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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., (© 2024. The Author(s).)

A pregnant female in her early 30s presented with cyanosis and oxygen saturation of 78%. She ingested isopropyl nitrate mistaking it for cannabidiol. Her arterial blood gas showed a methaemoglobin of >30% (outside the measuring range). She was treated with 120 mg of methylthioninium chloride (2 mg/kg) and symptoms improved. Her pregnancy progressed but was induced at 36 weeks because her child was small for gestational age. Methaemoglobinaemia is a rare presentation in pregnancy. There have been no reported cases of isopropyl nitrate-induced methaemoglobinaemia in pregnancy. Historically, intra-amniotic methylthioninium chloride was used in amniocentesis but use stopped after links to fetal malformations and neonatal death were made. There is no evidence outlining the risks of isopropyl nitrate in pregnancy and limited data on fetal effects from maternal exposure to intravenous methylthioninium chloride. This case adds to the evidence that treating methaemoglobinaemia may outweigh the risks of maternal exposure to methylthioninium chloride., Competing Interests: Competing interests: None declared., (© BMJ Publishing Group Limited 2024. No commercial re-use. See rights and permissions. Published by BMJ.)

Introduction: Methemoglobinemia represents an uncommon but potentially serious cause of presentation to the emergency department, resulting in hypoxemia and even death. The symptoms and clinical findings in this condition can be nonspecific and therefore methemoglobinemia can be easily missed if the clinician is not familiar with it. This report presents a case caused by recreational drug use which has rarely been documented previously., Case Report: A 23-year-old male with a history of asthma presents to the emergency department for an episode of syncope after inhalation of amyl nitrite "poppers". He had normal vitals other than tachycardia but was found to have nailbed and perioral cyanosis, a classic but uncommon presentation that is demonstrated in the included clinical image. He was found to have methemoglobinemia caused by his use of amyl nitrite and received supportive care but did not require methylene blue., Conclusion: Emergency physicians should familiarize themselves with the classic physical exam findings in methemoglobinemia in order to identify and treat this condition promptly. While this patient had a good outcome with only supportive care and observation, his presentation and the etiology of his condition offer an important teaching point. The possibility of methemoglobinemia after recreational "popper" use should be considered when working up a patient who presents with cyanosis and hypoxemia.

Background: Methemoglobinemia is an excess of oxidized hemoglobin in the blood, affecting oxygen transportation. It is characterized by central cyanosis that does not respond to oxygen therapy. Prognosis is excellent when treated adequately and rapidly. We present a case report of a 38-year-old Caucasian man suffering from methemoglobinemia due to the use of poppers., Case Presentation: A 38-year-old Caucasian man known as a smoker and addicted to cocaine was admitted to the emergency department with dyspnea, agitation, and central cyanosis that started approximately 3 hours before admission. The persistent hypoxia despite high-flow oxygen therapy and a history of poppers use helped to reveal a condition known as methemoglobinemia., Conclusions: Our case highlighted a typical clinical presentation of methemoglobinemia. This possible life-threatening condition can occur after ingestion or inhalation of poppers, commonly sold in sex shops for recreational purposes. This can be easily confirmed by the methemoglobin level of the blood gases, provided the emergency physician considers this diagnosis. Rapid treatment with intravenous methylene blue is effective and leads to a favorable prognosis., (© 2022. The Author(s).)

Rationale: Sodium nitrite intoxication reportedly causes severe methemoglobinemia. Recent studies reported that most clinically significant cases resulted from intentional exposure in suicidal attempts. We describe 2 cases of severe methemoglobinemia secondary to intentional sodium nitrite intoxication in suicidal attempts., Patients Concerns: A 26-year-old man and 20-year-old woman attempted suicide by taking sodium nitrite, and were brought to the emergency department., Diagnosis: The male patient collapsed at the scene. He ingested approximately 18 g of sodium nitrate, and his methemoglobin level was 90.3%. The female patient was conscious, but was cyanotic. She ingested approximately 12.5 g of sodium nitrite, and her methemoglobin level was 54.6%., Interventions: The male patient received advanced cardiac life support in the emergency department. Methylene blue was immediately administered for the female patient., Outcomes: The male patient died despite aggressive resuscitation. The female patient's cyanosis resolved, and her methemoglobin level decreased to 1.2% 3 hours later., Lessons: The immediate administration of methylene blue in severe methemoglobinemia patients prevented fatal consequences. The public should be informed about the accessibility and toxicity of sodium nitrite., Competing Interests: The authors have no conflicts of interests to disclose., (Copyright © 2022 the Author(s). Published by Wolters Kluwer Health, Inc.)

