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Background: Methemoglobinemia requires early identification and treatment, but limited knowledge exists regarding the current therapeutic approach taken by clinicians as well as the outcomes that occur in children. Objectives: To determine the current prevalence of this rare disease in the pediatric population, evaluate the impact of methemoglobin and functional hemoglobin levels, and assess how this disease is approached by clinicians. We hypothesize that methemoglobinemia prevalence is low and more methylene blue use would be observed in subjects with functional hemoglobin levels less than 7 g/dL. Design: This was a retrospective observational cohort study utilizing deidentified TriNetX® electronic health record (EHR) data. Methods: Using a multicenter EHR database, we evaluated subjective characteristics, diagnostic, laboratory results, medication, and procedural codes. Results: Ninety-eight children (mean age 5.3 ± 5.3 years) from 53 healthcare organizations were included. Methemoglobinemia prevalence was 0.0015% with an overall 30-day mortality of 6.1%. Subjects with methemoglobin percentages greater than 20% had a higher frequency of methylene blue administration (70.6% versus 24.7%, P =.0005). Critical care service requirements and methylene blue administration were similar in the subjects with functional hemoglobin less than 7 g/dL and more than 7 g/dL groups. Overall, 13 (13.2%) subjects underwent glucose-6-phosphate dehydrogenase deficiency (G6PD) testing. Conclusion: In our study, we found methemoglobinemia prevalence in children is low, there is a low frequency of G6PD testing despite methylene blue hemolysis risk, and subjects appeared to be treated similarly despite a low functional hemoglobin. These findings highlight the continued critical nature of this disease and may highlight opportunities for education aimed at improving care in children diagnosed with methemoglobinemia, particularly related to G6PD testing. [ABSTRACT FROM AUTHOR]

Background: Potassium nitrate poisoning is a rare but potentially serious condition that can result in methemoglobinemia and subsequent cyanosis. This case report presents a unique instance of rapid-onset methemoglobinemia resulting from the ingestion of a traditional medicine preparation containing potassium nitrate, known as "kalmi shora." Case presentation: A 14-year-old Pakistani boy reported to the emergency department with a history of sudden-onset headache, drowsiness agitation, irritability, and generalized cyanosis. Pulse oximetry showed a concerning oxygen saturation level of 58%, whereas arterial blood gas analysis revealed a normal partial pressure of oxygen (90 mmHg). The profile of abrupt onset of symptoms, generalized cyanosis, and the discrepancy between the partial pressure of oxygen and oxygen saturation readings necessitated a comprehensive assessment including inquiries into potential toxins. The peculiar appearance of the blood, resembling chocolate in color, further indicated the possibility of methemoglobinemia. The patient was successfully treated with methylene blue, leading to a prompt resolution of symptoms. Conclusion: This case highlights the significance of considering toxin exposures, such as traditional-medicine-induced poisoning, in emergency settings. The report contributes to the medical literature by highlighting the potential risks associated with traditional remedies and emphasizes the critical role of prompt diagnosis and intervention in optimizing patient outcomes. Recognition of the specific etiology of methemoglobinemia, in this case, traditional medicine ingestion, is essential for effective management in emergency medicine. [ABSTRACT FROM AUTHOR]

Naphthalene, an aromatic hydrocarbon prevalent in mothballs and deodorizers, poses significant health risks upon exposure, primarily through ingestion or dermal absorption. Herein, we report the case of a previously healthy 28-year-old male who presented with hemolysis, methemoglobinemia, and acute renal failure. The patient had a history of ingestion of mothballs, mistaking them for candy, prompting consideration of naphthalene intoxication as the clinical diagnosis, which was subsequently confirmed by laboratory findings. Given concurrent hepatic dysfunction and a diagnosis of glucose-6-phosphate dehydrogenase (G6PD) deficiency, N-acetyl cysteine was administered instead of methylene blue. The patient's condition improved after he was managed with aggressive fluid resuscitation, noninvasive ventilation, blood transfusions, and hemodialysis. Naphthalene ingestion can result in hemolysis, methemoglobinemia, and acute kidney injury, with heightened susceptibility observed in patients with G6PD deficiency. [ABSTRACT FROM AUTHOR]

Since the FDA's approval of rasburicase use for treatment of tumor lysis syndrome (TLS), multiple cases of rasburicase-induced methemoglobinemia and hemolytic anemia have been reported among patients with G6PD deficiency. This study aims to provide a systematic review of cases reporting such adverse reactions to rasburicase. A literature review of published cases in PubMed, Embase, Cochrane, and Web of Science was conducted. Descriptive studies reporting cases of rasburicase-induced methemoglobinemia and/or hemolytic anemia in English were analyzed and summarized in this study. Forty-three cases, including a case from our institution, were included in this study. Most cases (60.5%) received rasburicase for TLS treatment. Almost all patients (93.8%) were tested for G6PD after rasburicase administration. The median time to symptom onset was 24 h. The median methemoglobin level was 10%, peaking after a median of 24 h. The median hemoglobin nadir was 6.1 g/dL, and most patients (n = 32) required blood transfusion. Out of 39 cases with reported outcomes, 35 patients (89.7%) recovered, while four patients (three females and one male) died. The median time to recovery was 4.5 days while the median time to death was 8 days. Screening for G6PD deficiency among high-risk patients is important but not practical in acutely severe settings. When prior screening for G6PD deficiency is not feasible, close monitoring for methemoglobinemia and hemolytic anemia is recommended. Exchange transfusion is increasingly reported as a potentially successful therapeutic modality. Ascorbic acid may provide limited benefits. Methylene blue should be avoided as it may exacerbate hemolysis among these patients. [ABSTRACT FROM AUTHOR]

Abstract Background Potassium nitrate poisoning is a rare but potentially serious condition that can result in methemoglobinemia and subsequent cyanosis. This case report presents a unique instance of rapid-onset methemoglobinemia resulting from the ingestion of a traditional medicine preparation containing potassium nitrate, known as “kalmi shora.” Case presentation A 14-year-old Pakistani boy reported to the emergency department with a history of sudden-onset headache, drowsiness agitation, irritability, and generalized cyanosis. Pulse oximetry showed a concerning oxygen saturation level of 58%, whereas arterial blood gas analysis revealed a normal partial pressure of oxygen (90 mmHg). The profile of abrupt onset of symptoms, generalized cyanosis, and the discrepancy between the partial pressure of oxygen and oxygen saturation readings necessitated a comprehensive assessment including inquiries into potential toxins. The peculiar appearance of the blood, resembling chocolate in color, further indicated the possibility of methemoglobinemia. The patient was successfully treated with methylene blue, leading to a prompt resolution of symptoms. Conclusion This case highlights the significance of considering toxin exposures, such as traditional-medicine-induced poisoning, in emergency settings. The report contributes to the medical literature by highlighting the potential risks associated with traditional remedies and emphasizes the critical role of prompt diagnosis and intervention in optimizing patient outcomes. Recognition of the specific etiology of methemoglobinemia, in this case, traditional medicine ingestion, is essential for effective management in emergency medicine.

