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PubMed1990

Use of analgesics in the elderly.

Basic and clinical research on the pathophysiology, neurophysiology, biochemistry, and psychology of pain and its management has enhanced our understanding of this complex field. Clinical applications of new knowledge have led to the development of more effective analgesics and better modes of administration in concert with improved technology. However, applications to pain problems unique to the elderly require greater attention. Unfortunately, state-of-the-art analgesic care is not widespread. Barriers exist in knowledge, skills, and attitudes among health care providers. To provide optimal analgesic care, management of each patient should be individualized. The prescribing of standard doses of analgesics should be condemned. An understanding of the various pain problems (acute and chronic) that afflict the elderly, the effects of aging on the pharmacokinetics and pharmacodynamics of analgesics, and the role of specific analgesics for specific pain states is necessary. In addition to analgesics, nonpharmacologic methods of pain control should be utilized. If needed, consultations or referrals to pain clinics or pain centers which provide expert evaluation, recommendations, and/or treatment are available.

Aged↗
PubMed1989

Pemedolac: a novel and long-acting non-narcotic analgesic.

Pemedolac [cis-1-ethyl-1,3,4,9-tetrahydro-4-(phenylmethyl)-pyrano [3,4-b]indole-1-acetic acid; AY-30,715] exhibited potent analgesic effects against chemically induced pain in rats and mice and against inflammatory pain in rats. In each of the animal models used the analgesic potency of pemedolac was defined by an ED50 of 2.0 mg/kg p.o. or less. Significant analgesic activity was detected in rats at 16 hr after administration of 1 mg/kg p.o. (paw pressure test) and at 10 hr after administration of 10 mg/kg p.o. to mice (p-phenylbenzoquinone writhing). Inasmuch as pemedolac was inactive in the hot plate and tail-flick tests; and its analgesic activity was not antagonized by naloxone (1 mg/kg s.c.), and tolerance did not develop upon multiple administration; this drug does not exert its analgesic effects through an opiate mechanism. Pemedolac differed from standard nonsteroidal anti-inflammatory drugs (NSAIDs) in that the doses which produced analgesia were much lower than those required for either anti-inflammatory or gastric irritant effects. In acute anti-inflammatory tests, pemedolac exhibited only weak activity as evidenced by an ED50 approximately 100 mg/kg p.o. in the carrageenan paw edema procedure. This demonstrates for pemedolac a separation of at least 50-fold between the acute analgesic and anti-inflammatory activities, which was greater than that observed with reference NSAIDs. The compound also had a low ulcerogenic liability with an acute UD50 = 107 mg/kg p.o. and a subacute UD50 estimated to be 140 mg/kg/day p.o. In contrast, the reference NSAIDS (piroxicam, indomethacin, naproxen and ibuprofen) exhibited similar dose-response relationships for the analgesic, anti-inflammatory and gastric irritant effects.(ABSTRACT TRUNCATED AT 250 WORDS)

Analgesics↗
PubMed1985

Metoprolol in acute myocardial infarction. Narcotic analgesics and other antianginal drugs. The MIAMI Trial Research Group.

The effect of metoprolol on chest pain has been assessed in terms of the duration and the use of narcotic analgesics, nitrates and calcium-channel blockers. Fewer metoprolol-treated patients in the MIAMI trial were given narcotic analgesics (49% of the placebo patients vs 44% of the metoprolol patients, p less than 0.001), nitrates (55% vs 53%, p = 0.10) and calcium-channel blockers (12% vs 9%, p less than 0.001). A total number of 6,697 dose equivalents of narcotic analgesics were given to the placebo group compared with 5,493 dose equivalents to the metoprolol group, a difference of 18% (p less than 0.001). Mean dose equivalents were 2.3 and 1.9, respectively. The analysis of the total use of the 3 types of treatment for ischemic chest pain showed a significantly less frequent use of treatment for chest pain in the metoprolol group than in the placebo group (p less than 0.004). The relative difference in the incidence of drug treatment tended to be more striking for patients with maximal therapy, i.e., receiving high doses of narcotic analgesics, nitrates and calcium-channel blockers. There were 22% fewer patients receiving 4 or more doses of narcotic analgesics in the metoprolol group than in the placebo group. A multivariate analysis disclosed that site of suspected infarction, delay time, entry systolic blood pressure and metoprolol treatment all had a significant effect on the use of narcotic analgesics. There was a nonsignificant tendency for heart rate to be of importance. In the placebo group the use of narcotic analgesics increased with decreasing delay time and increasing systolic blood pressure.(ABSTRACT TRUNCATED AT 250 WORDS)

Analgesics, Opioid↗
PubMed1985

[Mechanism of action of the analgesic flupirtine].