Toluidine is a known cause of bladder cancer, but it is less widely recognized as a cause of methemoglobinemia because methemoglobinemia is rare. We herein report a case of methemoglobinemia caused by toluidine in a 50-year-old man. A solution of toluidine overflowed from its container during transportation and adhered to the man's clothes, but he drove to his workplace 100 km away without changing his clothes or undergoing decontamination. Before arriving at his workplace, he developed dyspnea and called emergency services, and he was then transported to a local hospital. He had significant cyanosis upon arrival, and arterial blood gas analysis revealed a high methemoglobin level of 44%. He was diagnosed with toluidine-induced methemoglobinemia and was transported to our hospital, where he was admitted to the intensive care unit. Treatment for methemoglobinemia was started immediately after hospitalization, and the patient's symptoms and methemoglobin level improved. Methemoglobinemia should be considered in workers who handle toluidine and develop cyanosis and dyspnea.

Background: Methemoglobinemia is a rare cause of neonatal cyanosis in the newborn. It is considered a medical emergency. Failure of recognition or appropriated treatment could result in serious disease and neonatal death. Neonatal methemoglobinemia can be caused by both hereditary and acquired factors., Case Description: We present two cases of newborns who developed severe cyanosis a few hours after birth due to methemoglobinemia. This was thought to be related to the local maternal perineal infiltration of prilocaine during childbirth. Though rare, prilocaine is the most potent agent to induce methemoglobinemia compared to other local aneasthetics. After intravenous administration of methylene blue, both newborns fully recovered., Conclusion: Neonatal methemoglobinemia is a rare and potentially fatal complication of local anesthetics, particularly prilocaine, administered to the mother during childbirth. Midwives, obstetricians, gynecologists and pediatricians should be aware of this complication. The use of other local anesthetics, including lidocaine, should be considered.

