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PubMedDate not supplied

Repetitive microvolumetric sampling and analysis of acetaminophen and its toxicologically relevant metabolites in murine plasma and urine using high performance liquid chromatography.

Acetaminophen is a widely used, nonprescription analgesic and antipyretic drug which can cause severe hepatic and renal cellular necrosis. Analysis of plasma and urinary concentrations of acetaminophen metabolites can facilitate an understanding of the relation of enzymatic pathways involved in the bioactivation and detoxification of acetaminophen to its cellular toxicity. There is a marked interindividual variability in the activity of these enzymatic pathways which play a critical role in the modulation of acetaminophen toxicity. A similar interindividual variability occurs in the in vivo temporal disposition of acetaminophen and its metabolites. Accordingly, optimal in vivo methods would permit repetitive sampling from the same animals, as opposed to sacrificing groups of different animals for each time point. This is particularly difficult in smaller rodents such as the mouse, where generally a single blood sample is obtained by cardiac puncture, often under conditions of general anesthesia which can affect drug metabolism and toxicity. A microvolumetric technique for repetitive blood sampling in individual mice, combined with a simple, high performance liquid chromatographic assay for acetaminophen and its toxicologically relevant metabolites is reported here. Data are presented for the disposition of acetaminophen and its metabolites in murine plasma, feces, and urine.

Acetaminophen↗
PubMed2003

Hepatocellular damage from non-steroidal anti-inflammatory drugs.

Non-steroidal anti-inflammatory drugs (NSAIDs) are widely used for the management of rheumatological disorders, and as analgesics and antipyretics. Hepatotoxicity is an uncommon, but potentially lethal complication, which usually occurs within 12 weeks of starting therapy. It can occur with all NSAIDs, but appears to be more common with diclofenac and particularly sulindac. Female patients aged >50 years, with autoimmune disease, and those on other potentially hepatotoxic drugs, appear to be particularly susceptible. Liver function test abnormalities generally settle within 4-6 weeks of stopping the causative drug. However, some patients may develop acute liver failure and successful orthotopic liver transplantation may be undertaken in such patients. Recent in vitro animal studies have shown that the mechanism of diclofenac toxicity relates both to impairment of ATP synthesis by mitochondria, and to production of active metabolites, particularly n,5-dihydroxydiclofenac, which causes direct cytotoxicity. Mitochondrial permeability transition (MPT) has also been shown to be important in diclofenac-induced liver injury, resulting in generation of reactive oxygen species, mitochondrial swelling and oxidation of NADP and protein thiols. Physicians and hepatologists must be vigilant to the hepatotoxic potential of any NSAID, as increased awareness, surveillance and reporting of these events will lead to a better understanding of the risk factors and the pathophysiology of NSAID-related hepatotoxicity.

Animals↗
PubMed1979

The pharmacological properties of ketoprofen and its place in antirheumatic therapy.

The anti-inflammatory effects of ketoprofen (Alrheumat) in inflamed areas are achieved by antagonizing inflammation mediators or blocking their synthesis. In addition to this peripheral effect, central analgesic and antipyretic effects also are detectable. The pharmacodynamic and pharmacokinetic properties of ketoprofen clearly distinguish it from other non-steroidal anti-inflammatory agents. These properties could also explain the low number of side-effects.

Analgesia↗
PubMed1991

Therapy with and mechanisms of nonsteroidal anti-inflammatory drugs.

Nonsteroidal anti-inflammatory drugs have anti-inflammatory, analgesic, and antipyretic properties. Although most nonsteroidal anti-inflammatory drugs inhibit prostaglandin synthesis, these agents also have important pharmacologic actions unrelated to their effects on prostaglandins. Among these properties is the ability to inhibit the release of mediators of inflammation from neutrophils and macrophages. These effects are due to the ability of nonsteroidal anti-inflammatory drugs to intercalate into the lipid bilayer of the plasma membrane and thereby disrupt protein-protein and protein-lipid interactions critical for cell responses (eg, calcium translocations, membrane phospholipid turnover). Our data, for example, indicate that nonsteroidal anti-inflammatory drugs exert direct inhibitory actions at the regulatory GTP protein (G protein) within the plasma membrane. This exhibit examines the evidence for diverse mechanisms of action of nonsteroidal anti-inflammatory drugs including effects directed at the G protein as well as new evidence that nonsteroidal anti-inflammatory drugs regulate the expression of the cyclooxygenase enzyme at the level of gene transcription.

