Zoloft Recall Info

Selective Serotonin-Reuptake Inhibitors and Risk of Persistent Pulmonary Hypertension of the Newborn

Christina D. Chambers, Ph.D., M.P.H., Sonia Hernandez-Diaz, M.D., Dr.P.H., Linda J. Van Marter, M.D., M.P.H., Martha M. Werler, Sc.D., Carol Louik, Sc.D., Kenneth Lyons Jones, M.D., and Allen A. Mitchell, M.D.

N Engl J Med 2006; 354:579-587 February 9, 2006

Persistent pulmonary hypertension of the newborn (PPHN) occurs in an estimated 1 or 2 infants per 1000 live births and is associated with substantial morbidity and mortality. Despite treatment, 10 to 20 percent of affected infants will not survive. Newborns with PPHN are typically full-term or near-term infants without associated congenital anomalies who present shortly after birth with severe respiratory failure requiring intubation and mechanical ventilation. This disruption of the normal fetal-to-neonatal circulatory transition is characterized by postnatal persistence of elevated pulmonary vascular resistance, resulting in right-to-left shunting of blood through fetal channels (the patent ductus arteriosus, foramen ovale, or both), diminished pulmonary blood flow, and profound hypoxemia.

On pathological study, newborn infants with PPHN are found to have congenital pulmonary vascular remodeling involving increased muscularization of the pulmonary arterioles. This increased muscularization may be due to distal extension of hypertrophied or hyperplastic arteriolar smooth muscle. Possible mechanisms leading to the maintenance of high pulmonary vascular resistance after birth may include decreased production of, or responsiveness to, vasodilators such as nitric oxide and prostacyclin; increased production of, or responsiveness to, vasoconstrictors such as endothelin and platelet-derived growth factor; or changes in the production of, or responsiveness to, both vasoconstrictors and vasodilators. However, structural pulmonary vascular remodeling clearly has a role in the pathogenesis of at least some cases of PPHN.

These findings suggest that prenatal exposures can contribute to the pathogenesis of this disorder. However, few studies have focused on risk factors for the development of PPHN. Male sex, nonvertex presentation, meconium staining of the amniotic fluid, neonatal sepsis, and pneumonia have been suggested as potential risk factors.Maternal risk factors include a lower educational level, fever, urinary tract infection, diabetes, cesarean section, antenatal use of nonsteroidal antiinflammatory agents (NSAIDs), and possibly tobacco use.

The results of a previous small cohort study conducted by a teratogen-information service generated the hypothesis that maternal use of selective serotonin-reuptake inhibitors (SSRIs) in late pregnancy may be a risk factor for PPHN. Among 174 infants born to women who used fluoxetine for some portion of their pregnancies, the 73 who were exposed to fluoxetine up to the time of delivery were significantly more likely to have specific transient neonatal complications, including respiratory problems, jitteriness, and hypotonia, than the 101 infants whose prenatal exposure was restricted to the first trimester of pregnancy. Two of the 73 infants (2.7 percent) exposed to fluoxetine in late pregnancy had PPHN, as compared with none of the 101 exposed only in early pregnancy. We conducted a study to test the hypothesis that exposure to SSRIs during late pregnancy is associated with an increased risk of PPHN. Our study is part of a large case–control study of risk factors for PPHN, conducted within the Birth Defects Study of the Slone Epidemiology Center.

Methods

The Slone Epidemiology Center Birth Defects Study began interviewing mothers of malformed children in 1976. The present analyses are based on a specially designed study, nested within the Birth Defects Study, to evaluate risk factors for PPHN, with a specific focus on exposure to NSAIDs and SSRIs during late pregnancy. Study subjects from 97 institutions in four metropolitan areas (Boston; Philadelphia; San Diego, California; and Toronto) were identified between 1998 and 2003. To identify subjects, admission and discharge records from major referral hospitals and clinics were reviewed, logbooks from neonatal intensive care units were examined, and weekly telephone calls were made to collaborators at newborn nurseries in community hospitals; the calls to community hospitals were made to identify infants with PPHN who might not have been referred to major centers. Information on healthy newborns from the same centers was also collected. Prior approval for the study was obtained from the review boards of all participating institutions. All mothers who were interviewed gave oral consent and, when it was required by institutional review boards, written consent to participation in the study.

