TriLyte wih orange flavor packet. Side Effect occurred on 2009-02-28
Safety Information about Raptiva
Since the approval of Raptiva (efalizumab) in October 2003, the FDA has received reports of three confirmed cases and one possible case of progressive multifocal leukoencephalopathy (PML) in patients who were 47 to 73 years of age who were using Raptiva for the treatment of moderate to severe plaque psoriasis. Two of the patients with confirmed PML and one patient with possible PML died. All four patients were treated with Raptiva continuously for more than three years. None of the patients were receiving other treatments that suppress the immune system while taking Raptiva.
PML is a rare, serious, progressive neurologic disease caused by a virus that affects the central nervous system. When PML occurs, it is usually in people whose immune systems have been severely weakened and often results in an irreversible decline in neurologic function and death. There is no known effective treatment for PML.
Raptiva works by affecting T-cells in the immune system. The effects of Raptiva also decrease the function of the immune system and increase susceptibility to infections.
Raptiva was approved for the treatment of moderate to severe plaque psoriasis in 2003. There were no cases of PML seen in the clinical trials that supported the approval of Raptiva. At the time of approval, a total of 2,764 patients had been treated with Raptiva. Of those 2,764 patients, 2400 had been treated for three months, 904 for six months, and 218 for one year or more.
In October 2008, the labeling for Raptiva was changed to highlight, in a Boxed Warning, the risks of life-threatening infections, including PML. In addition, FDA directed Genentech, the manufacturer of Raptiva, to develop a Risk Evaluation and Mitigation Strategy, or REMS, to ensure that patients receive risk information about Raptiva.
The FDA is reviewing this latest information. The agency will take appropriate steps to ensure that the risks of Raptiva do not outweigh its benefits, that patients prescribed Raptiva are clearly informed of the signs and symptoms of PML, and that health care professionals carefully monitor patients for the possible development of PML.
Healthcare providers should, in the interim, be aware of the following information and advice:
- Raptiva increases the risk of PML. Longer, continuous use may further increase this risk.
- Inform patients using Raptiva of the potential risk of developing PML.
- There are no known screening tests that can reliably predict PML or medical interventions that can prevent or treat this disease.
- Monitor patients being treated with Raptiva for the onset of neurologic symptoms. Discontinue Raptiva if PML is suspected.
- Patients treated with Raptiva should be periodically re-evaluated to ensure that the benefit of treatment continues to outweigh the risks. Consideration should be given to use of other approved therapies to control the patients’ psoriasis.
- The effects of periodic or intermittent use of Raptiva, or the concomitant use of other immunosuppressant drugs on the risk for PML is not known.
Patients using Raptiva should:
- Be aware that Raptiva increases the risk of developing PML. PML is a disease that is fatal or causes severe disability.
- Talk with their healthcare provider about the benefits and risks of treatment with Raptiva.
- Be aware of the symptoms of PML which may include unusual weakness, loss of coordination, changes in vision, difficulty speaking and sometimes personality changes.
- Contact their healthcare provider immediately if they experience these symptoms.
- Understand that there are no laboratory screening tests for PML or medical interventions that can prevent or treat PML
The FDA asks health care providers and patients to report possible cases of PML to the FDA through the MedWatch program by phone (1-800-FDA-1088) or by the Internet at http://www.fda.gov/medwatch/index.html.
Salmonella and Turtle Safety
Reclast Side Effect occurred on 2009-02-15
Amias, levothyroxine, Side Effect occurred on 2009-02-05
Video: Ethex Corp. Recalls Several Generic Drugs
Watch video:
UPDATE: Ethex Corporation is also recalling a single lot (Lot #90219, Exp: 03/2010; NDC #58177-0620-04) of hydromorphone HCl tablets because they may be oversized. In addition, as a precautionary measure, the parent company of Ethex, KV Pharmaceutical, has announced that it is voluntarily suspending shipments of all FDA-approved drug products in tablet form.
The generic drug company Ethex Corporation has recalled certain lots of several products because these lots may contain oversized tablets. Oversized tablets may have as much as about twice the labeled amount of active ingredient.
The recall affects specific lots of dextroamphetamine sulfate tablets, propafenone HCl tablets, isosorbide mononitrate extended release tablets, and morphine sulfate immediate and extended release tablets. Affected lot numbers can be found at the “Additional Information” links, below. Overdoses of these drugs could have serious or life-threatening consequences. For example, a dextroamphetamine sulfate overdose could result in tachycardia and hypertension. Overdoses of morphine sulfate can cause respiratory depression and hypotension.