Anti-Inflammatory Agents, Non-Steroidal↗
PubMed1992

Treatment of gout and crystal arthropathies and uses and mechanisms of action of nonsteroidal anti-inflammatory drugs.

Nonsteroidal anti-inflammatory agents have anti-inflammatory, analgesic, and antipyretic actions. Nonsteroidal anti-inflammatory drugs are the preferred class of agents for the treatment of gout and other crystal-induced arthropathies. The use of colchicine for other than the prophylaxis of acute attacks is discouraged owing to side effects, which include death. The inhibition of the enzyme prostaglandin H synthase by most nonsteroidal anti-inflammatory drugs explains many of their effects and toxicities. However, it is likely that additional biologic actions are important. These include the inhibition of the transcription of the gene for prostaglandin H synthase, a direct central effect on peripheral inflammation, and the modulation of the functions of a variety of cells (eg, neutrophils, lymphocytes, and chondrocytes). This review focuses on the current controversy in the treatment of gout and discusses the recent literature on the actions of nonsteroidal anti-inflammatory drugs.

Anti-Inflammatory Agents, Non-Steroidal↗
PubMed1982

Cimetidine and acetylcysteine as antidote for acetaminophen overdose.

The incidence of acetaminophen overdose, often resulting in hepatotoxicity or even death, steadily increases as its use (instead of aspirin) as an antipyretic and analgesic increases. Acetaminophen-induced hepatotoxicity is though to be dependent on the dose ingested and the activity of the cytochrome P450 enzyme system. The actual hepatotoxic mechanism is believed to be the formation of a toxic tissue arylating metabolite(s). Current therapy attempts to inactivate this toxic metabolite(s) with acetylcysteine, as opposed to inhibiting its production. Because cimetidine can inhibit the cytochrome P450 mixed-function oxidase system, we believe it could decrease the production of the hepatotoxic acetaminophen metabolite(s) providing an effective antidote to be used in conjunction with acetylcysteine.

Acetaminophen↗
PubMed2006

A population-based case-control study of risk factors for neural tube defects in four high-prevalence areas of Shanxi province, China.

Shanxi province in Northern China has one of the highest reported prevalence rates of neural tube defects (NTD) in the world. To explore the risk factors for NTDs in Shanxi province, we carried out a population-based case-control study in four selected counties with prevalence rates >10 per 1000 births during 2003. Using a multi-logistic regression model analysis (alpha = 0.10), 158 NTD cases were compared with 226 control mothers. Maternal factors significantly associated with increased risk for an NTD were a primary school education or lower (adjusted odds ratio [OR] 2.32, 95% confidence interval [CI] 1.09, 4.97); a history of a previous birth defect-affected pregnancy (adjusted OR 5.27, 95% CI 0.98, 28.37); history of a fever or 'cold' (adjusted OR 3.36, 95% CI 1.68, 6.72); use of analgesic and antipyretic drugs (adjusted OR 4.89, 95% CI 0.92, 25.97); daily passive exposure to cigarette smoke (adjusted OR 1.60, 95% CI 0.94, 2.73); poor ventilation during heating (adjusted OR 3.91, 95% CI 0.75, 20.81); and consumption of >or= six meals per week containing pickled vegetables (adjusted OR 3.86, 95% CI 1.11, 13.47) during pregnancy. Factors which appeared to be protective were meat consumption one to three times per week (adjusted OR 0.62, 95% CI 0.37, 1.06), or >or= four times per week (adjusted OR 0.28, 95% CI 0.11, 0.77); and legume consumption >or= six times per week (adjusted OR 0.39, 95% CI 0.17, 0.89). Differences in risk were found between the two most common phenotypes, anencephaly and spina bifida. Most of the environmental factors had stronger positive and negative associations with risk for anencephaly rather than spina bifida, whereas history of a previous birth defect-associated pregnancy, as well as legume consumption, were more strongly associated with the risk for spina bifida than for anencephaly. The findings suggest that aetiological heterogeneity may exist between anencephaly and spina bifida.

Adult↗
PubMed2004

Henna (Lawsonia inermis Linn.) induced haemolytic anaemia in siblings.

