Evaluating the introduction of a computerized prior-authorization system on the completeness of drug exposure data

2013 ◽  
Vol 22 (5) ◽  
pp. 551-555 ◽  
Author(s):  
John-Michael Gamble ◽  
Jeffrey A. Johnson ◽  
Sumit R. Majumdar ◽  
Finlay A. McAlister ◽  
Scot H. Simpson ◽  
...  
Keyword(s):  
Drug Exposure ◽  
Prior Authorization ◽  
Exposure Data

Fetal Minoxidil Exposure

PEDIATRICS ◽  
1987 ◽  
Vol 80 (1) ◽  
pp. 120-120
Author(s):  
FRANZ W. ROSA ◽  
JUHANA IDANPAAN-HEIKKILA ◽  
RITA ASANTI
Keyword(s):  
Case Report ◽  
Drug Administration ◽  
Birth Defects ◽  
Drug Safety ◽  
Congenital Anomalies ◽  
Drug Exposure ◽  
Spontaneous Abortions ◽  
Multiple Congenital Anomalies ◽  
Exposure Data ◽  
National Drug

To the Editor.— Kaler et al (Pediatrics 1987;79:434-436) provided a case report of hypertrichosis and multiple congenital anomalies with maternal minoxidil use. Reports such as this contribute to alerting national drug safety offices of possible teratologic questions. Maternal drug exposure data, since 1979 when minoxidil was marketed, is available to the Food and Drug Administration (FDA) from 73,000 pregnancies (15,600 birth defects, 4,400 spontaneous abortions, and 53,000 normal outcomes). This yields, in addition to the report by Kaler et al, only two other births with maternal minoxidil exposures:

scholarly journals Assumptions made when preparing drug exposure data for analysis have an impact on results: An unreported step in pharmacoepidemiology studies

2018 ◽  
Vol 27 (7) ◽  
pp. 781-788 ◽  
Author(s):  
Stephen R. Pye ◽  
Thérèse Sheppard ◽  
Rebecca M. Joseph ◽  
Mark Lunt ◽  
Nadyne Girard ◽  
...  
Keyword(s):  
Drug Exposure ◽  
Exposure Data

scholarly journals Contemporary epidemiology of rising atrial septal defect trends across USA 1991–2016: a combined ecological geospatiotemporal and causal inferential study

2020 ◽  
Vol 20 (1) ◽  
Author(s):  
Albert Stuart Reece ◽  
Gary Kenneth Hulse
Keyword(s):  
Alcohol Abuse ◽  
Atrial Septal Defect ◽  
Congenital Anomalies ◽  
Drug Exposure ◽  
Septal Defect ◽  
Linear Models ◽  
Spatial Modelling ◽  
Cannabis Use ◽  
Inverse Probability ◽  
Exposure Data

Abstract Background Cardiovascular anomalies are the largest group of congenital anomalies and the major cause of death in young children, with various data linking rising atrial septal defect incidence (ASDI) with prenatal cannabis exposure. Objectives / Hypotheses. Is cannabis associated with ASDI in USA? Is this relationship causal? Methods Geospatiotemporal cohort study, 1991–2016. Census populations of adults, babies, congenital anomalies, income and ethnicity. Drug exposure data on cigarettes, alcohol abuse, past month cannabis use, analgesia abuse and cocaine taken from National Survey of Drug Use and Health (78.9% response rate). Cannabinoid concentrations from Drug Enforcement Agency. Inverse probability weighted (ipw) regressions. Analysis conducted in R. Results ASDI rose nationally three-fold from 27.4 to 82.8 / 10,000 births 1991–2014 during a period when tobacco and alcohol abuse were falling but cannabis was rising. States including Nevada, Kentucky, Mississippi and Tennessee had steeply rising epidemics (Time: Status β-estimate = 10.72 (95%C.I. 8.39–13.05), P < 2.0 × 10 − 16). ASDI was positively related to exposure to cannabis and most cannabinoids. Drug exposure data was near-complete from 2006 thus restricting spatial modelling from 2006 to 2014, N = 282. In geospatial regression models cannabis: alcohol abuse term was significant (β-estimate = 19.44 (9.11, 29.77), P = 2.2 × 10 − 4); no ethnic or income factors survived model reduction. Cannabis legalization was associated with a higher ASDI (Time: Status β-estimate = 0.03 (0.01, 0.05), P = 1.1 × 10 -3). Weighted panel regression interactive terms including cannabis significant (from β-estimate = 1418, (1080.6, 1755.4), P = 7.3 × 10 -15). Robust generalized linear models utilizing inverse probability weighting interactive terms including cannabis appear (from β-estimate = 78.88, (64.38, 93.38), P = 1.1 × 10 -8). Marginal structural models with machine-aided SuperLearning association of ASDI with high v. low cannabis exposure R.R. = 1.32 (1.28, 1.36). Model e-values mostly > 1.5. Conclusions ASDI is associated with cannabis use, frequency, intensity and legalization in a spatiotemporally significant manner, robust to socioeconomicodemographic adjustment and fulfilled causal criteria, consistent with multiple biological mechanisms and similar reports from Hawaii, Colorado, Canada and Australia. Not only are these results of concern in themselves, but they further imply that our list of the congenital teratology of cannabis is as yet incomplete, and highlight in particular cardiovascular toxicology of prenatal cannabinoid and drug exposure.

