Role of ascorbic acid in the treatment of methemoglobinemia

Sahu, Kamal Kant; Dhibar, Deba Prasad; Gautam, Archana; Kumar, Yogeesh; Varma, Subhash

doi:10.1016/j.tjem.2016.07.003

Cited by 31 publications

(18 citation statements)

References 3 publications

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“…Although the addition of sucrose could lead to protein stabilization , the amount of sugars that must be added may be sufficient to pose clinical problems for certain patients, such as diabetics . The addition of antioxidants, such as ascorbic acid , NADH , GSH , or dithionite , is also available for maintaining the non‐oxidation states of Hb. However, previously reported data have indicated that many of these antioxidants can be toxic at high doses , and some antioxidants like ascorbic acid and GSH even have prooxidant effects if the antioxidant concentration is not maintained within a proper range .…”

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confidence: 99%

Study on Oxidation Stability and Oxygen Affinity of Hemoglobin During Storage

Zhang

et al. 2018

Artificial Organs

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The factors affecting hemoglobin (Hb) oxidation in its short- and long-term storage were investigated. Porcine Hb with different levels of oxygen saturation was stored at 25°C or 4°C for 40 days. The methemoglobin (metHb) content increased rapidly when Hb was at half saturation with oxygen at 4°C, increased gradually with the increase in Hb oxygenation or deoxygenation, and was almost unchanged when Hb was highly oxygenated or deoxygenated. The Hb oxidation was more intense when stored at 25°C. This indicated that highly oxygenated or deoxygenated Hb can be stored short term at 4°C. The accelerated test showed that metHb content was almost unchanged when Hb was highly deoxygenated and stored at 37°C for 7 days; however, the metHb content rapidly increased when Hb was highly oxygenated and stored at 37°C, which indicated that only highly deoxygenated Hb is suitable for long-term storage. Then, the long-term oxidation stability of highly deoxygenated Hb and polymerized hemoglobin was verified; the metHb content of both did not show significant changes at 4°C for 18 months. Moreover, the results in this work indicated that a temperature increasing from 20 to 40°C clearly increased the partial oxygen pressure (P50), which represents decreased oxygen affinity and is beneficial to deoxygenation. Furthermore, P50 was increased when the pH decreased from 9 to 7. Therefore, we concluded that the appropriate high temperature and neutral condition in vitro are conducive to reducing the oxygen affinity of Hb to achieve efficient deoxygenation, which could promote the development of hemoglobin-based oxygen carriers.

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confidence: 99%

Study on Oxidation Stability and Oxygen Affinity of Hemoglobin During Storage

Zhang

et al. 2018

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“…Since the methemoglobin levels in our patient is less than 20% and as the patient the patient was asymptomatic we used ascorbic acid to treat our patient. Moreover ascorbic acid is an alternative treatment in Methemoglobinemia as it has got no major side effects [6][7][8].…”

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confidence: 99%

Management of Herbicide Induced Methemoglobinemia

Sudheer¹,

Krishnapriya²,

Kumar³

et al. 2018

J Drug Metab Toxicol

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Methemoglobinemia is an altered state of haemoglobin that leads to impaired oxygen delivery to the body tissues. Deliberate ingestion of certain herbicides may lead to this condition. Modern herbicides are often synthetic mimics of natural plant hormones that interfere with growth of the target plants. These modern herbicides act by various mechanisms some of them being Acetyl co-enzyme A carboxylase inhibition, aceto lactate synthase inhibition, photosystem II inhibition, 4-hydroxy phenyl pyruvate dioxygenase inhibition and so on. We report a case of Methemoglobinemia after deliberate ingestion of an herbicide marketed to be safe and containing only biological extracts and filters. The patient was treated with ascorbic acid successfully. Our paper emphasizes the use of ascorbic acid as an alternative method in the treatment of Methemoglobinemia. Ascorbic acid is the main stay of treatment in patients with G6PD deficiency.

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“…The dosages and duration of treatment vary widely across these cases ranging from 1 g ascorbic acid as a one-time dose [reportedly lowering the patient's methemoglobin level from 26.2% to 2.1% within 6 h of dosing] [22] to high-dose 10 g ascorbic acid every 6 h [22]. Dosing recommendations from four case reports of successful resolution of methemoglobinemia using only vitamin C have been outlined in a 2016 review by Sahu et al [23]. See Fig.…”

Section: Management Of Methemoglobinemiamentioning

confidence: 99%

Methemoglobinemia in the Operating Room and Intensive Care Unit: Early Recognition, Pathophysiology, and Management

et al. 2020

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The objectives of this review are to describe the acquired and hereditary causes of methemoglobinemia, to recommend the most sensitive diagnostic tests, and to enable critical care clinicians to rapidly detect and treat methemoglobinemia. To meet these objectives, Internet search engines were queried with the keywords to select articles for review that included case reports, case series, observational, longitudinal, and surveillance studies. The most common causes of methemoglobinemia include oxidizing reactions to cocaine-derived anesthetics, such as benzocaine and lidocaine, to antibiotics, such as dapsone and other sulfonamides, and to gases, such as nitric oxide. Additionally, CO-oximetry is superior to standard pulse oximetry in detecting methemoglobinemia. Finally, effective treatments for methemoglobinemia include intravenous administration of methylene blue, ascorbic acid, and riboflavin. In this manuscript we will discuss methemoglobinemia, how it occurs, and how to treat it.

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Role of ascorbic acid in the treatment of methemoglobinemia

Cited by 31 publications

References 3 publications

Study on Oxidation Stability and Oxygen Affinity of Hemoglobin During Storage

Study on Oxidation Stability and Oxygen Affinity of Hemoglobin During Storage

Management of Herbicide Induced Methemoglobinemia

Methemoglobinemia in the Operating Room and Intensive Care Unit: Early Recognition, Pathophysiology, and Management

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