Original Article
Phenylpropanolamine and the Risk of Hemorrhagic Stroke
N Engl J Med 2000; 343:1826-1832December 21, 2000
- Abstract
Background
Phenylpropanolamine is commonly found in appetite suppressants and cough or cold remedies. Case reports have linked the use of products containing phenylpropanolamine to hemorrhagic stroke, often after the first use of these products. To study the association, we designed a case–control study.
Methods
Men and women 18 to 49 years of age were recruited from 43 U.S. hospitals. Eligibility criteria included the occurrence of a subarachnoid or intracerebral hemorrhage within 30 days before enrollment and the absence of a previously diagnosed brain lesion. Random-digit dialing identified two matched control subjects per patient.
Results
There were 702 patients and 1376 control subjects. For women, the adjusted odds ratio was 16.58 (95 percent confidence interval, 1.51 to 182.21; P=0.02) for the association between the use of appetite suppressants containing phenylpropanolamine and the risk of a hemorrhagic stroke and 3.13 (95 percent confidence interval, 0.86 to 11.46; P=0.08) for the association with the first use of a product containing phenylpropanolamine. All first uses of phenylpropanolamine involved cough or cold remedies. For men and women combined, the adjusted odds ratio was 1.49 (95 percent confidence interval, 0.84 to 2.64; P=0.17) for the association between the use of a product containing phenylpropanolamine and the risk of a hemorrhagic stroke, 1.23 (95 percent confidence interval, 0.68 to 2.24; P=0.49) for the association with the use of cough or cold remedies that contained phenylpropanolamine, and 15.92 (95 percent confidence interval, 1.38 to 184.13; P=0.03) for the association with the use of appetite suppressants that contained phenylpropanolamine. An analysis in men showed no increased risk of a hemorrhagic stroke in association with the use of cough or cold remedies containing phenylpropanolamine. No men reported the use of appetite suppressants.
Conclusions
The results suggest that phenylpropanolamine in appetite suppressants, and possibly in cough and cold remedies, is an independent risk factor for hemorrhagic stroke in women.
Media in This Article
Table 1
Identification and Enrollment of Patients.Table 2
Characteristics of the Patients and the Control Subjects.Article Activity
- Article
Phenylpropanolamine is a synthetic sympathomimetic amine commonly found in appetite suppressants and cough and cold remedies. Each month, millions of Americans use products containing phenylpropanolamine. Since 1979, more than 30 case reports have been published that describe the occurrence of intracranial hemorrhage after the ingestion of phenylpropanolamine.1-9 Affected patients were most commonly adolescent girls or young women between the ages of 17 and 45 years who were using phenylpropanolamine-containing appetite suppressants, often for the first time.7-13 In addition to the published reports, between 1969 and 1991, the Food and Drug Administration (FDA) received 22 spontaneous reports of hemorrhagic stroke associated with phenylpropanolamine in appetite suppressants (in 16 cases) or cough and cold remedies (in 6 cases) (Jolson HM: personal communication).
In response to the concern aroused by these case reports, in 1992 we collaborated with the FDA and manufacturers of phenylpropanolamine to design the Hemorrhagic Stroke Project, a case–control study of men and women who were 18 to 49 years of age. The study had three prespecified aims: to estimate, among women, the association between hemorrhagic stroke and the use of appetite suppressants containing phenylpropanolamine and any first use of products containing phenylpropanolamine; to estimate, among men and women, the association between any use of phenylpropanolamine in either an appetitie suppressant or a cough or cold remedy and hemorrhagic stroke; and to estimate, among men and women, the association between hemorrhagic stroke and the type of exposure to phenylpropanolamine.
Methods
Recruitment and Classification of Patients with Hemorrhagic Stroke
Between December 1994 and July 1999, we identified patients with symptomatic subarachnoid or intracerebral hemorrhage from 43 hospitals in Connecticut, Massachusetts, Ohio, Kentucky, Rhode Island, and Texas (see the Appendix). A subarachnoid hemorrhage was diagnosed on the basis of clinical symptoms plus either evidence of subarachnoid bleeding on computed tomography (CT) or evidence of xanthochromia on lumbar puncture. An intracranial hemorrhage was diagnosed on the basis of clinical symptoms plus a CT or magnetic resonance imaging scan showing blood primarily in the parenchyma of the brain. Eligibility criteria for patients included an age of 18 to 49 years, the ability to communicate and complete the interview within 30 days after the stroke, the absence of a history of a brain lesion that would increase the risk of hemorrhage (i.e., an arteriovenous malformation, tumor, or aneurysm), and the absence of a history of stroke. Patients were recruited in person or by telephone as soon as they were identified, provided that their personal physician approved.
Recruitment of Control Subjects
We attempted to identify two matched control subjects for each patient through the use of random-digit dialing. Matching criteria included telephone exchange, sex, race (black or nonblack), and age (within 3 years in the case of patients who were younger than 30 years of age and within 5 years in the case of patients who were 30 or older). When a perfectly matched control could not be located, we enrolled an imperfectly matched control rather than excluded the patient from the study. All interviews with control subjects had to be completed within 30 days after the patient's stroke to minimize seasonal differences in exposure to products containing phenylpropanolamine.
Definition of Focal Time
For each patient, we identified the focal time, which we defined as the calendar day (i.e., the index day) and the time of day that marked the onset of symptoms that were plausibly related to hemorrhage and that caused the patient to seek medical attention. Some patients with subarachnoid or intracerebral hemorrhage may have a transient headache hours or days before the onset of symptoms that lead them to seek medical attention.14,15 The cause of these sentinel headaches is not known, although clinicians infer that some may be due to minor bleeding.16 Accordingly, for patients with such headaches we defined a modified focal time as the time of onset of the sentinel headache. We used this definition in a secondary analysis.
The focal time used for each control subject was matched to the day of the week and the time of day that corresponded to the patient's focal time. We interviewed the control subject within seven days after this date, to improve recall of exposures and thereby minimize the opportunity for recall bias.
Ascertainment of Data on Exposure and Other Information
Trained researchers used a structured questionnaire to obtain demographic, clinical, behavioral, and pharmaceutical information from all subjects. Interviews were conducted in person unless the subject refused or a meeting could not be arranged within 30 days after the focal time in the patients (in which case the interview took place by telephone). Subjects were asked to recall cold symptoms, medications used to treat them, and any other medications taken during the two weeks before the focal time. After all such responses had been recorded, subjects were asked whether they had taken several specific medications or classes of medications (e.g., aspirin, anticoagulants, and diet pills).
To verify information about exposure to medications, subjects were asked to pick out brand-name medications from a book containing photographs of packages. They were then asked to produce each medication so that the exact name and manufacturer's lot number could be recorded. If the container was not available, use of a brand-name medication was considered verified if the subject identified it in the book. Only verified exposures to medication were counted in the analysis.
To determine the active ingredients in each medication, we relied on published sources.17,18 For national brands and prescription drugs that may have had changes in formulation during the study period and for generic or store-brand medications, we verified active ingredients directly with the manufacturer.
