Excessive nitrite in food poses a serious threat to public health. This compound not only induces methemoglobinemia by interfering with oxygen transport in the blood but also serves as a precursor to carcinogenic N-nitrosamines, posing long-term cancer risks. Thus, the development of rapid and highly sensitive methods for nitrite detection is crucial for ensuring food safety. Laccase mimics, which have been widely used for the degradation and detection of phenolic compounds, have recently emerged as promising tools for sensing various food contaminants. However, their application for nitrite detection has not been reported to date.

Neonatal cyanosis is commonplace, usually from respiratory or cardiac causes. Consideration of alternative or combined aetiologies was required when a 3-hour-old term male neonate with central cyanosis, low oxygen saturation (SpO2), and persistent pulmonary hypertension of the newborn (PPHN) confirmed on echocardiography, failed to respond to PPHN interventions. The high oxygen saturation gap and methemoglobin (MetHb) level of 16.2% shifted the working diagnosis to methemoglobinaemia. Possible triggering drugs were stopped and methylene blue was given without effect, prompting testing for haemoglobin variants. Though the SpO2 remained in the mid-80s, MetHb levels decreased, pulmonary pressures normalised by day of life (DOL) 4, and he was discharged home on DOL 22. Diagnostic testing confirmed the haemoglobin F-M-Fort Ripley mutation (HBG2: c.277C>T), a variant that affects fetal haemoglobin only and is therefore self-limited. In this case, the concurrent presentation of PPHN and congenital methaemoglobinaemia created significant diagnostic and therapeutic challenges.

BACKGROUND Methemoglobinemia is an uncommon hemoglobinopathy caused by oxidation of heme iron from its ferrous (Fe[2+]) state to the ferric (Fe[3+]) state, resulting in functional anemia that does not improve with supplemental oxygen. "Poppers" is a slang term for recreational drugs marketed as nail polish removers or room deodorizers, often sold under brand names such as "Jungle Juice," which may cause methemoglobinemia due to their nitrite content. CASE REPORT A 67-year-old White woman accidentally ingested "Jungle Juice" nail polish remover containing isobutyl nitrite, resulting in severe methemoglobinemia. Clinical hallmarks included cyanosis, chocolate-colored blood, refractory hypoxemia unresponsive to supplemental oxygen, and a partial pressure of oxygen (PaO2)-saturation gap. CONCLUSIONS Methemoglobinemia is a potentially life-threatening hemoglobinopathy that causes functional anemia unresponsive to supplemental oxygen. "Poppers" can induce methemoglobinemia. Despite legislative efforts to regulate these products and prevent misuse, manufacturers continue to exploit regulatory loopholes by producing chemical analogs exempt from current drug laws. Additionally, there has been an emerging trend of sodium nitrite ingestion to induce methemoglobinemia in suicide attempts over recent years, driven by its accessibility and increasing online dissemination. Given the rise in "popper" use and sodium nitrite ingestion, emergency physicians should be aware of these trends and the associated products to facilitate early recognition and prompt treatment of this rare condition.

Methemoglobinaemia is a rare but important cause of hypoxia that may be overlooked, particularly in patients with complex comorbidities. We present a 76-year-old man with Multiple Myeloma undergoing chemotherapy who presented with recurrent syncope and exertional dyspnoea. Initial investigations revealed pancytopenia and hypoxia. Imaging excluded pulmonary embolism and infection. Arterial blood gas analysis demonstrated elevated methemoglobin levels (10.5%), confirming methemoglobinaemia. The patient was managed with supportive therapy, including oxygen, blood transfusion, and filgrastim, resulting in clinical improvement. This case highlights the importance of considering methemoglobinaemia in patients with unexplained hypoxia, especially when conventional investigations are unremarkable. The coexistence of severe anaemia can further exacerbate tissue hypoxia and complicate diagnosis.

