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Biomedical subjects

W S Bond

Publications and source records attributed to W S Bond.

At least 19 recordsLinked to original sources
PubMed1991

Ethnicity and psychotropic drugs.

The literature concerning the effect of race and ethnicity on the pharmacokinetics of psychotropic drugs is reviewed, and recommendations concerning the use of these agents are presented. While no differences in the pharmacokinetics of dosage requirements of antipsychotic drugs have been demonstrated among black, Hispanic, and white persons, Asians seem to have a lower threshold for both the therapeutic and adverse effects of antipsychotic drugs than do Caucasians. Use of lower than usual initial dosages of antipsychotic drugs in Asian patients appears to be prudent. Although ethnicity may have an effect on antidepressant drug pharmacology and dosage requirements, the available data are not sufficiently convincing to make any dosage recommendations. Claims that Asians require lower dosages of lithium than do other ethnic groups are not supported by the available evidence. Higher plasma benzodiazepine concentrations and lower drug clearance observed in Asians compared with Caucasians are consistent with clinical observations of lower dosage requirements for Asian patients; smaller than usual dosages of these agents are recommended for Asian patients. Interracial pharmacokinetic and pharmacodynamic differences for psychotropic drugs can affect clinical outcomes. Further study of this issue is warranted.

Antidepressive Agents↗
PubMed1991

Detection methods and strategies for improving medication compliance.

The reliability of compliance detection methods and practical strategies for improving patient compliance with drug therapy are reviewed. Detection of noncompliance is a necessary prerequisite for adequate treatment. Noncompliance can be detected by indirect methods (e.g., self-report, interview, therapeutic outcome, pill count, computerized compliance monitors) or direct methods (e.g., biologic markers, tracer compounds, biologic assay of body fluids). In general, the direct methods of detection have a higher sensitivity and specificity than the indirect methods. Computerized compliance monitors are the most recent and reliable of the indirect-detection methods. Strategies for improving compliance involve identification of risk factors for non-compliance; development, with the patient's participation, of an individualized treatment plan that simplifies the regimen as much as possible; education of the patient, including information about his or her illness, instructions on how to take the prescribed medication correctly, and an explanation of the benefits and possible adverse effects of the therapy; and, if necessary, use of compliance aids such as medication calendars, special containers, caps, and dispensing systems, or compliance packaging. The patient should be taught to monitor his or her own treatment regimen. Follow-up monitoring by health-care professionals, including pharmacists, will also help ensure that the patient is complying with the treatment regimen. Health-care practitioners need to understand factors that contribute to noncompliance and to use effective methods for assessing and monitoring compliance in conjunction with strategies aimed at increasing compliant behavior.

Biomarkers↗
PubMed1990

Persistent metronidazole-induced peripheral neuropathy.

We report the case of a young woman with Crohn's disease who developed a debilitating peripheral neuropathy when treated with metronidazole 2000 mg/d for 50 days. The patient's neuropathy improved considerably after the discontinuation of metronidazole, but still persists two years later. The current literature on this topic is reviewed. Reports such as this one underscore the need to closely monitor the neurologic status of patients undergoing chronic treatment with metronidazole.

Adult↗
PubMed1989

Midazolam for aggressivity and violence in three mentally retarded patients.

Midazolam was administered to three mentally retarded patients with acute and refractory aggressivity and violence. Midazolam was well tolerated without complications and provided dramatic control of the symptoms, suggesting an expanded role for it in the management of aggressive and violent behavior.

Adolescent↗
PubMed1987

Recognition and treatment of attention deficit disorder.

The proposed etiologies, clinical features, prognosis, and drug therapy of attention deficit disorder (ADD) are reviewed. Attention deficit disorder is a common neurobehavioral problem in children that manifests as hyperactivity, impulsivity, and inattention. It may persist into adolescence and adulthood and predispose the patient to antisocial and substance-abuse disorders. Stimulant agents are the drugs of first choice for pharmacologic treatment of ADD. Methylphenidate is the most frequently used stimulant because of its reduced potential for abuse and less troublesome adverse effects compared with dextroamphetamine. Stimulant medications are usually well tolerated, with nervousness and insomnia being the most common adverse effects. The potential for stimulant-induced growth suppression during long-term treatment should be dealt with prospectively by providing drug holidays. Tricyclic antidepressants and monoamine oxidase inhibitors may be used in patients who do not respond adequately to stimulant agents. Low doses of the antipsychotic agents haloperidol, chlorpromazine, or thioridazine may be used as adjunctive treatment for ADD symptoms of hyperactivity and aggressiveness. Attention deficit disorder is not a benign disorder that children necessarily outgrow. Pharmacologic therapy should be combined with nonpharmacologic therapy to provide the greatest long-term benefits.

Antidepressive Agents↗
PubMed1986

Pharmacotherapy of eating disorders: a critical review.

The pharmacotherapy of anorexia nervosa and bulimia are critically reviewed. No chemical treatment has been shown effective for anorexia nervosa. Antidepressants with a low incidence of annoying adverse reactions (e.g., desipramine) may be used as initial drug therapy in patients with concomitant depression. Cyproheptadine also is an attractive agent for initial therapy consideration in anorectics because of its relative safety. Both uncontrolled and controlled trials have found antidepressant drugs effective in bulimia, and they represent the pharmacotherapy of first choice. Alternative drug therapies include anticonvulsants (phenytoin and carbamazepine) and lithium. However, these agents need further controlled trials to substantiate their efficacy.

