Database : MEDLINE
Search on : Methemoglobinemia [Words]
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[PMID]: 29523272
[Au] Autor:Bahadoran Z; Mirmiran P; Azizi F; Ghasemi A
[Ad] Address:Nutrition and Endocrine Research Center, Research Institute for Endocrine Sciences, Shahid Beheshti University of Medical Sciences, Tehran, Iran. Electronic address: z.bahadoran@endocrine.ac.ir.
[Ti] Title:Nitrate-rich dietary supplementation during pregnancy: The pros and cons.
[So] Source:Pregnancy Hypertens;11:44-46, 2018 Jan.
[Is] ISSN:2210-7797
[Cp] Country of publication:Netherlands
[La] Language:eng
[Ab] Abstract:Inorganic nitrate (NO ) due to its potential endogenous conversion to nitric oxide (NO), is suggested as a compensatory fuel for disrupted NO pathways in the case of pathological stats during pregnancy. Dietary NO -rich supplement in the NO-deficient pregnant women is now suggested as a more appealing choice with fewer off-target effects which can attenuate hypertension and preeclampsia, improve placental blood flow and subsequently enhance maternal and neonatal health. There is also an increasing public interest and common health claims regarding beneficial effects of NO -rich dietary supplements like beetroot byproducts in pregnant women. Conversely, NO -rich dietary supplementation during pregnancy may be accompanied with a wide range of unexpected maternal and fatal adverse outcomes such as methemoglobinemia, alteration in embryonic cells and malignant transformation, as well as thyroid disorders. In conclusion, use of dietary inorganic NO as a common supplement during pregnancy is currently on a long way from bench to bedside.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:In-Process

  2 / 3050 MEDLINE  
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[PMID]: 29522394
[Au] Autor:Raiker R; Lippert WC; Chadha R
[Ad] Address:Junior Resident, Department of Internal Medicine, University of Kentucky Medical Center, Lexington, KY, USA.
[Ti] Title:Methemoglobinemia in an HIV patient.
[So] Source:Cleve Clin J Med;85(3):186-187, 2018 Mar.
[Is] ISSN:1939-2869
[Cp] Country of publication:United States
[La] Language:eng
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180309
[Lr] Last revision date:180309
[St] Status:In-Data-Review
[do] DOI:10.3949/ccjm.85a.17004

  3 / 3050 MEDLINE  
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[PMID]: 29519718
[Au] Autor:Faust AC; Guy E; Baby N; Ortegon A
[Ad] Address:Texas Health Presbyterian Hospital Dallas, Department of Pharmacy, Dallas, Texas.
[Ti] Title:Local Anesthetic-Induced Methemoglobinemia During Pregnancy: A Case Report and Evaluation of Treatment Options.
[So] Source:J Emerg Med;, 2018 Mar 05.
[Is] ISSN:0736-4679
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:BACKGROUND: Methemoglobinemia is a well-recognized adverse drug reaction related to the use of certain local anesthetic agents. The mainstay of treatment for methemoglobinemia is i.v. methylene blue, along with provision of supplemental oxygen; however, methylene blue is listed as a category X teratogen. This poses an issue should methemoglobinemia develop during pregnancy. CASE REPORT: A 35-year-old, 20-week and 5-day gravid female was transferred from an outpatient oral surgeon's office for hypoxia. She was undergoing extraction of 28 teeth and was administered an unknown, but "large" quantity of prilocaine during the procedure. Given this exposure, the concern was for methemoglobinemia. This was confirmed with co-oximetry, which showed 34.7% methemoglobin. The initial treatment plan was methylene blue; however, this drug is a category X teratogen. Thus, an interdisciplinary team deliberated and decided on treatment with high-dose ascorbic acid and transfusion of a single unit of packed red blood cells. The patient was managed with noninvasive ventilation strategies and a total of 8 g ascorbic acid. She was discharged on hospital day 3 with no obstetric issues noted. WHY SHOULD AN EMERGENCY PHYSICIAN BE AWARE OF THIS?: Intravenous ascorbic acid appears to be a potential alternative to methylene blue in this patient population. The data surrounding teratogenicity of methylene blue are mostly related to intra-amniotic or intra-uterine administration. In life-threatening cases of methemoglobinemia during pregnancy, the benefits of i.v. methylene blue may outweigh the risks.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180309
[Lr] Last revision date:180309
[St] Status:Publisher