Ethex Corporation has sent instructions to affected wholesalers and retailers for returning the recalled products and for contacting consumers who received them. Consumers and their caregivers should not use any tablets that appear to be larger than usual. If they experience any adverse reactions to these drugs, they should contact their healthcare provider immediately. For more information contact Ethex Customer Service at 1-800-748-1472.
Additional Information:
FDA MedWatch Safety Alert. Propafenone HCl Tablets, Isosorbide Mononitrate Extended Release, Morphine Sulfate Immediate Release, Dextroamphetamine Sulfate Tablets. November 10, 2008.
http://www.fda.gov/medwatch/safety/2008/safety08.htm#Ethex
FDA MedWatch Safety Alert. Hydromorphone HCl 2 mg Tablets. December 24, 2008.
http://www.fda.gov/medwatch/safety/2008/safety08.htm#Hydromorphone
Video: Serious Infections and Neurological Events with Raptiva
Watch video:
FDA is highlighting the risk of life-threatening infections in patients treated with Raptiva (efalizumab). Raptiva is an immunosuppressant approved as a once a week injection to treat certain adult patients with moderate to severe plaque psoriasis.
FDA has received reports of serious infections in patients treated with Raptiva, in some cases leading to hospitalization and even death. A new boxed warning will highlight the risk of bacterial sepsis, viral meningitis, invasive fungal disease, progressive multifocal leukoencephalopathy (PML) and other opportunistic infections.
Raptiva’s label will also be updated to include data from studies of juvenile mice. These data suggest that repeated administration of Raptiva to pediatric patients may lead to permanent suppression of the immune system. Raptiva is not approved for children under 18 years of age.
Prescribers should carefully evaluate the risk/benefit profile of Raptiva for patients who may be more susceptible to these risks. Before starting Raptiva, make sure patients are up-to-date on their vaccinations. During therapy, do not vaccinate patients with live or live attenuated vaccines. Also, giving inactivated vaccines during Raptiva treatment may not produce an adequate immune response.
Patients should be taught to recognize the signs and symptoms of serious infections, as well as neurological disorders, anemia, thrombocytopenia, or the worsening of their psoriasis. If any of these signs appear, they should be told to seek immediate medical attention.
FDA is requiring Raptiva’s manufacturer to submit a Risk Evaluation and Mitigation Strategy (REMS) which will include a medication guide for patients.
Additional Information:
FDA MedWatch Safety Alert. Raptiva (efalizumab). October 17, 2008.
http://www.fda.gov/medwatch/safety/2008/safety08.htm#Raptiva
Drug Safety Communications posted by FDA from September 1, 2008 to November 30, 2008
Drug Safety Communications posted by FDA from September 1, 2008 to November 30, 2008 (advisories are available at www.fda.gov/cder/drug/DrugSafety/DrugIndex.htm)
Footnotes:
- Early Communication about an Ongoing Safety Review.
- Inform patients to immediately contact their physician at the first sign or symptom of fatigue, loss of appetite, nausea, vomiting, pruritis, dark urine, jaundice of the sclerae or skin, right upper quadrant tenderness, or unexplained “flu–like” symptoms
- Determine liver enzyme levels when a patient presents with signs or symptoms of liver injury
- Discontinue and not resume atomoxetine treatment if patients present with jaundice or laboratory evidence of liver injury
- Report cases of serious liver injury to FDA’s MedWatch program (www.fda.gov/medwatch)
- Atomoxetine (Strattera) product labeling
http://www.fda.gov/cder/foi/label/2008/021411s024s025s026lbl.pdf
- Verispan Vector One®: National, Total Patient Tracker (TPT), 2002-2007, data extracted Sept 2007.
- Bangs ME, Ling J, Zhang S, et al. Hepatic events associated with atomoxetine treatment for attention deficit hyperactivity disorder. Drug Safety. 2008;31(4):345-54.
- Stojanovski SD, Casavant MJ, Hayat MM, et al. Atomoxetine-induced hepatitis in a child. Clin Toxicol (Phila). 2007;45(1):51-5.
- Lim JR, Faught PR, Chalasani NP. Severe liver injury after initiating therapy with atomoxetine in two children. J Pediatr. 2006;148(6):831-4.