Anorexia Nervosa↗
PubMed1986

Psychiatric indications for clonidine: the neuropharmacologic and clinical basis.

Clonidine's actions and efficacy in mental disorders are reviewed and examined. Its efficacy in suppressing acute opiate withdrawal symptoms and its role in preparing the opiate-dependent patient for transition from opiate agonist to naltrexone therapy are well documented. Studies also indicate clonidine's value in alcohol and tobacco withdrawal syndromes. Of special interest is evidence which suggests that clonidine can reduce the duration and cost of the withdrawal process. Also discussed is clonidine's utility for mania, anxiety and panic disorders, schizophrenia, and the symptoms of tardive dyskinesia. Although further documentation of its efficacy for these disorders is required, clonidine's efficacy as an antimanic agent and treatment for tardive dyskinesia is particularly exciting and worthy of further study.

Animals↗
PubMed1985

Severe withdrawal syndrome after substitution of a short-acting benzodiazepine for a long-acting benzodiazepine.

A severe withdrawal syndrome occurred in a patient after oxazepam 10 mg bid was substituted for diazepam 5 mg bid. The onset of symptoms was consistent with the rate of decline of diazepam and its active metabolite, desmethyldiazepam. Reintroduction of diazepam produced prompt symptom remission. This report and others suggest the need for caution when substituting a short-acting drug for a long-acting one, even when usual doses of each are used. The chronic use of benzodiazepines for eight months or longer prior to substitution or withdrawal appears to place the patient at a higher risk of incurring withdrawal phenomena. Slow and careful tapering of drug is required in such patients to reduce the risk of withdrawal symptoms.

Diazepam↗
PubMed1982

Persistent dysarthria with apraxia associated with a combination of lithium carbonate and haloperidol.

Reported is a 19-year-old manic-depressive patient who developed persistent dysarthria with coexisting apraxia while on a combination of high dose haloperidol and lithium carbonate. The speech disability occurred as a solitary symptom in a patient with normal serum lithium levels and no other signs or symptoms of lithium toxicity and persisted after lithium was discontinued and the neuroleptic changed. There were several factors which favored an association between the speech disability and the drug therapy. These included improvement during a drug-free trial: the absence of a prior history of a speech problem; the patient's marked psychotic state and anxiety: and the high dosage of haloperidol.

Adult↗
PubMed1978

Clinical relevance of the effect of hepatic disease on drug disposition.

The effect of hepatic disease on the metabolism of drugs is reviewed. Drugs discussed include those acting on the central nervous system (phenobarbital, pentobarbital, amobarbital, diazepam, chlordiazepoxide, oxazepam, clorazepate, chlorpromazine, morphine, meperidine, phenytoin); those acting on the cardiopulmonary system (digoxin, digitoxin, lidocaine, theophylline); antineoplastic agents (azathioprine, 6-mercaptopurine, doxorubicin), antimicrobials (carbenicillin, ampicillin, nafcillin, chloramphenicol, clindamycin, lincomycin, rifampin, isoniazid, aminosalicylic acid) and antiinflammatory agents (phenylbutazone, prednisone). The effect of hepatic dysfunction on drug disposition is not consistent or predictable. The efficiency with which drugs are metabolized by the liver, the extent of drug plasma binding, and the etiology and stage of the hepatic disorder are each important in determining whether drug disposition will be altered.

Anti-Infective Agents↗
PubMed1977

Toxic reactions and side effects of glucocorticoids in man.

The toxic reactions and side effects of glucocorticoids in humans are discussed. The effects reviewed include metabolic (muscle and skin, carbohydrates and lipids), cardiovascular, cellular, immunologic, skeletal and growth, gastrointestinal, nervous system, ocular, and hypothalmic-pituitary-adrenal.

Adrenal Glands↗
PubMedDate not supplied

Detection and management of the neuroleptic malignant syndrome.

Two patients who developed the neuroleptic malignant syndrome (NMS) are described, and pertinent literature is reviewed. A 30-year-old man developed NMS, apparently as a result of haloperidol treatment of chronic undifferentiated schizophrenia. Treatment with cooling blankets, acetaminophen, dantrolene sodium, and bromocriptine mesylate decreased abnormal vital signs, but catatonia continued. After 30 treatments with electroconvulsive therapy over a one-month period, the patient's catatonia was resolved, and he was discharged on no medication with the schizophrenia in remission. The second patient was a 22-year-old woman who developed NMS after five weeks of therapy with haloperidol and thiothixene for an acute episode of abnormal behavior. She did not respond to therapy with cooling blankets, acetaminophen, antibiotics, and amobarbital sodium. Dantrolene sodium therapy produced no improvement except for some relief of muscular rigidity. Electroconvulsive therapy (22 treatments over one month) successfully decreased the patient's elevated liver enzymes and leukocyte count, but periodic temperature elevations and catatonia continued. Prompt diagnosis and treatment of NMS are essential, as the mortality rate is 20%. Acute lethal catatonia and malignant hyperthermia are considered in differential diagnosis. Both central and peripheral pathophysiologic mechanisms are probably involved in NMS, and most cases are seen in patients with psychiatric illness. Onset of NMS does not seem related to duration of neuroleptic therapy and, in susceptible persons, additional factors may be required to trigger onset of NMS. Symptoms, including diffuse muscular rigidity, akinesia, and fever, develop within 24-72 hours. Neurologic symptoms may develop or worsen, and leukocytosis and elevated levels of liver enzymes occur. Death can result from respiratory or cardiovascular failure, and rhabdomyolysis can lead to acute renal failure.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