  4 / 3050 MEDLINE  
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[PMID]: 29513738
[Au] Autor:Bickler MP; Rhodes LJ
[Ad] Address:Department of Anesthesia and Perioperative Care, Hypoxia Research Laboratory, University of California, San Francisco, California, United States of America.
[Ti] Title:Accuracy of detection of carboxyhemoglobin and methemoglobin in human and bovine blood with an inexpensive, pocket-size infrared scanner.
[So] Source:PLoS One;13(3):e0193891, 2018.
[Is] ISSN:1932-6203
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Detecting life-threatening common dyshemoglobins such as carboxyhemoglobin (COHb, resulting from carbon monoxide poisoning) or methemoglobin (MetHb, caused by exposure to nitrates) typically requires a laboratory CO-oximeter. Because of cost, these spectrophotometer-based instrument are often inaccessible in resource-poor settings. The aim of this study was to determine if an inexpensive pocket infrared spectrometer and smartphone (SCiO®Pocket Molecular Sensor, Consumer Physics Ltd., Israel) accurately detects COHb and MetHb in single drops of blood. COHb was created by adding carbon monoxide gas to syringes of heparinized blood human or cow blood. In separate syringes, MetHb was produced by addition of sodium nitrite solution. After incubation and mixing, fractional concentrations of COHb or MetHb were measured using a Radiometer ABL-90 Flex® CO-oximeter. Fifty microliters of the sample were then placed on a microscope slide, a cover slip applied and scanned with the SCiO spectrometer. The spectrograms were used to create simple linear models predicting [COHb] or [MetHb] based on spectrogram maxima, minima and isobestic wavelengths. Our model predicted clinically significant carbon monoxide poisoning (COHb ≥15%) with a sensitivity of 93% and specificity of 88% (regression r2 = 0.63, slope P<0.0001), with a mean bias of 0.11% and an RMS error of 21%. Methemoglobinemia severe enough to cause symptoms (>20% MetHb) was detected with a sensitivity of 100% and specificity of 71% (regression r2 = 0.92, slope P<0.001) mean bias 2.7% and RMS error 21%. Although not as precise as a laboratory CO-oximeter, an inexpensive pocket-sized infrared scanner/smartphone detects >15% COHb or >20% MetHb on a single drop of blood with enough accuracy to be useful as an initial clinical screening. The SCiO and similar relatively low cost spectrometers could be developed as inexpensive diagnostic tools for developing countries.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180307
[Lr] Last revision date:180307
[St] Status:In-Data-Review
[do] DOI:10.1371/journal.pone.0193891