Moncef Ben Ghoulem Ben Saad, Arunabha Karmakar, Tayseer Salih Mohamed Salih, Wajeeha Arshad, Muhammad Jaffar Khan Department of Anesthesiology, Critical Care and Perioperative MedicineHamad Medical Corporation, Doha, QatarCorrespondence: Muhammad Jaffar Khan, Department of Anesthesiology, Critical Care and Perioperative Medicine, Hamad Medical Corporation, P.O. Box 3050, Doha, Qatar, Tel +97444394444, Email mkhan44@hamad.qaBackground: Methemoglobin is an altered state of hemoglobin where iron in hemoglobin is oxidized and incapable of binding oxygen; leading to complications such as cyanosis, dyspnea, headache, and heart failure. Methemoglobinemia can be congenital or acquired. Congenital methemoglobinemia is a rare disease and its worldwide incidence is unclear. We recently encountered the first documented case of congenital methemoglobinemia at our institution, necessitating perioperative care.Case Presentation: In the present case, a 22-year-old man with congenital methemoglobinemia underwent general anesthesia for dental extraction. The surgeon was informed to avoid local anesthetics and oxygenation was performed with FiO2 of 1.0. Arterial blood gas analysis showed a PH of 7.337, PaO2 of 302 mm Hg, PaCO2 of 44 mm Hg, oxyhemoglobin level of 63.4%, and methemoglobin level of 37.8%. The patient had a stable course. No methylene blue therapy was required, although cyanosis was observed during surgery.Conclusion: In summary, though rare, congenital methemoglobinemia poses fatal risks during surgery. Its management involves preoperative recognition and optimization, oxygenation status, multidisciplinary care, avoiding precipitating or oxidizing agents, discussing treatment options, maintaining cardiopulmonary stability, and ensuring perioperative safety measures with the medical team.Keywords: methemoglobinemia, general anesthesia, perioperative management, cyanosis, methylene blue

Methemoglobinemia is a potentially life-threatening condition caused by the formation of methemoglobin, a form of hemoglobin that cannot bind oxygen. While there are some rare congenital causes of methemoglobinemia, most cases are acquired from the effects of specific drugs or environmental exposures. In this retrospective study, we analyzed a large data set of whole blood samples analyzed for methemoglobin at an academic medical center in Midwestern United States that provides both pediatric and adult services. For a 14 year timeframe (May 2009- June 2023), we performed detailed chart analysis of all patients with a methemoglobin concentration of 3.1 % or higher. For an earlier 13 year timeframe (January 1996-April 2009), we performed chart review for all patients with a methemoglobin concentration of 10.0 % or higher. For the 2009–2023 data, dapsone was the most frequent cause of methemoglobinemia (methemoglobin 3.1 % or higher) in both pediatric (73.3 %, 115 clinical encounters, 105 unique patients) and adult (65.3 %, 195 clinical encounters, 190 unique patients) populations. Inhaled nitric oxide as medical therapy was the next most frequent cause in both pediatric (18.1 %) and adult (13.2 %) populations. Causes associated with two or more unique episodes with methemoglobin concentrations of 10.0 % and higher included the following: dapsone (n = 40 episodes), benzocaine (n = 10), recreational use of amyl or isobutyl nitrite (n = 3), suicide attempt with sodium nitrite (n = 3 with 1 fatality; all 3 cases within last 3 years), food contaminated with nitrates (n = 2), and sepsis (n = 2). A total of 18 patients received treatment with methylene blue including 5 cases associated with benzocaine and all of the cases associated with amyl nitrite, isobutyl nitrite, sodium nitrite, and contaminated food. Only 3 patients with dapsone-associated methemoglobinemia received methylene blue, reflecting primary management by dose reduction or discontinuation of drug. Overall, our data reinforce previous studies showing dapsone, inhaled nitric oxide, and nitrites as common agents causing methemoglobinemia in a patient population seen at a medical center. Our data also are consistent with recent epidemiology trends showing increase in suicide attempts using sodium nitrite.

Background: Methemoglobin is an altered state of hemoglobin where iron in hemoglobin is oxidized and incapable of binding oxygen; leading to complications such as cyanosis, dyspnea, headache, and heart failure. Methemoglobinemia can be congenital or acquired. Congenital methemoglobinemia is a rare disease and its worldwide incidence is unclear. We recently encountered the first documented case of congenital methemoglobinemia at our institution, necessitating perioperative care. Case Presentation: In the present case, a 22-year-old man with congenital methemoglobinemia underwent general anesthesia for dental extraction. The surgeon was informed to avoid local anesthetics and oxygenation was performed with FiO2 of 1.0. Arterial blood gas analysis showed a PH of 7.337, PaO2 of 302 mm Hg, PaCO2 of 44 mm Hg, oxyhemoglobin level of 63.4%, and methemoglobin level of 37.8%. The patient had a stable course. No methylene blue therapy was required, although cyanosis was observed during surgery. Conclusion: In summary, though rare, congenital methemoglobinemia poses fatal risks during surgery. Its management involves preoperative recognition and optimization, oxygenation status, multidisciplinary care, avoiding precipitating or oxidizing agents, discussing treatment options, maintaining cardiopulmonary stability, and ensuring perioperative safety measures with the medical team. [ABSTRACT FROM AUTHOR]

Purpose: Ascorbic acid has been proposed as an alternative treatment for methemoglobinemia in patients with glucose-6-phosphate dehydrogenase (G6PD) deficiency. However, its efficacy has never been compared to that of methylene blue given the inability of patients with G6PD deficiency to receive methylene blue. We present a case of methemoglobinemia treated with ascorbic acid in a patient without G6PD deficiency who had previously received methylene blue. Summary: A 66-year-old male was treated for methemoglobinemia deemed to be secondary to benzocaine throat spray. He received intravenous (IV) methylene blue but had a severe reaction: diaphoresis, lightheadedness, and hypotension. The infusion was stopped prior to completion. Approximately 6 days later he presented with methemoglobinemia following an additional overconsumption of benzocaine and was treated with ascorbic acid. In both instances his methemoglobin levels were >30% on arterial blood gas on admission and decreased to 6.5% and 7.8%, respectively, after administration of methylene blue and ascorbic acid. Conclusion: Ascorbic acid had a similar effect on decreasing the concentration of methemoglobin compared to methylene blue. Further research into use of ascorbic acid as a recommended agent for treatment of methemoglobinemia is warranted. [ABSTRACT FROM AUTHOR]

Le terme de méthémoglobinémie (MetHb) désigne l'état d'oxydation de l'ion Fer dit « ferreux » (Fe2+) en Fer dit « ferrique » (Fe3+) au sein de l'hème, molécule de l'hémoglobine (Hb). Cet état est physiologique si son taux reste contrôlé. L'état ferreux de la molécule d'hème se manifeste lors d'une agression oxydative importante. La physiopathologie de la MetHb implique la NADH, la NADPH et les enzymes du cycle du glucose comprenant le cytochrome-b5-reductase. La MetHb est le plus souvent acquise et plus rarement congénitale. Les causes secondaires regroupent les causes médicamenteuses comme les topiques anesthésiques, ou toxiques comme le « poppers » ou les nitrites. Les causes primaires sont liées à des déficits enzymatiques ou à des anomalies constitutionnelles de l'Hb. Une MetHb trop élevée provoque des symptômes d'intensité variable selon son taux et les comorbidités associées. Les signes cliniques sont dominés par la cyanose, reflet de l'hypoxie tissulaire, et peuvent conduire à des troubles métaboliques graves voire au décès. Le diagnostic peut être complexe car les anomalies biologiques peuvent passer inaperçues. Le traitement repose sur le retour à l'état physiologique de la molécule d'hème. Le bleu de méthylène est le principal antidote en cas de MetHb pathologique mais possède des précautions d'emploi particulières. Nous proposons une mise au point concernant la méthémoglobinémie avec le résumé de sa physiopathologie, ses signes cliniques associés, les examens complémentaires utiles et ses principes thérapeutiques. Methemoglobinemia (MetHb) refers to the state of oxidation of the iron ion "ferrous" (Fe2+) to iron "ferric" (Fe3+) within the heme molecule that makes up hemoglobin (Hb). This state is physiological if its level remains controlled. The ferrous state of the heme molecule occurs in the event of significant oxidative stress. The pathophysiology of MetHb involves NADH, NADPH and glucose cycle enzymes such as cytochrome-b5-reductase. MetHb can be acquired or more rarely, congenital. Acquired causes include drug-induced effects such as topical anesthetics, or toxic effects such as nitrites. Primary causes are linked to enzyme deficiencies or constitutional Hb abnormalities. Excessively high MetHb causes symptoms of varying intensity, depending on the level of MetHb and associated comorbidities. Clinical signs are dominated by cyanosis, indicative of tissue hypoxia, which can be complicated by severe metabolic disorders leading to death. Diagnosis can be complex, as the resulting biological abnormalities may go undetected. Treatment is mainly based on identifying the etiology and restoring the heme molecule to its physiological state. Methylene blue is the main antidote in cases of elevated MetHb, but precautions must be taken in its use, and its physico-chemical effects must be understood. We provide an update on methemoglobinemia, summarizing its pathophysiology and clinical presentations, complementary tests and therapeutic principles. [ABSTRACT FROM AUTHOR]