To answer the questions of mode and site of action partly supplementary, partly new investigations with flupirtine (Katadolon) were carried out which are described below. The investigation for opiate receptor affinity of flupirtine in rat brain homogenate did not show any reduction in 3He-etorphine binding up to the highest concentration of flupirtine of 10(-5) mol/1. This result suggests that flupirtine either has a very low opiate receptor affinity or lacks it fully. Therefore the analgesic activity of flupirtine is not based on opiate mechanism. The intracerebroventricular and intrathecal administration of flupirtine and the other analgesics tested showed dose dependent analgesic activity in doses which, when applied systemically, did not cause any analgesia in rats. Thus these substances show cerebral or spinal analgesic activity. In relation to the effective doses (ED50 in micrograms/rat) flupirtine was of the same efficacy in both kinds of administration. Pethidine tested comparatively was found to be less potent by intrathecal than by intracerebroventricular application. On the other hand, morphine was weaker by intracerebroventricular than by intrathecal application. As in the experiments by oral administration, naloxone did not show any effect on the analgesic activity of flupirtine, neither by intracerebroventricular nor by intrathecal application. On the other hand, the analgesic effects of pethidine and morphine were completely suppressed by naloxone. These results demonstrate that the analgesic activity of flupirtine is not caused by the opiate mechanism.(ABSTRACT TRUNCATED AT 250 WORDS)

Aminopyridines↗
PubMed1988

Is analgesic nephropathy still a problem in Belgium?

End-stage renal failure due to analgesic nephropathy still frequently occurs in Belgium. In a study conducted at the end of 1984 including 53 of the 54 dialysis centres, a prevalence of analgesic nephropathy in dialysis patients of 17.9% was found. The epicentre of the disease was situated in a small area in the northern part of the country, the southern part showed a clearly lower prevalence. The annual consumption of analgesic preparations in 1983 was approximatively 25 g per capita, in the north as well as in the south. In the north analgesic mixtures in powder form had an important market share in some particular areas, where the prevalence of end-stage renal failure due to analgesic nephropathy is the greatest. A general population survey (n = 855) showed that 83% of subjects had analgesic medications at home. Abuse of these drugs was found in 2.1% of the studied population. Abusers were mainly females most commonly taking analgesic mixtures.

Adult↗
PubMed1978

[Tumors of the efferent parts of the urinary tract and abuse of analgesics].

Since 1965, when Swedish authors first suggested that analgesic abuse could cause uroepithelial tumors associated with or without analgesic nephropathy, an increasing number of cases have been reported from many parts of the world. In a retrospective analysis of all patients admitted to the medical department of the University Hospital in Basel from 1966 to 1976, records of 20 patients with analgesic nephropathy and tumors of the urinary tract (excluding hypernephroma) were found (17 uroepithelial tumors, 2 sarcomas, 1 chorionepithelioma). Typical symptoms, outcome and actuarial survival of the patients with uroepithelial tumors are summarized. Phenacetin as the common ingredient in analgesic mixtures has been regarded as carcinogenic, since some of its metabolites are similar in chemical structure to well-known industrial carcinogens. In animal experiments malignant tumors have in fact been induced with 2-hydroxylated metabolites and areneoxydes of phenacetin and paracetamol, and there is even more convincing evidence of the carcinogenic properties of N-oxydized metabolites such as N-hydroxy-phenetidine and N-hydroxy-phenacetin. Dimethylnitrosamine formed from aminophenazone appears to be improbable as a cause of uroepithelial tumors associated with analgesic abuse, since aminophenazone has not been a common ingredient of analgesic mixtures in Australia, where the incidence of uroepithelial tumors appears to be as high as in Sweden, where abuse of aminophenazone-containing analgesics has been massive.

Acetaminophen↗
PubMed1985

Patterns of analgesic prescription and consumption in a university-affiliated community hospital.

To assess the patterns of prescription and consumption of analgesic and psychotropic medications, we reviewed the medication records of all 311 adult medical and surgical patients at a university-affiliated community hospital. Acetaminophen combinations and meperidine accounted for 85% of all analgesics prescribed. Analgesic use declined with advancing age. Two or more analgesics were prescribed to 18% of medical patients, compared with 44% in surgical patients. Less than one third of the patients with cancer received analgesics more frequently than every six hours. Nearly all psychotropic prescriptions were for sedative-hypnotics. Our data suggest that (1) physicians prescribe a limited number of analgesics, despite the variety available; (2) elderly patients receive fewer analgesics; (3) polypharmacy occurs often; (4) pain in patients with cancer is probably undertreated; and (5) psychotropic medications are used infrequently for analgesia.