The participation rate was 69 percent for mothers of subjects with PPHN and 68 percent for mothers of controls. After exclusion of mothers who could not be located and invited to participate, the rates were 73 percent and 71 percent, respectively.

Selection of Patients and Controls

The diagnostic criteria for PPHN were a gestational age of more than 34 weeks, presentation shortly after birth with severe respiratory failure, and evidence of pulmonary hypertension. Severe respiratory failure was defined as the need for intubation and mechanical ventilation. The exclusion criteria were evidence of any cardiac anomaly except for patent ductus arteriosus, patent foramen ovale, an atrial septal defect, or a single, small, muscular ventricular septal defect. Subjects with an atrial septal defect were included because right-to-left atrial hemodynamic shunting commonly occurs among infants with PPHN, and neonatal echocardiographic studies often do not distinguish between atrial septal defects and patent foramen ovale. Infants who had isolated small muscular ventricular septal defects were not excluded, because the abnormality was thought to be a hemodynamically insignificant finding.

Pulmonary hypertension was documented either by a 5 percent or greater gradient between preductal and postductal oxygen saturation or by echocardiographic evidence. Among those who underwent echocardiography, infants were designated as having PPHN if any of the following criteria were met: the cardiologist assigned the diagnosis of PPHN or noted significant or marked pulmonary hypertension, the echocardiogram showed right-to-left hemodynamic shunting at the ductus arteriosus or at the patent foramen ovale, or the echocardiogram showed bidirectional hemodynamic shunting accompanied by leftward bowing of the ventricular septum to a degree consistent with a pulmonary arterial pressure more than half of the systemic pressure.

Records for all infants admitted to the neonatal intensive care units at participating hospitals were screened by nurses or by respiratory therapists specially trained to identify PPHN. One of the authors, a neonatologist, who was blinded to the history of maternal exposure to medications, reviewed the medical records of all patients with potential PPHN, including infants with diagnostic codes for asphyxia, cyanotic congenital heart disease, respiratory distress syndrome, pneumonia, meconium aspiration, transient tachypnea of the newborn, or pulmonary hypertension.
The control group consisted of infants born after 34 weeks of gestation without malformations who were matched with patients according to the hospital in which they were born and their date of birth (±30 days). The intended ratio of patients to controls was 1:2. After the final classification of patients with confirmed PPHN and completion of the interviews, controls who were matched with these patients and whose mothers had completed the interview were selected for the analyses.

Assessment of Exposure

Within six months of delivery, trained study nurses who were unaware of the study hypothesis interviewed the mothers of the patients and the mothers of the control infants. The telephone interview was detailed and structured, and it included questions on demographic characteristics, the mother's medical and obstetrical history, the parents' habits and occupations, and the use of all medications (prescription and over-the-counter) during the period from two months before conception to the end of the pregnancy. The interviewer entered the mother's responses directly into the computer. During the interview, the interviewer had access to computerized dictionaries of drugs and diagnoses, and responses were instantaneously coded. Quality-control procedures were conducted both manually and by computer.

The mothers were asked whether they had taken any medication for depression. A list of specific antidepressant drugs was read to each mother. Any report of medication use prompted a systematic series of questions, including the brand or generic name of the drug, the indication for which it was prescribed, the form and size of the dose, the starting and stopping dates, the frequency of dosing, and the number of pills taken per day. Recall of the timing of use was enhanced by the use of a calendar that highlighted the date of the woman's last menstrual period and the delivery date.

We classified antidepressants either as SSRIs or as other antidepressants. To be consistent with our hypothesis, we defined late-pregnancy exposure as the use of an antidepressant at any time in the second half of gestation (from 20 completed weeks after the first day of the last menstrual period until the date of delivery).

Statistical Analysis

Multivariate conditional logistic regression was used to estimate prevalence odds ratios (which approximate relative risks for rare outcomes) and 95 percent confidence intervals for PPHN in relation to antidepressant exposure. Risk estimates were adjusted for potential confounders. The analyses were performed with SAS for Windows (version 8.2).

Results

We enrolled 637 infants with possible PPHN; the diagnosis was confirmed in 377 of the infants, 12 of whom (3.2 percent) were born after a multiple pregnancy. These 377 patients were matched with 836 controls, 17 of whom (2.0 percent) were born after a multiple pregnancy, for a case–control ratio of 1:2.2. Of the 377 patients, 60 were preterm (born after a gestation period of >34 through <37 weeks). Among infants born at term, 265 were born with a patent ductus arteriosus. The frequency of infant death up to the time of the maternal interview was 3.0 percent in the PPHN group and 0 percent in the control group.