Henna is a traditional cosmetic agent and is used worldwide. It is used worldwide not only as a cosmetic agent to stain the hair, skin and nails but also is applied to the body on lesions in the treatment of seborrheic dermatitis or fungal infections. Different pathologies have been described as caused by henna. The aim of this study is to draw attention to the adverse effects of henna, applied over the whole body, observed in glucose-6-phosphate dehydrogenase (G6PD) enzyme deficient siblings. In the present paper, we report on two siblings with G6PD deficiency who developed haemolytic anaemia following topical application of henna to their whole body to treat skin lesions. Their parents were also found to be G6PD deficient. Even though anti-inflammatory, analgesic and antipyretic effects of henna have been shown, it may cause severe side-effects in some cases. For this reason, especially, in the regions where G6PD enzyme deficiency is common, people should be informed about the side-effects of topical henna application and clinicians should be aware of these manifestations.

Administration, Topical↗
PubMedDate not supplied

The world's longest surviving paediatric practices: some themes of Aboriginal medical ethnobotany in Australia.

Contemporary paediatric practices of Australian Aboriginal men and women, in more than 100 Aboriginal Language Groups, comprise a living discipline whose origins predate Western medicine by tens of millennia. The history of paediatrics acknowledges this surviving continuum of the world's oldest child-care practices. Because of the inextricable nexus between Aboriginal men and women and the land in which they live, medical ethnobotany forms a major part of the medical aspects of Aboriginal child care. Traditional tribal healers, called 'Nungungi' in some language groups of Central Australia, are identified as such whilst still young children and are given special education in the healing arts, especially that of medical ethnobotany, by older healers. Distinct from this specialized role, all Aboriginal men and women (and in particular grandmothers) in traditional communities use a sophisticated botanical materia medica in the treatment of sick and injured children. In cultures in transition, medical ethnobotanical practices may persist long after the local use of flora as sources of traditional food, weaponry, totemic identity and religious rites have disappeared. Some selected botanical 'cures' were adopted by early European settlers and a number of such relict uses have become part of mainstream Western life today, particularly as this applies to self-medication. Drugs and medicaments used in the treatment of children are obtained from leaves, bark, roots and flowers, usually as fresh preparations. They are prepared as infusions, decoctions and macerations and may be enjoined with emollients such as emu or kangaroo fat for topical application. Botanical drugs and medicaments are usually prepared fresh for each administration and are rarely stored. Contemporary Australian ethnobotany exploits the medicinal properties of more than 100 genera - using such extracts as antiseptics, analgesics, astringents, antipyretics, sedatives, hypnotics, expectorants and carminatives. Their widespread use, by the world's oldest surviving cultures, reflect perhaps 50 millennia of acute observation and clinical interpretation, trial and error, serendipidity and experimentation. Australian medical ethnobotany generally, and that used specifically for children, is characterized by several features including (i) the multipurpose or 'broad-spectrum' use of many floral species; (ii) a paradigm of the use of botanical material to treat symptoms and symptom-complexes rather than disease-based treatment; (iii) the widespread and universal medical knowledge of botanical remedies by all members of local Aboriginal communities, not only traditional community or tribal healers and (iv) the use of botanical material in the context of preventive medicine. Seventy per cent of the world's population uses traditional herbal remedies in the treatment of sick or injured children. In this context, the detailed and extensive ethnobotanical pharmacopoeia of the Aboriginal Peoples of Australia holds an important place.

Australia↗
PubMed2001

Hu 210: a potent tool for investigations of the cannabinoid system.

The synthetic compound HU 210 displays a multiplicity of biochemical, pharmacological, and behavioral effects, most of which have been demonstrated to be dependent on a selective agonistic activity at CB(1) and CB(2) cannabinoid receptors and to involve the main neurotransmitter systems. Results obtained in various studies suggest a potential clinical application of this highly potent drug (e.g., as antipyretic, antiinflammatory, analgesic, antiemetic, and antipsychotic agent) as well as its usefulness in research aimed to develop a better understanding of the involvement of the endogenous cannabinoid system in a number of physiopathological functions.

Analgesia↗
PubMed2005

National estimates of medication use in nursing homes: findings from the 1997 medicare current beneficiary survey and the 1996 medical expenditure survey.