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[PMID]: 29482478
[Au] Autor:Kedar PS; Gupta V; Warang P; Chiddarwar A; Madkaikar M
[Ad] Address:a National Institute of Immunohematology , Indian Council of Medical Research , Mumbai , India.
[Ti] Title:Novel mutation (R192C) in CYB5R3 gene causing NADH-cytochrome b5 reductase deficiency in eight Indian patients associated with autosomal recessive congenital methemoglobinemia type-I.
[So] Source:Hematology;:1-7, 2018 Feb 27.
[Is] ISSN:1607-8454
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:OBJECTIVE: To investigate the cause of recessive congenital methemoglobinemia (RCM) in Indian families and to identify molecular defect associated with RCM. METHODS: Eight cases of RCM have been addressed to our laboratory in order to investigate the cause of cyanosis associated with genetic disorders. NADH-cytochrome b5 reductase (cytb5r) enzyme activities were measured by standard methods, and molecular analysis was performed by polymerase chain reaction (PCR) followed by DNA sequencing. The interpretation of mutation effect and the molecular modeling were performed by using specific software DEEP VIEW SWISS-PDB VIEWER and Pymol molecular graphics program. RESULTS AND DISCUSSION: Eight index cases from four unrelated families were referred for the cause of cyanosis. All patients showed mild to moderate cyanosis without mental retardation or any neurologic abnormalities. The methemoglobin levels were in the range of 11.5-22.41% with 50-70% reduction in CYTB5R activity. Spectroscopic analysis of the hemolysate showed normal peaks suggesting the absence of Hb-M. Molecular characterization showed a novel homozygous mutation p.Arg192Cys in CYB5R3 gene is an evolutionarily conserved position located in exon 7 in all eight index cases. The substitution of Cys is located on the interface of two domains of NADH-binding domain and is close proximity to the adenosine moiety would preclude the reciprocal ionic interaction (salt bridge) between Arg192 and Ile97 and may influence binding of the NADH coenzyme is hypothesized to cause disruption of hydrogen bonding and instability. Our study indicated that novel homozygous mutation p.Arg192Cys in CYB5R3 gene present in eight cases and the possibility of high prevalence of heterozygous in Indian population causing Type I RCM.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1802
[Cu] Class update date: 180227
[Lr] Last revision date:180227
[St] Status:Publisher
[do] DOI:10.1080/10245332.2018.1444920

  6 / 3050 MEDLINE  
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[PMID]: 29451035
[Au] Autor:Haouzi P; Gueguinou M; Sonobe T; Judenherc-Haouzi A; Tubbs N; Trebak M; Cheung J; Bouillaud F
[Ad] Address:a Division of Pulmonary and Critical Care Medicine , Pennsylvania State University College of Medicine , Hershey , PA , USA.
[Ti] Title:Revisiting the physiological effects of methylene blue as a treatment of cyanide intoxication.
[So] Source:Clin Toxicol (Phila);:1-13, 2018 Feb 16.
[Is] ISSN:1556-9519
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:BACKGROUND: Although methylene blue (MB) had long been proposed to counteract the effects of cyanide (CN) intoxication, research on its mechanisms of action and efficacy has been abandoned for decades. Recent studies on the benefits of MB in post-anoxic injuries have prompted us to reexamine the relevance of this historical observation. METHODS: Our study was performed in adult male Sprague-Dawley rats and on HEK293T epithelial cells. First, the effects and toxicity of MB (0-80 mg/kg) on circulation and metabolism were established in four urethane-anesthetized rats. Then nine rats received a lethal infusion of a solution of KCN (0.75 mg/kg/min) and were treated by either saline or MB, at 20 mg/kg, a dose that we found to be innocuous in rat and to correspond to a dose of about 4 mg/kg in humans. MB was also administered 5 min after the end of a sub-lethal exposure to CN in a separate group of 10 rats. In addition, ATP/ADP ratio, ROS production, mitochondrial membrane potential (Δψm) and cellular O consumption rate (OCR) were determined in HEK293T cells exposed to toxic levels of CN (200 µM for 10 min) before and after applying a solution containing MB (1-100 µM for 10 min). RESULTS: Methylene blue was found to be innocuous up to 50 mg/kg. KCN infusion (0.75 mg/kg/min) killed all animals within 7-8 min. MB (20 mg/kg) administered at the same time restored blood pressure, cardiac contractility and limited O deficit, allowing all the animals to survive, without any significant methemoglobinemia. When administered 5 min after a non-lethal CN intoxication, MB sped up the recovery of lactate and O deficit. Finally, MB was able to decrease the production of ROS and restore the ATP/ADP ratio, Δψm as well as OCR of epithelial cells intoxicated by CN. CONCLUSIONS: The present observations should make us consider the potential interest of MB in the treatment of CN intoxication. The mechanisms of the antidotal properties of MB cannot be accounted for by the creation of a cyanomethemoglobinemia, rather its protective effects appears to be related to the unique properties of this redox dye, which, depending on the dose, could directly oppose some of the consequences of the metabolic depression produced by CN at the cellular level.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1802
[Cu] Class update date: 180218
[Lr] Last revision date:180218
[St] Status:Publisher
[do] DOI:10.1080/15563650.2018.1429615