The specific SSRI medications that study participants reported using were citalopram, fluoxetine, paroxetine, and sertraline. Among non-SSRI antidepressants, participants reported using tricyclic antidepressants (namely, amitriptyline, imipramine, and nortriptyline), bupropion, venlafaxine, and trazodone.

Maternal factors significantly associated with PPHN in unadjusted analyses included lower educational level, black or Asian race, higher prepregnancy body-mass index (the weight in kilograms divided by the square of the height in meters), and diabetes mellitus; male infants also had increased risk.  Table 1Selected Demographic, Maternal, and Fetal Characteristics of Study Subjects.). The factors associated in unadjusted analyses with SSRI use in the control group included tobacco and alcohol use, maternal diabetes, a body-mass index of more than 27, and white race (data not shown). These factors have previously been associated with the use of antidepressants.
Table 2 Use of SSRIs and Other Antidepressants during Pregnancy by Mothers of Infants with PPHN and Matched Controls. presents the matched odds ratios and 95 percent confidence intervals for antidepressant use relative to no antidepressant use during pregnancy. The crude risk of PPHN associated with the use of any antidepressant at any time in pregnancy was not significantly elevated (odds ratio, 1.3; 95 percent confidence interval, 0.7 to 2.2), nor was the use of SSRIs alone at any time in pregnancy significantly associated with PPHN (odds ratio, 1.5; 95 percent confidence interval, 0.8 to 2.9). However, when the comparison was stratified according to the timing of exposure in pregnancy, use of any antidepressant after the 20th week of gestation was significantly associated with PPHN (odds ratio, 2.9; 95 percent confidence interval, 1.3 to 6.5). Further analysis demonstrated that this association was entirely attributable to the subgroup of infants with late exposure to SSRIs (odds ratio for SSRI use after the 20th week of gestation relative to no use in the pregnancy, 5.1; 95 percent confidence interval, 1.9 to 13.3). There was no increased risk of PPHN when SSRI use was restricted to the first half of the pregnancy (odds ratio, 0.3; 95 percent confidence interval, 0.1 to 1.1).

Adjustment in a multivariate analysis for maternal diabetes (pregestational or gestational, with or without treatment), maternal race or ethnic group, and body-mass index did not attenuate the association between exposure to SSRIs late in pregnancy and PPHN, which remained significantly elevated (adjusted odds ratio, 6.1; 95 percent confidence interval, 2.2 to 16.8).  Inclusion of other factors in the multivariate model, such as use of NSAIDs in late pregnancy, smoking, and alcohol intake, did not substantially change the results (data not shown). The proportion of SSRI-exposed women taking another psychoactive drug in the second half of the pregnancy was similar for mothers of patients (29 percent) and mothers of controls (33 percent). Furthermore, restriction of analyses to full-term births (infants born at 37 weeks of gestation or later) resulted in a similar estimate of the odds ratio (adjusted odds ratio, 5.6; 95 percent confidence interval, 2.0 to 15.4). The association was also similar for patients with and without patent ductus arteriosus and after exclusion of mothers whose infants died (data not shown).

Although our predefined cutoff point for exposure in late pregnancy was 20 weeks of gestation, 12 of the 14 mothers with late SSRI exposure whose infants had PPHN continued use of their medication at least into the eighth month of pregnancy. Post hoc analysis using a cutoff point of 26 weeks of gestation yielded identical results (adjusted odds ratio, 6.1; 95 percent confidence interval, 2.2 to 16.8). The numbers were too small to permit examination of the effects of dose size, specific SSRI used, or reduction of the length of exposure before delivery.

Discussion

This large case–control epidemiologic study focusing on risk factors for PPHN showed a significant association between exposure of a mother to an SSRI during late pregnancy and the occurrence of PPHN in her infant. This finding is consistent with an earlier observation in a small cohort study.

Although our study cannot establish causality, several possible mechanisms suggest that a causal association is plausible. The lung acts as a reservoir for antidepressant drugs, and substantial accumulation of SSRIs in the lungs has been reported. Serotonin not only has vasoconstrictive properties that increase pulmonary vascular resistance, but also has mitogenic and comitogenic effects on pulmonary smooth-muscle cells.Thus, higher circulating levels of serotonin in the fetus and accumulation of serotonin in the fetal lung might result in the proliferation of smooth-muscle cells that is characteristic of PPHN.

