{"title":"Aerosol pentamidine for Pneumocystis carinii pneumonia.","authors":"C P Stoner","doi":"10.1177/106002808802201127","DOIUrl":"https://doi.org/10.1177/106002808802201127","url":null,"abstract":"anion gap (Na[CI+ HCO,)) was20 mEq/L (normal 8-16 mEq/L). The measured serum osmolarity on admission was 423 mOsmol/kg. The calculated serum osmolarity (2Na+ BUN/28 + glucose/I 8) was 306mOsmol/kg (normal 280-295 mOsmol/kg) for an osmolar gap of 117 mOsmol/kg. Urinalysis showedthe urine to beclearand yellow; witha specificgravityof 1.020;pH 6.0; no ketones, blood, albumin, crystals, or casts; and a WBC count of one per high-powered field. Toxicological analysis revealed an initial ethanol blood level of 297 mg/dL and an ethylene glycol blood level of 2100 mg/L (210 mg/dL). Ethyleneglycollevelswerereportedas milligrams per literbythe laboratory throughout this case. The treatment courseof this patient includedan ethanol infusionand hemodialysis.Figure I summarizesthe useof ethanol and the timingof hemodialysis procedures. The presence of a high ethanol concentration on admission is believed to have aided in preventingthis patient from developing a potentially severemetabolicacidosisby inhibiting the metabolismof ethyleneglycol.The initial infusionrate of ethanolchosen(7.5g/h) waslowfor thisyoungalcoholic patient with normal liverfunction. Compensationfor ethanol removedduring hemodialysis was also inadequate, as shown in Figure I. The ethanol infusion wascontinued without change on days 3 and 4; ethanol serum concentrations on these days were again subtherapeutic. Figure I also summarizesall blood concentrationsof ethanol and ethyleneglycolobtained and their relationshipto ongoingtherapy. BEN M. LOMAESTRO, B.S.Pharm. Clinical Specialist Intensive Care Albany Medical Center Albany, New York 12208","PeriodicalId":77709,"journal":{"name":"Drug intelligence & clinical pharmacy","volume":"22 11","pages":"916-7"},"PeriodicalIF":0.0,"publicationDate":"1988-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1177/106002808802201127","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"14395801","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Chlorpromazine accumulation and sudden death in a patient with renal insufficiency.","authors":"P G Dorson, M L Crismon","doi":"10.1177/106002808802201007","DOIUrl":"https://doi.org/10.1177/106002808802201007","url":null,"abstract":"<p><p>Sudden death has been reported in psychiatric patients before and after the advent of antipsychotic medications. A case of sudden death following chlorpromazine administration in a schizophrenic patient is presented. After receiving a mean daily dose of 780 mg for five days, the patient died suddenly. Laboratory work on day 2 of hospitalization indicated a calculated creatinine clearance of 14 ml/min. The autopsy was noncontributory except for a blood chlorpromazine concentration of 1534 ng/ml. The potential cause of death in this patient and the proposed mechanisms of sudden death in psychiatric patients are discussed. The effect of renal and hepatic disease on chlorpromazine plasma concentrations is presented. This case is the first report of sudden death in a psychiatric patient with a documented elevated antipsychotic plasma concentration. It is also the first report of an elevated chlorpromazine blood concentration in a patient with renal insufficiency.</p>","PeriodicalId":77709,"journal":{"name":"Drug intelligence & clinical pharmacy","volume":"22 10","pages":"776-8"},"PeriodicalIF":0.0,"publicationDate":"1988-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1177/106002808802201007","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"14357496","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Comment: liquid dosage form of chloroquine.","authors":"","doi":"10.1177/106002808802201029","DOIUrl":"https://doi.org/10.1177/106002808802201029","url":null,"abstract":"above which the study drug must demonstrate improvement. For the specific study question of the effectiveness of propranolol (or another beta-blocker) in the management of frequently occurring negative behaviors that are not adequately controlled by psychotropic agents, the following criteria should be met: I. Patients who are severely disabled and require long-term hospitalization are the most suitable candidates for the studies. Sixto 12month studies would be feasible in this subpopulation. 2. A lengthening of the individual blocks of the study design, perhaps in the range of 6-12 weeks, would allow adequate time for the observation of the slowly changing outcome measure. 