Adolescent↗
PubMedDate not supplied

[Pain-alleviating action of gidifen and its combinations with analgesics].

The analgesic effect of gidifen, a new tranquilizer belonging to the group of organophosphorus compounds, manifests itself in relatively high doses (1/3 of the LD50). The quantitative characteristics of the analgesic action depends on the method for evaluating the analgesic action of the drug. On combined use of gidifen and analgesics applied in a definite dosage range the analgesic effect is potentiated. If the tranquilizer under study is combined with non-narcotic analgesics, the above potentiation is accompanied with an increase in the toxicity and myorelaxant activity of gidifen. On combination of the latter with morphine the parameters under consideration are unchanged. According to the pattern of interaction with analgesics gidifen does not differ in principle from benzodiazepine tranquilizers. However, the drug is not superior to benzodiazepines in this respect.

Analgesics↗
PubMed1976

Effect of narcotic analgesics on the striatal homovanillic acid content in mice; relation to antinociceptive effect.

The effects of various narcotic analgesics on striatal homovanillic acid (HVA) content, hot plate time and rectal temperature in mice were compared in relation to dose and time. The hypothermia induced by narcotic analgesics did not correlate with the striat"al HVA increase. Pentazocine, cyclazocine and thebaine had no effect on the hot plate time. The maximum prolongation of hot plate time induced by morphine, methadone or piminodine occurred before the highest HVA increase. The highest increase induced by narcotic analgesics in striatal HVA content was twice the original concentration. This occurred 2 hr after 40 mg/kg of morphine; 2 hr after 20 mg/kg of methadone; 1/2 hr after 20 mg/kg of piminodine; and 1 hr after 60 mg/kg of pentazocine. Cyclacozine (10 and 20 mg/kg) and thebaine (10 mg/kg) did not alter the HVA content. With the exception of pentazocine, those doses of narcotic analgesics that caused equal increases in striatal HVA content were also equianalgesic. These results suggest that there are similarities in the structural requirements for antinociceptive and striatal HVA-increasing effects of narcotic analgesics. The neuroleptic compound haloperidol (0.5 mg/kg) caused a fourfold increase in striatal HVA content making it twice as efficient as narcotic analgesics. This finding suggests that narcotic analgesics do not act on the same sites as neuroleptics when causing an increase in striatal HVA content.

Analgesics, Opioid↗
PubMed1980

[Narcotic analgesics and endorphins and the release of pituitary hormones (author's transl)].

This report concerns a review of the neuroendocrine effects of narcotic analgesics and endorphins. Acute administration of narcotic analgesics to rats increases the blood levels of ACTH, GH and prolactin, and decreases levels of LH and TSH, however, there is no general consensus regarding changes in serum FSH, ADH and oxytocin as induced by narcotics in rats. In humans, the narcotic analgesic increases in serum prolactin, decreases in serum LH and has no effect on the release of other known pituitary hormones. Endorphins mimic morphine regarding hormonal effects. Effects of naloxone on the basal levels of prolactin, LH or GH were inverse to the effects seen with narcotics and endorphins, therefore endorphins may play a role in regulating the basal levels of these hormones. Narcotics analgesics depress the increased blood levels of prolactin, gonadotropins or TSH elicited by specific measures. While chronic administration of morphine results in tolerance to the stimulant effect of ACTH, and possibly of prolactin secretion, tolerance does not develop to the stimulant effect on GH secretion. The analgesic potency of narcotic analgesics correlates with their suppressive effect on the pituitary-gonadal system and the potency with which endorphins bind to the opiate receptors correlates with their prolactin releasing activity. It is assumed that narcotic analgesics and endorphins exert their hormonal effects by altering the release of neurotransmitters in the CNS. Thus, a release of hypothalamic releasing hormones is involved rather than a direct action on the pituitary. The central neurotransmitter systems involved in the hormonal effects of narcotics are now being intensively investigated by various groups of workers.

Adrenocorticotropic Hormone↗
PubMed1982

Beta 2-microglobulin excretion and urinary cytology in analgesic nephropathy.

