Phenylpropanolamine and Intracranial Hemorrhage Risk in a Mexican Population

Abstract

Background and Purpose: Phenylpropanolamine (PPA) has been associated with an increased risk of intracranial hemorrhage (ICH). The aim of this study was to assess the association between PPA intake and ICH in a Mexican population. Methods: We included all patients with ICH aged 18 to 51 years, with no known structural etiology, diagnosed from January 1991 to December 2000. Three to 4 controls per patient matched by sex, age (within 5 years) and place of residence were included. Patients and controls were asked about use of cold medication or appetite suppressant medications within the previous year before the interview. We considered a PPA related hemorrhage when there was a temporal relationship between the use of medication and the development of the hemorrhage, and when other causes could be ruled out. Associated risks for PPA use and other possibly related variables were estimated. Results: 177 patients (mean age 39 ± 12 years) were included; 58 (33%) were diagnosed with subarachnoid hemorrhage (SAH) and 119 (67%) with ICH. 41.2% (73 of 177) of patients had documented use of PPA within the past year and 10 (5.7%) of them had a temporal relationship between ingestion of PPA and ICH. In control subjects 42.4% (422 of 996) had been exposed to PPA and none of them developed hemorrhage. The time from PPA exposure to the onset of ICH varied from 30 minutes to 24 hours. The risk of PPA exposure for hemorrhage was not significant in cases or controls, OR 0.95 (95% CI, 0.68 to 1.34; p = 0.77). No subjects (cases or controls) reported use of PPA as an appetite suppressant. Conclusions: We found no association between ingestion of PPA and cerebral hemorrhage with respect to ingestion of PPA in the previous year. When recent use was looked at an apparent risk was evident.

Risk of stroke in prescription and other amphetamine‐type stimulants use: A systematic review

“…The CCS by Arauz et al . did not find any association. The failure to stratify by periods of ATS exposure, instead grouping together all exposures in the last 12 months, could have biased the results towards the null.…”

“…Arauz et al . did not find a significant association when considering exposure in the 12 months previous to H‐stroke [aOR = 0.95 (95% CI = 0.68, 1.34)].…”

“…Arauz et al . reported 150 mg. The only study investigating ephedra‐containing products stratified results by dose (≤32 and >32 mg).…”

“…Morgenstern et al [55] concluded that ephedracontaining products are not associated with an increased risk of H-stroke after adjusting for dose and time elapsed between last exposure and stroke onset: ≤32 mg day À1 and 3 days [aOR = 1.00 (95% CI = 0.32, 3.11)], ≤32 mg day À1 and 1 day [aOR = 1.11 (95% CI = 0.34, 3.56)], >32 mg day À1 and 3 days [aOR = 3.59 (95% 13.80)] and showed a significant trend towards increasing risk of H-stroke in more recent (P = 0.02), lasting (P = 0.01) and intense (higher doses) (P = 0.02) exposures. Arauz et al [57] did not find a significant association when considering exposure in the 12 months previous to H-stroke [aOR = 0.95 (95% CI = 0.68, 1.34)].…”

Unusual Causes of Ischaemic Stroke and Transient Ischaemic Attack

“…Other sympathomimetic drugs (often found in nasal decongestants and appetite suppressants) may cause stroke in similar ways to amphetamines: • ephedrine and pseudoephedrine; 459 • ephedra alkaloids (ma huang); 460 • phenylpropanolamine; [461][462][463] • oxymetazoline; • diethylproprion; • phentermine; • fenfluramine; • methylene dioxymethylamphetamine ('ecstasy'). [464][465][466] Cannabis has been associated with ischaemic stroke in a handful of case reports but whether this is a causal relationship, and if so what the mechanism is, is unknown.…”