- Shear NH, Milpied B, Bruynzeel DP, Phillips EJ. A review of drug patch testing and implications for HIV clinicians. AIDS. 2008;22(9):999-1007.
- Escaut L, Liotier JY, Albengres E, et al. Abacavir rechallenge has to be avoided in case of hypersensitivity reaction. AIDS. 1999;13(11):1419-20.
- Hernandez J, Cutrell A, Bonny T, et al. Diagnosis of abacavir hypersensitivity reactions among patients not receiving abacavir in two blinded studies. Antivir Ther. 2003;8:L88.
- Mallal S, Nolan D, Witt C, et al. Association between presence of HLA-B*5701, HLA-DR7, and HLA-DQ3 and hypersensitivity to HIV-1 reverse-transcriptase inhibitor abacavir. Lancet. 2002;359(9308):727-32.
- Hetherington S, Hughes AR, Mosteller M, et al. Genetic variations in HLA-B region and hypersensitivity reactions to abacavir. Lancet. 2002;359(9312):1121-2.
- Abacavir product labeling. http://www.fda.gov/cder/foi/label/2008/020977s017,020978s020lbl.pdf
- Mallal S, Phillips E, Carosi G, et al. HLA-B*5701 screening for hypersensitivity to abacavir. N Engl J Med. 2008; 358:568–79.
- Saag M, Balu R, Phillips E, et al. High sensitivity of Human Leukocyte Antigen-B*5701 as a marker for immunologically confirmed abacavir hypersensitivity in white and black patients. Clin Infect Dis. 2008;46:1111-18.
Atomoxetine (Marketed as Strattera): Serious Liver Injury
FDA continues to receive reports of serious liver injury in patients given atomoxetine. Atomoxetine received FDA approval on November 26, 2002 as the first non-stimulant medication used for the treatment of attention deficit hyperactivity disorder (ADHD) in children (ages 6 years and above) and adults.1 Atomoxetine’s therapeutic action is believed to be due to its selective inhibition of norepinephrine reuptake. From the year 2002 to 2007, approximately 3.3 million patients received a prescription for atomoxetine in the United States. Of those, approximately 2.1 million patients (64%) were children ages 17 years and younger.2
While a signal for serious liver injury was not detected during premarket clinical trials of atomoxetine, two published postmarket reports did identify instances of atomoxetine-induced hepatitis.3,4 In one of these reports, there was a positive rechallenge with atomoxetine. Subsequent to these reports, a bolded warning was added in 2004 to the atomoxetine label indicating an increased risk for severe liver injury.
Since the 2004 labeling change, FDA received six additional reports of serious liver injury in patients taking atomoxetine. Following an evaluation of the information from the drug sponsor and additional literature articles submitted to FDA, the atomoxetine product label was again revised in 2007. The Warnings and Precautions section of the drug label advises prescribers about the risk for severe liver injury with this drug.1 Healthcare professionals and patients should be watchful for serious liver injury associated with the use of atomoxetine and report cases to FDA’s MedWatch.
Box 1
|
What is drug-induced liver injury? The liver is the main organ for metabolizing, activating and/or deactivating drugs prior to excretion via the bile or urine. Sometimes the drug (or its metabolites) can cause chemical injury to liver cells. This injury can vary in severity from asymptomatic elevations of blood enzyme activities to liver failure with a need for transplantation. This injury can also result in death. Drug-induced liver injury (DILI) is now the most frequent cause for acute liver failure in the United States, exceeding all other causes (e.g., viral, alcoholic, autoimmune, ischemic) combined. It is also one of the main reasons for not approving new drugs, or for removing drugs from the market after they were approved for clinical use. The mechanisms causing DILI are not well understood. There are several ways the injury can present in patients including jaundice, nausea and vomiting, abdominal pain, bleeding, mental confusion, and/or kidney failure. Although exceedingly rare for most drugs, almost any drug can cause DILI. Still, some drugs are more likely than others to result in this injury. The main determinant for DILI may be individual differences in constitution or manner of responding to the drug. That is, some patients may be more sensitive than others to DILI. Injuries due to individual differences are generally called “idiosyncratic reactions.” Severe idiosyncratic reactions, while generally rare, may occur at much lower doses than those that are well-tolerated and handled by most people. The FDA, along with partners in academia and industry, is engaged in research into questions about DILI and sponsors an annual public conference on this topic. The proceedings from the conference can be found at www.fda.gov/cder/livertox. |
The following paragraphs summarize FDA’s analysis of these six Adverse Event Reporting System (AERS) cases of atomoxetine-associated liver injury. These reports were received between January 2005 and March 19, 2008. Two of the six cases are described in the medical literature.3,4,5
Table 1 summarizes some of the characteristics of these cases. Five of the six cases were among patients 17 years of age and younger.