Patients with analgesic nephropathy are at risk from uro-epithelial malignancy. Enhanced secretion of beta 2-microglobulin occurs from epithelial cancer cells. In order to find a screening test for malignancy in analgesic nephropathy, urinary levels of this protein were measured in patients with analgesic nephropathy with urine cytological abnormalities and were compared to a control group with glomerulonephritis. Mean fractional excretion of beta 2-microglobulin was higher (8.61 +/- 1.76 SEM) in patients with analgesic nephropathy than in those with glomerulonephritis (1.13 +/- 0.76) (P less than 0.025). Those patients with analgesic nephropathy who had malignant cells in the urine had higher mean fractional excretion (18.56 +/- 5.77) than those with only atypical cells (8.5 +/- 2.0) (P less than 0.05) who in turn had higher mean values than those with normal cytology (2.12 +/- 0.62) (P less than 0.0025). It is suggested that the increased beta 2-microglobulin excretion in analgesic nephropathy is due to secretion from abnormal urothelial cells as well as reduced tubular catabolism. Beta 2-microglobulin may be of use as a screening test for malignancy in analgesic nephropathy.

Adult↗
PubMed1982

[Analgesic and narcotic antagonist effects of buprenorphine (author's transl)].

Pharmacological properties of buprenorphine were studied in comparison with those of morphine and pentazocine. Buprenorphine was more potent than morphine and pentazocine in analgesic tests, using chemical, thermal, pressure, and electrical stimulation as the nociceptive stimuli. Buprenorphine exhibited analgesic activity in the D' Amour-Smith's test at high stimulus intensity and in the Haffner's test, while pentazocine exhibited little or no analgesic action in these tests. Buprenorphine showed a bell-shaped dose-response curve in the mouse D'Amour-Smith's test at high stimulus intensity. Analgesic action of buprenorphine was antagonized by naloxone administered before buprenorphine, but not antagonized by naloxone administered after buprenorphine. Duration of the analgesic action of buprenorphine was longer than those of morphine and pentazocine. Buprenorphine decreased the amplitudes of evoked potentials which were recorded from the nucleus ventralis posteromedialis, nucleus centralis lateralis, and periaquaductal central gray. As a naloxone antagonist, Buprenorphine was equivalent or less potent than naloxone and more potent than pentazocine. Tolerance developed to the analgesic activity of buprenorphine, but development of tolerance to buprenorphine was less than that of tolerance to morphine. It was concluded that buprenorphine may be a useful analgesic drug because of its high intrinsic activity and long duration of action.

Analgesics↗
PubMed1981

Analgesic ingestion and chronic peptic ulcer.

The patterns of analgesic ingestion in gastric and duodenal ulcer patients were compared with those of matched community controls in order to ascertain differences that may exist between ulcer and nonulcer subjects of comparable age and sex. The differences sought concerned amounts and types of analgesics ingested. The types of analgesics studied were aspirin and acetaminophen, ingested either alone or together. Analgesics such as dextropropoxyphene and codeine were disregarded. It was found that there was a strong positive association between heavy analgesic intake and chronic gastric ulcer with a relative risk of 29.5. The association was most marked in female patients (relative risk = 51.8). The involvement of aspirin-containing and acetaminophen-containing drugs was of similar significance with relative risk of 17.3 and 24.4, respectively. Aspirin alone was the least frequently ingested. The association was only partly related to painful nonulcer health problems and to ulcer pain. No association was found between chronic duodenal ulcer and analgesic intake. The strong association found between gastric ulcer and heavy analgesic intake does not, per se, necessarily indicate a causal relationship.

Acetaminophen↗
PubMed1994

[Evaluation of the analgesic effect of naftidrofuryl in permanent ischemia in patients with arterial diseases. Double-blind versus placebo study].

Ischemic rest pain, with or without trophic disorders and occurring very frequently at night, is responsible for insomnia and complications such as positional oedema. The pathophysiological mechanisms underlying the analgesic effect of naftidrofuryl led us to evaluate the efficacy of this treatment. 37 selected patients were given 2 daily infusions of 400 mg of naftidrofuryl for 8 days, under double-blind conditions. Evaluation criteria were pain assessment using a visual analogue scale, analgesic consumption considering both the power (WHO scale: level I paracetamol, level II dextropropoxyphene, level III morphine) and the dosage of the analgesic used (analgesic score), index of therapeutic success including the level of pain reduction and the absence of analgesic use. The results showed a significant difference in favour of naftidrofuryl for: reduction of pain, difference in the course of the analgesic score, the distribution of the population according to the index of therapeutic success. Three patients discontinued treatment due to inefficacy, but all 3 belonged to the placebo group. This study demonstrates the benefit of naftidrofuryl in pain reduction which was assessed, in particular, by the reduction of analgesic consumption.

Aged↗
PubMed1994

Postoperative analgesic prescription and administration in a pediatric population.

