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Biomedical subjects

M Bourin

Publications and source records attributed to M Bourin.

At least 163 records · Page 9Linked to original sources
PubMed1979

[Acute overdosage with benzodiazepine derivatives (author's transl)].

The study of 210 cases of voluntary intoxications by benzodiazepines alone, out of a total of 2080 intoxicated patients admitted at the Hospital of Tours, shows that when no other drugs is associated the prognosis is good, both for children and for adults. The association with ethanol does not change the prognosis. The clinical symptoms alone cannot prove the nature of the gravity of the intoxications. After having analysed the drugs present in the gastric juice, and after having checked that only benzodiazepines are implied, the patient can usually be taken care of on a non specialized ward.

Adolescent↗
PubMed1979

[Value of the intravenous route for the use of phenobarbital in asphyxiated full term newborn infants].

Phenobarbital (20 mg/kg) was given intravenously to asphyxiated full term neonates who were less than 48 hours old. Further doses were given for 4 days (5 mgs/kg/d). Plasma levels were within the therapeutic range from 5 to 36 hours after the first injection but the maintenance dose always resulted in overdose by 5th day. The exact maintenance dose needs to be determined.

Asphyxia Neonatorum↗
PubMed1979

[Bromide encephalopathies (author's transl)].

Bromide encephalopathies are frequently reported in Northern America and Great Britain. There is no characteristic clinical pattern, the neurological symptoms are multiple, this is readily explained by the diffusion of bromide ions to all regions in the central nervous system. An accurate history (bromide intake, followed by the slow onset of digestive and neuropsychiatric symptoms) as well as an apparent hyperchloremia are of the greatest aid in suggesting the diagnosis. The incidence of this type of intoxication is greater in women over 50. The association of a salt free diet to bromide therapy favors the onset of clinical symptoms because of the competition between bromide and chloride at the choroid plexus and at the renal tubule.

Brain Diseases↗
PubMedDate not supplied

Pharmacological comparison of antipsychotic drugs and sigma-antagonists in rodents.

We compared antipsychotic drugs (haloperidol, chlorpromazine and clozapine) and sigma antagonists (remoxipride, cinuperone, alpha-(4-fluorophenyl)-4-(-fluoro-2-pyrimidinyl)-1-piperazine butanol (BMY 14802) and rimcazole) in the radio-ligand binding and behavioural experiments in rodents. A good correlation was established between the affinity of compounds at dopamine2-receptors in the striatum and their ability to block apomorphine-, amphetamine- and quipazine-induced behavioural effects in rodents. By contrast, no correlation was found between the behavioural effects of these drugs and their affinity at dopamine1-5-HT2- and sigma receptors. The rank order of potency among the studied antipsychotic drugs in the behavioural tests and at dopamine2-receptors was following: haloperidol >> chlorpromazine > or = clozapine. The effectiveness of chlorpromazine and clozapine was nearly similar against apomorphine-induced aggressiveness and yawning, whereas at 5-HT2-receptors clozapine was more active than chlorpromazine. The weak activity of sigma antagonists at dopamine2 receptors could be a possible reason why these compounds were less effective in the behavioural studies compared to antipsychotic drugs. However, the antagonism of remoxipride against apomorphine-induced stereotypy and aggressiveness is not related to its activity at sigma receptors, because the other sigma antagonists did not block these effects of apomorphine. It is probable that remoxipride exerts its action through blocking of dopamine2 receptors. In conclusion, the present study revealed only weak activity of sigma antagonists in the behavioural models widely used to study the antipsychotic drugs. Therefore, the antipsychotic activity of sigma antagonists is doubtful.

Animals↗
PubMedDate not supplied

Clinical methodology for testing of anxiolytic drugs.

Diagnostic criteria and classification are changing. It is no longer acceptable to include patients with a general diagnosis of any anxiety, or neurotic anxiety. Regardless of the reference system used, DSM IV or ICD 10, anxiety disorders are now detailed in separate entities. General anxiety disorder, GAD, which is pivotal for the evaluation of new products, can only be claimed after the elimination of all the others, and is relatively rare. The inclusion of such outpatients is further complicated, as comorbidity is frequently associated with GAD--alcoholism, major depression, dysthymia, personality disorders, somatic disease likely to interfere with patient evaluation--and leads to exclusions, and also because the requested duration for the syndrome, prior to inclusion, is six months, which means six months without psychotropic drugs, including excessive alcohol consumption. As to patient evaluation, the reference scale remains the HAM-A. It should show a score above 20 at baseline. It has been designed to assess the level of anxiety of patients presenting with the diagnosis of anxiety, but not the diagnosis of GAD, and, clearly, in relation to the expected results obtained with BZD, which are still the standard reference drugs. The same is true for the other investigator scales and self-rating scales. Moreover, the criteria defining clinical improvement are still discussed. More generally, clinical testing in comparison with placebo and reference drugs is particularly important for anxiolytic drugs. The optimal dose range should be investigated in phase I, evidence of sedative or disinhibiting effects, and in phase II, defining the minimal active dose. Longer duration of treatment should be scrutinized in phase III, in order to check on long-term efficacy, recurrences and relapses. The effects of drug withdrawal should also be studied: withdrawal syndrome, rebound, recurrence, dependence. It currently looks difficult to market new anxiolytic drugs, and clinical research mainly provides an extension of the indications for antidepressant drugs in anxiety.