Table 1. Characteristics of the six cases of atomoxetine-associated severe liver injury
| Age (years) | Median | 10.5 |
|---|---|---|
| Range | 6-26 | |
| Sex | Male | n = 4 |
| Female | n = 2 | |
| Dose (n = 4): | Median | 32.5 mg |
| Range | 10 – 80 mg | |
| Time to onset (days) | Median | 62.5 |
| Range | 21 – 730 | |
| Reports | U.S | n = 5 |
| Non-U.S. | n = 1 | |
| Serious Outcome | Hospitalization | n = 5 |
| Death | n = 1 |
In four cases, the patients presented with jaundice and one or more symptoms, including fatigue, lack of appetite, abdominal pain, nausea, or vomiting. Acute impairment of liver function, as manifested by the inability to synthesize sufficient prothrombin (PT) to produce a normal INR or the inability to clear bilirubin, was observed at the time of diagnosis in three of the six patients. Two patients had significant increases in hepatic enzymes. In one case, profiled in Box 2, peak AST and ALT levels were 6619 IU/L [73 x upper limit of normal (ULN)] and 5182 IU/L (86 x ULN), respectively; peak total bilirubin (TB) was 14.7 mg/dl. Viral titers for hepatitis A, B, and C, Epstein-Barr virus (EBV), and cytomegalovirus (CMV) IgM were negative in two cases with elevated hepatic enzymes. Liver biopsies showed hepatic inflammation/fibrosis in one patient and inflammation with moderate piecemeal necrosis in the other.
Although the majority of patients were hospitalized, none required a liver transplant. Four patients recovered after atomoxetine was discontinued. One adult, male patient died due to hepatic and renal failure. Because there were limited details available about this case, the role of atomoxetine in this patient’s death could not be determined. Over the course of two years, this patient had alternated atomoxetine 80 mg/day with methylphenidate in order to manage his ADHD.
Three patients in this case series reported a history of occasional acetaminophen use, the use of a recent, single dose of mebendazole, or concomitant quetiapine use. None of these drugs were felt to have contributed to the liver injury.
Two representative cases illustrating the relationship between atomoxetine and serious liver injury are summarized in Box 2. The cases were selected based on a temporal relationship between initiation of atomoxetine and onset of symptoms indicative of a liver injury. Both patients presented with elevated hepatic enzymes and jaundice, and had extensive clinical work-ups, including liver biopsies and tests to rule out non-drug causes of liver injury. Both patients recovered upon atomoxetine discontinuation. The two cases are also described in the medical literature.3,4,5
Box 2
|
Case 1 A 12-year-old female diagnosed with ADHD experienced jaundice and elevation of liver enzymes when she restarted atomoxetine 40 mg daily following a 6-week interruption of a year-long therapy. This patient had no history of liver disease, or exposure to hepatitis or any known hepatotoxins. Three weeks after restarting atomoxetine, she was hospitalized for jaundice, abdominal pain, diarrhea, and vomiting. Upon admission, she had stable vital signs, conjunctival icterus, and tenderness in her right upper quadrant. She had no hepatosplenomegaly. She was evaluated for acute hepatitis. Over the course of the event, her peak liver biomarkers were AST: 3505 U/L (78 x ULN), ALT: 3264 U/L (65 x ULN), TB: 9.8 mg/dL (~10 x ULN), GGT: 108 U/L (normal reference range: 12-43), and PT: 14.1 seconds (normal reference range: 10.8–13.7). Her serum alkaline phosphatase (AP) was normal. A liver biopsy confirmed hepatic inflammation and fibrosis. Testing for hepatitis A, B, C, CMV, and EBV were negative. An antinuclear antibody (ANA) titer was positive (1:160; normal reference range: < 1:40). Smooth muscle antibodies were negative, ceruloplasmin and alpha-1 antitrypsin were normal. The diagnosis of drug-induced liver injury by atomoxetine was made. Atomoxetine was discontinued. Four weeks later, she had an AST of 800 U/L, ALT of 1438 U/L, and TB of 2.6 mg/dL. Serum transaminase and bilirubin levels returned to normal approximately 6 months after discontinuation of atomoxetine. Case 2 An 8-year-old female with ADHD was being treated with atomoxetine 25 mg/day and developed vomiting, abdominal pain, jaundice, and very high serum aminotransferases approximately five weeks after starting therapy. She was hospitalized and atomoxetine was discontinued. She had no known history of liver disease. The child occasionally received therapeutic doses of acetaminophen