Definition of Exposure to Phenylpropanolamine
The window of exposure to phenylpropanolamine refers to the interval before the focal time when a subject's exposure status is defined. For all analyses except those involving the first use of a product containing phenylpropanolamine, the window of exposure was defined as the index day before the focal time and the preceding three calendar days. For the first use of a product containing phenylpropanolamine, a subject was considered to have been exposed if he or she had used a product containing phenylpropanolamine within 24 hours before the focal time and had not used any other such products during the preceding two weeks. To maintain a consistent reference group, nonexposure for all analyses was defined by the absence of the use of products containing phenylpropanolamine within two weeks before the focal time.
Statistical Analysis
The sample size was based on the need to determine whether the first use of products containing phenylpropanolamine increased the risk of hemorrhagic stroke among women who were 18 to 49 years of age. Using available market data, we estimated that 0.502 percent of control subjects would report an exposure to phenylpropanolamine within 24 hours before the focal time. We specified one-tailed statistical tests because the focus of this research was the effect of phenylpropanolamine in increasing the risk of stroke. For a one-tailed test of significance at the 0.05 level and for the study to have a power of 80 percent to detect among women an odds ratio of 5.0 for hemorrhagic stroke after the first use of a product containing phenylpropanolamine, 324 female patients and 648 female control subjects were required. Because our research interest extended to the effects of phenylpropanolamine in men, we doubled our sample size to include 350 male and 350 female patients and 1400 controls.
In the first phase of the analysis, we compared demographic and clinical features of patients and control subjects using the chi-square test or Fisher's exact test (SAS Institute, Cary, N.C.). In the second phase, we estimated odds ratios and 95 percent confidence intervals for the association between hemorrhagic stroke and exposure to phenylpropanolamine using conditional logistic models for matched sets. Because of the low incidence rate of hemorrhagic stroke, the odds ratio is a close approximation of the relative risk. We calculated unadjusted and adjusted estimates using exact methods and asymptotic methods, respectively. We adjusted for black race (because not all patients and control subjects were successfully matched for this factor), presence or absence of a history of hypertension, and current smoking status. We also adjusted for features that, when added to this model, changed the matched odds ratio by at least 10 percent. All logistic models were estimated with use of the LogXact Program (version 2.1, Cytel Software, Cambridge, Mass.). Although we used a one-sided test of significance at the 0.05 level to estimate sample size, for the results we present two-sided P values and 95 percent confidence intervals.
An autonomous external scientific advisory group reviewed the protocol and research progress, developed criteria for early termination, and evaluated interim and final analyses. Two interim analyses of the data were conducted. Because of the (conservative) O'Brien–Fleming spending function we used to assess the associations between phenylpropanolamine use and hemorrhagic stroke during the interim analyses, no adjustment has been made in the P values and confidence intervals computed with all the data and presented in this report.
Results
Study Participants
Between December 1994 and July 1999, 1714 patients with hemorrhagic stroke were identified (Table 1Table 1
Identification and Enrollment of Patients.). Among these, 784 patients were ineligible for enrollment, 222 were eligible but were not enrolled, and 708 were enrolled. Six of those who were enrolled were not included in the analysis: there were no matched control subjects for three, two were interviewed more than 30 days after the stroke, and in the case of one patient the index day could not be determined. Thus, the analysis included 702 patients: 425 (61 percent) had had a subarachnoid hemorrhage and 277 (39 percent) had had an intracerebral hemorrhage.A total of 674 patients (96 percent) had two matched control subjects apiece, and 28 patients (4 percent) each had one matched control subject. All control subjects were matched to their respective patients for sex and telephone exchange. Age matching was successful in the case of 1367 controls (99 percent), and 1321 controls (96 percent) were matched for race. On average, for each patient, we called 151 telephone numbers (range, 3 to 1119) and identified 2.8 eligible persons (range, 1 to 12) for each control enrolled.
As compared with control subjects, patients were significantly (P<0.05) more likely to be black and to report lower levels of education, current cigarette smoking, a history of hypertension, a family history of hemorrhagic stroke, regular alcohol use (more than two drinks per day), and recent cocaine use (Table 2Table 2
Characteristics of the Patients and the Control Subjects.). Patients were less likely to report the use of nonsteroidal antiinflammatory drugs and more likely to report the use of pharmaceutical agents that contained caffeine and nicotine (Table 3Table 3
Frequency of Exposure to Pharmacologic Agents Other Than Phenylpropanolamine during the Three-Day Window of Exposure.).To identify variables for inclusion in multivariable models, we sequentially tested each feature listed in Table 2 and Table 3 in the basic model, which included race (black vs. nonblack), presence or absence of hypertension, and current smoking status. Under any definition of exposure to phenylpropanolamine, only the level of education changed the adjusted odds ratio for the association with hemorrhagic stroke by more than 10 percent.
Association between Phenylpropanolamine and Hemorrhagic Stroke
Table 4Table 4
Association between the Use of Products Containing Phenylpropanolamine and the Risk of Hemorrhagic Stroke. shows the results of analyses of the relation between the use of products containing phenylpropanolamine and the risk of hemorrhagic stroke for women and men separately and for all subjects combined. Frequencies are shown in an unmatched format for patients and control subjects, with adjusted matched odds ratios provided.For women, analysis of the association between the use of phenylpropanolamine in appetite suppressants within three days before the focal time and the risk of hemorrhagic stroke yielded an adjusted odds ratio of 16.58 (95 percent confidence interval, 1.51 to 182.21; P=0.02). With respect to the risk of a hemorrhagic stroke after the first use of a product containing phenylpropanolamine, the adjusted odds ratio was 3.13 (95 percent confidence interval, 0.86 to 11.46; P=0.08). All first uses of a product containing phenylpropanolamine involved cough or cold remedies.
For men and women combined, analysis of the association between any use of a product containing phenylpropanolamine within three days before the focal time and the risk of a hemorrhagic stroke yielded an adjusted odds ratio of 1.49 (95 percent confidence interval, 0.84 to 2.64; P=0.17). With respect to the risk of a hemorrhagic stroke within three days after the use of a cough or cold remedy containing phenylpropanolamine, the adjusted odds ratio was 1.23 (95 percent confidence interval, 0.68 to 2.24; P=0.49), and for the risk associated with the use of an appetite suppressant containing phenylpropanolamine within three days before the focal time, the adjusted odds ratio was 15.92 (95 percent confidence interval, 1.38 to 184.13; P=0.03).
The results of the analyses shown in Table 4 indicate that with respect to the use of cough or cold remedies containing phenylpropanolamine, the adjusted odds ratio for the risk of a hemorrhagic stroke was lower for men than for women (0.62 vs. 1.54), indicating that sex may modify the effect of phenylpropanolamine on the risk of hemorrhagic stroke. We present the results of the analysis of all subjects because it was a prespecified aim. No men were exposed to phenylpropanolamine through the use of an appetite suppressant. With respect to the risk associated with the first use of a product containing phenylpropanolamine, the adjusted odds ratios for men and women were similar (2.95 and 3.13, respectively).
In supplementary analyses, we examined the relation between the recency of exposure to phenylpropanolamine and the risk of hemorrhagic stroke. For these analyses, the definition of current use was consumption within 24 hours before the focal time, and both men and women were included. The adjusted odds ratio associated with current use (1.61; 95 percent confidence interval, 0.83 to 3.10; P=0.16) was slightly higher than that associated with the use of products containing phenylpropanolamine two or three days before the focal time (1.16; 95 percent confidence interval, 0.40 to 3.38; P=0.79). When current use was further stratified according to whether or not it was the first use, the risk was concentrated among first-time users (adjusted odds ratio for first-time use, 3.14; 95 percent confidence interval, 0.96 to 10.28; P=0.06; adjusted odds ratio for use other than first-time use, 1.20; 95 percent confidence interval, 0.54 to 2.67; P=0.66).