Dear Editor, Dapsone is a dual-function drug with antimicrobial and antiprotozoal effects and anti-inflammatory features (1). In dermatology, it is a first choice for conditions such as leprosy, IgA pemphigus, dermatitis herpetiformis, and linear IgA bullous dermatosis, or an adjunctive treatment for, e.g. bullous pemphigoid (BP) and pemphigus vulgaris (1). However, dapsone is associated with some adverse effects, including methemoglobinemia (1). Methemoglobin (MetHb) concentrations of less than 15% usually cause no symptoms in patients with normal hemoglobin concentrations (2). Herein, we report the case of a patient with BP who developed dyspnea because of dapsone-induced methemoglobinemia that was as mild as 4.7%. A 93-year-old man was diagnosed with BP based on skin manifestations (Figure 1, a and b), histopathological findings (Figure 1, c and d), and anti-BP180 NC16A antibody titer determined by chemiluminescence enzyme immunoassay (279 U/mL) 3 years earlier. His comorbidities included diabetes mellitus, chronic heart failure, right pleural effusion, and brain infarction. The patient had been successfully treated with oral prednisolone, so the steroid was tapered to 4 mg/day. The blisters recurred, however, and new ones kept developing even though the prednisolone was increased to 25 mg/day. Dapsone (75 mg/day) was begun as adjunctive treatment, and new blister formation ceased. At one week from dapsone initiation, the patient developed dyspnea, and his oxygen saturation as measured by pulse oximetry decreased to 88% on room air. At presentation, his blood pressure was 118/78 mmHg, the heart rate was 95 beats/minute, and axillary temperature was 36.3 °C. Neurological examination and consciousness findings remained unchanged compared with findings before dyspnea onset. Chest examination showed normal breath and heart sounds, but lip and peripheral cyanosis was present. Blood tests revealed a white blood cell count of 12,920/μl; red blood cells, 370×104/μl; hemoglobin, 11.7 g/dl; and CMV antigenemia (or C7-HRP), negative. Chest CT and echocardiography indicated no remarkable change compared with imaging from one year earlier. Arterial blood gas analysis showed a pH of 7.454, PaO2 63.1 mmHg, PaCO2 35.4 mmHg, HCO3- 24.3 mmol/L, SaO2 92.4%, and MetHb of 4.7%. These findings indicated a saturation gap (difference between SpO2 and SaO2) induced by MetHb. Upon cessation of dapsone, MetHb levels and SpO2 returned to normal and the dyspnea resolved, implicating dapsone in the methemoglobinemia (Figure 1, e). Differential diagnoses were pulmonary disease, heart disease, neuromuscular disease, sepsis, and drug intoxication. These possibilities were ruled out by the physical examination, drug history, vital signs, blood tests, and chest CT and echocardiography. In normal individuals, MetHb levels are less than 1% (2). Healthy patients with normal hemoglobin concentrations develop cyanosis at MetHb level of 15-20%, dyspnea at 20-50%, and coma at 50-70%, and die at more than 70% (2). However, patients with hematologic disease, acidosis, or cardiopulmonary diseases, for example, present with symptoms even with MetHb levels less than 15% (2,3). We inferred that our patient presented with dyspnea even under mild methemoglobinemia because he had anemia, chronic heart failure, and right pleural effusion. The occurrence of dapsone-induced methemoglobinemia with obvious symptoms is rare (1,4). Clinicians should be aware that methemoglobinemia symptoms are influenced not only by MetHb concentrations but also by comorbidities.

Background: Terlipressin, a long-acting synthetic analogue of vasopressin has been used in the adult population for various indications including hepatorenal syndrome (HRS-AKI), esophageal variceal hemorrhage (EVH) and shock, but its use in pediatrics is still limited to individualized cases and data on safety and efficacy is scant., Methods: We reviewed the patient records of children with liver disease and Acute Kidney Injury requiring terlipressin admitted to the Paediatric Intensive Care Unit (PICU) of King's College Hospital, London from January 2010-December 2017, with special emphasis on its effect on renal parameters and adverse event profile., Results: Twenty-one terlipressin administration records in a total of 16 patients (median) (IQR) 10 years (6.1-14.4) were included. The drug was initially given as a bolus dose in all cases, followed by either bolus or infusion with median dosage being 5.2 (3.8-6.7) mcg/kg/hour. After administration, a sustained increase of mean arterial pressure was observed. There was an improvement in serum creatinine (Cr) (at 24 h; p = 0.386) and increase in urine output (UO), especially in the hepatorenal syndrome subgroup (HRS-AKI). We found minimal evidence of gastrointestinal side effects including feeding intolerance and vasoconstrictive side effects including cyanosis / ischaemia of extremities., Conclusion: Terlipressin was found to be safe in critically sick children with liver disease with positive impact on renal parameters which might be taken as a surrogate marker of HRS reversal, though effects on outcomes are difficult to ascertain. It is important to be aware of all its side-effects and actively watch for them. Future prospective studies are warranted to validate these findings.

Purpose: Carfentanil is a synthetic opioid with an estimated potency that is 10,000 times more than that of morphine and 100 times more than that of fentanyl. Although there is a paucity of evidence, when considering the potency of carfentanil, it is reasonable to speculate that larger doses of naloxone may be required to resuscitate patients after carfentanil ingestion. This case report discusses the use of high-dose naloxone in 2 patients with suspected carfentanil overdose presenting to a small community hospital., Summary: Two patients with suspected carfentanil overdose presented to a 30-bed emergency department at a community hospital in New Hampshire. Cyanosis and respiratory distress were noted in both instances, and airway intervention was ultimately deemed necessary. Patient 1 required a total of 12 mg of naloxone to be successfully resuscitated, while patient 2 required a total of 10 mg for resuscitation. Both patients were successfully resuscitated with high doses of naloxone. The use of high-dose naloxone prevented the need for intubation in these patients., Conclusion: While more robust studies should be considered, emergency personnel should be comfortable using higher-than-standard doses of naloxone in appropriate cases., (© American Society of Health-System Pharmacists 2019. All rights reserved. For permissions, please e-mail: journals.permissions@oup.com.)