from a parent (~10 times/month) for soccer-related musculoskeletal pains. She also received one dose of mebendazole for a pinworm infection nine days after starting atomoxetine therapy. Upon admission to the hospital, her physical exam was significant for scleral icterus, jaundice, and hepatomegaly. The peak values of liver markers were AST: 6619 U/L (73 x ULN), ALT: 5182 U/L (86 x ULN), TB: 14.7 mg/dL (~14 x ULN), AP: 528 U/L (3.5 x ULN), and GGPT: 196 U/L (2.5 x ULN). Testing for hepatitis A, B, C, CMV, and EBV were negative. An abdominal ultrasound showed mild hepatomegaly with no gallstones or ductal dilatation. Liver biopsy showed mixed portal inflammation and moderate piecemeal necrosis. Infectious, autoimmune and metabolic causes of liver injury were ruled out. No serum acetaminophen was detected. She received vitamin K, diphenhydramine, ursodiol, and fresh frozen plasma. The patient’s transaminases and bilirubin serum levels began to improve approximately 13 days into her hospitalization. Within two months of her hospital discharge, her AST and ALT serum levels had decreased to 276 U/L (normal reference range: 25-45) and 178 U/L (normal reference range: 0-50), respectively. |
Postmarket reports indicate that atomoxetine is associated with serious idiosyncratic liver injury. Some of the cases reported additional confounding factors, such as occasional acetaminophen use. Some of the cases lacked sufficient clinical detail to convincingly detail the relationship between the use of atomoxetine and liver injury. The mechanism of atomoxetine-induced liver injury remains unknown. FDA continues to monitor AERS for reports of serious liver injury in association with atomoxetine.
FDA encourages physicians to:
References
Abacavir (Marketed as Ziagen) and Abacavir-Combination Products (Marketed as Trizivir and Epzicom): Hypersensitivity Reaction, HLA-B*5701, and Skin Patch Testing
Abacavir (ABC) sulfate (Ziagen; also in the combination products Trizivir and Epzicom), a nucleoside reverse transcriptase inhibitor indicated for treatment of HIV-1 infection, has been associated with a unique, serious, and sometimes fatal hypersensitivity reaction (HSR). ABC HSR is a multi-organ syndrome which typically occurs within six weeks of initiating ABC treatment.1 The most common symptoms of an ABC HSR include fever (~80% of cases), rash (~70% of cases), malaise/fatigue, nausea, and vomiting. Other signs and symptoms of an ABC HSR may include myalgia or arthralgia, headache, diarrhea, pruritis, hypotension, and various respiratory symptoms. Development of an ABC HSR requires immediate and permanent discontinuation of the drug, as rechallenge can be fatal.2
Correctly diagnosing an ABC HSR is critical given the severe consequences of this reaction to the patient and the utility of this drug in managing HIV. Unfortunately, the diagnosis of an ABC HSR can be difficult. An ABC HSR may mimic common infections, or may be confused with adverse events seen with other concomitant or prophylactic medications used for the treatment of HIV, or with opportunistic infections commonly seen in patients with HIV. A review of literature indicates that misdiagnosis of an ABC HSR can occur in approximately two to seven percent of patients, independent of whether patients are even taking ABC.1,3
One risk factor that has been shown to be associated with the development of an ABC HSR is the presence of the human leukocyte allele, HLA-B*5701.4,5 In one prospective, randomized clinical trial (PREDICT-1), not treating patients positive for HLA-B*5701 with abacavir significantly reduced the incidence of clinically suspected cases of an ABC HSR from 7.8% to 3.4%.6 Data from this study suggest that 61% of HLA-B*5701 positive subjects may develop an abacavir HSR during the course of therapy compared with 4.5% of HLA-B*5701 negative subjects. As of July 2008, the Boxed Warning on the abacavir product labeling recommends that patients be screened for HLA-B*5701 prior to initiating abacavir treatment.6
Even with genetic screening for HLA-B*5701, and refraining from initiating abacavir treatment in those patients positive for this allele, some patients may develop an ABC HSR. As noted above, HLA-B*5701 is not 100% predictive of an ABC HSR. Some patients negative for this allele may still develop signs and symptoms suggestive of an ABC HSR. For this reason, healthcare professionals should closely monitor patients taking abacavir for potential signs and symptoms of this reaction (see Table 1).