This case report describes a female in her late 80s who presented with progressive dyspnoea and marked hypoxia. Notably, the hypoxia was refractory to high-flow supplemental oxygen. Her medical history included myeloperoxidase (MPO) positive vasculitis, vitamin B12 deficiency with a baseline haemoglobin of 88g/dL and well-controlled hypertension. A venous blood gas showed a MetHb of 10.2% [< 2%], which was initially overlooked. She was admitted to the ward and remained refractory to supplementary oxygen. A subsequent arterial blood gas (ABG) revealed an oxygen saturation (SaO2) of 95% and a methaemoglobin (MetHb) level of 10.7%. On review of her drug history, it was noted that she was taking 100 mg of dapsone once daily for Pneumocystis jirovecii pneumonia (PCP) prophylaxis. Dapsone was discontinued; her symptoms and hypoxia rapidly improved, and she was discharged 48 hours later.

Methemoglobinemia is a rare but potentially serious complication of lidocaine (LDC) use for local anesthesia in infants and young children, yet its prevalence during continuous systemic infusion for neonatal seizures remains unclear. Given the increasing use of LDC as add-on therapy for neonatal seizures, this retrospective cohort study evaluated methemoglobin (MetHb) levels in 51 neonates with (serial) measurements within 96 h before and after LDC infusion. Methemoglobinemia was defined as MetHb > 2% in arterial or capillary blood gas samples. Prevalence increased from 6% (3/51) before LDC to 47% (24/51) after administration (p < 0.001). Most neonates had mildly elevated MetHb levels (< 5%); three had a MetHb level > 5%, with a highest peak of 9.5%. In one neonate LDC was discontinued due to hypoxemia, the others were asymptomatic. In neonates who developed methemoglobinemia after LDC, the mean time to peak MetHb was 29.1 h (95% CI 11.1-73.3), and mean time to recover to < 2% after the peak was 27.5 h (95% CI 8.4-75.5). Over half of neonates receiving regimen III (> 36 weeks without therapeutic hypothermia [TH]) developed methemoglobinemia, compared to none on regimen IV (with TH). This suggests an association with a higher cumulative dose and longer infusion duration.Conclusion: In conclusion, methemoglobinemia occurred in nearly half of neonates receiving continuous LDC for seizures and was associated with the dosing regimen. It is important to be aware of this complication, especially in infants who develop respiratory deterioration and oxygenation problems following continuous LDC administration.

Methemoglobinemia is a rare but potentially life-threatening condition caused by oxidation of hemoglobin iron from the ferrous to ferric state, impairing oxygen delivery to tissues; early recognition is crucial as clinical manifestations may be disproportionate to pulse oximetry readings. We describe a case of a three-year-old female child who presented with acute onset cyanosis and hypoxia unresponsive to supplemental oxygen, despite a normal cardiopulmonary examination and persistently low oxygen saturation on pulse oximetry. Blood gas analysis revealed a discrepancy between low oxygen saturation and oxygen levels, raising suspicion of methemoglobinemia, which was subsequently confirmed by elevated methemoglobin levels. The child was managed with prompt supportive care, including high-flow oxygen therapy, followed by intravenous methylene blue, due to significant symptoms and elevated methemoglobin levels, which resulted in rapid clinical and biochemical improvement. She made a complete recovery without residual complications. This case underscores the importance of considering methemoglobinemia in young children presenting with unexplained hypoxia refractory to oxygen therapy, as timely diagnosis and appropriate treatment can be life-saving.

Glucose-6-phosphate dehydrogenase (G6PD) deficiency is among the most common enzyme disorders affecting red blood cells. It often remains unnoticed until the individual is exposed to oxidative stress, which can trigger rapid hemolysis. Methemoglobinemia develops when hemoglobin becomes oxidized into a form that cannot efficiently transport oxygen. This leads to impaired oxygen delivery to tissues and cyanosis that does not improve despite supplemental oxygen. Although uncommon, methemoglobinemia can develop as a serious complication during episodes of severe oxidative stress. We describe the case of an 11-month-old boy who developed acute hemolysis together with methemoglobinemia shortly after his first exposure to peanuts.