  7 / 3050 MEDLINE  
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[PMID]: 29258784
[Au] Autor:Dhibar DP; Sahu KK; Jain S; Kumari S; Varma SC
[Ad] Address:Department of Internal Medicine, Post Graduate Institute of Medical Education and Research (PGIMER), Chandigarh, India.
[Ti] Title:Methemoglobinemia in a Case of Paint Thinner Intoxication, Treated Successfully with Vitamin C.
[So] Source:J Emerg Med;54(2):221-224, 2018 Feb.
[Is] ISSN:0736-4679
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:BACKGROUND: Methemoglobin (MetHb) is an oxidized form of hemoglobin. It is a poor transporter of oxygen and is unable to deliver oxygen to the tissue. Globally, drug & toxin induced methemoglobinemia is more common as compared with the congenital form. Methemoglobinemia caused by paint thinner intoxication is rare. Methylene blue is well established as the first-line therapy for severe methemoglobinemia. CASE REPORT: A 25-year old man was brought to the Emergency Department after accidental consumption of paint thinner. On clinical examination, he had cyanosis and there were discrepancies in his pulse oximetry and arterial blood gas (ABG) analysis results. With this clue and supporting laboratory investigations, the diagnosis of toxin-induced methemoglobinemia was made. Due to the unavailability of methylene blue, alternative treatment with high-dose vitamin C was attempted, to which the patient responded. WHY SHOULD AN EMERGENCY PHYSICIAN BE AWARE OF THIS?: The role of vitamin C in the treatment of methemoglobinemia has not been well established, with only a few published case reports. This patient had severe methemoglobinemia, with MetHb of 46.4%, which responded dramatically to vitamin C therapy, with no side effects. This case shows that high-dose vitamin C is safe and has the potential to be an effective alternative for the treatment of severe methemoglobinemia. In the presence of cyanosis, mismatch of pulse-oximetry and ABG-analysis are the key for the physician to suspect methemoglobinemia.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1712
[Cu] Class update date: 180211
[Lr] Last revision date:180211
[St] Status:In-Data-Review

  8 / 3050 MEDLINE  
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[PMID]: 29356095
[Au] Autor:Shino H; Otsuka-Yamasaki Y; Sato T; Ooi K; Inanami O; Sato R; Yamasaki M
[Ad] Address:Department of Veterinary Medicine, Faculty of Agriculture, Iwate University, Morioka, Iwate, Japan.
[Ti] Title:Familial Congenital Methemoglobinemia in Pomeranian Dogs Caused by a Missense Variant in the NADH-Cytochrome B5 Reductase Gene.
[So] Source:J Vet Intern Med;32(1):165-171, 2018 Jan.
[Is] ISSN:1939-1676
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:BACKGROUND: In veterinary medicine, congenital methemoglobinemia associated with nicotinamide adenine dinucleotide (NADH)-cytochrome b5 reductase (b5R) deficiency is rare. It has been reported in several breeds of dogs, but little information is available about its etiology. OBJECTIVES: To analyze the NADH-cytochrome b5 reductase gene, CYB5R3, in a Pomeranian dog family with methemoglobinemia suspected to be caused by congenital b5R deficiency. ANIMALS: Three Pomeranian dogs from a family with methemoglobinemia were analyzed. Five healthy beagles and 5 nonrelated Pomeranian dogs without methemoglobinemia were used as controls. METHODS: Methemoglobin concentration, b5R activity, and reduced glutathione (GSH) concentration were measured, and a turbidity index was used to evaluate Heinz body formation. The CYB5R3 genes of the affected dog and healthy dogs were analyzed by direct sequencing. RESULTS: Methemoglobin concentrations in erythrocytes of the affected dogs were remarkably higher than those of the control dogs. The b5R activity of the affected dogs was notably lower than that of the control dogs. DNA sequencing indicated that this Pomeranian family carried a CYB5R3 gene missense variant (ATC→CTC at codon 194) that resulted in the replacement of isoleucine (Ile) by leucine (Leu). CONCLUSIONS AND CLINICAL IMPORTANCE: This dog family had familial congenital methemoglobinemia caused by b5R deficiency, which resulted from a nonsynonymous variant in the CYB5R3 gene. This variation (c.580A>C) led to an amino acid substitution (p.Ile194Leu), and Ile194 was located in the proximal region of the NADH-binding motif. Our data suggested that this variant in the canine CYB5R3 gene would affect function of the b5R in erythrocytes.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1801
[Cu] Class update date: 180209
[Lr] Last revision date:180209
[St] Status:In-Process
[do] DOI:10.1111/jvim.15031