BACKGROUND Hepatorenal syndrome (HRS), which is a type of functional renal impairment, is one of the most serious complications in patients with liver cirrhosis. Terlipressin can induce splanchnic vasoconstriction, which increases the renal blood flow and has beneficial effects on HRS. However, terlipressin administration may cause serious ischemic complications such as skin ischemia, peripheral gangrene, and ischemic bowel necrosis. Here, we report a case of peripheral cyanosis following terlipressin administration in a cirrhotic patient with HRS. CASE REPORT The patient was a 65-year-old male. He was considered to have type-1 HRS, and thus, terlipressin was administered. However, peripheral cyanosis involving the fingers, toes, area around an umbilical hernia, and scrotum was noted. Thus, terlipressin administration was discontinued. Subsequently, his condition rapidly improved. CONCLUSIONS We reported a case of peripheral cyanosis following terlipressin administration, which resolved after discontinuation of terlipressin administration. It is important to recognize the early signs of side effects and discontinue the administration of the suspected drug immediately.

Methemoglobinemia is a condition characterized by a high blood concentration of methemoglobin. Methemoglobinemia is a disorder that occurs when hemoglobin in the blood is oxidized to form methemoglobin, rendering it unable to transport oxygen. Although it can be congenital in cyanotic newborn, it is more often an adverse medication effect. The aim is to report a pediatric methemoglobinemia case, assisted in Magdalena V. de Martínez Hospital, with cyanosis in face and limb, in poor condition, that consumed dapsone accidentally. Her methemoglobin concentration was 35%. Intravenous methylene blue was administered with favorable outcome., (Sociedad Argentina de Pediatría.)

Rationale: Acute kidney injury (AKI) with hyperparathyroidism caused by nitrite was rare, and renal function and parathyroid hormone (PTH) decreased to normal range after therapy., Patient Concerns: Acute kidney injury was diagnosed in a 40-year-old male with hyperparathyroidism and cyanosis of his hands and both forearms., Diagnoses: The patient ate some recently pickled vegetables, and he experienced nausea, vomiting and diarrhoea without oliguria or anuria; Additionally, his hands and both forearms had a typical blue ash appearance. After admission, the laboratory findings indicated theincreasing serum creatinine (Scr) and parathyroid hormone (PTH). He was diagnosed as acute kidney injury with hyperparathyroidism caused by nitrite., Interventions: The patient stopped eating the pickled vegetables and was given rehydration, added calories and other supportive therapy without any glucocorticoids., Outcomes: According to his clinical manifestations, laboratory findings and imaging results, the patient was diagnosed with acute kidney injury with secondary hyperparathyroidism. He was given symptomatic supportive care therapy. After one week, the serum creatinine, parathyroid hormone (PTH), hypercalcemia, hyperphosphatemia, proteinuria, and urine red blood cell values decreased to normal range., Lessons: Nitrite-induced acute kidney injury with secondary hyperparathyroidism was relatively rare. After therapy, the function of the kidney and parathyroid returned to normal. This case suggests that detailed collection of medical history, physical examination and correct symptomatic treatment is very important.

Although the use of topical local anesthetics is generally safe, several potentially fatal complications have been reported. Methemoglobinemia is a rare but potentially fatal complication. Methemoglobin is a naturally occurring oxidized metabolite of hemoglobin, and physiologic levels (<1%) are normal. Methemoglobinemia can be congenital or acquired. Several drugs including topical anesthetic agents like benzocaine can induce this condition. Sudden appearance of cyanosis, with a disproportionately better oxygen saturation of 85% after use of local anesthetics can be a helpful for diagnosis.

