metabolic Acidosis owing to increased H^+ load (including lactic Acidosis, ketoAcidosis, ingestion of various substances, administration of hyperalimentation solutions and massive rhabdomyolysis) and Metabolic Acidosis due to HCO_3 ^− loss (including gastrointestinal loss and type II renal tubular Acidosis). Determinations of arterial blood gases, the serum anion gap and, in some circumstances, the serum osmolar gap are helpful in delineating the pathogenesis of the acid-base disorder. In all cases of drug-related Metabolic Acidosis, discontinuation of the culprit medications and avoidance of readministration is advised.
-
Pharmacologically-Induced Metabolic Acidosis A Review
Drug safety, 2010Co-Authors: George Liamis, Haralampos J. Milionis, Moses ElisafAbstract:Metabolic Acidosis may occasionally develop in the course of treatment with drugs used in everyday clinical practice, as well as with the exposure to certain chemicals. Drug-induced Metabolic Acidosis, although usually mild, may well be life-threatening, as in cases of lactic Acidosis complicating antiretroviral therapy or treatment with biguanides. Therefore, a detailed medical history, with special attention to the recent use of culprit medications, is essential in patients with acid-base derangements. Effective clinical management can be handled through awareness of the adverse effect of certain pharmaceutical compounds on the acid-base status. In this review, we evaluate relevant literature with regard to Metabolic Acidosis associated with specific drug treatment, and discuss the clinical setting and underlying pathophysiological mechanisms. These mechanisms involve renal inability to excrete the dietary H+ load (including types I and IV renal tubular acidoses), Metabolic Acidosis owing to increased H+ load (including lactic Acidosis, ketoAcidosis, ingestion of various substances, administration of hyperalimentation solutions and massive rhabdomyolysis) and Metabolic Acidosis due to HCO3- loss (including gastrointestinal loss and type II renal tubular Acidosis). Determinations of arterial blood gases, the serum anion gap and, in some circumstances, the serum osmolar gap are helpful in delineating the pathogenesis of the acid-base disorder. In all cases of drug-related Metabolic Acidosis, discontinuation of the culprit medications and avoidance of readministration is advised.
Haralampos J. Milionis - One of the best experts on this subject based on the ideXlab platform.
-
Pharmacologically-Induced Metabolic Acidosis
Drug Safety, 2010Co-Authors: George Liamis, Haralampos J. Milionis, Moses ElisafAbstract:Metabolic Acidosis may occasionally develop in the course of treatment with drugs used in everyday clinical practice, as well as with the exposure to certain chemicals. Drug-induced Metabolic Acidosis, although usually mild, may well be life-threatening, as in cases of lactic Acidosis complicating antiretroviral therapy or treatment with biguanides. Therefore, a detailed medical history, with special attention to the recent use of culprit medications, is essential in patients with acid-base derangements. Effective clinical management can be handled through awareness of the adverse effect of certain pharmaceutical compounds on the acid-base status. In this review, we evaluate relevant literature with regard to Metabolic Acidosis associated with specific drug treatment, and discuss the clinical setting and underlying pathophysiological mechanisms. These mechanisms involve renal inability to excrete the dietaryH^+ load (including types I and IV renal tubular acidoses), Metabolic Acidosis owing to increased H^+ load (including lactic Acidosis, ketoAcidosis, ingestion of various substances, administration of hyperalimentation solutions and massive rhabdomyolysis) and Metabolic Acidosis due to HCO_3 ^− loss (including gastrointestinal loss and type II renal tubular Acidosis). Determinations of arterial blood gases, the serum anion gap and, in some circumstances, the serum osmolar gap are helpful in delineating the pathogenesis of the acid-base disorder. In all cases of drug-related Metabolic Acidosis, discontinuation of the culprit medications and avoidance of readministration is advised.
-
Pharmacologically-Induced Metabolic Acidosis
Drug Safety, 2010Co-Authors: George Liamis, Haralampos J. Milionis, Moses ElisafAbstract:Metabolic Acidosis may occasionally develop in the course of treatment with drugs used in everyday clinical practice, as well as with the exposure to certain chemicals. Drug-induced Metabolic Acidosis, although usually mild, may well be life-threatening, as in cases of lactic Acidosis complicating antiretroviral therapy or treatment with biguanides. Therefore, a detailed medical history, with special attention to the recent use of culprit medications, is essential in patients with acid-base derangements. Effective clinical management can be handled through awareness of the adverse effect of certain pharmaceutical compounds on the acid-base status. In this review, we evaluate relevant literature with regard to Metabolic Acidosis associated with specific drug treatment, and discuss the clinical setting and underlying pathophysiological mechanisms. These mechanisms involve renal inability to excrete the dietaryH^+ load (including types I and IV renal tubular acidoses), Metabolic Acidosis owing to increased H^+ load (including lactic Acidosis, ketoAcidosis, ingestion of various substances, administration of hyperalimentation solutions and massive rhabdomyolysis) and Metabolic Acidosis due to HCO_3 ^− loss (including gastrointestinal loss and type II renal tubular Acidosis). Determinations of arterial blood gases, the serum anion gap and, in some circumstances, the serum osmolar gap are helpful in delineating the pathogenesis of the acid-base disorder. In all cases of drug-related Metabolic Acidosis, discontinuation of the culprit medications and avoidance of readministration is advised.