We also examined the possibility of a dose effect. Among 21 male and female control subjects with current use of products containing phenylpropanolamine, the median dose of phenylpropanolamine was 75 mg. Analyses showed that the point estimate of the odds ratio was higher for current use involving doses above the median dose of 75 mg (adjusted odds ratio, 2.30; 95 percent confidence interval, 0.96 to 5.54; P=0.06) than for current use involving lower doses (adjusted odds ratio, 1.01; 95 percent confidence interval, 0.36 to 2.80; P=0.98).
To examine the potential effect of ambiguity in the focal time, we recalculated the odds ratios after excluding 154 patients who were classified as having a definite sentinel headache (76 patients) or a possible sentinel headache (78) and their matched controls. The adjusted odds ratios for women were 12.6 (95 percent confidence interval, 1.01 to 157.75; P=0.05) for the use of appetite suppressants containing phenylpropanolamine within three days before the focal time and 3.32 (95 percent confidence interval, 0.72 to 15.2; P=0.12) for the first use. The adjusted odds ratios for men and women combined were 1.33 for any use of a product containing phenylpropanolamine within three days before the focal time (95 percent confidence interval, 0.70 to 2.55; P=0.39), 1.12 for the use of cough or cold remedies containing phenylpropanolamine (95 percent confidence interval, 0.57 to 2.20; P=0.74), 12.10 for the use of appetite suppressants containing phenylpropanolamine (95 percent confidence interval, 0.92 to 159.14; P= 0.06), and 3.34 for the first use of a product containing phenylpropanolamine (95 percent confidence interval, 0.87 to 12.87; P=0.08).
Discussion
Among women between the ages of 18 and 49 years, the use of a product containing phenylpropanolamine as an appetite suppressant was associated with an increased risk of hemorrhagic stroke. There was also a suggestion of an association in women with any first use of phenylpropanolamine, which involved only cough or cold remedies. No significantly increased risk of hemorrhagic stroke was observed among men who used a cough or cold remedy that contained phenylpropanolamine. Because no male subject reported the use of appetite suppressants containing phenylpropanolamine and only two reported the first use of a product containing phenylpropanolamine, we could not determine whether men are at increased risk for hemorrhagic stroke under these conditions.
Before our study, published information concerning the association between the use of phenylpropanolamine and the risk of hemorrhagic stroke came from one epidemiologic study19 and several case reports.1 The epidemiologic study found no association, but design limitations reduced its contribution to the assessment of the safety of phenylpropanolamine. Although the case reports called attention to a possible association between the use of phenylpropanolamine and the risk of hemorrhagic stroke, the absence of control subjects meant that these studies could not produce evidence that meets the usual criteria for valid scientific inference. Our study provides strong epidemiologic evidence of the association between the use of phenylpropanolamine and the risk of hemorrhagic stroke.
Other than a valid association between the use of phenylpropanolamine and the risk of stroke, possible explanations for our findings include chance, residual confounding, and other forms of bias. Regarding chance, the lower bound of the 95 percent confidence interval is greater than 1 for the odds ratio pertaining to the use of products containing phenylpropanolamine as an appetite suppressant among women. The lower bound falls at or just below 1 for odds ratios pertaining to any use of products containing phenylpropanolamine among women (not a prespecified research aim) and the first use among women. Although these two odds ratios are not statistically significant by conventional criteria (95 percent confidence interval excluding 1), their associated probabilities are sufficiently low to arouse concern regarding safety.
Residual confounding refers to incomplete adjustment for factors related to both exposure and outcome. Although there may have been residual confounding in the Hemorrhagic Stroke Project, our data provide little support for the presumption that it significantly distorted the observed association between phenylpropanolamine and hemorrhagic stroke. In particular, adjustment for known potential confounders did not produce odds ratios that were markedly different from the unadjusted figures. As in any research study, however, it is possible that unmeasured confounders contributed to the observed association between phenylpropanolamine and hemorrhagic stroke.
Biases that might have affected our study include temporal-precedence bias, recall bias, and selection bias. Temporal-precedence bias refers to a systematic error in which an exposure is counted although the exposure occurs after the onset of the disease under study, often in response to disease symptoms.20 We checked for temporal-precedence bias with specific analytic strategies for patients with sentinel headache and found no evidence that it distorted the main findings.
Recall bias refers to the tendency of case subjects, as compared with control subjects, to have more or less accurate recall of exposures. Because of the potential importance of recall bias, we used several safeguards, including a highly structured interview and the blinding of subjects to the study's phenylpropanolamine hypothesis. In addition, to overcome greater stimulation for recall among patients, we used a shorter interval between the focal time and interview dates for control subjects.
Selection bias refers to the preferential referral to a case–control study of patients or control subjects with (or without) the exposure under study.21 Publicity about phenylpropanolamine and stroke might have led physicians to preferentially seek a diagnosis of hemorrhage or to refer a patient to our study if there had been a history of phenylpropanolamine use.22 Although case–control studies cannot assuredly avoid such biases, we adopted several strategies to reduce the possibility of bias in the selection of patients, including active case surveillance and objective determination of eligibility.
Several features of the Hemorrhagic Stroke Project provide evidence of the validity of the associations found between the use of phenylpropanolamine and the risk of hemorrhagic stroke. First, uniform procedures to determine the eligibility of the subjects minimized bias in enrollment. Second, extensive procedures for ascertaining and verifying exposure to phenylpropanolamine were successfully implemented to reduce error and bias in exposure classification. Third, the odds ratios for the prespecified study aims regarding the use of appetite suppressants in women (16.58) and first use (3.13) were large. Fourth, the data suggest an association with hemorrhagic stroke for the two major formulations of phenylpropanolamine (i.e., cough or cold remedy and appetite suppressant).
Although data from the Hemorrhagic Stroke Project cannot be used to estimate individual risk, they can be used to estimate the number of people who must be exposed to phenylpropanolamine in order to observe one occurrence of hemorrhagic stroke (number needed to harm). Using a daily incidence rate of hemorrhagic stroke of 0.6 per million for persons 35 to 54 years of age23 and assuming a range of odds ratios from 1.51 to 16.58, we estimate that 1 woman may have a stroke due to phenylpropanolamine for every 107,000 to 3,268,000 women who use products containing phenylpropanolamine as an appetite suppressant within a three-day window.
In conclusion, the results of the Hemorrhagic Stroke Project suggest that phenylpropanolamine in appetite suppressants, and possibly also as a cold and cough remedy, is an independent risk factor for hemorrhagic stroke in women. For both persons considering the use of phenylpropanolamine and for policy makers, our study provides important data for a contemporary assessment of risks associated with the use of this common medication.
Supported by Novartis Consumer Health (formerly Ciba Consumer Pharmaceuticals), Thompson Medical Company, and Chattem.