A previously well 4-year-old boy presented to the emergency room with progressive cyanosis, pallor and vomiting over the last 5 h. Oxygen saturation on pulse oximetry was 87-89% despite 9 L/min of supplemental oxygen. He was tachypnoeic and had a systolic heart murmur, with no other findings on clinical examination. In his medical history, there was record of a restrictive atrial septal defect, with a normal echocardiogram from 3 years before. He had no relevant family history. His shoes appeared to have been recently painted, which raised the suspicion of methaemoglobinaemia, presumptively caused by aniline-containing shoe dye. The shoes were removed promptly and his feet washed profusely. After confirming the diagnosis, methylene blue was started. The level of methaemoglobin decreased rapidly and the boy made a full recovery., (2015 BMJ Publishing Group Ltd.)

Purple glove syndrome is a rare and poorly understood complication of phenytoin use, occurring almost always with its intravenous formulation. This syndrome comprises of pain, purple discoloration, and edema distal to the site of intravenous administration of phenytoin. We hereby report an unusual case, wherein purple glove syndrome was seen on oral formulation of phenytoin in its therapeutic dose.

We describe a case of acquired methaemoglobinaemia due to frequent use of the 'legal high' known as 'Pink Panthers'. This contains 5,6-Methylenedioxy-2-aminoindane and 2-Aminoindane, both amphetamine analogues with the potential to cause methaemoglobinaemia. Furthermore, the most common 'cutting agent' for legal highs in the UK is benzocaine, also known to cause methaemoglobinaemia. Given the increasing prevalence of legal highs, particularly those containing added benzocaine, such presentations may become more common. Furthermore, in one case series, benzocaine gel used for toothache was the second most common reason for hospitalisation due to acquired methaemoglobinaemia after dapsone use. Indeed, the Federal Drug Agency has issued as public warning as to the risk of these products. We therefore think that clinicians and the public should be made more aware of the risk associated with such agents., (Published by the BMJ Publishing Group Limited. For permission to use (where not already granted under a licence) please go to http://group.bmj.com/group/rights-licensing/permissions.)

Background: Toxin-induced methemoglobinemia is seen in poisoning with oxidizing agents. We report the clinical features and outcome of patients admitted with severe methemoglobinemia due to intentional ingestion of toxicants., Methods: In this observational case series, patients admitted with toxin-induced methemoglobinemia between September 2011 and January 2014 were identified from the institutional poisoning database. Clinical profile and outcome of patients with methemoglobin concentration greater than or equal to 49% is reported., Results: Of the 824 patients admitted with poisoning, 5 patients with methemoglobin concentration greater than or equal to 49% were included. The implicated compounds were nitrobenzene, benzoylphenylurea, flubendamide and Rishab(TM). One patient refused to name the compound. All patients were managed in the intensive care unit. Altered sensorium [Glasgow coma scale (GCS) < 10] was common (80%); 2 patients presented with a GCS greater than 4. All patients manifested cyanosis, low oxygen saturation and chocolate-brown-colored blood despite supplemental oxygen therapy. The median methemoglobin concentration was 64.7% (range 49.8-91.6%); 2 patients had methemoglobin concentration greater than 70%. One patient needed inotropes. Four patients required mechanical ventilation for 4-14 days. All patients were treated with methylene blue; 4 received more than one dose. Three patients also received intravenous ascorbic acid 500 mg, once daily, for 3 days. Following treatment, there was evidence of haemolysis in all patients; 2 required blood transfusion. All patients survived., Conclusion: Patients with severe toxin-induced methemoglobinemia present with altered sensorium and cyanosis and may require ventilatory support and inotropes. Though methemoglobin concentrations greater than 70% are considered fatal, aggressive management with methylene blue and supportive therapy can lead to survival.

