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Query: UMLS:C0012833 (dizziness)
 9,689 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

On rare occasions benzocaine has produced methemoglobinemia from oral, rectal and dermal exposures. There is disagreement whether this is an idiosyncratic event or a dose-related event. To gain a better perspective on this problem we retrospectively reviewed cases at 4 large regional poison centers of children <18-y of age from 1993-1996. One hundred and eighty-eight benzocaine exposures were reported. Mean and median ingested dosage were 86.8 (+/- 89.5) mg/kg and 50 mg/kg, respectively. Fifty-eight patients (30%) were managed in the emergency department; 8 patients had methemoglobin levels determined. One child had a methemoglobin level of 19%; all others were <1%. One hundred and seventy-three patients (92%) remained asymptomatic. Other symptoms were minor: oral numbness (8), vomiting (3), and 1 each of oral irritation, dizziness and nausea. In this series of accidental ingestions of benzocaine-containing products cyanosis was rare and apparently not dose related. These cases may be safely managed at home with telephone follow up for at least 2 h. If there is evidence of cyanosis, dusky pallor, shortness of breath, or change in mental status direct medical evaluation should be recommended.
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PMID:Multi-center retrospective evaluation of oral benzocaine exposure in children. 1092 90

Methemoglobinemia and hemolysis are the most prominent side-effects of exposure to a wide variety of arylamine drugs, including agricultural and industrial chemicals. Recent studies with aniline and dapsone have identified N-hydroxyl metabolites as the red blood cell (RBC) mediators. This study examines the time-course methemoglobinemic potential of several halogenated aniline phenylhydroxylamines. Symptoms of aniline poisoning include headache, fatigue, dizziness, respiratory and cardiac arrest, and possibly death. Initial studies indicated that the parent compounds are converted to their toxic metabolites (N-hydroxylamine), which enter the RBC and react with oxyhemoglobin. Consequent reduction of molecular oxygen to active oxygen species occurs, leading to RBC damage. Our laboratory is investigating the role of redox cycling and an alternative hypothesis--that a "hydroxylamine-centered" radical formed during arylhydroxylamine-oxyhemoglobin reaction results in RBC injury. The methemoglobinemic capacities of several structurally related N-hydroxy derivatives of aniline--phenylhydroxylamine (PHA), p-fluoro-, p-chloro-, p-bromo-, and p-iodo-PHA--were studied spectrophotometri-cally by treating washed rat RBC at concentrations ranging from 30 to 300 microM of the test compounds for up to 240 minutes. The results showed dose- and time-dependent changes in the induction of methemoglobin (MetHb) by aniline derivatives. The MetHb levels peaked to as high as 75% and remained elevated up to 240 minutes, depending on the electronegativity of halogenated phenylhydroxylamine aniline. This study supports the previous findings that there may be several aniline-derived metabolites other than PHA that are capable of inducing MetHb. The minimum dose required to induce this effect and duration of the MetHb may vary with the test agent.
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PMID:Aniline derivative-induced methemoglobin in rats. 1571 9

The athletic performance supplement industry is a multibillion-dollar business and one popular category claims to increase nitric oxide (NO) production. We report three patients presenting to the emergency department with adverse effects. A 33-year-old man presented with palpitations, dizziness, vomiting, and syncope, after the use of NO(2) platinum. His examination and electrocardiogram (ECG) were normal. The dizziness persisted, requiring admission overnight. A 21-year-old man with palpitations and near syncope had used a "nitric oxide" supplement. He was tachycardic to 115 bpm with otherwise normal examination. Laboratory values including methemoglobin, and ECG were unremarkable. He was treated with 1 L of saline with no change in heart rate. He was admitted for observation. A 24-year-old man presented after taking NO-Xplode with palpitations and a headache. His examination, laboratory values, and ECG were normal. He was discharged. The purported active ingredient in these products is arginine alpha-ketoglutarate (AAKG), which is claimed to increase NO production by supplying the precursor L-arginine. The symptoms could be due to vasodilation from increased levels of NO, though other etiologies cannot be excluded. AAKG containing supplements may be associated with adverse effects requiring hospital admission.
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PMID:Adverse effects associated with arginine alpha-ketoglutarate containing supplements. 1975 57

Nitrite stores decrease after exercise in patients with peripheral artery disease (PAD) and diabetes represents decreased nitric oxide (NO) bioavailability that may contribute to endothelial dysfunction and limit exercise duration. The primary objective of this placebo-controlled study was the safety and tolerability of multiple doses of oral sodium nitrite in patients with PAD, predominantly with diabetes, over a period of 10 weeks. The primary efficacy endpoint was endothelial flow-mediated dilatation (FMD) and secondary efficacy endpoints included a 6-minute walk test and quality of life assessment. Of the 55 subjects, the most common side effects attributed to sodium nitrite were a composite of headache and dizziness occurring in 21% with the 40 mg dose and 44% with the 80 mg dose. There was no clinically significant elevation of methemoglobin. FMD non-significantly worsened in the placebo and 40 mg groups, but was stable in the 80 mg group. Diabetic patients receiving 80 mg had significantly higher FMD compared with the placebo and 40 mg groups. There was no significant change in 6-minute walk test or quality of life parameters over time compared to placebo. In conclusion, sodium nitrite therapy is well tolerated in patients with PAD. The possible clinical benefit of sodium nitrite should be studied in a larger and fully powered trial.
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PMID:Sodium nitrite in patients with peripheral artery disease and diabetes mellitus: safety, walking distance and endothelial function. 2436 2

The authors report a case of acute methemoglobinemia in a patient treated with naproxen for the common cold. A 42-year-old Asian woman began taking naproxen sodium and methocarbamol formylagia, chills, and coughing. On the day prior to her emergency department (ED) admission,the patient was taking lorazepam, trazodon, and paroxetine in addition to the naproxen and methocarbamol prescribed for the cold symptoms, and she also ingested approximately 300 mL of 20% alcohol. Upon awakening the next morning, the patient experienced dyspnea and dizziness. At the hospital, she was diagnosed with severe methemoglobinemia. After initiation of methylene blue therapy, the patient's symptoms improved substantially and her serum methemoglobin levels decreased. After 10 days in the hospital, the patient was discharged without any complications.Naproxen is known to cause oxidative stress. Alcohol is known to reduce G6PD activity, and thus it is hypothesized that the administration of naproxen in an alcohol-dependent patient caused methemoglobinemia.
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PMID:Naproxen-induced methemoglobinemia in an alcohol-dependent patient. 2485 47