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Biomedical subjects

J Desmeules

Publications and source records attributed to J Desmeules.

At least 19 recordsLinked to original sources
PubMed2006

[Preparing a drug list for primary care].

To limit drug adverse effects, the use of a limited choice of drugs is desirable. We identified 29 frequent health problems and selected first and second choice medication based on the following criteria: clinical efficacy based on medical evidence or expert consensus, safety profile, and costs. For each substance, adverse effect, contraindication, interaction risk, specific dosing, and safety use during pregnancy and lactation were reviewed. More than seventy substances were identified. This list is available for download at the following address (in French): http://www.hcuge.

Formularies, Hospital as Topic↗
PubMed2006

[Behavioural and psychological symptoms of dementia (BPSD): pharmacological management].

BPSD affect all demented patients during their illness. They are part of the process of the disease and can be correlated to neurotransmitter dysfunctions as well as to the coping difficulties due to the patient's cognitive decline. The major consequences of BPSD are a decreased quality of life of both patient and caregivers and an increased need of professional care. Physicians should exclude precipitating factors such as intercurrent somatic, psychiatric or drug-related problems first and then proceed with behavioural or environment therapy. Introduction of a pharmacological treatment should be the last resort. This systematic review discusses the causes and consequences of BPSD and focuses on the evidence-based pharmacological approach. Only three drugs can be recommended at the present time: risperidone, olanzapine and donepezil.

Aged, 80 and over↗
PubMed2006

[A link between sodium sensitivity and pharmacogenomics of antihypertensive drugs].

Pharmacogenomics studies the links between polymorphisms (genetic variants) and the variability of the response to some treatments in a given individual. Pharmacogenomics thus allows to explore polymorphisms that could potentially explain heterogeneous efficacy of diuretics, ACE inhibitors or angiotensin receptor blockers, beta-blockers and calcium channel blockers among populations of varied ethnical origin. There have been many studies on the relation between the efficacy of these treatments and the specific polymorphisms involved in the regulation of blood pressure. So far, no unique mutation is by itself predictive of the therapeutic response to these drugs; more elaborated polygenetic models are required so that pharmacogenomics can one day offer an individualized prescription for a complicated disease such as high blood pressure.

Antihypertensive Agents↗
PubMed2005

[Treating hypertension: a challenge for the general practitioner].

Hypertension is associated with a greater risk of developing a stroke or a coronary heart disease, but remains, for the meanwhile, undertreated in a vast majority of patients. Non pharmacological interventions can reduce blood pressure and should be recommended to every patient suffering from hypertension. Nevertheless, a drug therapy must often be introduced. The threshold at which a treatment should be started depends mostly on the cardiovascular risk of each patient and the benefit of antihypertensive drug therapy depends primarily on the reduction of the blood pressure itself.

Antihypertensive Agents↗
PubMed2005

[The selection of a drug in a defined therapeutic class: the case of the HMG-CoA reductase inhibitors].

The HMG-CoA reductase inhibitors have similar therapeutic targets and indications. However, their potential pharmacokinetic drug-drug interaction profile may play a significant role in their safety profile in polymedicated and polymorbid patients and can serve as a selection criterion. If their utility is clearly demonstrated in selected conditions, their safety profile remains of concern. Beside dose-related hepatic and muscular injury, other rare and important adverse drug reactions have been reported after prolonged administration such as polyneuropathy, fibrotic interstitial pulmonary disease and lupus-like syndrome. Teratogenicity has also been associated with statin therapy.

Humans↗
PubMed2004

Fibromyalgia: a randomised, controlled trial of a treatment programme based on self management.

OBJECTIVE: To evaluate the efficacy of a treatment programme for patients with fibromyalgia (FM) based on self management, using pool exercises and education. METHODS: Randomised controlled trial with a 6 month follow up to evaluate an outpatient multidisciplinary programme; 164 patients with FM were allocated to an immediate 6 week programme (n = 84) or to a waiting list control group (n = 80). The main outcomes were changes in quality of life, functional consequences, patient satisfaction and pain, using a combination of patient questionnaires and clinical examinations. The questionnaires included the Fibromyalgia Impact Questionnaire (FIQ), Psychological General Well-Being (PGWB) index, regional pain score diagrams, and patient satisfaction measures. RESULTS: 61 participants in the treatment group and 68 controls completed the programme and 6 month follow up examinations. Six months after programme completion, significant improvements in quality of life and functional consequences of FM were seen in the treatment group as compared with the controls and as measured by scores on both the FIQ (total score p = 0.025; fatigue p = 0.003; depression p = 0.031) and PGWB (total score p = 0.032; anxiety p = 0.011; vitality p = 0.013,). All four major areas of patient satisfaction showed greater improvement in the treatment than the control groups; between-group differences were statistically significant for "control of symptoms", "psychosocial factors", and "physical therapy" No change in pain was seen. CONCLUSION: A 6 week self management based programme of pool exercises and education can improve the quality of life of patients with FM and their satisfaction with treatment. These improvements are sustained for at least 6 months after programme completion.