  9 / 3050 MEDLINE  
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[PMID]: 29293483
[Au] Autor:Mathew PJ; Gupta A; Natarajan V; Ganesan R; Sharma R
[Ti] Title:Failure of Pulse Oximetry and Cooximetry as Monitors in a Patient With Hemoglobin MIwate: A Case Report.
[So] Source:A A Pract;, 2017 Dec 28.
[Is] ISSN:2575-3126
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:We present the perioperative details of a 2-year-old child scheduled for cleft palate repair. Low pulse oximetry readings after induction of anesthesia and before surgery led to the diagnosis of HbMIwate, a rare congenital methemoglobinemia due to mutation in the α-globin gene. We explored the utility of noninvasive cooximetry to monitor methemoglobin and oxygenation during anesthesia and found that noninvasive cooximetry is not useful to monitor oxygenation or to detect the percentage of methemoglobin arising from congenital variants like HbMIwate.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1801
[Cu] Class update date: 180206
[Lr] Last revision date:180206
[St] Status:Publisher
[do] DOI:10.1213/XAA.0000000000000689

  10 / 3050 MEDLINE  
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[PMID]: 29245041
[Au] Autor:Varlet V; Ryser E; Augsburger M; Palmiere C
[Ad] Address:Forensic Chemistry and Toxicology Unit, University Centre of Legal Medicine Lausanne - Geneva, CH-1011 Lausanne, Switzerland. Electronic address: vincent.varlet@chuv.ch.
[Ti] Title:Stability of postmortem methemoglobin: Artifactual changes caused by storage conditions.
[So] Source:Forensic Sci Int;283:21-28, 2018 Feb.
[Is] ISSN:1872-6283
[Cp] Country of publication:Ireland
[La] Language:eng
[Ab] Abstract:Hemoglobin is the protein in red blood cells that carries and distributes oxygen to the body. Methemoglobinemia is a blood disorder in which an abnormal amount of methemoglobin (MetHb), a form of hemoglobin (Hb), is produced from either inadequate MetHb reductase activity or too much MetHb production or by exposure to oxidizing agents. This could lead to anoxia and death if it is not treated. However, this parameter has not been investigated as a valid post-mortem indicator because random MetHb levels have been observed in various studies: MetHb increases can be observed due to autoxidation during storage, and MetHb decreases can be observed due to MetHb reductase or microbial activity in post-mortem samples. MetHb variations can also come from the blood state and can interfere in the optical measurements of MetHb. We have studied the post-mortem MetHb concentrations according to various storage conditions. Based on our results, both the post-mortem delay and the delay before analysis should be reduced whenever possible to avoid changes in MetHb. If the analysis is delayed for a short period of time (two weeks), the blood sample taken at autopsy should not be frozen but collected in EDTA preservative and stored under refrigeration (4-6°C) until analysis. If the analysis is delayed for a longer period (more than two weeks), the blood sample should be frozen with cryoprotectant at -80°C or -196°C.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1712
[Cu] Class update date: 180124
[Lr] Last revision date:180124
[St] Status:In-Process


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