Another potential pathway is through the inhibitory effect of SSRIs on the synthesis of nitric oxide, a vasodilator that appears to have a role in the regulation of vascular tone and reactivity both in utero and during postnatal life.In one study, the release of nitric oxide was inhibited in a dose-dependent fashion in synovial-cell culture medium treated with fluoxetine.In a sample of patients with cardiac disease who were treated with paroxetine, the activity of nitric oxide synthase was inhibited and the serum levels of nitrite and nitrate were significantly decreased as compared with pretreatment levels.

Our findings may be consistent with some of the transient neonatal complications noted to occur in 20 to 30 percent of newborns with late prenatal exposure to SSRIs. Mild respiratory distress, transient tachypnea of the newborn, failure to cry, and cyanosis are among the complications that are reported with increased frequency. It is possible that these respiratory problems represent the less severe end of the spectrum in a range of outcomes consistent with PPHN.

We found a nonsignificant reduction in the risk of PPHN when SSRI exposure was limited to the first half of gestation; however, this estimate was based on only two exposed patients. Our study was specifically designed to assess the association of PPHN with SSRI use in the second half of pregnancy. An alternative explanation for our results is confounding, particularly confounding by indication. However, exposure to non-SSRI antidepressants was not associated with PPHN, nor was there an association between PPHN and SSRIs when exposure was limited to the first half of gestation; these observations suggest that maternal depression was not independently associated with PPHN. Controlling for other potential confounders, including maternal body-mass index, smoking, use of NSAIDs in late pregnancy, and diabetes, did not attenuate the association between SSRI use in late pregnancy and PPHN. Although residual confounding cannot be ruled out, we believe it is unlikely that it could account for an elevated risk of this size. On the other hand, it is important to note that our findings, although statistically significant, are based on a relatively small number of exposed mothers with affected infants.

A potential limitation of this study is the retrospective design, which introduces the possibilities of inaccurate recall or recall bias. However, all interviews were conducted within six months after delivery, antidepressants are prescription medications taken over the long term, and the study interviewers specifically and similarly questioned both mothers of patients and mothers of controls regarding their use of antidepressants. The likelihood of recall bias is reduced by the fact that neither the interviewers nor the mothers were aware of the study hypothesis at the time of the interview. In addition, it seems implausible that there would be differential recall of the gestational timing of exposure to SSRIs and that of exposure to other antidepressants.

It is important to replicate these findings in other studies. In addition, further research should assess the relationship of different types and dosages of SSRIs with PPHN and with milder respiratory complications in newborns. Studies should also be undertaken to investigate whether there is any association between SSRIs and PPHN in the offspring of women who discontinue SSRI use late in pregnancy. Furthermore, to better identify patients who may be at risk, investigations should explore interactions between environmental and genetic factors, the latter including polymorphisms affecting the production or regulation of enzymes involved in the metabolism of SSRIs, as well as mutations related to PPHN.

The prevalence of major depressive disorders among women of reproductive age is estimated to be between 10 and 15 percent. SSRIs are among the most common medications used to treat these disorders, and continued treatment may be needed throughout pregnancy for the health of the mother. Our findings might be factored into an assessment of the benefit and risk for a particular mother. On the assumption that the relative risk of 6.1 for PPHN observed in our study is true, and that the relation is causal, the absolute risk among those who use SSRIs late in pregnancy is relatively low (about 6 to 12 per 1000 women); to put it in other terms, about 99 percent of women exposed to one of these medications late in pregnancy will deliver an infant unaffected by PPHN. Pending further studies to confirm these findings, clinicians and their patients must consider both the benefits of SSRIs in the treatment of depression and the potential risk of PPHN relative to the risks and benefits of alternative treatments or nontreatment.

Supported by a grant (HL50763) from the National Heart, Lung, and Blood Institute and by the National Center for Birth Defects Research and Prevention and the Massachusetts Department of Public Health.

Dr. Chambers and Dr. Jones report having received research support from Apotex, Barr Laboratories, Par Pharmaceutical, Teva Pharmaceuticals, and Sandoz; Dr. Louik and Dr. Werler, research support from GlaxoSmithKline; and Dr. Mitchell, research support from GlaxoSmithKline, Barr Laboratories, and Genpharm. No other potential conflict of interest relevant to this article was reported.