OBJECTIVES: To provide the first nationwide estimates of medication use in nursing homes (NHs) and to introduce a new data set for examining drug use in long-term care facilities. DESIGN: Cross-sectional comparison. SETTING: NH medication files from two nationally representative data sets, the 1997 Medicare Current Beneficiary Survey (MCBS) and the 1996 Medical Expenditure Panel Survey-Nursing Home Component (MEPS-NHC). PARTICIPANTS: NH residents in the MCBS (n=929, weighted n=2.0 million) and MEPS-NHC (n=5,899, weighted n=3.1 million). MEASUREMENTS: Estimates include characteristics of facilities and residents, average number of drugs used per person per month, and the prevalence and duration of use by select therapeutic drug classes. RESULTS: NH residents received, on average, seven to eight medications each month (7.6 MCBS, 7.2 MEPS-NHC). About one-third of residents had monthly drug regimens of nine or more medications (31.8% MCBS, 32.4% MEPS-NHC). The most commonly used medications in NHs, in descending order, were analgesics and antipyretics, gastrointestinal agents, electrolytic and caloric preparations, central nervous system agents, anti-infective agents, and cardiovascular agents. CONCLUSION: These estimates serve as examples of the first national benchmarks of prescribing patterns in NHs. This study highlights the usefulness of the MCBS as an important new resource for examining medication use in NHs.

Activities of Daily Living↗
PubMed1997

Aspirin for the second hundred years: new uses for an old drug.

The history of aspirin can be traced back to ancient Egypt where extract of willow bark was used to treat inflammation. The active component of the extract was identified as the glucoside of salicylic alcohol. The severe gastric side effects associated with the use of sodium salicylate prompted the synthesis of the o-acetyl-derivative as a possible pro-drug. In fact, acetylsalicylic acid was antiinflammatory, analgesic and antipyretic but also ulcerogenic to the stomach. Acetylsalicylic acid was synthesized one hundred years ago, and was mass-produced under the commercial name of 'Aspirin' (Dreser, 1899) by the German company Bayer for the treatment of fever and rheumatism.

Alzheimer Disease↗
PubMed1985

Clinical pharmacology and therapeutic uses of non-steroidal anti-inflammatory drugs in the horse.

Weak organic acids possessing anti-inflammatory, analgesic and antipyretic properties--commonly known as aspirin-like drugs--have been used in equine medicine for almost 100 years. These non-steroidal anti-inflammatory drugs (NSAIDs) may be classified chemically into two groups; the enolic acids such as phenylbutazone and carboxylic acids like flunixin, meclofenamate and naproxen. All NSAIDs have similar and possibly identical modes of action accounting for both their therapeutic and their toxic effects. They block some part of the cyclo-oxygenase enzyme pathway and thereby suppress the synthesis of several chemical mediators of inflammation, collectively known as eicosanoids. The available evidence indicates that some of the newer NSAIDs have a reasonable safety margin but further studies are required. The toxicity of phenylbutazone in the horse has been investigated very thoroughly in recent years and it has been shown to cause renotoxicity and, most significantly, ulceration of the gastrointestinal tract when relatively high doses are administered. Several factors may predispose towards phenylbutazone toxicity in the horse, including breed and age, but high dosage is considered to be particularly important. The absorption into, and fate within, the body of NSAIDs are considered and particular attention is drawn to the ways in which these pharmacokinetic properties relate to the drugs' toxicity and clinical efficacy. In reviewing current knowledge of the clinical pharmacology of this important group of drugs, it is hoped to provide the clinician with a rational, scientific basis for their safe and effective use in equine practice.

Animals↗
PubMed2003

Inhibition of prostaglandin H2 synthases by salicylate is dependent on the oxidative state of the enzymes.

At antipyretic and analgesic doses, salicylate has no antiplatelet or anti-inflammatory effects, unlike typical inhibitors of the prostaglandin H synthases (PGHSs). We demonstrated that salicylate inhibits PGHS-1 and -2 with a potency inversely related to ambient hydroperoxide concentrations. Salicylate inhibition of PGHS-1 was prevented by 12-hydroperoxyeicosatetraenoic acid (12-HPETE). Increasing the production of prostaglandin G2 (the peroxide product of PGHS-cyclooxygenase activity) by elevating the concentration of either enzyme or substrate reversed inhibition. Using analogs of benzoic acid differing only at the hydroxyl position, we revealed the importance of this moiety to salicylate's inhibitory mechanism. Unlike typical phenolic inhibitors, e.g., acetaminophen, salicylate was ineffective as a reducing cosubstrate for PGHS-peroxidase activity, implicating the cyclooxygenase site as its putative target. PGHS-cyclooxygenase activity depends upon the oxidation of an active site tyrosine by electron transfer to the oxidized ferriprotoporphyrin of the peroxidase. The PGHS-1 apoenzyme reconstituted with manganese protoporphyrin instead of iron protoporphyrin has very little peroxidase activity. 12-HPETE does not prevent the inhibition of Mn-PGHS-1 by salicylate, indicating that reversal of salicylate inhibition by hydroperoxides depends upon electron transfer between the cyclooxygenase and peroxidase active sites. These results are consistent with an inhibitory action of salicylate at the PGHS-cyclooxygenase site that is dependent on the PGHS-peroxidase activity.