Source Information
From the Departments of Internal Medicine (W.N.K., C.M.V., R.I.H.), Neurology (L.M.B.), and Epidemiology and Public Health (L.M.B., R.I.H.), Yale University School of Medicine, New Haven, Conn.; the Department of Neurology, University of Cincinnati, Cincinnati (J.P.B.); the Department of Neurology, Mayo Clinic, Jacksonville, Fla. (T.B.); the Department of Neurology, Brown University School of Medicine, Providence, R.I. (E.F., J.L.W.); and the Department of Neurology and School of Public Health, University of Texas, Houston (L.B.M.).
Address reprint requests to Dr. Kernan at the Department of Medicine, Yale University School of Medicine, P.O. Box 208025, New Haven, CT 06520-8025.
Appendix
The following regional centers, hospitals, coordinators, and institutional investigators participated in the Hemorrhagic Stroke Project: Clinical centers: University of Cincinnati (17 hospitals, 233 patients; principal investigators: J.P. Broderick, T. Brott; study coordinators: L. Sauerbeck, J. Carrozzella) — Bethesda North Hospital, Bethesda Oak Hospital, Clermont Mercy Hospital, Deaconess Hospital, Good Samaritan Hospital, Mercy Hospital (Anderson), Mercy Hospital (Fairfield), Mercy Franciscan Hospital (Western Hills), Mercy Franciscan Hospital (Mount Airy), Saint Elizabeth Medical Center (South), Saint Elizabeth Medical Center (North), Saint Luke Hospital (West), Saint Luke Hospital (East), Christ Hospital, Jewish Hospital, University Hospital and Veterans Affairs Medical Center, Cincinnati; University of Texas Medical School (1 hospital, 136 patients; principal investigator: L.B. Morgenstern; study coordinator: M. Cox) — Hermann Hospital: L.B. Morgenstern; and Brown University (2 hospitals, 109 patients; principal investigators: E. Feldmann, J.L. Wilterdink; study coordinators: C. Cirillo, N. Thovmasian) — Miriam Hospital: E. Feldmann; Rhode Island Hospital: E. Feldmann. Coordinating Center: Yale University School of Medicine (23 hospitals, 268 patients; principal investigators: L.M. Brass, R.I. Horwitz, W.N. Kernan, C.M. Viscoli; study coordinator: K. Krompf) — Bridgeport Hospital: K.N. Sena; Danbury Hospital: J.M. Murphy; Gaylord Hospital: R. Stein; Greenwich Hospital: W.A. Camp; Griffin Hospital: J.B. Butler; Hartford Hospital: R.H. Simon; Hospital for Special Care: S. Yoon-DeLuca; Hospital of Saint Raphael: P.S. Dickey; Lawrence and Memorial Hospital: L.I. Radin; Manchester Memorial Hospital: R.H. Berland; Middlesex Hospital: K.J. Kiwak; New Britain General Hospital: B.G. Spass; Norwalk Hospital: R.A. Levine; Rehabilitation Hospital of Connecticut: D. Feingold; Saint Francis Hospital and Medical Center (Saint Francis Campus): P.B. Wade; Saint Francis Hospital and Medical Center (Mount Sinai Campus): G.H. Belt; Saint Joseph Medical Center: E.D. Xistris; Saint Mary's Hospital: K.A. Kaplove; Saint Vincent's Medical Center: P. Shear; Stamford Hospital: M.H. Camel; Waterbury Hospital: J.O. Bizzozero; William W. Backus Hospital: C. Salame; and Yale–New Haven Hospital: R.I. Horwitz. Scientific Advisory Group: L.C. Lasagna (chair), S. Suissa, and J.P. Mohr.
- References
References
1
Lake CR ,Gallant S ,Masson E ,Miller P . Adverse drug effects attributed to phenylpropanolamine: a review of 142 case reports. Am J Med 1990;89:195-208
CrossRef | Web of Science | Medline2
King J . Hypertension and cerebral haemorrhage after trimolets ingestion. Med J Aust 1979;2:258-258
Web of Science | Medline3
Morgan JP. Phenylpropanolamine: a critical analysis of reported adverse reactions and overdosage. Fort Lee, N.J.: Jack K. Burgess, 1986:105.
4
Kikta DG ,Devereaux MW ,Chandar K . Intracranial hemorrhages due to phenylpropanolamine. Stroke 1985;16:510-512
CrossRef | Web of Science | Medline5
Fallis RJ ,Fisher M . Cerebral vasculitis and hemorrhage associated with phenylpropanolamine. Neurology 1985;35:405-407
Web of Science | Medline6
Johnson DA ,Etter HS ,Reeves DM . Stroke and phenylpropanolamine use. Lancet 1983;2:970-970
CrossRef | Web of Science | Medline7
McDowell JR ,LeBlanc HJ . Phenylpropanolamine and cerebral hemorrhage. West J Med 1985;142:688-691
Medline8
Maher LM . Postpartum intracranial hemorrhage and phenylpropanolamine use. Neurology 1987;37:1686-1686[Erratum, Neurology 1987;37:1890.]
Web of Science | Medline9
Forman HP ,Levin S ,Stewart B ,Patel M ,Feinstein S . Cerebral vasculitis and hemorrhage in an adolescent taking diet pills containing phenylpropanolamine: case report and review of literature. Pediatrics 1989;83:737-741
Web of Science | Medline10
Stoessl AJ ,Young GB ,Feasby TE . Intracerebral haemorrhage and angiographic beading following ingestion of catecholaminergics. Stroke 1985;16:734-736
CrossRef | Web of Science | Medline11
Kase CS ,Foster TE ,Reed JE ,Spatz EL ,Girgis GN . Intracerebral hemorrhage and phenylpropanolamine use. Neurology 1987;37:399-404
Web of Science | Medline12
Traynelis VC ,Brick JF . Phenylpropanolamine and vasospasm. Neurology 1986;36:593-594
Web of Science | Medline13
Chung Y-T ,Hung D-Z ,Hsu C-P ,Yang D-Y ,Wu T-C . Intracerebral hemorrhage in a young woman with arteriovenous malformation after taking diet control pills containing phenylpropanolamine: a case report. Chung Hua I Hsueh Tsa Chih (Taipei) 1998;61:432-43514
Linn FHH ,Wijdicks EFM ,van der Graaf Y ,Weerdesteyn-van Vliet FAC ,Bartelds AIM ,van Gijn J . Prospective study of sentinel headache in aneurysmal subarachnoid hemorrhage. Lancet 1994;344:590-593
CrossRef | Web of Science | Medline15
Mayer PL ,Awad IA ,Todor R , et al. Misdiagnosis of symptomatic cerebral aneurysm: prevalence and correlation with outcome at four institutions. Stroke 1996;27:1558-1563
CrossRef | Web of Science | Medline16
Edlow JA ,Caplan LR . Avoiding pitfalls in the diagnosis of subarachnoid hemorrhage. N Engl J Med 2000;342:29-36
Full Text | Web of Science | Medline17
Physicians' desk reference. Montvale, N.J.: Medical Economics, 1999.
18
Knodel LC, Young LL, Kendall SCE. Nonprescription products: formulations and features ('98-'99). Washington, D.C.: American Pharmaceutical Association, 1997.