Source Information

From the Departments of Pediatrics (C.D.C., K.L.J.) and Family and Preventive Medicine (C.D.C.), University of California, San Diego, La Jolla; the Slone Epidemiology Center, Boston University School of Public Health, Boston (S.H.-D., M.M.W., C.L., A.A.M.); and Children's Hospital and Brigham and Women's Hospital, Harvard Medical School, Boston (L.J.V.M.).

Address reprint requests to Dr. Chambers at the University of California, San Diego, Medical Center, 200 W. Arbor Dr., Mail Code 8446, San Diego, CA 92103, or at chchambers@ucsd.edu.

We are indebted to Dawn Jacobs, R.N., M.P.H., Rachel Wilson, M.P.H., Fiona Rice, M.P.H., Rita Krolak, R.N., Sally Perkins, R.N., Kathleen Sheehan, R.N., Karen Bennett Mark, R.N., Deborah Kasindorf, R.N., Clare Coughlin, R.N., Geraldine Ellison, R.N., Joan Shander, Diane Gallagher, Nastia Dynkin, Nancy Rodriquez-Sheridan, Cecelia Stadler, Meghan Malone-Moses, Irene Shephard, R.N., Melody Kisor, Dawn Taggett, M.P.H., Sherlonda Allen, Michelle Hose, R.N., Beth Smith, R.N., Patricia Maloney, R.N., Merianne Mitchell, R.T., Valerie Hillis, Steven Rivers, and John Farrell for their assistance in data collection and computer programming. We also thank the medical and nursing staff of the following participating hospitals. Boston area: Baystate Medical Center, Beth Israel Deaconess Medical Center, Boston Medical Center, Brigham and Women's Hospital, Brockton Hospital, Cambridge Hospital, Caritas Good Samaritan Medical Center, Charlton Memorial Hospital, Children's Hospital, Emerson Hospital, Falmouth Hospital, Haverhill–Hale Hospital, Jordan Hospital, Kent Hospital, Lawrence General Hospital, Lowell General Hospital, Melrose–Wakefield Hospital, Metro West Medical Center–Framingham, Mt. Auburn Hospital, New England Medical Center, Newton–Wellesley Hospital, North Shore Medical Center, Rhode Island Hospital, Saints Memorial Medical Center, South Shore Hospital, Southern New Hampshire Medical Center, St. Elizabeth's Medical Center, St. Luke's Hospital, St. Vincent Hospital, UMass Memorial Health Care, and Women and Infants' Hospital. Philadelphia area: Abington Memorial Hospital, Albert Einstein Medical Center, Alfred I. duPont Hospital for Children, Bryn Mawr Hospital, Chester County Hospital, Children's Hospital of Philadelphia, Christiana Care Health Services, Community Hospital of Lancaster, Crozer–Chester Medical Center, Doylestown Hospital, Frankford Hospital, Hahnemann University Hospital, the Hospital of the University of Pennsylvania, Lankenau Hospital, Lancaster General Hospital, Lehigh Valley Hospital, Nanticoke Memorial Hospital, Pennsylvania Hospital, Sacred Heart Hospital, St. Christopher's Hospital for Children, St. Mary Medical Center, Temple University Health Sciences Center, Reading Hospital and Medical Center, and Thomas Jefferson University Hospital. Toronto area: Grand River Hospital, Guelph General Hospital, Hamilton Health Sciences Corporation, the Hospital for Sick Children, Humber River Regional Hospital–Church Site, Humber River Regional Hospital–Finch Site, Joseph Brant Memorial Hospital, Lakeridge Health Corporation, London Health Sciences Center, Mt. Sinai Hospital, North York General Hospital, Oakville Trafalgar Memorial Hospital, Scarborough Hospital–General Division, Scarborough Hospital–Grace Division, St. Joseph's Health Centre–London, St. Joseph's Health Centre–Toronto, St. Joseph's Healthcare–Hamilton, St. Michael's Hospital, Sunnybrook and Women's College Health Sciences Center, Toronto East General Hospital, Toronto General Hospital, Trillium Health Center, William Osler Heath Centre, York Central Hospital, and York County Hospital. San Diego area: Alvarado Hospital, Balboa Naval Medical Center, Camp Pendleton Naval Hospital, Children's Hospital and Health Center, Kaiser Zion Medical Center, Palomar Medical Center, Pomerado Hospital, Scripps Memorial Hospital–Encinitas, Scripps Memorial Hospital–Chula Vista, Scripps Memorial Hospital–La Jolla, Scripps Mercy Hospital, SharpChula Vista Hospital, Sharp Coronado Hospital, Sharp Grossmont Hospital, Sharp Mary Birch Hospital, Tri-City Medical Center, and UCSD Medical Center.

