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Biomedical subjects

T J Meredith

Publications and source records attributed to T J Meredith.

At least 37 records · Page 2Linked to original sources
PubMed1984

Epidemiology of analgesic overdose in England and Wales.

The number of deaths from acute poisoning in England and Wales has remained constant at approximately 4000 per annum for the last 10 years despite major changes in the agents responsible. Deaths due to carbon monoxide and barbiturate and non-barbiturate hypnotics have fallen, while those due to psychotropic and analgesic drugs have risen. The number of hospital admissions in England and Wales due to analgesics taken in overdose has risen from 15 940 in 1968 to 24 930 in 1980, with aspirin and paracetamol being the preparations most commonly ingested. Currently, the mortality from salicylate intoxication is falling while that due to paracetamol is rising. In 1980, the Office of Population Censuses and Surveys recorded 790 deaths from analgesic poisoning, of which 181 were due to salicylates and 152 to paracetamol alone. A further 269 deaths were attributed to paracetamol and dextropropoxyphene, and an additional 132 deaths were thought to be due to paracetamol in combination with other drugs. An important factor in the changing mortality from salicylate and paracetamol poisoning is the trend observed in the sales and usage of these agents. Since 1979, the number of analgesic tablets containing aspirin sold in the UK (except Northern Ireland), excluding hospital use, has fallen by 326 X 10(6), while sales of those containing paracetamol have increased by 395 X 10(6) tablets.

Acetaminophen↗
PubMed1984

Deaths from paracetamol and dextropropoxyphene (Distalgesic) poisoning in England and Wales in 1979.

Paracetamol and dextropropoxyphene were implicated on clinical and analytical grounds in 237 poison deaths in England and Wales in 1979. In addition to paracetamol, dextropropoxyphene and ethanol, other agents were detected in 61 of these cases (26%). Analytical evidence suggests that very substantial overdoses of paracetamol and dextropropoxyphene were ingested in the majority of cases; their mean plasma concentrations in those ingesting no other agents were 252 and 8.64 mg/l respectively. Significant quantities of ethanol were ingested in 133 of 237 cases (56%). The mean ethanol concentration in those in whom quantitative estimations of paracetamol, dextropropoxyphene and ethanol were undertaken and who had not ingested other drugs, was 1588 mg/l. There was no analytical support for the diagnosis of paracetamol and dextropropoxyphene poisoning in 74 of 305 cases (24%) of H.M. Coroners' returns to the Office of Population, Censuses and Surveys for the period 1 January-31 December 1979. In addition, dextropropoxyphene was detected analytically in six cases classified as being due to paracetamol alone.

Acetaminophen↗
PubMed1982

Retrospective comparison of 'Cheno' and 'Urso' in the medical treatment of gallstones.

In two groups of gallstone patients ideally suited for medical treatment, the effect of six to 18 months' therapy was compared retrospectively in 52 given chenodeoxycholic acid (CDCA) and 46 given ursodeoxycholic acid (UDCA). The minimum dose (mg kg-1 day-1) required to desaturate bile consistently was 10.1 for UDCA and 14.3 for CDCA. In patients completing six months' treatment, 23 of 35 (66%) taking a mean of 7.7 (+/- SEM 0.5) mg UDCA and 34 of 42 (81%) taking 14.7 +/- 0.2 mg CDCA showed partial or complete dissolution of gallstones. The mean dose in the UDCA-treated patients, however, was artefactually lowered by previous dose-response studies: in those who had not taken multiple doses, the mean UDCA intake in the 'responders' at six months was 9.1 +/- 0.3 mg kg-1 day-1. At six months, more UDCA (five of 35 or 14.3%) than CDCA (four of 42 or 9.5%)-treated patients showed complete dissolution of gallstones, but, by one year, the situation was reversed, 20 of 41 (49%) CDCA-treated and eight of 30 (27%) UDCA-treated patients showing complete dissolution of gallstones. Cumulative efficacy at one year had risen to 76% for UDCA and 89% for CDCA. Both treatments reduced the frequency of dyspepsia and biliary colic; 37% of CDCA and 2.6% of UDCA-treated patients showed hypertransaminasaemia; diarrhoea developed in 60% of the CDCA group but in none of the UDCA group.

Chenodeoxycholic Acid↗
PubMed1981

Treatment of acetaminophen poisoning. The use of oral methionine.