We present a case of acquired methaemoglobinaemia related to the prolonged use of dapsone in a patient with chronic hypoxia. The patient was initially successfully treated for infective exacerbation of chronic obstructive pulmonary disease (COPD). However, he remained persistently hypoxic on pulse oximetry despite a normal PaO2 on arterial blood gas sampling. His fraction of methaemoglobin (FMetHb) was found to be elevated at 13%. After cessation of dapsone, his clinical cyanosis recuperated, his exercise tolerance and functional capacity improved and his FMetHb normalised to 1%.

A 25-year man presented to the Accident and Emergency Department complaining of dizziness and shortness of breath after taking 70 grams of cocaine over 10 hours. He said a friend had noticed that his skin had turned dark blue. On examination the patient was severely centrally and peripherally cyanosed. His pulse oximeter oxygen saturations were 88% on air. An arterial blood gas showed a methaemoglobin level of 45.6%. The patient was diagnosed with cocaine-induced methaemoglobinaemia and given methyl thioninium chloride (methylene blue). He made an uneventful recovery.

A 39-year-old man presented to the emergency department after falling downstairs after he consumed a large quantity of alcohol. On examination, he had altered mental state (GCS 14), central cyanosis and low oxygen saturation of 86%, despite 100% oxygen being administered. His arterial blood gas confirmed diagnosis of methaemoglobinaemia with a methaemoglobin percentage of 14.08. He was treated successfully with methylthioninium chloride. The patient later admitted to use of recreational poppers (amyl nitrates) the previous evening. The emergency physician is challenged by the presentation of a patient with altered mental state and unexplained low oxygen saturation with concurrent alcohol intoxication but must have a high index of suspicion for methaemoglobinaemia particularly with a history of recreational drug ingestion.

Dinitrotoluene (DNT) is a nitroaromatic explosive used in propellant mixtures and in the production of plastics. Isomers of DNT were administered daily via oral gavage to male Sprague-Dawley rats for 14 days to determine the subacute toxicity of individual isomers of DNT. The 3,5-DNT isomer was the most toxic isomer, inducing weight loss and mortality within 3 days. Cyanosis and anemia were observed for all isomers. Exposure to 2,4-, 2,6-, and 3,5-DNT resulted in decreased testes mass and degenerative histopathological changes. Increased splenic mass was observed for 2,4-, 2,6-, and 2,5-DNT. Extramedullary hematopoiesis of the spleen was noted for all isomers, while lymphoid hyperplasia of the spleen was noted for all isomers except 2,5-DNT. Increased liver mass was observed for 2,3-DNT and 3,4-DNT. Hepatocellular lesions were observed for 2,6-DNT and 2,4-DNT. Neurotoxic effects were noted for 3,4-DNT, 2,4-DNT, and 3,5-DNT.

The safety and tolerability of primaquine (PQ) administered as a short higher-dose (30mg twice daily for 7 days) regimen in 203 Australian Defence Force personnel was evaluated in an open-label presumptive anti-relapse therapy study. No clinically significant differences were measured in the subjects' haematological and biochemical indices before and after PQ treatment. The most common adverse events were nausea, abdominal pain, headache and insomnia, many of which were mild in severity (30%; 60/203) and transient; 19% of subjects (39/203) experienced moderate (with some interference with daily duties requiring no or minimal medical therapy) adverse events. Two subjects (1%) had severe gastrointestinal adverse events requiring cessation of medication, but neither was seriously ill. Ten subjects (5%) had peripheral cyanosis (blueness of the lips), but none reported any respiratory compromise. These findings suggest that the short higher-dose PQ regimen is safe and well tolerated, which could improve PQ compliance and effectiveness., (Crown Copyright © 2011. Published by Elsevier Ltd. All rights reserved.)

Peptide deformylase (PDF) inhibitors represent a potential new class of antibiotics targeting a large number of bacterial species. We studied the pharmacokinetics and safety of LBM415, a novel PDF inhibitor, administered as a single oral dose at 100-3,000 mg in the fasted state and at 1,000 mg in the fed state in healthy volunteers. LBM415 was then administered at dosages ranging from 100 mg q.d. to 1,000 mg t.i.d. for 11 days. Dose-proportional pharmacokinetics was observed, with a peak plasma concentration (C(max)) of 17.85 ± 5.96 µg/ml at 1,000 mg b.i.d. (the projected therapeutic dose) and an area under the concentration-time curve (AUC)(0-24h) of 36.83 ± 10.36 µg/ml·h. The half-life, as determined after a 1,000-mg single dose, was 2.18 ± 0.61 h. The compound was well tolerated at low doses, but at the highest dose, 1,000 mg t.i.d., reversible cyanosis and low oxygen saturation, attributable to methemoglobinemia, were detected on day 11. Oxygen saturation was as low as 88% in one subject on day 11.