Cyanosis is a bluish discoloration of the tissues due to increased levels of deoxygenated hemoglobin in capillaries. It is a common finding in newborn infants that can be caused by different diseases, including pulmonary, cardiac, infectious, and hematological disorders. Methemoglobinemia is a rare cause of cyanosis, in which hemoglobin is oxidized, changing its heme iron configuration from the ferrous (Fe2 +) to the ferric (Fe3 +) state, creating methemoglobin (Met-Hb), a form that does not bind oxygen, leading to decreased oxygen delivery to the tissues and cyanosis. We report a rare case of a preterm newborn, who developed cyanosis and worsening hypoxemia on day ten of life, she was found to have elevated Met-Hb percentage in blood gas analysis that required treatment with intravenous methylene blue. Her symptoms resolved after a period of maintenance treatment with oral methylene blue and ascorbic acid, and the etiology of her disease remains unclear. [ABSTRACT FROM AUTHOR]

AbstractHemoglobin (Hb) Chile, a variant of Hb M, is produced by a point mutation of CTG→ATG on codon 29 (legacy codon 28) of the Hb β locus gene, which results in an amino acid substitution of Leu→Met. It has been identified in two families worldwide and is inherited in an autosomal dominant manner. Here, we report a case of Hb Chile in which a de novo mutation was detected in the proband. A 17-year-old male presented to the outpatient clinic with a pale appearance. There was cyanosis on his lips and fingers. Blood tests indicated the existence of hemolysis, but complete blood counts revealed no anemia. Peripheral arterial oxygen saturation on pulse oximetry was 80% on room air and did not improve with oxygen supplementation. The level of methemoglobin was 15.4%. Targeted next-generation sequencing identified a heterozygous NM_000518.4(HBB):c.85C > A mutation, indicating Hb Chile. The Hb Chile mutation, on the other hand, was not discovered in his parents, implying that it arose as a result of a de novo mutation. This case highlights the necessity of suspecting Hb gene mutations in patients with unexplained chronic methemoglobinemia, even if there is no family history. [ABSTRACT FROM AUTHOR]

The article presents a case of a preterm neonate who developed methemoglobinemia following repeated lidocaine administration for chest drain placements. Topics discussed include the identification and treatment of methemoglobinemia, the potential risks of lidocaine in preterm infants, and the need for careful monitoring of methemoglobin levels in such cases.

Aim and background: Acquired Methemoglobinemia, is one of the least common differential diagnoses while evaluating a cyanotic and hypoxemic patient. Typically results from toxin exposure, leading to significant morbidity and mortality if not promptly diagnosed and treated. Case description: A 38-year-old woman presented with altered consciousness, and respiratory distress, 13 hours after ingesting emamectin benzoate. She exhibited refractory hypoxemia, cyanosis with a "saturation gap", and a co-oximetric methemoglobin level of 33%. Treatment included methylene blue infusion, Vitamin C, and N-acetylcysteine. Her mentation and oxygen saturation improved gradually, and she was discharged on the sixth day. Conclusion: Methemoglobinemia following pesticide ingestion is rare but fatal. Physicians should consider it in cases of refractory hypoxemia and a "saturation gap". Treatment with antidotes is crucial and continued monitoring is essential to detect and manage potential relapse. Clinical significance: This is the first case report of methemoglobinemia followed by emamectin benzoate poisoning. [ABSTRACT FROM AUTHOR]

IntroductionUrea is one of the nitrogen chemical fertilizers for vegetable production in soil. But it is seldom used in soilless cultures. Leafy vegetables such as Lettuce (Lactuca sativa L.) contain high levels of nitrate and attempts have been made to reduce the nitrate concentration in this crop for human consumption. Using reduced forms of nitrogen, i.e. urea, is one of the applied strategies for reducing nitrate accumulation in lettuce. Little information is available concerning urea as a source of nitrogen for production of leafy vegetables such as lettuce in soilless culture. This experiment was conducted to investigate the effect of different ratios of urea:nitrate in nutrient solution on the growth indices, yield and nitrate accumulation of red French lettuce (Lactuca sativa L. cv. Lolla Rossa) in soilless culture. Materials and MethodsA hydroponic experiment using completely randomized design was carried out with seven ratios of urea:nitrate in nutrient solution and four replications in the research greenhouse of Shahrekord University. Urea:nitrate ratios in nutrient solution were: 0:100, 10:90, 20:80, 30:70, 40:60, 50:50 and 60:40. Lettuce seedlings were grown in 2 L plastic pots (one plant per pot) containing mixture of cocopeat + perlite at the ratio of 2:1 (v/v) and were manually fertigated with nutrient solutions on a daily basis. Four weeks after transplanting, lettuce plants were harvested and fresh weights of shoot and root were determined. Plant growth indices including of plant height, plant diameter, leaf length, leaf width, leaf number, leaf greenness index and leaf brix level were measured. After measuring the growth indices, the leaves were grouped separately according to leaf numbers 1-10=outer leaves, >11= inner leaves. The samples were dried in an oven at 60 °C and were ground. Nitrate concentrations in samples were determined calorimetrically using a spectrophotometer at a wavelength of 410 nm. Analysis of variance was performed using SAS software version 9.4. Means comparison was conducted using least significant difference test at 0.05 probability level. Results and DiscussionThe results indicated that application of different ratios of urea to nitrate in nutrient solution had not significant effect on the lettuce growth indices including of plant diameter, leaf length, leaf width, leaf number, leaf greenness index and leaf brix level in comparison with 0:100 of urea:nitrate ratio. Also, root and shoot fresh weights were not affected by urea:nitrate ratio in nutrient solution. The greatest quantity of shoot fresh weight (141 g per plant) was obtained with a 50:50 urea:nitrate ratio. However, this was not significantly different from the shoot fresh weight (125 g per plant) observed when urea was not included in the nutrient solution. Shoot nitrogen concentration (except for plants nourished with a 50:50 urea:nitrate ratio) was not affected by increasing the urea:nitrate ratio in the nutrient solution. The results revealed that application of urea in nutrient solution effectively provided the nitrogen requirement of lettuce. This indicates that lettuce plants can efficiently hydrolyze urea and use it efficiently as a nitrogen source. Application of urea in the nutrient solution led to significant decrease in the nitrate concentration of lettuce root (P< 0.05). Moreover, increasing urea:nitrate ratio in nutrient solution resulted in significant decrease of the nitrate concentration of outer leaves, inner leaves and all leaves of lettuce (P< 0.01). The highest and lowest nitrate concentration in inner, outer and all leaves of lettuce were obtained in plants nourished with 0:100 and 50:50 urea:nitrate ratio in nutrient solution, respectively. Application of urea:nitrate ratio of 50:50 led to the meaningful decrease of nitrate concentration in root (43%), outer leaves (41%), inner leaves (44%) and all leaves (43%) of lettuce in comparison with 0:100 of urea:nitrate ratio. Urea had a repressive effect on nitrate influx and decreased its uptake by plants. Also, after urea uptake by plant root, it is first degraded by cytosolic ureases and then ammonium is incorporated via the GS-GOGAT (Glutamine Synthetase- Glutamine α-OxoGlutarate Amino Transferaze) cycle. Therefore, application of urea in nutrient solution can lead to the reduction of nitrate accumulation in plants. ConclusionBased on the shoot fresh weight and nitrate concentration in lettuce leaves, replacing 50% of nitrate in nutrient solution with urea is recommended for red French lettuce production in hydroponic culture under the conditions of the present study. Compared to other nitrogen fertilizers, urea has a lower price and its application in nutrient solution is useful in reducing production costs.