One hundred thirty-two cases of severe acetaminophen (paracetamol) poisoning were treated with oral methionine. Seven of 96 patients who received the antidote within ten hours of ingestion of the overdose had severe liver damage (aspartate transaminase level, greater than 1,000 IU/L), but none of these patients died. Thirty-six patients received methionine between ten and 24 hours of ingestion; severe liver damage occurred in 47%, and two patients died. The treatment protocol for oral methionine is simple, and therapy is complete within 12 hours as compared with three days for oral acetylcysteine and 20 hours for intravenous acetylcysteine. Side effects from methionine were unimportant. Oral methionine is as effective as acetylcysteine in preventing severe liver damage and death after acetaminophen overdose. However, as with acetylcysteine, it must be given within ten hours of ingestion to be effective.

Acetaminophen↗
PubMed1981

The epidemiology of acute acetaminophen poisoning in England and Wales.

The mortality from analgesic poisoning in England and Wales has risen markedly during the last five years, but only a small increase in mortality from acetaminophen poisoning has been seen in the same period. Two separate epidemiologic studies of acetaminophen-overdose patients were undertaken during the two years from 1977 to 1978. Eighty-five percent of 1,644 patients and 95% of 341 patients arrived at the hospital within 12 hours of ingestion of an acetaminophen overdose. Although most patients who ingested hepatotoxic doses of acetaminophen were asymptomatic--347 (66%) of 667 and 26 (51%) of 51 patients--the absence of symptoms did not adversely affect the time of their arrival at the hospital.

Acetaminophen↗
PubMed1980

Baclofen overdose.

A 57-year-old woman suffering from multiple sclerosis took an estimated 1500 mg of baclofen. She became deeply unconscious with generalized flaccid muscle paralysis and absent tendon reflexes. Toxicological analysis confirmed the presence of baclofen together with small amounts of paracetamol and glutethimide. Supportive therapy, including assisted ventilation for 3 days, led to complete recovery; anticonvulsant drugs were necessary for the treatment of grand mal fits. The clinical features and treatment of baclofen overdose are discussed.

Baclofen↗
PubMed1980

Paracetamol.

Paracetamol is an analgesic and antipyretic agent which was first marketed for use as a drug in the U.K. in 1956. It has since become popular with the medical profession and the general public as an alternative to aspirin.

Acetaminophen↗
PubMedDate not supplied

Acute poisoning due to non-steroidal anti-inflammatory drugs. Clinical features and management.

Despite the widespread use of non-steroidal anti-inflammatory drugs (NSAIDs), the current number of reported cases of poisoning is small. However, with the introduction of 'over-the-counter' preparations of NSAIDs in some countries (e.g. ibuprofen in the UK and USA) an increased incidence of acute poisoning from this group of drugs can be expected. Conventionally, NSAIDs are divided into the following groups based on their chemical structure: arylpropionic acids, indole and indene acetic acids, heteroarylacetic acids, fenamates, phenylacetic acids, pyrazolones and oxicams. Unless NSAIDs are ingested in substantial overdose, acute poisoning with these agents does not usually result in significant morbidity or mortality. In most cases the clinical features are mild and confined to the gastrointestinal and central nervous systems, though acute renal failure, hepatic dysfunction, respiratory depression, coma, convulsions, cardiovascular collapse and cardiac arrest may complicate severe poisoning. Arylpropionic acid derivatives were thought initially to have a low order of toxicity in overdose but, in addition to anticipated gastrointestinal symptoms, headache, tinnitus, hyperventilation, sinus tachycardia, hypoprothrombinaemia, haematuria, proteinuria and acute renal failure have been described. In addition, drowsiness, coma, nystagmus, diplopia, hypothermia, hypotension, respiratory depression and cardiac arrest have been reported in severe cases of poisoning. Oxyphenbutazone and phenylbutazone are considerably more toxic in overdose. Complications of severe poisoning include coma, convulsions, hepatic dysfunction, acute renal failure, sodium and water retention, haematuria, cardiovascular collapse, respiratory alkalosis, metabolic acidosis, hypoprothrombinaemia and thrombocytopenia. In contrast, indomethacin appears to be much less toxic. In addition to gastrointestinal symptoms, indomethacin taken in overdose induces headache, tinnitus, dizziness, lethargy, drowsiness, confusion, disorientation and restlessness. Only 1 case of acute sulindac poisoning has been reported in the literature. A 16-year-old boy was admitted with hypokalaemia (2.2 mmol/L), transient granulocytosis and 'scanty' haematemesis after ingesting 12 g sulindac. No case of acute tolmetin poisoning have been reported. The fenamates (flufenamic acid, meclofenamic acid, mefenamic acid, tolfenamic acid) are, with the exception of mefenamic acid, not as widely prescribed as other groups of NSAIDs. In overdose, mefenamic acid may result in nausea, vomiting, diarrhoea, muscle twitching, convulsions and coma.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