Adult↗
PubMed2003

Clinical pharmacology and rationale of analgesic combinations.

BACKGROUND AND OBJECTIVE: Oral fixed drug combination analgesics have potential advantages over monotherapy, but these can only be attained through careful design. RESULTS: The main reasons for developing combination analgesics are to gain efficacy and to reduce toxicity. Analgesic combinations interact pharmacokinetically, or pharmacodynamically, or both, in positive or negative terms. The t(max) value for both enantiomers of tramadol occur two hours following administration, and that for the active, (+)-M1 metabolite occurs after three hours. Thus, pairing tramadol with acetaminophen, a rapid-onset analgesic, represents a pharmacokinetically rational combination. Analgesic combinations should satisfy two important pharmacodynamic criteria: the components of the combination should display additive or synergistic analgesia; and this interaction should allow lower doses of each substance to be used in combination, resulting in an improved safety profile. Clinical studies of the pharmacodynamic between oral tramadol and acetaminophen in third molar extraction and cold pressor models have provided evidence that this combination provides better efficacy than either individual component of the combination. CONCLUSIONS: In summary, combination analgesics can play a valuable role in pain management. However, dubious combinations (directed against the same targets or with unwanted interactions) and 'old fashioned' fixed-dose multiple analgesic agent combinations should be avoided. Fixed-dose combination analgesics are of value only when they have been developed according to rational pharmacokinetic and pharmacodynamic criteria, and when claims for their benefits have been supported by evidence-based data and well-designed clinical studies.

Analgesics↗
PubMed1998

[Influence of sex on reporting pain].

In many epidemiological pain studies, women more frequently report more intense, frequent and long-lasting or chronic transient pain than men. In our retrospective study including hospitalised patients referred to a pain centre, prevalence of headaches, musculoskeletal pain and somatoform pain was observed in women, as described in the literature. Generally pain intensity was higher in women and pain was more frequently controlled in men, but when intensity and pain control were compared according to the pain aetiologies, no gender difference was found. Drug treatments were adapted to pain aetiologies, which accounted for the observed differences. In hospitalised patients the significant differences observed in intensity, pain control and treatment reflect the heterogeneity of pain aetiologies rather than gender differences.

Adult↗
PubMed1998

[Factors associated with refractory cancer pain].

Cancer pain can be effectively controlled in most patients by classical pharmacological treatment. We retrospectively studied the characteristics and factors associated with non responsive pain. Between 1989 and 1996, 1767 patients were referred to our pain center; 831 (47%) had cancer pain and from 787 evaluable cases 118 (15%) experienced non-controlled pain whereas good pain control was achieved within a few days in 669 (85%) patients. Gender, age, cancer type, metastasis, initial pain intensity, nociceptive or neuropathic components and administration of adjuvant therapies were similar in both groups. On the other hand, diffuse pain, abdominal pain, terminal care, near death and doses of strong opioids were significantly different. Factors associated with therapeutic failure were conflicts, life and complications and breakthrough pain. In the presence of refractory cancer pain the factors predictive of therapeutic failure should be identified in order to optimize individual pain treatment.

Adult↗
PubMed1998

[Genetic and environmental effects on neuromodulation and the antinociceptive effect of dextromethorphan].

Administration of NMDA antagonists leads to attenuation or disappearance of some symptoms of central sensitization, such as secondary hyperalgesia. However, the side effects of NMDA antagonists to a large extent counterbalance the expected benefits, thus preventing wide or prolonged use. Dextromethorphan and its metabolite dextrophan, on the other hand, are established and safe drugs. Experimentally they both antagonize the NMDA receptor. This study evaluates the effects of dextromethorphan and its metabolite in pain models using electrical stimulation for testing the antinociceptive effect and capsaicin-induced hyperalgesia. Dextromethorphan shows clear antinociceptive as well as neuromodulary effects, both depending heavily on the cytochrome P450 2D6 phenotype (CYP2D6).