19
Jick H ,Aselton P ,Hunter JR . Phenylpropanolamine and cerebral haemorrhage. Lancet 1984;1:1017-1017
CrossRef | Web of Science | Medline20
Horwitz RI ,Feinstein AR ,Harvey MR . Temporal precedence and other problems of the exposure-disease relationship. Arch Intern Med 1984;144:1257-1259
CrossRef | Web of Science | Medline21
Breslow NE, Day NE. Statistical methods in cancer research. Vol. 1. The analysis of case-control studies. Lyon, France: International Agency for Research on Cancer, 1980. (IARC scientific publications no. 32.)
22
Jick H ,Vessey MP . Case-control studies in the evaluation of drug-induced illness. Am J Epidemiol 1978;107:1-7
Web of Science | Medline23
Broderick JP ,Brott T ,Tomsick T ,Huster G ,Miller R . The risk of subarachnoid and intracerebral hemorrhages in blacks as compared with whites. N Engl J Med 1992;326:733-736
Full Text | Web of Science | Medline
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Lisa L. Ioannides-Demos, Loretta Piccenna, John J. McNeil. (2011) Pharmacotherapies for Obesity: Past, Current, and Future Therapies. Journal of Obesity 2011, 1-18
CrossRef11
Tadaaki KAWANABE, Ryota TANAKA, Yohei SAKAGUCHI, Osamu AKIYAMA, Hideki SHIMURA, Yukimasa YASUMOTO, Masanori ITO, Nobutaka HATTORI, Shigeki TANAKA. (2011) Posterior Reversible Encephalopathy Syndrome Complicating Intracranial Hemorrhage After Phenylpropanolamine Exposure. Neurologia medico-chirurgica 51:8, 582-585
CrossRef12
Mariela Glandt, Itamar Raz. (2011) Present and Future: Pharmacologic Treatment of Obesity. Journal of Obesity 2011, 1-13
CrossRef13
John C.M. Brust. 2011. Stroke and Substance Abuse. , 790-813.
CrossRef14
Scott E. Kasner, Brett L. Cucchiara. 2011. Treatment of “Other” Stroke Etiologies. , 1084-1105.
CrossRef15
J. González Fernández, V. García Morales, J.M. Trejo Gabriel y Galán. (2010) Hemorragia de núcleo caudado por anestesia dental. Neurología 25:9, 586-588
CrossRef16
Stéphanie Noël, Stéphanie Claeys, Annick Hamaide. (2010) Acquired urinary incontinence in the bitch: Update and perspectives from human medicine. Part 2: The urethral component, pathophysiology and medical treatment. The Veterinary Journal 186:1, 18-24
CrossRef17
C. Tabernero García. (2010) Neurocatástrofes farmacológicas. Neurología 25, 68-79
CrossRef18
2010. Bibliography. , 321-339.
CrossRef19
M A Valentino, J E Lin, S A Waldman. (2010) Central and Peripheral Molecular Targets for Antiobesity Pharmacotherapy. Clinical Pharmacology & Therapeutics 87:6, 652-662
CrossRef20
Stéphanie Noël, Carole Cambier, Kris Baert, Pascal Gustin, Raphael Denooz, Laurent Massart, Annick Hamaide. (2010) Combined pharmacokinetic and urodynamic study of the effects of oral administration of phenylpropanolamine in female Beagle dogs. The Veterinary Journal 184:2, 201-207
CrossRef21
Frank L. Greenway, George A. Bray. (2010) Combination Drugs for Treating Obesity. Current Diabetes Reports 10:2, 108-115
CrossRef22
Rex Watson, Ryan Woodman, Warren Lockette. (2010) Ephedra alkaloids inhibit platelet aggregation. Blood Coagulation & Fibrinolysis 21:3, 266-271
CrossRef23
Paul Nyquist. (2010) Management of acute intracranial and intraventricular hemorrhage. Critical Care Medicine 38:3, 946-953
CrossRef24
Kenneth J. Broadley. (2010) The vascular effects of trace amines and amphetamines. Pharmacology & Therapeutics 125:3, 363-375
CrossRef25
Robhash Kusam Subedi, Jun-Ho Jang, Jae-Il Kim, Young-Joon Park, Hoo-Kyun Choi. (2010) Formulation and Evaluation of Transdermal Patch Containing Sibutramine. Journal of Korean Pharmaceutical Sciences 40:1, 33-38
CrossRef26
Noboru Imai, Nobuyasu Yagi, Takashi Konishi, Masahiro Serizawa, Masahiro Kobari. (2010) Ischemic Stroke Associated with Cough and Cold Preparation Containing Methylephedrine and Supplement Containing Chinese Herbal Drugs. Internal Medicine 49:4, 335-338
CrossRef27
J. González Fernández, V. García Morales, J.M. Trejo Gabriel y Galán. (2010) Caudal nucleus haemorrhage due to dental anaesthesia. Neurología (English Edition) 25:9, 586-588
CrossRef28
James C. Johnston. (2009) Life threatening intracerebral hemorrhage with isometheptene mucate, dichlorophenazine and acetaminophen combination therapy. Journal of Forensic and Legal Medicine 16:8, 489-491
CrossRef29
Daniel J. Caruso, Christopher S. Gomez, Angelo E. Gousse. (2009) Medical management of stress urinary incontinence: Is there a future?. Current Urology Reports 10:5, 401-407
CrossRef30
Lori M. Dickerson, Peter J. Carek. (2009) Pharmacotherapy for the Obese Patient. Primary Care: Clinics in Office Practice 36:2, 407-415
CrossRef31
Anastasios Athanasopoulos, Petros Perimenis. (2009) Pharmacotherapy of urinary incontinence. International Urogynecology Journal 20:4, 475-482
CrossRef32
Akira Furuta, Koji Asano, Shin Egawa, William C. de Groat, Michael B. Chancellor, Naoki Yoshimura. (2009) Role of α2-Adrenoceptors and Glutamate Mechanisms in the External Urethral Sphincter Continence Reflex in Rats. The Journal of Urology 181:3, 1467-1473
CrossRef33
Tsan-Hon Liou, Nicole Huang, Chih-Hsing Wu, Yiing-Jenq Chou, Yiing-Mei Liou, Pesus Chou. (2009) Weight loss behavior in obese patients before seeking professional treatment in Taiwan. Obesity Research & Clinical Practice 3:1, 35-43
CrossRef34
(2009) Position of the American Dietetic Association: Weight Management. Journal of the American Dietetic Association 109:2, 330-346
CrossRef35
Nobuhiro OOBA, Kiyoshi KUBOTA. (2009) Rinsho yakuri/Japanese Journal of Clinical Pharmacology and Therapeutics 40:1, 17-21
CrossRef36