This study is a replication of the classic work conducted by Eland (1974) that investigates the prescription and administration of postoperative analgesics in a pediatric population. This study was conducted to compare and contrast results over almost 20 years to determine whether any changes have occurred in analgesic administration of children in the same large midwestern teaching hospital. This study retrospectively reviewed 25 patient charts matched by age grouping and surgical diagnosis to the original sample. Findings of the original study (Eland, 1974) showed that of the 25 children studied, 4 children did not have orders for pain medications. Only 12 children received an analgesic during hospitalization. The 12 children who were administered analgesics received a total of 24 doses (range 1 to 5 doses). Findings of the current study showed that all 25 children in the sample had orders for pain medications postoperatively and 23 children had orders for narcotic pain medications. All 25 children received an analgesic medication during hospitalization, and 20 children received narcotic pain medications. The total number of analgesics administered to this group was 968 doses (range 1 to 280 doses). The average number of doses administered was 3.3 doses per day. When examining only the first 48 postoperative hours, the average number of doses administered was 4.36 doses per day. The investigator concludes that the prescription and administration of analgesics in the pediatric population at this facility has improved dramatically over the past 18 years.

Adult↗
PubMed1994

Chronic headache: appropriate use of opiate analgesics.

The question of the appropriate use of opiate analgesics in the management of chronic headache pain is under debate. Often, the management of headache pain is complicated by the overuse of dependency-promoting analgesics. Because of confusion about the use of analgesics in pain management, some patients are denied access to necessary opioid analgesia, whereas others receive large quantities of combination analgesics. The proper use of opiate analgesics is presented here, including a review of the pharmacology of these agents. Signs of analgesic dependence, analgesic rebound headache, and methods of withdrawal are also presented. The potential use of such new treatment modalities as butorphanol nasal spray is discussed.

Analgesics↗
PubMed1977

Unreliable drug histories, analgesics, and changes in renal function.

One hundred and nine outpatients were questioned on their use of analgesics and asked to provide urine and blood samples. Forty-one per cent said they used analgesics daily and 54% said they had ingested analgesics during the 3 days before questioning. The analgesics used were mainly aspirin or paracetamol, alone or in combination. Five (42%) of the patients who denied the use of analgesics, and 10 (29%) of those who denied intake during the preceding week, had detectable amounts of paracetamol or aspirin in their urine. Mean serum urea, although still within the normal range, increased with increasing use of analgesics. The mean serum urea of patients who used aspirin and paracetamol in combination was significantly higher than that of those who used either of the drugs alone. The findings suggest that one should not rely heavily on the history of analgesic use, and that by replacing phenacetin with paracetamol one might not have achieved much as far as renal function is concerned.

Acetaminophen↗
PubMed1997

The competitive alpha-amino-3-hydroxy-5-methylisoxazole-4-propionate receptor antagonist LY293558 attenuates and reverses analgesic tolerance to morphine but not to delta or kappa opioids.

Antagonists of the NMDA type of excitatory amino acid (EAA) receptor attenuate or reverse the development of tolerance to the analgesic effects of the mu opioid agonist morphine, the delta-1 opioid agonist DPDPE but not the kappa-1 agonist U50,488H or the kappa-3 agonist naloxone benzoylhydrazone. The role of the AMPA subtype of EAA receptor in analgesic tolerance was examined using LY293558, a selective competitive antagonist that is active after systemic administration. Administration of morphine, DPDPE, or U50,488H three times daily for 3 days according to an escalating dosing schedule resulted in analgesic tolerance as indicated by an increase in analgesic ED50 values using the tail-flick test in mice. Analgesic tolerance was attenuated when mice received a continuous subcutaneous infusion of LY293558 at doses of 30, 45 or 60 mg/kg/24 hr via an osmotic pump concurrent with the morphine treatment. Continuous subcutaneous infusion of LY293558 (45 mg/kg/24 hr) also reversed established morphine tolerance. In contrast, continuous subcutaneous infusion of the highest dose of LY293558 (60 mg/kg/24 hr) was ineffective in preventing the development of analgesic tolerance to DPDPE or U50,488H. Continuous subcutaneous infusion of LY293558 (60 mg/kg/24 hr) for 3 days protected mice from generalized convulsions produced by the selective AMPA agonist ATPA, indicating that the dosage of LY293558 that attenuated morphine tolerance was effective as an antagonist at AMPA receptors. These results demonstrate that AMPA receptors may play a role in the development and maintenance of morphine, but not DPDPE or U50,488H, analgesic tolerance.

3,4-Dichloro-N-methyl-N-(2-(1-pyrrolidinyl)-cycloh↗