-
Pharmacologically-Induced Metabolic Acidosis A Review
Drug safety, 2010Co-Authors: George Liamis, Haralampos J. Milionis, Moses ElisafAbstract:Metabolic Acidosis may occasionally develop in the course of treatment with drugs used in everyday clinical practice, as well as with the exposure to certain chemicals. Drug-induced Metabolic Acidosis, although usually mild, may well be life-threatening, as in cases of lactic Acidosis complicating antiretroviral therapy or treatment with biguanides. Therefore, a detailed medical history, with special attention to the recent use of culprit medications, is essential in patients with acid-base derangements. Effective clinical management can be handled through awareness of the adverse effect of certain pharmaceutical compounds on the acid-base status. In this review, we evaluate relevant literature with regard to Metabolic Acidosis associated with specific drug treatment, and discuss the clinical setting and underlying pathophysiological mechanisms. These mechanisms involve renal inability to excrete the dietary H+ load (including types I and IV renal tubular acidoses), Metabolic Acidosis owing to increased H+ load (including lactic Acidosis, ketoAcidosis, ingestion of various substances, administration of hyperalimentation solutions and massive rhabdomyolysis) and Metabolic Acidosis due to HCO3- loss (including gastrointestinal loss and type II renal tubular Acidosis). Determinations of arterial blood gases, the serum anion gap and, in some circumstances, the serum osmolar gap are helpful in delineating the pathogenesis of the acid-base disorder. In all cases of drug-related Metabolic Acidosis, discontinuation of the culprit medications and avoidance of readministration is advised.
Nuno Ribeiro Ferreira - One of the best experts on this subject based on the ideXlab platform.
-
Metabolic Acidosis Due To Pyroglutamic Acid.
European Journal of Case Reports in Internal Medicine, 2018Co-Authors: M.j. Serpa, Luís Falcão, Susana Franco, Diana Repolho, Nuno Ribeiro FerreiraAbstract:Metabolic Acidosis is a common clinical disturbance due to increased plasma acidity caused by a primary decrease in serum HCO3- concentration. It is classified as normal or high anion gap Metabolic Acidosis. High anion gap Metabolic Acidosis can result from either a decrease in unmeasured cations (K+, Ca2+, Mg2+) or an increase in unmeasured anions (PO43−, albumin). However, other anions such as lactic acid or keto acids may cause this acid-base disorder. It can also result from renal failure and intoxication (salicylate, methanol, ethylene glycol), or more rarely, from massive rhabdomyolysis and pyroglutamic (5-oxoproline) acidemia. Acidemia due to pyroglutamic acid should be considered when no other aetiology is found. High anion gap Metabolic Acidosis is diagnosed in children with inherited defects in enzymes of the γ-glutamyl cycle. In adults, this disorder from pyroglutamic acid has been described in association with chronic acetaminophen misuse. We report a case of pyroglutamic Acidosis in a woman with acute misuse of acetaminophen concurrent with chronic use. LEARNING POINT Paracetamol is an easily available drug with potentially harmful consequences. Accumulation of pyroglutamic acid (5-oxoproline) may be a cause of high anion gap Metabolic Acidosis. Reporting cases of 5-oxoprolinemia Acidosis contributes to better understanding of the condition. Keywords: High anion gap Metabolic Acidosis, 5-oxoprolinemia, pyroglutamic acidemia, acetaminophen, paracetamol CASE DESCRIPTION A 55-year-old woman was brought to the emergency department after ingestion of more than 10 g of acetaminophen the same day, with little relief of pain. The patient had a 12-year history of breast cancer treated with chemotherapy and radiotherapy, with chronic pain from bone metastasis diagnosed the year previously (rib cage, sacroiliac joint and pubic bone). Her medications included hormones, opioids and non-prescribed analgesics. On examination, the patient was alert, her blood pressure was 156/80 mmHg, her temperature was 36oC, and she was tachycardic (120 beats per minute) and short of breath (respiratory rate of 40 per minute, with 98% oxygen saturation on room air). The remaining physical examination was unremarkable except for cachexia. The results of her initial laboratory evaluation were: severe Metabolic Acidosis (pH 7.15, pCO2 10 mmHg, pO2 112 mmHg, bicarbonate 3.5 mmol/l, lactate 7 mg/dl (reference range 