3. Carryover effects can be handled in a manner similar to that of Greendyke et al. in their A-B design case study, which is very much in the model we are advocating.' In essence, one builds in upward and downward titration periods for introduction and removal (washout) of the study drug. In summary, aside from the difficulty of maintaining staff interest in the quantitative measurement of negative behaviors, there seem to be only advantages for applying rigorous standards to the evaluation of drug effects in individual patients.","PeriodicalId":77709,"journal":{"name":"Drug intelligence & clinical pharmacy","volume":"22 10","pages":"828-9"},"PeriodicalIF":0.0,"publicationDate":"1988-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1177/106002808802201029","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"14359412","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Rho Chi lecture. The pharmaceutical sciences as academic disciplines.","authors":"A P Lemberger","doi":"10.1177/106002808802201020","DOIUrl":"https://doi.org/10.1177/106002808802201020","url":null,"abstract":"<p><p>Recent studies of higher education in America have raised concern over the lack of integrity and coherence, the absence of vigorous intellectual exchange, and the dominance of careerism in the undergraduate curriculum. Observations and recommendations emanating from studies of pharmaceutical education acknowledge the importance of problem-solving abilities but emphasize the inculcation of knowledge relevant to professional functions and the development of skill in contemporary practice. The current emphasis placed on training students for pharmacy practice found in the pharmacy curriculum causes the objective of achieving intellectual growth to be overshadowed. Balance must be restored. The pharmaceutical sciences, taught for their value as academic disciplines and for their integrity with other branches of science, could serve as the stimulus for intellectual growth of students. An academic baccalaureate program with a major in pharmaceutical sciences as the required base for professional education is proposed as a remedy.</p>","PeriodicalId":77709,"journal":{"name":"Drug intelligence & clinical pharmacy","volume":"22 10","pages":"807-12"},"PeriodicalIF":0.0,"publicationDate":"1988-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1177/106002808802201020","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"14359405","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
B H Chen, E H Taylor, B H Ackerman, K Olsen, A A Pappas
{"title":"Effect of pH on free quinidine.","authors":"B H Chen, E H Taylor, B H Ackerman, K Olsen, A A Pappas","doi":"10.1177/106002808802201023","DOIUrl":"https://doi.org/10.1177/106002808802201023","url":null,"abstract":"TO THE EDITOR: Protein binding of quinidine has been noted to be pH-dependent with equilibrium dialysis;' however, this relationship has not been examined using ultrafiltration to separate free from protein-bound quinidine. Thus, the implication of pH dependency on protein ultracentrifugation from experiments run at unphysiological or unknown pH may be irrelevant to the in vivo conditions. The pHdependent protein binding in human serum is also found with other drugs including warfarin,\" lidocaine,\" propranolol,\" and disopyramide.\" Weused pooled serum from patients with normal liverand renal functions, and spiked the serum with either 2 or 10 mg/L of quinidine sulfate. After adjusting the pH of 10 ml of pooled serum, according to the procedure of Ponganis and Stanski,' with 0.5 M phosphoric acid (15-120I'L), the total and free quinidine concentrations were determined by fluorescence polarization immunoassayon theTDx. Freequinidineanalysiswasperformedbyultrafiltration method using an Amicon centrifree filter. The pH was determined by a Corning pH meter model 10,whichwascalibrated at 22°C. The pH dependence of serum binding of quinidine is shown in Figure I. The free fraction decreased with increasing pH. For the spiked total 10 mg/L quinidine concentration, the free fraction percentages were 25.6 ±0.69, 2.2 ± .05, 14.8 ±0.64, and 8.80 ± 0.38 percent REFERENCES","PeriodicalId":77709,"journal":{"name":"Drug intelligence & clinical pharmacy","volume":"22 10","pages":"826"},"PeriodicalIF":0.0,"publicationDate":"1988-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1177/106002808802201023","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"14359408","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
L A Shimp, T J Wells, C A Brink, A C Diokno, G L Gillis