Victoria L. Cooper, Roger Hainsworth. (2008) Head-up sleeping improves orthostatic tolerance in patients with syncope. Clinical Autonomic Research 18:6, 318-324
CrossRef37
Daniel Refai, James A. Botros, Russell G. Strom, Colin P. Derdeyn, Aseem Sharma, Gregory J. Zipfel. (2008) Spontaneous isolated convexity subarachnoid hemorrhage: presentation, radiological findings, differential diagnosis, and clinical course. Journal of Neurosurgery 109:6, 1034-1041
CrossRef38
J. Hallas, L. Bjerrum, H. Stovring, M. Andersen. (2008) Use of a Prescribed Ephedrine/Caffeine Combination and the Risk of Serious Cardiovascular Events: A Registry-based Case-Crossover Study. American Journal of Epidemiology 168:8, 966-973
CrossRef39
Bikash Sharma, David C Henderson. (2008) Sibutramine: current status as an anti-obesity drug and its future perspectives. Expert Opinion on Pharmacotherapy 9:12, 2161-2173
CrossRef40
Jemima R. Ingle, Kenneth W. Busch, Marianna A. Busch. (2008) Chiral analysis by multivariate regression modeling of spectral data using cyclodextrin guest–host complexes—Methods for determining enantiomeric composition with varying chiral analyte concentration. Talanta 75:2, 572-584
CrossRef41
Robert A. Nathan. (2008) The pathophysiology, clinical impact, and management of nasal congestion in allergic rhinitis. Clinical Therapeutics 30:4, 573-586
CrossRef42
Hugo H. Davila, Justin Parker, J. Christopher Webster, Jorge L. Lockhart, Rafael E. Carrion. (2008) Subarachnoid Hemorrhage as Complication of Phenylephrine Injection for the Treatment of Ischemic Priapism in a Sickle Cell Disease Patient. The Journal of Sexual Medicine 5:4, 1025-1028
CrossRef43
John H. Krouse. (2008) Allergic Rhinitis—Current Pharmacotherapy. Otolaryngologic Clinics of North America 41:2, 347-358
CrossRef44
Roy Freeman. (2008) Current pharmacologic treatment for orthostatic hypotension. Clinical Autonomic Research 18:S1, 14-18
CrossRef45
George A. Bray. (2008) Are Non-prescription Medications Needed for Weight Control?. Obesity 16:3, 509-514
CrossRef46
Timothy L Siu, John W Morley, Minas T Coroneo. (2008) Toxicology of the retina: advances in understanding the defence mechanisms and pathogenesis of drug- and light-induced retinopathy. Clinical & Experimental Ophthalmology 36:2, 176-185
CrossRef47
Marvin S. Medow, Julian M. Stewart, Sanjukta Sanyal, Arif Mumtaz, Domenic Sica, William H. Frishman. (2008) Pathophysiology, Diagnosis, and Treatment of Orthostatic Hypotension and Vasovagal Syncope. Cardiology in Review 16:1, 4-20
CrossRef48
Soon Jib Yoo. (2008) Pharmacological Treatment of Obesity. Journal of Korean Endocrine Society 23:4, 223
CrossRef49
(2008) CrossRef Listing of Deleted DOIs. CrossRef Listing of Deleted DOIs
CrossRef50
Artyom Sedrakyan, Chuck Shih. (2007) Improving Depiction of Benefits and Harms. Medical Care 45:Suppl 2, S23-S28
CrossRef51
Anne T. Berg. (2007) Hypotheses, tests, methods, and innovation: The balancing act in research. Epilepsia 0:0, 070916052732004-???
CrossRef52
Cristina Bianchi, Giuseppe Penno, Fabiola Romero, Stefano Del Prato, Roberto Miccoli. (2007) Treating the metabolic syndrome. Expert Review of Cardiovascular Therapy 5:3, 491-506
CrossRef53
Raj S Padwal. (2007) Antiobesity drug therapy: a call for more rigorous end-point evaluation. Therapy 4:3, 221-226
CrossRef54
Frank Greenway, Alok Gupta. 2007. Safety of Obesity Drugs. , 199-217.
CrossRef55
Hatzimouratidis Konstantinos, Konstantinidou Eleni, Hatzichristou Dimitrios. (2007) Dilemmas in the management of female stress incontinence: the role of pelvic floor muscle training. International Urology and Nephrology 38:3-4, 513-525
CrossRef56
Mitchell SV Elkind. (2007) Why now? Moving from stroke risk factors to stroke triggers. Current Opinion in Neurology 20:1, 51-57
CrossRef57
Julie K. Byron, Philip A. March, Dennis J. Chew, Stephen P. DiBartola. (2007) Effect of Phenylpropanolamine and Pseudoephedrine on the Urethral Pressure Profile and Continence Scores of Incontinent Female Dogs. Journal of Veterinary Internal Medicine 21:1, 47-53
CrossRef58
Eduardo Benarroch, Roy Freeman, Horacio Kaufmann. 2007. Autonomic Nervous System. , 383-404.
CrossRef59
John C.M. Brust. 2007. Amphétamine et autres psychostimulants. , 129-170.
CrossRef60
Neal Benowitz. 2006. Medical Complications of Drug Abuse. , 597-694.
CrossRef61
2006. Stress Urinary Incontinence. .
CrossRef62
David M. Schnee, Kathy Zaiken, William W. McCloskey. (2006) An update on the pharmacological treatment of obesity. Current Medical Research and Opinion 22:8, 1463-1474
CrossRef63
K. Abbasi, M.I. Bhanger, M.Y. Khuhawar. (2006) Capillary gas chromatographic determination of phenylpropanolamine in pharmaceutical preparation. Journal of Pharmaceutical and Biomedical Analysis 41:3, 998-1001
CrossRef64
Nissen, Steven E., . (2006) ADHD Drugs and Cardiovascular Risk. New England Journal of Medicine 354:14, 1445-1448
Full Text65
Joel Lexchin. (2006) Withdrawals of drugs for safety reasons. Adverse Drug Reaction Bulletin &NA;:236, 903-906
CrossRef66
Konstantinos Spengos, Georgios Tsivgoulis, Nikolaos Zakopoulos. (2006) Blood Pressure Management in Acute Stroke: A Long-Standing Debate. European Neurology 55:3, 123-135
CrossRef67
Wael A. AlJaroudi, John L. Petersen. (2006) Obesity, diabetes, and associated risk factors. Current Treatment Options in Cardiovascular Medicine 8:1, 67-78
CrossRef68
Byron G. Stier, Charles H. Hennekens. (2006) Phenylpropanolamine and Hemorrhagic Stroke in the Hemorrhagic Stroke Project: A Reappraisal in the Context of Science, the Food and Drug Administration, and the Law. Annals of Epidemiology 16:1, 49-52