Abstract Introduction This case study reports on a suicide attempt involving indoxacarb and vitamin C. Indoxacarb is a neurotoxic insecticide used in agriculture and as a flea controller in pets. Cotton, vegetables, and fruits are treated with indoxacarb, an insecticide that can be applied both indoors and outdoors. It causes skin allergies, methemoglobinemia, and hemolytic anemia. It is also attributed to allergic reactions through ingestion, inhalation, physical contact, and translaminar action. This case report highlights use of vitamin C in methemoglobinemia caused by indoxacarb poisoning. Indoxacarb poisoning has the potential to be extremely serious and even lethal. In this instance, the patient initially had no symptoms after ingesting a substance containing indoxacarb in an attempt at suicide. However, further tests revealed methemoglobinemia and low oxygen levels. Case presentation A 28-year-old south-east Asian female patient ingested an insecticide containing 5.25% novaluron, 4.5% indoxacarb, and 25% thiamethoxam, and reported that she noticed muddy brown urine but presented with no active signs or symptoms of poisoning. Upon examination, the patient was fully conscious, alert, and hemodynamically stable, but had an oxygen saturation of 84%. Gastric lavage was performed, and blood investigations revealed a muddy-brown-colored blood sample and methemoglobin levels of 12%. The patient was treated with high-dose vitamin C and showed significant improvement, with a drop in methemoglobin levels to 1.2% and an increase in oxygen saturation to 97%. Discussion Indoxacarb poisoning can cause severe methemoglobinemia. Vitamin C may be a useful treatment option for methemoglobinemia caused by indoxacarb, particularly in cases in which traditional treatment with methylene blue is contraindicated or not tolerated. Hence high doses of ascorbic acid, that is, vitamin C, were administered to the patient, which lowered their methemoglobin levels and improved oxygen levels without much safety concerns. Conclusion This example emphasizes the significance of early indoxacarb poisoning detection and treatment as well as the possible advantages of utilizing ascorbic acid in the management of methemoglobinemia, and highlights the use of vitamin C in the treatment of methemoglobinemia caused by indoxacarb poisoning. Therefore, it is important for healthcare professionals to be aware of the potential for indoxacarb to cause methemoglobinemia and to consider vitamin C as a treatment option.

Introduction: Methemoglobinemia is a potentially life-threatening condition characterized by the reduced oxygen-carrying capacity of hemoglobin. With the increasing popularity of natural and herbal biopesticides, there is a growing risk of exposure to substances that can induce this dyshemoglobinemia. This case report highlights the importance of recognizing and promptly treating methemoglobinemia in the context of biopesticide exposure, a concern relevant to various healthcare professionals. Case description: A 70-year-old male presented to the emergency department (ED) in an unresponsive state following suspected ingestion of an unknown quantity of an organic biopesticide labeled ''Bull Fight''. Initial management included fluid resuscitation, endotracheal intubation and mechanical ventilation. The patient developed significant hypoxia and hypotension. Abnormal blood color and a saturation gap raised suspicion of methemoglobinemia, which was confirmed by co-oximetry (68.7 % MetHb). Treatment with methylene blue was initiated, leading to initial improvement. However, the patient experienced rebound methemoglobinemia, requiring additional doses of methylene blue. Despite treatment, the patient ultimately succumbed to pneumonia. Discussion: This case underscores the potential dangers of organic biopesticides and the importance of considering methemoglobinemia in patients with unexplained cyanosis, saturation gap, and abnormal blood color. The increasing use of natural and herbal products in agriculture may expose individuals to undisclosed ingredients capable of inducing methemoglobinemia. Healthcare professionals across various specialities, including emergency medicine, critical care, toxicology, and primary care, must remain vigilant and maintain a high index of suspicion for this condition, especially in cases of biopesticide exposure. Conclusion: Awareness of methemoglobinemia and its association with biopesticide exposure is crucial for all healthcare providers who may encounter such cases. Prompt recognition and treatment can be lifesaving. As natural biopesticide use increases, clinicians should be prepared to diagnose and manage methemoglobinemia effectively. Careful monitoring is crucial to detect and prevent rebound methemoglobinemia. Ongoing education and preparedness are essential to address risks associated with emerging agricultural practices and products.

BackgroundThe appearance of bite cells associated with methemoglobinemia can be caused by oxidizing drugs such as dapsone in patients with glucose-6-phosphate dehydrogenase (G6PD) deficiency or high drug serum levels. Bite cells are often pathognomonic for oxidant injury in patients with G6PD deficiency and suggest active hemolysis.Case presentationWe report a case of a woman with no prior history of G6PD deficiency who presented with anemia, methemoglobinemia and bite cells on peripheral blood smear after dapsone therapy for new onset idiopathic urticaria. Laboratory tests for G6PD, blood count and liver function were within normal limits prior to initiation of therapy. During the patient's hospital course, moderate methemoglobinemia and anemia were identified despite mildly increased serum G6PD level. These pathologies were reversed upon stopping dapsone therapy.ConclusionThis case highlights the potential for therapeutic levels of dapsone to induce side effects in patients without G6PD deficiency and highlights the importance of routine blood monitoring for anemia and hemolysis during the course of drug therapy.

BackgroundGlucose-6-phosphate dehydrogenase deficiency is a rarely recognized predisposing factor for rhabdomyolysis. Rhabdomyolysis with coronavirus disease 2019 has been increasingly seen during the pandemic. We report the uncommon occurrence of coronavirus disease 2019 pneumonia, severe rhabdomyolysis, and acute renal failure in the setting of glucose-6-phosphate dehydrogenase deficiency.Case presentationA 19-year-old African American male presented with myalgias, diaphoresis, and dark urine. Testing for severe acute respiratory syndrome coronavirus 2 was positive. He had severe rhabdomyolysis with creatine kinase levels up to 346,695 U/L. He was oliguric and eventually required hemodialysis. Progressive hypoxemia, methemoglobinemia, and hemolytic anemia occurred following one dose of rasburicase for hyperuricemia. Glucose-6-phosphate dehydrogenase deficiency was diagnosed. Full recovery followed a single volume exchange transfusion and simple packed red blood cell transfusions.ConclusionsGlucose-6-phosphate dehydrogenase deficiency may predispose individuals to rhabdomyolysis due to severe acute respiratory syndrome coronavirus 2, presumably due to altered host responses to viral oxidative stress. Early screening for glucose-6-phosphate dehydrogenase deficiency can be useful for management of patients with rhabdomyolysis.