Animals↗
PubMed2002

Cyclooxygenase-2--10 years later.

The enzyme cyclooxygenase (COX) catalyzes the first step of the synthesis of prostanoids. In the early 1990s, COX was demonstrated to exist as two distinct isoforms. COX-1 is constitutively expressed as a "housekeeping" enzyme in most tissues. By contrast, COX-2 can be up-regulated by various pro-inflammatory agents, including lipopolysaccharide, cytokines, and growth factors. Whereas many of the side effects of nonsteroidal anti-inflammatory drugs (NSAIDs) (e.g., gastrointestinal ulceration and bleeding, platelet dysfunctions) are caused by a suppression of COX-1 activity, inhibition of COX-2-derived prostanoids facilitates the anti-inflammatory, analgesic, and antipyretic effects of NSAIDs. During the past few years specific inhibitors of the COX-2 enzyme have emerged as important pharmacological tools for treatment of pain and arthritis. However, although COX-2 was initially regarded as a source of pathological prostanoids only, recent studies have indicated that this isoenzyme mediates a variety of physiological responses within the organism. The present review assesses recent advances in COX-2 research, with particular emphasis on new insights into pathophysiological and physiological functions of this isoenzyme.

Animals↗
PubMed2006

Targeting PGE2 receptor subtypes rather than cyclooxygenases: a bridge over troubled water?

Prostaglandins (PG) are synthesized by the sequential action of phosholipases, cyclooxygenases (COX)-1 and COX-2, and specific terminal synthases, and exert their diverse biological effects through several membrane receptors. In particular, PGE2 is involved in many normal and pathological pathways that are mediated by four different E prostanoid receptors (EP1-4). Selective COX-2 inhibitors (Coxibs) have analgesic and antipyretic effects that are indistinguishable from those of nonsteroidal anti-inflammatory drugs (NSAIDs), but some possess hazardous cardiovascular side effects. Recent results indicate that EP1 and EP4 antagonists might prove useful for inhibiting the unwanted actions of COX-2. Has the time come for research to examine earnestly the selective antagonism of EP subtypes rather than further the development of direct COX-2 inhibitors?

Animals↗
PubMed2005

Mefenamic acid shows neuroprotective effects and improves cognitive impairment in in vitro and in vivo Alzheimer's disease models.

Nonsteroidal anti-inflammatory drugs (NSAIDs) exert anti-inflammatory, analgesic, and antipyretic activities and suppress prostaglandin synthesis by inhibiting cyclooxygenase, an enzyme that catalyzes the formation of prostaglandin precursors from arachidonic acid. Epidemiological observations indicate that the long-term treatment of patients suffering from rheumatoid arthritis with NSAIDs results in reduced risk and delayed onset of Alzheimer's disease. In this study, we investigated the therapeutic potential for Alzheimer's disease of mefenamic acid, a commonly used NSAID that is a cyclooxygenase-1 and 2 inhibitor with only moderate anti-inflammatory properties. We found that mefenamic acid attenuates the neurotoxicities induced by amyloid beta peptide (Abeta)(1-42) treatment and the expression of a Swedish double mutation (KM595/596NL) of amyloid precursor protein (Swe-APP) or the C-terminal fragments of APP (APP-CTs) in neuronal cells. We also show that mefenamic acid decreases the production of the free radical nitric oxide and reduces cytochrome c release from mitochondria induced by Abeta(1-42), Swe-APP, or APP-CTs in neuronal cells. In addition, mefenamic acid up-regulates expression of the antiapoptotic protein Bcl-X(L). Moreover, our study demonstrates for the first time that mefenamic acid improves learning and memory impairment in an Abeta(1-42)-infused Alzheimer's disease rat model. Taking these in vitro and in vivo results together, our study suggests that mefenamic acid could be used as a therapeutic agent in Alzheimer's disease.

Alzheimer Disease↗
PubMed2001

Niflumic acid and cutaneous reactions in children.

In a case control study of adverse drug reactions in children, the odds ratio of developing a serious mucocutaneous event among users of niflumic acid, adjusted for concomitant use of all other drugs, was 4.9 (95% CI 1.9 to 12.8). Given the availability of safer analgesics and antipyretics, there is no indication, in our opinion, that requires the prescription of substances which bear an increased risk.

Anti-Inflammatory Agents, Non-Steroidal↗