{"title":"Relationship between drug use and urinary incontinence in elderly women.","authors":"L A Shimp, T J Wells, C A Brink, A C Diokno, G L Gillis","doi":"10.1177/106002808802201012","DOIUrl":"https://doi.org/10.1177/106002808802201012","url":null,"abstract":"<p><p>Two hundred older women with urinary incontinence were studied to observe the influence of their prescription and nonprescription drug use on symptoms of incontinence. Ninety percent of women reported using medication, with an average use of four drugs. Medications statistically associated with urinary incontinence symptomatology were prostaglandin inhibitors, diuretics, and estrogen therapy. Further studies are needed to clarify the relationship between medication usage and the presence and severity of urinary incontinence.</p>","PeriodicalId":77709,"journal":{"name":"Drug intelligence & clinical pharmacy","volume":"22 10","pages":"786-7"},"PeriodicalIF":0.0,"publicationDate":"1988-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1177/106002808802201012","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"14359400","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Education of manpower for future pharmaceutical care and research.","authors":"P H Vlasses","doi":"10.1177/106002808802201018","DOIUrl":"https://doi.org/10.1177/106002808802201018","url":null,"abstract":"","PeriodicalId":77709,"journal":{"name":"Drug intelligence & clinical pharmacy","volume":"22 10","pages":"800-3"},"PeriodicalIF":0.0,"publicationDate":"1988-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1177/106002808802201018","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"14359404","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Monoamine oxidase inhibitors and weight gain.","authors":"T G Cantú, J S Korek","doi":"10.1177/106002808802201002","DOIUrl":"https://doi.org/10.1177/106002808802201002","url":null,"abstract":"<p><p>Weight gain associated with antidepressant therapy is a common problem that often results in noncompliance. Some authors suggest that monoamine oxidase inhibitors (MAOI) are less likely to produce weight gain than tricyclic antidepressants. This paper addresses the relative potential for weight gain with the MAOI. Assessing the potential for antidepressant-induced weight gain necessitates separating the weight changes associated with alterations in mood disorders from those due to drug-induced alterations in appetite control. The mechanisms of appetite control are reviewed briefly followed by proposed mechanisms by which the MAOI may alter this control. A literature review suggests that phenelzine is the MAOI most likely to induce weight gain; reports of isocarboxazid-induced weight gain are less common. There are no cases of tranylcypromine-induced weight gain in the literature that are clearly associated with the drug. The MAOI probably have different effects on the mechanisms of appetite control.</p>","PeriodicalId":77709,"journal":{"name":"Drug intelligence & clinical pharmacy","volume":"22 10","pages":"755-9"},"PeriodicalIF":0.0,"publicationDate":"1988-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1177/106002808802201002","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"14199911","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Effect of infusion rate on amphotericin B-associated febrile reactions.","authors":"J D Cleary, D Weisdorf, C V Fletcher","doi":"10.1177/106002808802201005","DOIUrl":"https://doi.org/10.1177/106002808802201005","url":null,"abstract":"<p><p>Our objective was to prospectively study febrile and chill reactions associated with two amphotericin B (AB) infusion rates, slow (2-hour) versus rapid (45 minute). Seventeen consenting bone marrow transplant recipients in whom AB was to be initiated for documented or suspected fungal infections were recruited. After standardized premedication, patients received eight daily AB infusions (0.5 mg/kg/d, concentration 0.25 mg/ml). Rate was assigned using a randomized, crossover pair design. Axillary temperature, chills, and meperidine dose required to resolve chills were monitored for each infusion. For the first pair of infusions, fever (defined as a rise of 1 degree C) occurred frequently, in 12 of 17 (70.5 percent) and 13 of 17 patients (76.4 percent), with a mean rise of 1.7 degrees C (range 1.1-3.7) and 1.7 degrees C (1.1-3.5) degrees for the 45-minute and 2-hour infusions, respectively (p greater than 0.10). Chills were observed in 15 of 17 (88.2 percent) and 14 of 17 (82.3 percent) recipients of the 45-minute and 2-hour infusions, respectively. The time of onset (p greater than 0.10) and the duration of chills (p = 0.08) were similar for both infusion rates. Meperidine requirements for rapid and slow infusions were similar as well (p = 0.12). These data suggest that for patients free of preexisting renal and cardiac disease, rapid AB infusions are well tolerated and produce adverse reactions (fever and chills) similar in nature and severity to slower infusions.</p>","PeriodicalId":77709,"journal":{"name":"Drug intelligence & clinical pharmacy","volume":"22 10","pages":"769-72"},"PeriodicalIF":0.0,"publicationDate":"1988-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1177/106002808802201005","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"14199912","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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