IntroductionUrea is one of the nitrogen chemical fertilizers for vegetable production in soil. But it is seldom used in soilless cultures. Leafy vegetables such as Lettuce (Lactuca sativa L.) contain high levels of nitrate and attempts have been made to reduce the nitrate concentration in this crop for human consumption. Using reduced forms of nitrogen, i.e. urea, is one of the applied strategies for reducing nitrate accumulation in lettuce. Little information is available concerning urea as a source of nitrogen for production of leafy vegetables such as lettuce in soilless culture. This exfaiment was conducted to investigate the effect of different ratios of urea:nitrate in nutrient solution on the growth indices, yield and nitrate accumulation of red French lettuce (Lactuca sativa L. cv. Lolla Rossa) in soilless culture. Materials and MethodsA hydroponic exfaiment using completely randomized design was carried out with seven ratios of urea:nitrate in nutrient solution and four replications in the research greenhouse of Shahrekord University. Urea:nitrate ratios in nutrient solution were: 0:100, 10:90, 20:80, 30:70, 40:60, 50:50 and 60:40. Lettuce seedlings were grown in 2 L plastic pots (one plant fa pot) containing mixture of cocopeat + falite at the ratio of 2:1 (v/v) and were manually fertigated with nutrient solutions on a daily basis. Four weeks after transplanting, lettuce plants were harvested and fresh weights of shoot and root were determined. Plant growth indices including of plant height, plant diameter, leaf lenth, leaf width, leaf number, leaf greenness index and leaf brix level were measured. After measuring the growth indices, the leaves were grouped separately according to leaf numbers 1-10=outer leaves, >11= inner leaves. The samples were dried in an oven at 60 °C and were ground. Nitrate concentrations in samples were determined calorimetrically using a spectrophotometer at a wavelenth of 410 nm. Analysis of variance was faformed using SAS software version 9.4. Means comparison was conducted using least significant difference test at 0.05 probability level. Results and DiscussionThe results indicated that application of different ratios of urea to nitrate in nutrient solution had not significant effect on the lettuce growth indices including of plant diameter, leaf lenth, leaf width, leaf number, leaf greenness index and leaf brix level in comparison with 0:100 of urea:nitrate ratio. Also, root and shoot fresh weights were not affected by urea:nitrate ratio in nutrient solution. The greatest quantity of shoot fresh weight (141 g fa plant) was obtained with a 50:50 urea:nitrate ratio. However, this was not significantly different from the shoot fresh weight (125 g fa plant) observed when urea was not included in the nutrient solution. Shoot nitrogen concentration (except for plants nourished with a 50:50 urea:nitrate ratio) was not affected by increasing the urea:nitrate ratio in the nutrient solution. The results revealed that application of urea in nutrient solution effectively provided the nitrogen requirement of lettuce. This indicates that lettuce plants can efficiently hydrolyze urea and use it efficiently as a nitrogen source. Application of urea in the nutrient solution led to significant decrease in the nitrate concentration of lettuce root (P< 0.05). Moreover, increasing urea:nitrate ratio in nutrient solution resulted in significant decrease of the nitrate concentration of outer leaves, inner leaves and all leaves of lettuce (P< 0.01). The highest and lowest nitrate concentration in inner, outer and all leaves of lettuce were obtained in plants nourished with 0:100 and 50:50 urea:nitrate ratio in nutrient solution, respectively. Application of urea:nitrate ratio of 50:50 led to the meaningful decrease of nitrate concentration in root (43%), outer leaves (41%), inner leaves (44%) and all leaves (43%) of lettuce in comparison with 0:100 of urea:nitrate ratio. Urea had a repressive effect on nitrate influx and decreased its uptake by plants. Also, after urea uptake by plant root, it is first degraded by cytosolic ureases and then ammonium is incorporated via the GS-GOGAT (Glutamine Synthetase- Glutamine α-OxoGlutarate Amino Transferaze) cycle. Therefore, application of urea in nutrient solution can lead to the reduction of nitrate accumulation in plants. ConclusionBased on the shoot fresh weight and nitrate concentration in lettuce leaves, replacing 50% of nitrate in nutrient solution with urea is recommended for red French lettuce production in hydroponic culture under the conditions of the present study. Compared to other nitrogen fertilizers, urea has a lower price and its application in nutrient solution is useful in reducing production costs. [ABSTRACT FROM AUTHOR]

The design and development of a novel approach for the administration of a drug to the targeted area within the therapeutic dosage have been an ongoing progression for the last few decades. Developing biopolymer-based hydrogels as site-specific drug delivery devices is one such strategy gaining lots of attention. Herein, the present study reports the synthesis of novel, pH-responsive hydrogel using whole barley grain (Hordeum vulgare L.) and a biocompatible monomer, 2-acrylamido-2-methylpropanesulfonic acid through copolymerization method. The synthesized polymeric material has been characterized using various characterization methods and detailed swelling studies. After exploring the pH-responsive behavior and appreciable swelling at pH 7.4 (3925%) and pH 4.0 (3033%), suitable for blood-related ailments and anticancer studies, respectively. The synthesized superabsorbent has been explored as a drug delivery device using methylene blue (MB) as a drug against methemoglobinemia. MB dosage has been regulated within the therapeutic dosage (1–2 mg/kg) using synthesized material loaded at varied initial MB concentrations (50–500 ppm). The release mechanism has been determined using various kinetic models: zero-order, first-order, Higuchi, Korsmeyer–Peppas, and Hixson–Crowell. It was found that the release mechanism followed the Korsmeyer–Peppas model with 'n' values of 0.78 (500 ppm), 0.84 (300 ppm), 0.77 (100 ppm), 0.34 (50 ppm) at pH 7.4 and 0.69 (500 ppm), 0.86 (300 ppm), 0.73 (100 ppm) and 0.31 (50 ppm) at pH 4.0, respectively, at 37 °C in 7 h, which significantly depicted non-Fickian diffusion with controlled release of MB. [ABSTRACT FROM AUTHOR]

Methemoglobinemia is a potentially life-threatening, rare condition in which the oxygen-carrying capacity of hemoglobin is diminished. We present the case of a 3-year-old boy treated for T-cell acute lymphoblastic leukemia (T-ALL) who developed methemoglobinemia (MetHb 57.1%) as a side effect of ifosfamide administration. Due to his critical condition, the patient was transferred to the intensive care unit (ICU). The therapy included methylene blue administration, an exchange transfusion, catecholamine infusion, and steroids. Improving the general condition allowed for continuing chemotherapy without ifosfamide and completion of the HR2 block. Vigilance for methemoglobinemia as a very rare side effect should be widespread when using ifosfamide in the treatment protocols. [ABSTRACT FROM AUTHOR]

Key Clinical Message: Nitrobenzene poisoning is a rare yet life‐threatening contention. The ensuing acute methemoglobinemia has a high fatality rate, hence early prompt intervention is required. Methylene blue (intravenous or oral) and ascorbic acid are the cornerstones of management. They must be administered to suspected patients without tardiness. An aromatic organic chemical used in paints and the printing industry is nitrobenzene. Its poisoning causes potentially fatal methemoglobinemia. One aspect of its management involves reducing the iron moiety from its ferric to ferrous form by administering intravenous methylene blue. A 23‐year‐old man who had deliberately consumed nitrobenzene presented to us with a history of headache and vomiting. He was diagnosed to have methemoglobinemia on the basis of clinical grounds and was managed successfully with intravenous methylene blue and vitamin C. [ABSTRACT FROM AUTHOR]