Important Warnings in Antidepressant Drug Labeling

FDA Patient Safety News: Show #31, September 2004

We told you that FDA was working with antidepressant drug manufacturers to add new warnings to their drugs' labels. The drugs that are the focus of these changes are: Prozac (fluoxetine), Zoloft (sertraline), Paxil (paroxetine), Luvox (fluvoxamine), Celexa (citalopram), Lexapro (escitalopram), Wellbutrin (bupropion), Effexor (venlafaxine), Serzone (nefazodone), and Remeron (mirtazapine).

A number of the manufacturers have already changed the labeling for their drugs, and have notified health care professionals about the changes.

The new labeling says that both adult and pediatric patients with major depressive disorder may experience a worsening of their depression or start to have suicidal thoughts, and that this can happen whether or not they're taking antidepressant drugs.

Even though a causal link hasn't been established between these behaviors and the drugs, patients on antidepressants should be observed closely for clinical worsening or suicidality. This is especially important at the beginning of treatment or when the dose is either increased or decreased.

Patients who develop suicidal thoughts for the first time when they take these drugs should be carefully monitored to determine whether to discontinue or modify the drug therapy. The same holds true for patients whose depression becomes persistently worse, or whose suicidality is severe or abrupt in onset.

The warning also points out that patients should be observed for anxiety, agitation, panic attacks, and other behavioral symptoms known to be associated with antidepressant therapy. Although FDA hasn't concluded that these symptoms are a precursor to worsening depression or suicidal impulses, patients who experience these symptoms may be at increased risk.

Again, therapy should be evaluated and medications may need to be stopped if the patient has symptoms that are severe, abrupt in onset, or weren't part of the presenting symptoms.

Patients and caregivers also have an important role to play in monitoring, and that includes the parents of pediatric patients. They should be told to look for these kinds of symptoms or suicidal thoughts and report them immediately to health care providers.

On a different note, Wyeth Pharmaceuticals, the maker of Effexor, has notified health professionals about other labeling changes. Neonates who were exposed to Effexor late in the third trimester of pregnancy have developed complications requiring prolonged hospitalization, respiratory support, and tube feeding. Practitioners treating pregnant women with Effexor in their third trimester should carefully weigh the potential risks and benefits of treatment, and may wish to consider tapering Effexor use during that time. These complications can also occur with other Serotonin and Norepinephrine Reuptake Inhibitors (SNRIs) or Selective Serotonin Reuptake Inhibitors (SSRIs).

And finally, Bristol-Meyers Squibb has revised the product labeling for Serzone to reinforce the importance of doing a thorough risk-benefit analysis when considering whether to prescribe this drug. The labeling now says that when deciding among alternative treatments for depression, the prescriber should consider the risk of hepatic failure associated with Serzone treatment. In many cases, this would mean that drugs other than Serzone should be tried first.

 


Verdicts & Settlements

Scott has been involved in numerous and diverse settlements and verdicts throughout his 18 year legal career.  He prides himself on taking care of the injured people he represents.  Scott has represented individuals from almost every state in the country and can point to settlements involving millions of dollars. Whether it be a faulty medical device, a flawed manufacturing process, a failed prescription drug or some other issue that has caused personal injury, Scott has the experience, determination and the integrity to represent a client’s interests aggressively and see that justice is served. The following examples are but a few of recent notable accomplishments:

  • Hundreds of Scott’s clients from numerous states received monetary awards in the Silicone breast implant litigation. These cases involved defective leaking or ruptured silicone implants which caused significant injury, illness and/or damage to women who relied on the manufactures of the implants.  Scott worked with the women all the way through to verdict or settlement and was responsible for ultimately settling client cases for millions of dollars.