If an ABC HSR is suspected, healthcare professionals are directed to discontinue ABC immediately and not rechallenge patients with the drug or by any other means.
Table 1. This table lists the systems and signs and symptoms involved in the “> 2 signs and symptoms from 2 systems” rule used in the clinical diagnosis of ABC HSR.
| System | Signs and Symptoms |
|---|---|
| Group 1 | Fever |
| Group 2 | Rash |
| Group 3 | Nausea, Vomiting, Diarrhea, Abdominal Pain |
| Group 4 | Malaise, Tiredness, Myalgias, or Arthralgias |
| Group 5 | Shortness of Breath, Cough, Sore Throat |
Several research reports have emerged that have used skin patch testing to immunologically confirm suspected cases of ABC HSR.7,8 Specifically, in an analysis of race differences in ABC HSRs among black and white subjects positive for HLA-B*5701, white HLA-B*5701 positive subjects with a HSR were more likely to be skin patch test positive than black HLA-B*5701 positive subjects with a HSR.8 Among the 10 HLA-B*5701 positive black subjects, 5 were skin patch test positive and 5 were skin patch test negative. These data suggest that skin patch testing was not predictive for an ABC HSR in patients positive for the HLA-B*5701 allele. Conversely, only 32.3% (42/130) of white and 7.2% (5/69) of black patients who were skin patch tested and who met criteria for clinically suspected ABC HSR had a positive skin patch test for an ABC HSR. Healthcare professionals must be aware that the use of skin patch testing to immunologically confirm cases of an ABC HSR remains in the realm of research and that skin patch testing has not been clinically validated. Skin patch testing may miss cases of true ABC HSR or provide false positive results. The accuracy of skin patch testing results is unknown in a broad population.
Given the risks associated with rechallenging patients with ABC when a case of HSR is suspected, that is, an increased risk of mortality, the diagnosis of an ABC HSR must remain a clinical one in all patients (see Table 1). Although skin patch testing appears to be a simple solution to aid in the diagnosis of a clinical syndrome with diagnostic uncertainty, the positive and negative predictive value of the abacavir skin patch test are not fully understood, making its use to justify a potentially fatal systemic abacavir rechallenge a risky endeavor.
Relevant Web Sites
Information sheet on Abacavir and Abacavir-containing medications
www.fda.gov/cder/drug/InfoSheets/HCP/abacavirHCP.htm
Abacavir (Ziagen) product labeling
http://www.fda.gov/cder/foi/label/2008/020977s017,020978s020lbl.pdf
Abacavir sulfate; lamivudine (Epzicom) product labeling
http://www.fda.gov/cder/foi/label/2007/021652s005lbl.pdf
Abacavir sulfate; lamivudine ; zidovudine (Trizivir) product labeling
http://www.fda.gov/cder/foi/label/2007/021205s018lbl.pdf
Medication Guide for Abacavir products
http://www.fda.gov/cder/Offices/ODS/MG/abacavirMG.pdf
Guidelines for the Use of Antiretroviral Agents in HIV-1-Infected
Adults and Adolescents
http://www.aidsinfo.nih.gov/ContentFiles/AdultandAdolescentGL.pdf
References
PatientsVille.com – Latest Comments- Re: Myslee Side Effects|3 February 12, 2012
- Re: Nitrofurantoin Side Effects February 12, 2012
- Re: Implanon Side Effect Report#3661 itching, redness & swelling February 12, 2012
- Re: Mucinex DM Side Effect Report#5687 Dilated pupils, dizziness, confusion, altered consciousness, inability to concentrate, nausea, fatigue, general feeling of intoxication, incoordination, disinhibi... February 12, 2012
- Re: Sucralfate Side Effects February 12, 2012
- Re: Antabuse Side Effects February 12, 2012
- Re: Lovan Side Effects February 11, 2012
- Re: Miralax Questions and Answers | Patient Discussion Forum 2 February 11, 2012
- Re: Boniva Side Effects|5 February 11, 2012
- Re: Klacid Side Effects February 11, 2012
Subscribe to RSS Feed