Anti-Anxiety Agents↗
PubMedDate not supplied

Warning! One buflomedil may hide another one!

A 75-year-old woman experienced fever and convulsions. She was treated for diabetes mellitus, angina pectoris and also for arteritis with Buflomedil Merck (3 tab/d). Further investigations failed to find any aetiology. Buflomedil dosage was elevated to 6.3 mg/l (N = 4-4.5 mg/l). The drug was discontinued and there was no recurrence of symptoms. There was no evidence of error in dosage or interaction. A failure of the generic product was suspected. Only a pharmacist solved the problem. Fonzylane (buflomedil) had recently been switched to Buflomedil Merck. The patient misunderstood the change and took both drugs! Our purpose is not to report a known effect but to emphasize the importance of extending the information given to the patient and the risk of misuse of the generic product.

Adrenergic alpha-Antagonists↗
PubMedDate not supplied

[Results of a French nationwide survey of cutaneous side effects of ketoprofen gel reported between September 1996 and August 2000].

A French nation-wide pharmacovigilance survey of ketoprofen topic collated, from September 1996 to August 2000, 770 cutaneous side-effects. The frequency varies from 0.013@1000 to 0.028@1000 according to the commercial gel. Analysis concerns spontaneous notifications of French nation-wide pharmacovigilance. Sex ratio is well distributed, population is young. Treatment lasted about 12 days, the side-effects appearing after about 13 days, 25 per cent of cases are delayed to discontinuance of treatment, mainly after exposure to sunlight. Co-administered drugs are in most cases systemic or topical NSAIDs and/or fibrates and then increase the seriousness of the iatrogenic pathology. 75 per cent of cutaneous side-effects appear in summer, 50 per cent have been reported as "photosensitivity". Reactions are severe in 30 per cent of the cases. More than 80 per cent of cases present an extension beyond the site of application. The course is usually favourable and neither topical nor systemic corticosteroid treatment influence the duration of evolution. Photopatchtests testing in 23 per cent of cases show evidence of photoallergy to ketoprofen and crossed photoallergy with tiaprofenic acid, fenofibrate, oxybenzone and benzophenone. These results confirm that photoallergy is due to the common benzoylketone structure but not to their arylpropionic function. Some cases of persistent or recurrent photosensitivity must be more explored. The results lead to request a modification of marketing authorizations.

Glycine↗
PubMedDate not supplied

[Characteristics of hypersensitivity syndrome to lamotrigine: review of one case reported in the Regional Center of Pharmacovigilance of Nantes].

Drug-induced hypersensitivity syndrome is an uncommon but potentially life-threatening idiosyncratic drug reaction. In the literature, about five cases have been reported concerning hypersensitivity syndrome with lamotrigine. Most cases concern aromatic anticonvulsants but we report a case induced by lamotrigine which is a non aromatic anticonvulsant. A 73-year-old man was treated with lamotrigine for epilepsy due to a cerebrovascular stroke for 5 weeks. After 2 weeks with a single oral dose of 50 mg lamotrigine, the patient received 100 mg. Quickly thereafter fever, erythema and edema involving the periorbital area appeared. He was then admitted to hospital and lamotrigine was immediately discontinued. He developed acute hepatic and renal failure. During his hospital stay, he was treated with systemic and topical corticosteroids. After slow improvement, he was discharged 4 weeks later. Concerning this typical case, we review the characteristics of hypersensitivity syndrome and the different etiopathogenesis. The hypersensitivity syndrome typically develops two to six weeks after a drug is first administered, later than most other serious skin reactions. This syndrome manifests as rash, fever, tender lymphadenopathy, hepatitis and eosinophilia. The mechanism of hypersensitivity syndrome is unknown. Several theories have been proposed. The reaction is secondary to circulating antibodies or concerns toxic metabolities. On the other hand, association of human herpes virus 6 infection may play a role in the development of hypersensitivity syndrome. Hypersensitivity reactions to the aromatic antiepileptic drugs appear to have an immune etiology much like lamotrigine: bioactivation, detoxification, covalent adduct formation, processing and presentation of antigen to the immune system, and consequent formation of antibody and T-cell immune effectors. Another theory involves toxic metabolites; the aromatic antiepileptic agents are metabolised by cytochrome P-450 to an arene oxide metabolite. This is normally detoxified by epoxide hydrolase. This enzyme may be lacking or mutated in persons that develop the syndrome, and this is genetically determined. Lamotrigine is mainly metabolised by hepatic glucuronidation, but hypersensitivity may involve similar processes such aromatic antiepileptic drugs, except that the toxic metabolite has not yet been found. Because of slow evolution and clinical similarity to many infectious illnesses, the diagnosis of hypersensitivity syndrome may be delayed. Prompt recognition and withdrawal of the suspected drug is essential. The goal of research is to describe a "susceptibility profile" identifying individuals at risk for these forms of drug toxicity.

Aged↗