Central nervous system toxicity due to mefenamic acid.

Mefenamic acid is a fenamate nonsteroidal anti-inflammatory (NSAI) drug, which is used for several years for pain management. However, it has been rarely reported that, mefenamic acid can induce central nervous system toxicity both in toxic doses and therapeutic usage. We report a case of a 27-year-old female who presented to the emergency department (ED) with altered mental status and vomiting. On admission to the ED, she was lethargic and disoriented. Her vital signs were normal and her physical examination was completely normal except dysarthric speech. The etiology of altered mental status was investigated with electrolyte levels, cranial computed tomography, cranial magnetic resonance imaging and EEG, however the results were normal. Her blood gas analysis revealed a deep metabolic acidosis with a pH of 7.14. Neither etiologic agent nor drug use history was provided at the presentation; she had only osteogenesis imperfecta since several years and she had been using various NSAI drugs. However, her relatives later stated that, she took mefenamic acid for her pains since two weeks. After her admission to intensive care unit, her neurologic state was improved gradually after plasmapheresis and she was discharged healthy. Although mefenamic acid has been considered as one of the safe NSAI drugs, its effects due to central nervous system toxicity should be cautiously handled.

Central nervous system toxicity of mefenamic acid overdose compared with other NSAIDs: an analysis of cases reported to the United Kingdom National Poisons Information Service.

AIMS: Case reports and small case series suggest increased central nervous system (CNS) toxicity, especially convulsions, after overdose of mefenamic acid, compared with other nonsteroidal anti-inflammatory drugs (NSAIDs), although comparative epidemiological studies have not been conducted. The current study compared rates of CNS toxicity after overdose between mefenamic acid, ibuprofen, diclofenac and naproxen, as reported in telephone enquiries to the UK National Poisons Information Service (NPIS). METHODS: NPIS telephone enquiries related to the four NSAIDs, received between January 2007 and December 2013, were analysed, comparing the frequency of reported CNS toxicity (convulsions, altered conscious level, agitation or aggression, confusion or disorientation) using multivariable logistic regression. RESULTS: Of 22 937 patient-specific telephone enquiries, 10 398 did not involve co-ingestion of other substances (mefenamic acid 461, ibuprofen 8090, diclofenac 1300, naproxen 547). Patients taking mefenamic acid were younger and more commonly female than those using other NSAIDs. Those ingesting mefenamic acid were more likely to experience CNS toxicity than those ingesting the other NSAIDs combined [adjusted odds ratio (OR) 7.77, 95% confidence interval (CI) 5.68, 10.62], especially convulsions (adjusted OR 81.5, 95% CI 27.8, 238.8). Predictors of CNS toxicity included reported dose and age, but not gender. CONCLUSIONS: Mefenamic acid overdose is associated with a much larger and dose-related risk of CNS toxicity, especially convulsions, compared with overdose of other NSAIDs. The benefit-risk profile of mefenamic acid should now be re-evaluated in light of effective and less toxic alternatives.

Acute renal failure from hemoglobinuric and interstitial nephritis secondary to iodine and mefenamic acid.

Mefenamic acid ingestion, usually in excess and over prolonged period is known to produce interstitial nephritis, or less commonly papillary necrosis, with acute renal failure. However, it is not dose-dependent for the induction of tubulointerstitial damage. Excess iodine ingestion is known to produce toxicity and possible death, but acute renal failure is rare. There is evidence from clinical and experimental data that iodine has toxic effect on tubular epithelial cells. Iodine has not been documented to produce red cell hemolysis and hemoglobinuria. We present a unique case of acute renal failure from hemoglobinuric and acute interstitial nephritis secondary to suicidal ingestion of potassium iodide solution and also ingestion of a few mefenamic acid tablets. These agents led to potentiation of the renal injury from hemoglobinuric tubulopathy, probably from the iodine, and renal dysfunction from alteration of renal perfusion by selective COX-1 inhibition of prostaglandin production, and induction of acute interstitial nephritis from mefenamic acid, leading to acute renal failure which was reversible by hemodialysis and supportive therapy.

A case of intravenous and oral mefenamic acid poisoning.

A 22 year old heroin addict was admitted with tonic-clonic seizures, confusion and agitation 10 hours after taking mefenamic acid 5 grams orally and 2.25 grams intravenously. This appears to be the first recorded case of intravenous mefenamic acid abuse and, although not fatal, is a cause of concern. This is a commonly used drug and its seizure inducing potential is well recognised. It may therefore be worthwhile considering the possibility of intravenous abuse of mefenamic acid in heroin addicts admitted with confusion or seizures.

Severe mefenamic acid poisoning. A case report.

An 18-year-old girl was admitted to hospital after deliberately ingesting about 90 capsules of mefenamic acid 250 mg (Ponstan). The management is discussed.

Trends in analgesic self-poisoning in West-Fife, 1971-1985.

All admissions for analgesic self-poisoning to a district poisons unit over a 15-year period have been reviewed. During this time overdose with analgesic drugs increased to represent almost half of all admissions for self-poisoning. The types of analgesics taken in overdose also changed significantly during the period of this review. Aspirin and Distalgesic poisoning declined in incidence and more cases of self-poisoning by paracetamol and non-steroidal anti-inflammatory agents were seen. The impact of these changes on the medical management and outcome of deliberate self-poisoning is analysed. The reasons behind the trends described in this paper are assessed and their implications for future prevention and treatment are discussed.

Clinical features and management of analgesic poisoning.

Analgesic poisoning is a common medical emergency, and these drugs account for about 30% of self-poisoning in adults. Aspirin and paracetamol are taken most often, and can cause significant morbidity and mortality. However, problems with the hepatotoxicity of paracetamol have been greatly reduced by the introduction of effective treatment with agents such as N-acetylcysteine. The non-steroidal anti-inflammatory analgesics are not commonly taken in overdosage but the incidence of self-poisoning with mefenamic acid is increasing at an alarming rate. With the exception of phenylbutazone and mefenamic acid these drugs rarely seem to cause serious toxicity. The narcotic analgesics can cause profound respiratory depression and are the most dangerous drugs in overdosage.