scholarly journals Epidemiological overview of multidimensional chromosomal and genome toxicity of cannabis exposure in congenital anomalies and cancer development

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Albert Stuart Reece ◽  
Gary Kenneth Hulse
Keyword(s):  
Congenital Anomalies ◽  
Drug Exposure ◽  
Experimental Studies ◽  
Cancer Data ◽  
Pancreatic Cancers ◽  
Exposure Data ◽  
Deletion 22Q11.2 ◽  
Causal Criteria ◽  
Linear Effects ◽  
Inverse Probability Weighted

AbstractCannabis and cannabinoids are implicated in multiple genotoxic, epigenotoxic and chromosomal-toxic mechanisms and interact with several morphogenic pathways, likely underpinning previous reports of links between cannabis and congenital anomalies and heritable tumours. However the effects of cannabinoid genotoxicity have not been assessed on whole populations and formal consideration of effects as a broadly acting genotoxin remain unexplored. Our study addressed these knowledge gaps in USA datasets. Cancer data from CDC, drug exposure data from National Survey of Drug Use and Health 2003–2017 and congenital anomaly data from National Birth Defects Prevention Network were used. We show that cannabis, THC cannabigerol and cannabichromene exposure fulfill causal criteria towards first Principal Components of both: (A) Down syndrome, Trisomies 18 and 13, Turner syndrome, Deletion 22q11.2, and (B) thyroid, liver, breast and pancreatic cancers and acute myeloid leukaemia, have mostly medium to large effect sizes, are robust to adjustment for ethnicity, other drugs and income in inverse probability-weighted models, show prominent non-linear effects, have 55/56 e-Values > 1.25, and are exacerbated by cannabis liberalization (P = 9.67 × 10–43, 2.66 × 10–15). The results confirm experimental studies showing that cannabinoids are an important cause of community-wide genotoxicity impacting both birth defect and cancer epidemiology at the chromosomal hundred-megabase level.

EPC2407, a new beta-tubulin vascular disrupting agent with potent apoptosis and cell growth inhibition

2007 ◽  
Vol 25 (18_suppl) ◽  
pp. 14043-14043 ◽  
Author(s):  
S. P. Anthony ◽  
D. Von Hoff ◽  
J. K. Whisnant ◽  
B. Y. Tseng
Keyword(s):  
Drug Exposure ◽  
Safety Issue ◽  
Parent Compound ◽  
Safety Margin ◽  
Therapeutic Index ◽  
Cancer Therapies ◽  
Vascular Disrupting Agent ◽  
Exposure Data ◽  
Vascular Disrupting

14043 Background: Compounds which bind to colchicine-like sites of microtubules have contributed greatly to the armamentarium of cancer therapies. But new modes of administration of taxanes and potent new vascular disruption agent molecules such as combretastatin continue to challenge drug development for ways to improve the therapeutic index in this important class. EPC2407 is a novel 4-aryl chromene of nM anti-tumor potency; it is crossing the translational bridge based on an array of preclinical anti-tumor pharmacology and supported by multiple toxicology trials which included drug exposure data. Methods: Vascular disrupting agents demand careful preclinical workup. What we have done is summarized in the table below. This data is from cellular metabolic, cell proliferation, vascular endothelial, in vivo tumor, and animal toxicokinetic and safety studies. Results: Please see table below of the preclinical experiments. Conclusions: A Phase I clinical trial has been designed and initiated to replicate the safety margin shown by the analysis of preclinical drug exposure data. The critical safety issue for human dosing was the dose exposure which might produce the well known ECG abnormality of delayed repolarization or prolonged QTc. A dose related QTc effect was demonstrated in cynomolgus monkeys after a 2 min infusion which achieved acute plasma exposures higher than 3836 nM. These effects were dose related and persisted only through 4 short half-lives of the parent compound. Initial human analysis fails to show any prolongation of the QTc. [JW1] [JW1]THE END HERE, all else was draft. [Table: see text] No significant financial relationships to disclose.

Prior Authorization

2010 ◽  
Vol 43 (14) ◽  
pp. 49
Author(s):  
JOSEPH S. EASTERN
Keyword(s):  
Prior Authorization
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