CrossRef69
2006. Phenylpropanolamine (norephedrine). , 2811-2813.
CrossRef70
2006. Ergot derivatives. , 1230-1235.
CrossRef71
Lisa L Ioannides-Demos, Joseph Proietto, Andrew M Tonkin, John J McNeil. (2006) Safety of Drug Therapies Used for Weight Loss and Treatment of Obesity. Drug Safety 29:4, 277-302
CrossRef72
Neeraj Badjatia, Jonathan Rosand. (2005) Intracerebral Hemorrhage. The Neurologist 11:6, 311-324
CrossRef73
Ayrn D. O'Connor, Daniel E. Rusyniak, Askiel Bruno. (2005) Cerebrovascular and Cardiovascular Complications of Alcohol and Sympathomimetic Drug Abuse. Medical Clinics of North America 89:6, 1343-1358
CrossRef74
Frank L Greenway, Mary K Caruso. (2005) Safety of obesity drugs. Expert Opinion on Drug Safety 4:6, 1083-1095
CrossRef75
A. Desai, S. Patel, W. Book. (2005) “Myocardial Infarction” in Adolescents: Do We Have the Correct Diagnosis?. Pediatric Cardiology 26:5, 627-631
CrossRef76
&NA;. (2005) Older pharmacological therapies for stress urinary incontinence are often unreliable, but duloxetine is a promising new option. Drugs & Therapy Perspectives 21:6, 12-15
CrossRef77
Frank Greenway. (2005) Another Type of Intervention: Treating Obesity with Medication. Journal of the American Dietetic Association 105:6, 895-898
CrossRef78
Karen W. Phinney, Toshihide Ihara, Lane C. Sander. (2005) Determination of ephedrine alkaloid stereoisomers in dietary supplements by capillary electrophoresis. Journal of Chromatography A 1077:1, 90-97
CrossRef79
Bokyung Min, Brian F. McBride, Michael J. Kardas, Agron Ismali, Vinnita Sinha, Jeffrey Kluger, C. Michael White. (2005) Electrocardiographic Effects of an Ephedra-Free, Multicomponent Weight-Loss Supplement in Healthy Volunteers. Pharmacotherapy 25:5, 654-659
CrossRef80
G BRAY. (2005) Drug Treatment of Obesity. Psychiatric Clinics of North America 28:1, 193-217
CrossRef81
E. S. McDonald, J. I. Lane. (2005) Dietary Supplements and Stroke. Mayo Clinic Proceedings 80:3, 315-315
CrossRef82
Matthew J. Seamon, Kevin A. Clauson. (2005) Ephedra. Journal of Herbal Pharmacotherapy 5:3, 67-86
CrossRef83
Lars Viktrup, Stephanie Koke, Kathryn L. Burgio, Joseph G. Ouslander. (2005) Stress Urinary Incontinence in Active Elderly Women. Southern Medical Journal 98:1, 79-89
CrossRef84
Yih-Shou Hsieh, Jeng-Dong Hsu, Shun-Fa Yang, Dong-Yih Kuo. (2004) Immunohistochemical and genomic evidence for the involvement of hypothalamic neuropeptide Y (NPY) in phenylpropranolamine-mediated appetite suppression. Peptides 25:12, 2155-2161
CrossRef85
Nasser Mikhail, Soma Wali, Irwin Ziment. (2004) Use of Alternative Medicine Among Hispanics. The Journal of Alternative and Complementary Medicine 10:5, 851-859
CrossRef86
F. Pesce. (2004) Current management of stress urinary incontinence. BJU International 94:s1, 8-13
CrossRef87
Stephan Krähenbühl. 2004. Adverse Effects and Drug–Drug Interactions. , 285-296.
CrossRef88
George Bray. 2004. Noradrenergic, Serotonergic, Antiepileptic, and Herbal Drugs. , 267-284.
CrossRef89
Amal Kaddoumi, Mihoko N Nakashima, Mitsuhiro Wada, Kenichiro Nakashima. (2004) Pharmacokinetic interactions between phenylpropanolamine, caffeine and chlorpheniramine in rats. European Journal of Pharmaceutical Sciences 22:2-3, 209-216
CrossRef90
Atul Pathak, Jean-Michel Senard. (2004) Pharmacology of orthostatic hypotension in Parkinson’s disease: from pathophysiology to management. Expert Review of Cardiovascular Therapy 2:3, 393-403
CrossRef91
Amal Kaddoumi, Toyomi Mori, Mihoko N. Nakashima, Mitsuhiro Wada, Kenichiro Nakashima. (2004) High performance liquid chromatography with fluorescence detection for the determination of phenylpropanolamine in human plasma and rat’s blood and brain microdialysates using DIB-Cl as a label. Journal of Pharmaceutical and Biomedical Analysis 34:3, 643-650
CrossRef92
John C.M. Brust. 2004. Stroke and Substance Abuse. , 725-745.
CrossRef93
Carlos S. Kase, J.P. Mohr, Louis R. Caplan. 2004. Intracerebral Hemorrhage. , 327-376.
CrossRef94
Keith M Blechman, Steven B Karch, Boyd G Stephens. (2004) Demographic, pathologic, and toxicological profiles of 127 decedents testing positive for ephedrine alkaloids. Forensic Science International 139:1, 61-69
CrossRef95
Scott E. Kasner. 2004. Treatment of "Other" Causes of Stroke. , 1059-1077.
CrossRef96
Jason M. Enders, Paul P. Dobesh, James N. Ellison. (2003) Acute Myocardial Infarction Induced by Ephedrine Alkaloids. Pharmacotherapy 23:12, 1645-1651
CrossRef97
ROGER R. DMOCHOWSKI, JOHN R. MIKLOS, PEGGY A. NORTON, NORMAN R. ZINNER, ILKER YALCIN, RICHARD C. BUMP. (2003) Duloxetine Versus Placebo for the Treatment of North American Women With Stress Urinary Incontinence. The Journal of Urology 170:4, 1259-1263
CrossRef98
Bernhard Schuessler, Kaven Baessler. (2003) Pharmacologic treatment of stress urinary incontinence: expectations for outcome. Urology 62:4, 31-38
CrossRef99
Melissa E. Huggins, Narender N. Bhatia, Donald R. Ostergard. (2003) Urinary incontinence: newer pharmacotherapeutic trends. Current Opinion in Obstetrics and Gynecology 15:5, 419-427
CrossRef100
Dudley Robinson, Linda D Cardozo. (2003) The role of estrogens in female lower urinary tract dysfunction. Urology 62:4, 45-51
CrossRef101
Norman R Zinner. (2003) Duloxetine: a serotonin-noradrenaline re-uptake inhibitor for the treatment of stress urinary incontinence. Expert Opinion on Investigational Drugs 12:9, 1559-1566
CrossRef102
Janice B. Schwartz. (2003) Gender-Specific Implications for Cardiovascular Medication Use in the Elderly. Cardiology in Review 11:5, 275-298
CrossRef103
Federico Martinón-Torres. (2003) Current treatment for acute viral bronchiolitis in infants. Expert Opinion on Pharmacotherapy 4:8, 1355-1371
CrossRef104
Carl V. Phillips. (2003) Quantifying and Reporting Uncertainty from Systematic Errors. Epidemiology 14:4, 459-466
CrossRef105
Mittie K Doyle, Marta L Cuellar. (2003) Drug-induced vasculitis. Expert Opinion on Drug Safety 2:4, 401-409
CrossRef106
JESSE WEINBERGER, WILLIAM H. FRISHMAN, DAWN TERASHITA. (2003) Drug Therapy of Neurovascular Disease. Cardiology in Review 11:3, 122-146
CrossRef107
Sterling G. West. (2003) Central nervous system vasculitis. Current Rheumatology Reports 5:2, 116-127
CrossRef108
(2003) International Society of Hypertension (ISH). Journal of Hypertension 21:4, 665-672
CrossRef109
Catherine Wubbel, Albert Faro. (2003) Chronic Cough in Children. Pediatric Case Reviews 3:2, 95-104
CrossRef110
Joel Handler. (2003) Drug-Induced Hypertension. The Journal of Clinical Hypertension 5:1, 83-85
CrossRef111
Lars Viktrup, Richard C. Bump. (2003) Pharmacological agents used for the treatment of stress urinary incontinence in women. Current Medical Research and Opinion 19:6, 485-490
CrossRef112
Enzo Nisoli, Michele O Carruba. (2003) A Benefit-Risk Assessment of Sibutramine in the Management of Obesity. Drug Safety 26:14, 1027-1048
CrossRef113
Wilson Y.S Leung, G Neil Thomas, Juliana C.N Chan, Brian Tomlinson. (2003) Weight management and current options in pharmacotherapy: Orlistat and sibutramine. Clinical Therapeutics 25:1, 58-80
CrossRef114
William H. Frishman, Victor Azer, Domenic Sica. (2003) Drug Treatment of Orthostatic Hypotension and Vasovagal Syncope. Heart Disease 5:1, 49-64
CrossRef115
Askiel Bruno. (2003) Cerebrovascular complications of alcohol and sympathomimetic drug abuse. Current Neurology and Neuroscience Reports 3:1, 40-45
CrossRef116
Nalini Samuel, Luis D'Olhaberriague, Steven R. Levine, Lawrence M. Brass. 2003. Illicit Drugs and Stroke. , 359-362.