4.5–18 mg/dl)) in arterial blood gas; creatinine 2.15 mg/dl, sodium 138 mmol/l, potassium 5.2 mmol/l, chloride 104 mmol/l, ionized calcium 8.2 mg/dl, phosphate 2.6 mg/dl, magnesium 2.1 mg/dl, albumin 3 mg/dl, anion gap 40 mmol/l; aspartate aminotransferase 66 U/l, alanine aminotransferase 69 U/l, alkaline phosphatase 120 U/l, γ-glutamyl transferase 160 U/l and total bilirubin 0.19 mg/dl, with no coagulation abnormalities. Lactate dehydrogenase was 356 U/l and CK was normal (rhabdomyolysis was excluded). The acetaminophen concentration was 103.4 mg/l. Ethanol, salicylate and beta-hydroxybutyrate levels were undetectable. The N-acetylcysteine protocol was initiated as well as intravenous fluids with sodium bicarbonate. Two hours after admission and initial treatment, the patient deteriorated with worsened Kussmaul breathing, a respiratory rate of 44 per minute, arterial blood gas with decreased bicarbonate (3 mmol/l) and pCO2 9 mmHg, lactate 13 mg/dl despite medical treatment. The patient required mechanical ventilation and was admitted to the ICU. She was started on hydration, bicarbonate and N-acetylcysteine. The patient improved over the following days and was extubated. Her transaminase levels and renal function had returned to normal by the third day, which obviated the need for dialysis. Her pH normalized, the anion gap reduced to 13 mmol/l and the acetaminophen level decreased to 37 mg/l. The diagnosis of high anion gap Metabolic Acidosis secondary to 5-oxoprolinemia (pyroglutamic acidemia) was considered due to the lack of any other unifying diagnosis. An anion gap of 40 mmol/l clearly indicates the presence of an organic acid, while the absence of lactic, keto and other acids suggested accumulation of 5-oxoproline as an explanation for the severe Acidosis.
-
Metabolic Acidosis Due To Pyroglutamic Acid
SMC MEDIA SRL, 2018Co-Authors: M.j. Serpa, Luís Falcão, Susana Franco, Diana Repolho, Nuno Ribeiro FerreiraAbstract:Metabolic Acidosis is a common clinical disturbance due to increased plasma acidity caused by a primary decrease in serum HCO3- concentration. It is classified as normal or high anion gap Metabolic Acidosis. High anion gap Metabolic Acidosis can result from either a decrease in unmeasured cations (K+, Ca2+, Mg2+) or an increase in unmeasured anions (PO43-, albumin). However, other anions such as lactic acid or keto acids may cause this acid-base disorder. It can also result from renal failure and intoxication (salicylate, methanol, ethylene glycol), or more rarely, from massive rhabdomyolysis and pyroglutamic (5-oxoproline) acidemia. Acidemia due to pyroglutamic acid should be considered when no other aetiology is found. High anion gap Metabolic Acidosis is diagnosed in children with inherited defects in enzymes of the γ-glutamyl cycle. In adults, this disorder from pyroglutamic acid has been described in association with chronic acetaminophen misuse. We report a case of pyroglutamic Acidosis in a woman with acute misuse of acetaminophen concurrent with chronic use.
Bryan S. Judge - One of the best experts on this subject based on the ideXlab platform.
-
Differentiating the causes of Metabolic Acidosis in the poisoned patient.
Clinics in laboratory medicine, 2006Co-Authors: Bryan S. JudgeAbstract:Numerous drugs and toxins may induce the development of a Metabolic Acidosis. The treating physician should be cognizant of the many compounds that can produce Metabolic Acidosis following an overdose or an accidental exposure, or with therapeutic use. Knowledge and comprehension of the substances associated with Metabolic Acidosis will facilitate the diagnosis and treatment of poisoned patients.
-
Metabolic Acidosis: differentiating the causes in the poisoned patient.
The Medical clinics of North America, 2005Co-Authors: Bryan S. JudgeAbstract:Metabolic Acidosis may arise from several drugs and toxins through a variety of mechanisms. Differentiating the causes of Metabolic Acidosis in the poisoned patient is an indispensable skill in clinical practice. Comprehension of toxin-induced Metabolic Acidosis, combined with a thorough history, physical examination, appropriate use of laboratory tests, and a stepwise approach, should aid the clinician in determining the cause of Metabolic Acidosis in the poisoned patient. When confronted with such a patient, it is imperative that one administer appropriate antidotal therapy, when necessary, and provide the patient with exceptional supportive care.