Unlabelled: In previous years, several publications have reported cases of infants presenting neurological and gastrointestinal symptoms after ingestion of star anise tea. Such teas are sometimes given in various cultures for the treatment of infant colic pains. In most cases, the cause of intoxication was contamination of Chinese star anise (Illicium verum) by Japanese star anise (Illicium anisatum). Indeed, the toxicity of Illicium anisatum, also known as Shikimi, is caused by its content in potent neurotoxins (anisatin, neoanisatin, and pseudoanisatin), due to their activity as non-competitive antagonists of GABA receptors. The main reasons explaining the frequent contaminations are the strong macroscopic resemblance of the 2 substances, as well as the fact that the fruits are often sold partially broken or in ground form. Therefore, in most cases, chemical analysis is required to determine the possible adulterations., Case Report: A 2-month-old infant, in good general health, was brought to the emergency unit after 3 consecutive episodes of central cyanosis and tetany of the limbs with spontaneous recovery the same afternoon. The child was also very irritable, regurgitated a lot, and positioned himself in opisthotonos. Between these episodes, the neurological exam showed some perturbations (horizontal nystagmus and Bell's phenomenon, hypertony of the extensor muscles, and mild hypotony of the axial flexor muscles) with slow improvement over the following hours. The remaining clinical exam, the laboratory work (complete blood count, renal, hepatic, and muscular tests, capillary blood gas, plasmatic amino acids, and urinary organic acids), and the electroencephalogram findings were all normal. In the course of a detailed interview, the parents reported having given 3 bottles to their child, each one containing 200 mL of an infusion with 4 to 5 fruits of star anise, in the hours preceding the symptoms to relieve colic pains. The last seizure-like event took place approximately 8h after the last ingestion. We could prove the ingestion of anisatin, the toxic substance found in Japanese star anise, and the contamination of Chinese star anise by the Japanese species. Indeed, the anisatin analysis by liquid chromatography and mass spectroscopy (LC-MS) in a urine sample taken 22 h after the last infusion ingestion showed trace amounts of the substance. In another urine sample taken 33 h after ingestion, no anisatin could be detected. Furthermore, the analysis of the fruit sample gave an anisatin concentration of 7800 μg/kg while the maximum tolerance value in Switzerland is 1000 μg/kg., Conclusion: The evaluation of ALTE in infants should always include the possibility of intoxication. Star anise is generally considered a harmless medicine. Nevertheless, it can sometimes cause a severe intoxication resulting in various neurological and gastrointestinal symptoms. To prevent such events, not only the parents, but also the care personnel and pharmacists must be informed about the possible adverse effects caused either by the overdose of Chinese star anise or by the eventual contamination of herbal teas with Japanese star anise. A better control of the substances by the health authorities is also necessary., (Copyright © 2011. Published by Elsevier SAS.)

Ergotamine-induced limb ischemia is rare and usually results from an accidental overdose. Several agents, including erythromycin and tetracycline, raise serum ergotamine levels and augment its effect. We present a case of acute lower limb ischemia with characteristic angiography findings of diffuse arterial spasm resulting from use of ergotamine and an erythromycin derivative, clarithromycin. The history of the patient and classic features seen on angiography helped us establish the diagnosis. The patient was successfully treated with low molecular heparin and epidural infusion of bupivacain. Since ergot vasospasm is a self limited and medically treatable condition, interventional radiologists must be aware of ergotamine-induced acute limb ischemia to avoid any unnecessary interventional procedures, unless necrosis and gangrene are imminent.