CrossRef117
Christine Bond, Philip Hannaford. (2003) Issues Related to Monitoring the Safety of Over-The-Counter (OTC) Medicines. Drug Safety 26:15, 1065-1074
CrossRef118
N. Finer. (2002) Pharmacotherapy of obesity. Best Practice & Research Clinical Endocrinology & Metabolism 16:4, 717-742
CrossRef119
Roger E. Kelley. (2002) Perioperative stroke: Evaluation, management, and possible preventive measures. Comprehensive Therapy 28:4, 230-234
CrossRef120
Timothy G. Schuster, Dana A. Ohl. (2002) Diagnosis and treatment of ejaculatory dysfunction. Urologic Clinics of North America 29:4, 939-948
CrossRef121
W. Glenn Lyle. (2002) Pharmacological Treatment of Obesity. Plastic and Reconstructive Surgery 110:6, 1577-1580
CrossRef122
M. Ammar Hatahet, Nikhil V. Dhurandhar. (2002) Antiobesity drugs: Current and future issues. Current Diabetes Reports 2:5, 409-415
CrossRef123
Donald RJ Singer, Teck K Khong. (2002) Adverse drug reactions: current issues and strategies for prevention and management. Expert Opinion on Pharmacotherapy 3:9, 1289-1300
CrossRef124
Yoshiharu Ohyama, Kazuhiro Funao, Eri Kawabe, Doubun Hayashi, Tsutomu Yamazaki, Tatsuji Iga, Daisuke Koide, Kazuhiko Ohe, Kiyoshi Kubota. (2002) Calcium channel blockers and myocardial infarction: a case-control study in a Japanese hospital. Pharmacoepidemiology and Drug Safety 11:6, 487-492
CrossRef125
Alan J Wein, Eric S Rovner. (2002) Pharmacologic management of urinary incontinence in women. Urologic Clinics of North America 29:3, 537-550
CrossRef126
Julian E. Bailes, Robert C. Cantu, Arthur L. Day. (2002) The Neurosurgeon in Sport: Awareness of the Risks of Heatstroke and Dietary Supplements. Neurosurgery 51:2, 283-288
CrossRef127
Ron Bouchard, Anna R. Weber, Jonathan D. Geiger. (2002) Informed Decision-Making on Sympathomimetic Use in Sport and Health. Clinical Journal of Sport Medicine 12:4, 209-224
CrossRef128
Leah A. Cohn, John R. Dodam, Balazs Szladovits. (2002) Effects of selegiline, phenylpropanolamine, or a combination of both on physiologic and behavioral variables in healthy dogs. American Journal of Veterinary Research 63:6, 827-832
CrossRef129
Thomas A. Tami, Sung J. Chung. (2002) Advances in treating the common cold: an update for otolaryngologists. Current Opinion in Otolaryngology & Head and Neck Surgery 10:3, 179-183
CrossRef130
Carla A. Luque, Jose A. Rey. (2002) The discovery and status of sibutramine as an anti-obesity drug. European Journal of Pharmacology 440:2-3, 119-128
CrossRef131
Stanley Tuhrim. (2002) Management of hemorrhagic stroke. Current Cardiology Reports 4:2, 158-163
CrossRef132
Robert F. Kushner, Hazel Manzano. (2002) Obesity pharmacology: past, present, and future. Current Opinion in Gastroenterology 18:2, 213-220
CrossRef133
Wood, Alastair J.J., , Yanovski, Susan Z., Yanovski, Jack A., . (2002) Obesity. New England Journal of Medicine 346:8, 591-602
Full Text134
Marta Lucia Cuellar. (2002) Drug-induced vasculitis. Current Rheumatology Reports 4:1, 55-59
CrossRef135
Stephen E Nadeau. (2002) Neurologic Manifestations of Systemic Vasculitis. Neurologic Clinics 20:1, 123-150
CrossRef136
Maxime Lamarre-Cliche. (2002) Drug Treatment of Orthostatic Hypotension Because of Autonomic Failure or Neurocardiogenic Syncope. American Journal of Cardiovascular Drugs 2:1, 23-35
CrossRef137
Peter C. Austin, Muhammad Mamdani, Ivan J. Williams. (2002) Adverse Effects of Observational Studies When Examining Adverse Outcomes of Drugs. Drug Safety 25:9, 677-687
CrossRef138
Albert Figueras, Joanramon Laporte. (2002) Regulatory Decisions in a Globalised World. Drug Safety 25:10, 689-693
CrossRef139
Dorsey M. Bass, Mary Prevo, Deborah S. Waxman. (2002) Gastrointestinal Safety of an Extended-Release, Nondeformable, Oral Dosage Form (OROS??)*. Drug Safety 25:14, 1021-1033
CrossRef140
B. M. Curtis, J. H. O'Keefe. (2002) Autonomic Tone as a Cardiovascular Risk Factor: The Dangers of Chronic Fight or Flight. Mayo Clinic Proceedings 77:1, 45-54
CrossRef141
(2001) Current Awareness. Pharmacoepidemiology and Drug Safety 10:3, 263-278
CrossRef142
(2001) Phenylpropanolamine and Hemorrhagic Stroke. New England Journal of Medicine 344:14, 1094-1095
Full Text143
(2001) Dietary Supplements Containing Ephedra Alkaloids. New England Journal of Medicine 344:14, 1095-1097
Full Text144
Pamela Talalay, Paul Talalay. (2001) The Importance of Using Scientific Principles in the Development of Medicinal Agents from Plants. Academic Medicine 76:3, 238-247
CrossRef145
Michael D. Murray, Kurt Kroenke. (2001) Polypharmacy and Medication Adherence. Small Steps on a Long Road. Journal of General Internal Medicine 16:2, 136-139
CrossRef146
Michael D. Murray, Kurt Kroenke. (2001) Polypharmacy and medication adherence. Journal of General Internal Medicine 16:2, 137-139
CrossRef147
C. T. Rhodes. (2001) SOME IMPLICATIONS OF THE PHENYLPROPANOLAMINE PROBLEM. Clinical Research and Regulatory Affairs 18:1-2, 1-16
CrossRef148
Jean-Michel Senard, Christine Brefel-Courbon, Olivier Rascol, Jean-Louis Montastruc. (2001) Orthostatic Hypotension in Patients with Parkinson??s Disease. Drugs & Aging 18:7, 495-505
CrossRef149
Fleming, G. Alexander, . (2000) The FDA, Regulation, and the Risk of Stroke. New England Journal of Medicine 343:25, 1886-1887
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