Adult↗
PubMed1998

Lack of acetaminophen ceiling effect on R-III nociceptive flexion reflex.

OBJECTIVE: The analgesic efficacy of intravenous doses of acetaminophen (paracetamol) 0.5 g, 1 g and 2 g (administered as propacetamol) was assessed in 11 healthy subjects in a randomised, double-blind, placebo-controlled crossover study. The antinociceptive effect was assessed over 8 h by measurement of the nociceptive flexion reflex threshold (R-III) in response to selective transcutaneous electrical stimulations. RESULTS: After acetaminophen 0.5 g, R-III increased to a mean maximum of 23% over baseline values; after 1 g to 28%, and after 2 g to 40%. The AUC(0-8 h) of the analgesic effects and the AUC(0-8 h) of plasma concentrations closely correlated and were dose-dependent: rs = 0.37, for R-III and rs = 0.94, for the plasma concentrations. Intravenous acetaminophen exerted a dose-dependent central antinociceptive effect.

Acetaminophen↗
PubMed1998

Use of the label "litigation neurosis" in patients with somatoform pain disorder.

The use of the term "litigation neurosis"--a condition with controversial clinical significance--might correspond to the expression for a difficult physician-patient relationship. The characteristics of patients with a DSM-III-R diagnosis of somatoform pain disorder who had been labeled "litigation neurosis" by their physicians were explored. Among 74 patients referred to a pain clinic, 30% had been labeled litigation neurosis, and among 81 patients referred while claiming disability benefits, 19% had been thus categorized. The attribution of this label was neither correlated to actually being involved in a claim for disability benefits nor to involvement in legal action. Patients who had been designated with litigation neurosis were characterized by a lower educational level, a higher rate of DSM-III-R major depression, and a much higher frequency of personality disorders than patients who were not thus labeled. We postulate that the communication style of patients with this constellation of characteristics, in particular the presence of psychiatric comorbidity, may have engendered a difficult doctor-patient relationship, leading physicians to use the label in the absence of objective evidence of litigation or involvement in legal action. We agree that the inappropriate use of labels such as "litigation neurosis" should be questioned.

Adult↗
PubMed1998

Sodium stibogluconate (pentostan) overdose in a patient with acquired immunodeficiency syndrome.

A 32-year-old man with acquired immunodeficiency syndrome (AIDS) admitted to the hospital for treatment of visceral leishmaniasis was inadvertently given 10 times the prescribed first dose of sodium stibogluconate ([Sb] 6.5 g instead of 0.65 g). He experienced no immediate major toxicity during the first 48 hours, but a significant rise of pancreatic enzyme activities was observed (amylase at 10 times the upper limit of normal, lipase at 50 times the upper limit of normal) without clinical signs or indications on computed tomography (CT) of pancreatitis. The third day after the overdose, he developed appendicitis, which appeared coincidental; he recovered uneventfully from surgery. Most of the overdose of Sb was eliminated within the first few hours. Pharmacokinetics remained linear; the rapid, long elimination half-lives (2.7 hours and 54 hours, respectively) were similar to those in previously published results. The administration of a chelating agent, dimercaptosuccinic acid (DMSA), 72 hours after the Sb overdose did not modify the pharmacokinetics of the medication.

Acquired Immunodeficiency Syndrome↗
PubMed1998

Rhabdomyolysis after correction of hyponatremia due to psychogenic polydipsia possibly complicated by clozapine.

OBJECTIVE: To report a case of rhabdomyolysis related to rapid correction of hyponatremia attributable to compulsive drinking of water, possible complicated by clozapine use. CASE SUMMARY: A 42-year-old white man treated with clozapine for schizophrenia was admitted for a generalized seizure. Marked hyponatremia due to psychogenic polydipsia was present. He developed a marked elevation of creatine kinase concentrations after correction of hyponatremia with hyperosmolar sodium solution, without clinical signs of rhabdomyolysis. DISCUSSION: Rhabdomyolysis associated with hyponatremia due to water intoxication has been reported in 17 patients to date. A possible explanation may lie within the framework of the calcium-sodium exchange across the skeletal muscle cell membrane. By increasing muscle cell permeability, clozapine treatment may possibly enhance the destruction of muscle cells. CONCLUSIONS: Hyponatremia due to water intoxication and concurrent use of clozapine should be considered in the differential diagnosis of rhabdomyolysis, especially in the severely psychiatrically disabled population.