  • Scott represented clients in the Rezulin litigation which involved a drug used by diabetics. The FDA ultimately removed the drug from the market due to liver and cardiac adverse events. Scott was involved in hundreds of hours of document review and depositions in the U.S. and Europe.  He deposed corporate witnesses who designed, manufactured, marketed and sold the drug and his clients received exceptional settlements.

  • Scott and his partner Ed Blizzard were involved in representing hundreds of individuals who suffered as a result of defective Sulzer hip and knee implant replacement joints.  Scott and Ed worked at both the state and federal level and were instrumental in developing documents and deposing corporate witnesses so that ultimately a global settlement of all claims was announced.  Scott and Ed were able to secure millions in settlement for their clients.

  • Scott represented many clients who encountered problems as a result of the diet drugs Pondimin and Redux.  He was involved with discovery committees, reviewed thousands of documents and deposed many corporate witnesses.  He tried many of these cases to verdict receiving large settlements for his clients. In December 2000, Scott tried a case in Philadelphia for two ladies from Utah who developed heart valve damage after taking the diet drug combination known as Fen-Phen. After a two week trial the jury awarded each of his clients $100 million dollars. This $200 million dollar verdict stands today as the largest Fen-Phen valvular heart disease verdict in the country. Because of this verdict, Scott was inducted into the Million Dollar and the Multi-Million Dollar Advocates Forum.

  • Scott’s clients in the Ephedra litigation were compensated well for the damages they suffered.  These cases involved  products such as Herbalife, Dexatrim, Stacker and Hydroxicut that were associated with heart attacks and strokes. He was heavily involved in developing justification documents and taking corporate depositions that ultimately led to large dollar settlements for his clients.  

Most recently, Scott began working on Paxil birth defect cases. Paxil is an antidepressant still used by millions of Americans daily.  In recent years, however, it has been associated with significant heart defects when ingested by women during the first trimester of a pregnancy.  Scott has been actively prosecuting these cases against GSK, maker of the drug. One of his cases was the first to be set for trial.  The case was resolved in favor of Scott’s client.

Name
Comment
Phone
Email

Current Litigation:

Celexa
  • Heart Defects
  • Lung Defects

Zoloft
  • Heart Defects
  • Lung Defects

Prozac
  • Heart Defects
  • Lung Defects

DARVON & DARVOCET
  • Heart Rhythm

PAXIL
  • Birth Defects

REGLAN
  • Tardive Dyskinesia
  • Tardive Dystonia

ACCUTANE

ACTOS

DEPAKOTE

DePuy

MERIDIA

WELLBUTRIN

On the Web:



Office Location:

Lyric Centre
440 Louisiana, Suite 1710
Houston TX 77002-1689
our toll free # 800-349-0127
phone # 713-844-3750
fax # 713-844-3755

Visit us on Facebook
Visit us on Twitter

Map | Email Us


* Verdicts and settlement amount does not reflect client portion

Blizzard, McCarthy & Nabers, LLP represents clients in mass tort and primary pulmonary hypertension lawsuits nationwide, including Alabama, Alaska, Arizona, Arkansas, California, Colorado, Connecticut, Delaware, Florida, Georgia, Hawaii, Idaho, Illinois, Indiana, Iowa, Kansas, Kentucky, Louisiana, Maine, Maryland, Massachusetts, Michigan, Minnesota, Mississippi, Missouri, Montana, Nebraska, Nevada, New Hampshire, New Jersey, New Mexico, New York, North Carolina, North Dakota, Ohio, Oklahoma, Oregon, Pennsylvania, Rhode Island, South Carolina, South Dakota, Tennessee, Texas, Utah, Vermont, Virginia, Washington, West Virginia, Wisconsin and Wyoming.

We also serve the cities of New York, Los Angeles, Chicago, Houston, Phoenix, Philadelphia, San Antonio, San Diego, Dallas, San Jose City, Detroit, Jacksonville, Indianapolis, San Francisco, Columbus, Austin, Memphis, Fort Worth, Baltimore, Charlotte, Boston, Seattle, Washington, Milwaukee, Denver, Louisville, Las Vegas, Nashville, Oklahoma City, Portland, Tucson, Albuquerque, Atlanta, Long Beach, Fresno, Sacramento, Mesa, Kansas City, Cleveland, Virginia Beach, Omaha, Miami, Oakland, Tulsa, Honolulu, Minneapolis, Colorado Springs, Arlington and Wichita.