Key Clinical Message: Treatment of congenital chyloperitoneum is a challenge. Conservative methods may be ineffective. Preoperative visualization of the site of lymphatic leakage is crucial, but radiological imaging is technically complicated and may not provide sufficient information, especially in small patients. To ease the detection of lymphatic leakage during surgery, preoperative feeding with fat‐rich formula with Sudan Black has been recommended. However, administration of Sudan Black may result in life‐threatening methemoglobinemia and liver damage without any advantage of revealing leakage during surgery. We recommend preoperative feeding with pure fat‐rich formula. [ABSTRACT FROM AUTHOR]

Introduction and aim. In India, the utilization of agricultural pesticides for intentional self-poisoning is a prevalent method, and it is associated with substantially higher fatality rates compared to other self-poisoning approaches. Plethora, an agricultural insecticide containing novaluron (5.25%) and indoxacarb (4.5%), has recently been introduced and widely used in India and various other regions for its broad-spectrum lepidopteran control. While there have been documented cases of isolated self-poisoning involving indoxacarb, there is currently no literature reporting incidents of human poisoning specifically related to novaluron. Description of the case. An 83-Year-old male was presented to the emergency department (ED) with a history of consumption of 50 mL of an insecticide suspension concentrate called 'PLETHORA' to commit suicide. He had one episode of vomiting and dizziness after the ingestion. There was associated cyanosis, and the patient was put on high-flow oxygen at 10 L/min through a face mask. The patient was diagnosed to have methemoglobinemia and was successfully treated with methylene blue and ascorbic acid. One hour post methylene blue injection showed a methemoglobin level of 1%, and the patient gradually improved. Patients presenting with novaluron and indoxacarb poisoning require supportive treatment as there is no specific antidote. There should be a high index of suspicion for methemoglobinemia in such patients, and timely management is necessary to prevent further complications. The patient was successfully managed and discharged after the 3rd day of admission. Conclusion. The management of patients with novaluron and indoxacarb poisoning primarily involves supportive care, as there is currently no specific antidote available for these substances. Maintaining a high suspicion index for the development of methemoglobinemia and timely management of other complications is crucial for the best possible patient outcomes. [ABSTRACT FROM AUTHOR]

Introduction: This case study reports on a suicide attempt involving indoxacarb and vitamin C. Indoxacarb is a neurotoxic insecticide used in agriculture and as a flea controller in pets. Cotton, vegetables, and fruits are treated with indoxacarb, an insecticide that can be applied both indoors and outdoors. It causes skin allergies, methemoglobinemia, and hemolytic anemia. It is also attributed to allergic reactions through ingestion, inhalation, physical contact, and translaminar action. This case report highlights use of vitamin C in methemoglobinemia caused by indoxacarb poisoning. Indoxacarb poisoning has the potential to be extremely serious and even lethal. In this instance, the patient initially had no symptoms after ingesting a substance containing indoxacarb in an attempt at suicide. However, further tests revealed methemoglobinemia and low oxygen levels. Case presentation: A 28-year-old south-east Asian female patient ingested an insecticide containing 5.25% novaluron, 4.5% indoxacarb, and 25% thiamethoxam, and reported that she noticed muddy brown urine but presented with no active signs or symptoms of poisoning. Upon examination, the patient was fully conscious, alert, and hemodynamically stable, but had an oxygen saturation of 84%. Gastric lavage was performed, and blood investigations revealed a muddy-brown-colored blood sample and methemoglobin levels of 12%. The patient was treated with high-dose vitamin C and showed significant improvement, with a drop in methemoglobin levels to 1.2% and an increase in oxygen saturation to 97%. Discussion: Indoxacarb poisoning can cause severe methemoglobinemia. Vitamin C may be a useful treatment option for methemoglobinemia caused by indoxacarb, particularly in cases in which traditional treatment with methylene blue is contraindicated or not tolerated. Hence high doses of ascorbic acid, that is, vitamin C, were administered to the patient, which lowered their methemoglobin levels and improved oxygen levels without much safety concerns. Conclusion: This example emphasizes the significance of early indoxacarb poisoning detection and treatment as well as the possible advantages of utilizing ascorbic acid in the management of methemoglobinemia, and highlights the use of vitamin C in the treatment of methemoglobinemia caused by indoxacarb poisoning. Therefore, it is important for healthcare professionals to be aware of the potential for indoxacarb to cause methemoglobinemia and to consider vitamin C as a treatment option. [ABSTRACT FROM AUTHOR]

Methemoglobinemia is a serious hematological disease characterized by the incapability of sufficient oxygen delivery to tissues and cyanosis when iron within hemoglobin in ferrous form (Fe+2) is oxidized to ferric form (Fe+3). Methemoglobinemia may be congenital or acquired. While prilocaine-induced methemoglobinemia can be seen in newborns and early pediatric ages, it is a rare condition in adults. We aimed to investigate prilocaine-induced adult methemoglobinemia with four cases. [ABSTRACT FROM AUTHOR]

We describe a series of six patients with naphthalene ball intentional poisoning in adult patients. A 41‑year‑old male developed methemoglobinemia, intravascular hemolysis, and hemoglobinuria. The patient was managed by intravenous methylene blue, ascorbic acid, N‑acetylcysteine, and packed red blood cell transfusion. Rest of the patients had mild symptoms and were managed symptomatically. All the patients had a favorable outcome. The relationship between features of the toxidrome and serum levels of methemoglobin is analyzed. The supportive role of gastric lavage and methylene blue is being discussed. [ABSTRACT FROM AUTHOR]

Nitrate pollution of water sources has been increasing due to the expansion of agriculture and human activities. The use of electrodialysis (ED) technologies has expanded significantly in recent years. In this study, an ED system with current circulation was built, and it was converted to electrodeionization (EDI) by adding resin to its dilute chambers. The EDI and ED systems by examining different operating parameters such as initial concentration, voltage, and flow rate, and their effects on the removal rate were compared. Flow rates of 10, 20, and 30 ml/min, voltages of 5, 10, and 15 V, and various nitrate concentrations (75, 100, 150, and 200 ppm) to assess the nitrate removal percentage were considered. The results showed that the average nitrate removal in the EDI process was significantly higher than in the ED process (P < 0.001) at all voltage, flow rate, and concentration levels. In the denitrification process by EDI, the osmotic property did not affect the membrane ion exchange process. The research results showed that the EDI process has better functionality to reduce nitrate concentration in water. The results also revealed that osmotic properties do not affect the membrane ion exchange process in the nitrate removal process by continuous electrodeionization. Additionally, the amount of nitrate removal increased with increasing voltage, while increasing the flow rate through the electro-ionization system decreased the amount of nitrate removal, thereby increasing the remaining nitrate. Furthermore, the highest rate of nitrate removal of 99.7% in the continuous electrodeionization system was achieved at the minimum initial concentration, minimum flow rate, and maximum voltage. As a fundamental technology for in situ remediation for groundwater contamination, the EDI process proved feasible and provided a foundation for further research. [ABSTRACT FROM AUTHOR]

Introduction . Methemoglobinemia is a rather rare cause of hypoxemia and hypoxia, however, with a severe course of the disease and an increase in the concentration of methemoglobin in the blood of more than 20 %, this can cause the development of multi-organ dysfunction and death.The objective was to descript the case of methemoglobinemia in a child with congenital epidermolysis bullosa with the use of a combined drug containing benzocaine.Materials and methods. Newborn premature baby boy, from the first pregnancy, gestation period 36 weeks, suffering from congenital epidermolysis. Birth weight 2850 g, height 47 cm. Apgar score in the first minute – seven, on the fifth – eight points. As a local treatment, an aerosol for external use «Olazol» was prescribed. At the age of 56 hours from the moment of birth, a sharp deterioration in the child’s condition was noted in the form of a decrease in SpO2 to 72–76 %, pronounced tachycardia, an increase in methemoglobin concentration in the blood (53.7 %).Results. A distinctive feature of this case was the presence of severe methemoglobinemia, which led to severe metabolic acidosis, venous hypoxemia and tissue hypoxia. Timely diagnosis and adequate therapy in the early stages of the pathological process contributed to the complete stabilization of the child’s condition and the normalization of the blood gas composition fifteen hours after the start of therapy.Conclusion. The use of drugs containing benzocaine in the early neonatal period is a risk factor for the development of methemoglobinemia, which requires a dynamic assessment of the level of methemoglobin in the blood in order to prevent tissue hypoxia.