Adult↗
PubMed1997

[Pharmacology of tramadol].

(+/-)-Tramadol is a synthetic 4-phenyl-piperidine analogue of codeine. It is a central analgesic with a low affinity for opioid receptors. Its selectivity for mu receptors has recently been demonstrated, and the M1 metabolite of tramadol, produced by liver O-demethylation, shows a higher affinity for opioid receptors than the parent drug. The rate of production of this M1 derivative (O-demethyl tramadol), is influenced by a polymorphic isoenzyme of the debrisoquine-type, cytochrome P450 2D6 (CYP2D6). Nevertheless, this affinity for mu receptors of the CNS remains low, being 6000 times lower than that of morphine. Moreover, and in contrast to other opioids, the analgesic action of tramadol is only partially inhibited by the opioid antagonist naloxone, which suggests the existence of another mechanism of action. This was demonstrated by the discovery of a monoaminergic activity that inhibits noradrenaline (norepinephrine) and serotonin (5-hydroxytryptamine; 5-HT) reuptake, making a significant contribution to the analgesic action by blocking nociceptive impulses at the spinal level. (+/-)-Tramadol is a racemic mixture of 2 enantiomers, each one displaying differing affinities for various receptors. (+/-)-Tramadol is a selective agonist of mu receptors and preferentially inhibits serotonin reuptake, whereas (-)-tramadol mainly inhibits noradrenaline reuptake. The action of these 2 enantiomers is both complementary and synergistic and results in the analgesic effect of (+/-)-tramadol. After oral administration, tramadol demonstrates 68% bioavailability, with peak serum concentrations reached within 2 hours. The elimination kinetics can be described as 2-compartmental, with a half-life of 5.1 hours for tramadol and 9 hours for the M1 derivative after a single oral dose of 100mg. This explains the approximately 2-fold accumulation of the parent drug and its M1 derivative that is observed during multiple dose treatment with tramadol. The recommended daily dose of tramadol is between 50 and 100mg every 4 to 6 hours, with a maximum dose of 400 mg/day; the duration of the analgesic effect after a single oral dose of tramadol 100mg is about 6 hours. Adverse effects, and nausea in particular, are dose-dependent and therefore considerably more likely to appear if the loading dose is high. The reduction of this dose during the first days of treatment is an important factor in improving tolerability. Other adverse effects are generally similar to those of opioids, although they are usually less severe, and can include respiratory depression, dysphoria and constipation. Tramadol can be administered concomitantly with other analgesics, particularly those with peripheral action, while drugs that depress CNS function may enhance the sedative effect of tramadol. Tramadol should not be administered to patients receiving monoamine oxidase inhibitors, and administration with tricyclic antidepressant drugs should also be avoided. Tramadol has pharmacodynamic and pharmacokinetic properties that are highly unlikely to lead to dependence. This was confirmed by various controlled studies and postmarketing surveillance studies, which reported an extremely small number of patients developing tolerance or instances of tramadol abuse. Tramadol is a central acting analgesic which has been shown to be effective and well tolerated, and likely to be of value for treating several pain conditions (step II of the World Health Organization ladder) where treatment with strong opioids is not required.

Administration, Oral↗
PubMed1996

[Drug-induced hepatic involvement, something to consider!].

A retrospective study over the last 5 years on drug-induced liver injury was performed in the Internal Medicine Department of the University Hospital of Geneva. According to WHO and Council for International Organizations of Medical Sciences (CIOMS) criteria for drug-induced liver adverse events, 142 cases were identified, with 255 drugs fulfilling causality criteria of certain, probable or possible. 63 patients (44%) suffered severe consequences of liver injury, including 9 deaths. Drugs reported belonged to the therapeutic classes of antibiotics (43%), cardiovascular (20%), analgesics (10%), gastrointestinal (9%), psychotropic (7%), and others (11%). Despite bias inherent to the retrospective methodology, only 10% of the side effects were spontaneously reported to the pharmaco-vigilance board. This is in accordance with the known reporting rate. It can be concluded that spontaneous reports are to be regarded only as signals.

Adult↗