Persistent left superior vena cava drain into the left atrium is frequently overlooked since it rarely has a major influence on haemodynamic in children. Therefore, it is frequently asymptomatic and accidentally found during catheterization and imaging modalities. It has the potential to mimic pulmonary disease, especially in individuals who do not have a congenital cardiac anomaly. We report the case of a five-year-old boy who had recurrent pneumonia with persistent hypoxaemia and was discovered to have persistent left superior vena cava into the left atrium by computer tomography pulmonary angiography. Due to the lifetime risk of emboli and bacteraemia from right to left shunting, the left superior vena cava must be terminated either percutaneously or surgically. [ABSTRACT FROM AUTHOR]

Methemoglobinemia (MetHb) is an uncommon and fatal condition. It is usually suspected when there is a discrepancy between the pulse oximetry reading and arterial blood gas analysis findings. Treatment depends on the level of MetHb and symptoms. Here, we present a case of an elderly male with lepromatous leprosy on regular therapy who developed influenza infection leading to the precipitation of erythema nodosum leprosum (ENL) and hypoxia due to drug-induced MetHb. [ABSTRACT FROM AUTHOR]

Background: Methemoglobinemia is one of the rare causes of cyanosis, encountered in the Emergency Department. It can be congenital or acquired, affecting the oxygen binding capacity of hemoglobin, thus shifting the oxyhemoglobin dissociation curve to the left. It is potentially life-threatening, but it responds well to specific therapies, if recognized and intervened early. MetHb levels >70% are often described as incompatible with life.Case: Here, we describe two cases of near-fatal MH (MetHb levels >70%), one with intentional and the other with accidental ingestion of substance-producing MH, and its management which highlights how timely diagnosis and prompt appropriate treatment in the Emergency Department can be lifesaving. Both cases were at physiological extremes on arrival to the ED. However, the early clinical suspicion and prompt diagnosis of methemoglobinemia, which was confirmed by blood co-oximetry, helped expedite the delivery of specific anti-dote for methemoglobin, i.e., intravenous methylene blue. Both patients responded well to the treatment and were hemodynamically stable within 6 hoursConclusion: Cyanosis, which does not respond to oxygen, and low saturation levels not responding to oxygen therapy should raise the suspicion of Methemoglobinemia (MH). Early diagnosis and prompt administration of methylene blue are the key factors for survival.

Abstract Background Hemoglobin (Hb) Chile [β28(B10) Leu > Met; HBB: c.85 C > A] is a rare hemoglobin variant caused by a missense mutation in the HBB gene. Only one case of Hb Chile has been reported worldwide so far. It is an unstable hemoglobin, characterized by cyanosis associated with chronic methemoglobinemia and hemolytic anemia induced by sulfonamides or methylene blue. Case presentation A 9-year-3-month-old girl had mild anemia of unknown etiology for more than 6 years. She had a slight pallor without other symptoms or signs. The complete blood count revealed normocytic normochromic anemia with a sometimes-elevated reticulocyte count, and the bone marrow cytology showed marked erythroid hyperplasia, but the tests related to hemolysis were normal. Therefore, the whole exome sequencing was performed and showed a heterozygous mutation for HBB: c.85 C > A. With asymptomatic methemoglobinemia confirmed later, she was eventually diagnosed with Hb Chile. Conclusions This is the first report of Hb Chile in China and the second worldwide. This case shows that Hb Chile is clinically heterogeneous and difficult to diagnose and expands our understanding on the clinical and hematological traits of the disease.

The case report describes a case of a severe dapsone (more than 200 tablets dapsone 100 mg) and mild methotrexate intoxication (10 tablets methotrexate 10 mg) as an attempt to commit suicide, resulting in severe cyanosis with elevation in methemoglobin concentration, treated with methylene blue, ascorbic acid, folinic acid, multidose activated charcoal and hemodialysis. Measurements of blood gases, dapsone and methotrexate levels were performed. Furthermore a hepatitis, pulmonary artery thrombus and a strange taste sensation were diagnosed, probably related to dapsone. The patient recovered and was discharged from hospital after five days. Acute intoxication from excessive dapsone intake is uncommon and clear treatment guidelines are lacking. We here report the treatment modalities as a result of a dapsone intoxication, including the effects on the overall condition of the patient.

Methylene blue is a versatile substance used for various medical purposes for years. It has shown promise as a diagnostic tool and a potential treatment option for illnesses such as methemoglobinemia, cyanide poisoning, and malaria, but primarily neurodegenerative diseases like Alzheimer's. The present study aimed to investigate the hypothesis that hydrogen peroxide-induced neuronal cell death debris could activate inflammation, leading to endothelial cell death. To test this hypothesis, we employed two innovative transwell models, the distant and adjacent models, to replicate intercellular interactions between endothelial and neuronal cells at varying brain ranges. We also analyzed the expression levels of pro-apoptotic genes BAX and BIK in three conditions. Our findings suggest that the proximity between endothelial and neuron cells is crucial in inducing endothelial cell death. We further found that the methylene blue treatment significantly decreased the percentage of cell death in both distant and adjacent models. Moreover, our analysis of IL-2, IL-8, and TNF-alpha expression levels using RT-PCR suggests that MBS may protect endothelial cells by blocking the inflammation pathway, which is critical in regulating inflammation and cell death pathways. Dysregulation of these cytokines and their downstream signaling pathways can lead to cell death and brain damage, contributing to the pathogenesis of inflammatory diseases. Therefore, methylene blue has potential therapeutic benefits as a treatment option for diseases involving neuronal and endothelial cell death. [ABSTRACT FROM AUTHOR]

Methemoglobinemia is due to oxidization of divalent ferro-iron of hemoglobin to ferri-iron of methemoglobin (MetHb) which is incapable of transferring oxygen to tissues. This disease may be acquired by intoxication with oxidizing agents or inherited with a mutation of CYB5R3, the gene coding for the methemoglobin reductase or cytochrome B5 reductase 3 responsible for the reduction of MetHb to hemoglobin. We report the case of 2 sisters aged respectively of 15 and 8 months. They were born to a second-degree consanguineous marriage with a history of precocious and unexplained deaths in 3 relatives. Both sisters presented neurological features including psychomotor retardation, microcephaly, and axial hypotonia. Cerebral magnetic resonance imaging revealed cerebral atrophy in both cases associated with hypoplasia of the corpus callosum in the younger child. The association of neurological disability, cyanosis, and hypoxemia prompted a search for methemoglobinemia, with MetHB levels respectively of 26% and 15.8%in the 2 sisters. Initial treatment was based on methylene blue, then ascorbic acid. The genetic study revealed a c.463+8G>C mutation of CYB5R3 confirming the diagnosis of methemoglobinemia type II. The diagnosis of methemoglobinemia, although rare, should be considered in the presence of psychomotor retardation with cyanosis and subacute onset hypoxemia, especially in the presence of a family history. [ABSTRACT FROM AUTHOR]

Congenital methemoglobinemia is a rare cause of cyanosis that is characterized by increased methemoglobin levels and caused by mutations in the cytochrome B5 reductase 3 (CYB5R3) gene resulting in deficiencies of the nicotinamide adenine dinucleotide-cytochrome b5 reductase enzyme. The congenital disease has two types: type I, in which the enzyme deficiency occurs only in the erythrocytes, and type II, in which all tissues are affected. Accordingly, cyanosis is the sole clinical manifestation in type I, whereas cyanosis is accompanied by such severe neurological findings as intellectual disability, microcephaly, generalized dystonia, and movement disorders. In this study, a case who presented with respiratory distress was found to have high methemoglobin levels and was diagnosed with type II congenital methemoglobinemia due to the presence of neurological findings was presented. The patient's treatment was adjusted, the methemoglobin level was reduced, and cyanosis regressed, but no change was observed in neurological findings. This untreatable, rare condition must be included in the differential diagnosis of patients with unexplained cyanosis and high methemoglobin levels, and genetic counseling must be provided to the family, because of its severity and 25% recurrence rate. [ABSTRACT FROM AUTHOR]

Methemoglobinemia occasionally causes cyanosis particularly in congenital methemoglobinemia. Avoidance of exposure to oxidizing agents is important for patients with congenital methemoglobinemia because of their deficient enzymatic pathways and decreased oxygen-carrying capacity. Here, we present a pediatric patient with preoperatively undiagnosed congenital methemoglobinemia who underwent catheterization with probably diagnosis of pulmonar hypertension under general anesthesia. The pediatric patient was a 10-year-old who displayed a low pulse oximetry reading of 92% prior to induction of anesthesia. Methemoglobinemia was first suspected intraoperatively because of a mismatch of SpO2 of finger pulse oximetry and SaO2 of arterial blood, and was later confirmed by multiplewavelength CO-oximetry. The pathophysiology, etiology, clinical manifestations, anesthetic considerations, and treatment options of methemoglobinemia are discussed. [ABSTRACT FROM AUTHOR]

Methemoglobinemia (MET) is a life-threatening condition resulting from the development of methemoglobin (MetHb), which binds oxygen irreversibly, causing refractory hypoxia and so-called "functional anemia". MET can be caused by hereditary or acquired processes. Acquired forms are the most common. Symptoms correlate with the MetHb level and range from cyanosis and dyspnea to dysrhythmias, metabolic acidosis, coma, and cardiac arrest. MetHb levels above 70% are fatal. Methylene blue (MB) is the specific antidote. In all cases, supportive treatment, including intravenous hydration, glucose correction, and oxygen supplementation, must be started immediately. Exchange transfusion has been used successfully to treat MET and may be appropriate in patients for whom MB is ineffective. We report the case of a 54-year-old woman who presented to our emergency department for the acute and sudden development of chest pain, shortness of breath, and severe cyanosis after drinking a significant amount of boiled courgette water. Arterial blood gas analysis revealed a MetHb level of 26%. She was treated immediately with MB, oxygen supplementation, and hydration with normalization of her MetHb in 12 hours. Our recommendation is to always investigate MET in patients with unexplained cyanosis and refractory hypoxia. [ABSTRACT FROM AUTHOR]

Objective The aim of this study was to assess the impact of hydroxocobalamin (OHCbl) infusion on arterial blood gas and oximetry values in patients with vasoplegic syndrome. Methods Blood samples collected from 95 patients receiving OHCbl infusion were assayed using the ABL90 FLEX Plus blood gas analyzer for the concentration of methemoglobin (MetHb), total hemoglobin (tHb), carboxyhemoglobin (COHb), arterial oxygen saturation (SaO2), arterial oxygen partial pressure (PaO2), and arterial carbon dioxide partial pressure (PaCO2). Interference of OHCbl on these variables was evaluated using the measured difference between the preinfusion and postinfusion samples. Results Blood MetHb (%) measured after the infusion of OHCbl (5g) were significantly higher than the baseline levels, with a median of 4.8 (IQR, 3.0−6.5) versus 1.0 (IQR, 1.0−1.2) (P <.001). Blood COHb (%) increased from a median of 1.3 (IQR, 1.0−1.8) to 1.7 (IQR, 1.3−2.2) (P <.001) following the OHCbl infusion. No differences were seen in median levels of tHb, PaO2, PaCO2, and SaO2 between pre- and post-OHCbl treatment. Conclusion The presence of OHCbl in blood clearly interfered with the oximetry measurements of the hemoglobin component fractions by falsely increasing the levels of MetHb and COHb. Blood levels of MetHb and COHb cannot be reliably determined by the co-oximetry when OHCbl is known or suspected. [ABSTRACT FROM AUTHOR]

Background: Hemoglobin (Hb) Chile [β28(B10) Leu > Met; HBB: c.85 C > A] is a rare hemoglobin variant caused by a missense mutation in the HBB gene. Only one case of Hb Chile has been reported worldwide so far. It is an unstable hemoglobin, characterized by cyanosis associated with chronic methemoglobinemia and hemolytic anemia induced by sulfonamides or methylene blue. Case presentation: A 9-year-3-month-old girl had mild anemia of unknown etiology for more than 6 years. She had a slight pallor without other symptoms or signs. The complete blood count revealed normocytic normochromic anemia with a sometimes-elevated reticulocyte count, and the bone marrow cytology showed marked erythroid hyperplasia, but the tests related to hemolysis were normal. Therefore, the whole exome sequencing was performed and showed a heterozygous mutation for HBB: c.85 C > A. With asymptomatic methemoglobinemia confirmed later, she was eventually diagnosed with Hb Chile. Conclusions: This is the first report of Hb Chile in China and the second worldwide. This case shows that Hb Chile is clinically heterogeneous and difficult to diagnose and expands our understanding on the clinical and hematological traits of the disease. [ABSTRACT FROM AUTHOR]

Background: Methemoglobinemia is one of the rare causes of cyanosis, encountered in the Emergency Department. It can be congenital or acquired, affecting the oxygen binding capacity of hemoglobin, thus shifting the oxyhemoglobin dissociation curve to the left. It is potentially life-threatening, but it responds well to specific therapies, if recognized and intervened early. MetHb levels >70% are often described as incompatible with life. Case: Here, we describe two cases of near-fatal MH (MetHb levels >70%), one with intentional and the other with accidental ingestion of substance-producing MH, and its management which highlights how timely diagnosis and prompt appropriate treatment in the Emergency Department can be lifesaving. Both cases were at physiological extremes on arrival to the ED. However, the early clinical suspicion and prompt diagnosis of methemoglobinemia, which was confirmed by blood co-oximetry, helped expedite the delivery of specific anti-dote for methemoglobin, i.e., intravenous methylene blue. Both patients responded well to the treatment and were hemodynamically stable within 6 hours. Conclusion: Cyanosis, which does not respond to oxygen, and low saturation levels not responding to oxygen therapy should raise the suspicion of Methemoglobinemia (MH). Early diagnosis and prompt administration of methylene blue are the key factors for survival. [ABSTRACT FROM AUTHOR]

This article addresses the increase in suicide rates in the US, emphasizing the emergence of sodium nitrite ingestion as a method of self-harm, particularly among adolescents and young adults influenced by social media. Given the rising incidence of sodium nitrite-related suicide attempts, healthcare providers must remain vigilant and prepared to respond effectively. [ABSTRACT FROM AUTHOR]