Excedrin Back & Body Extra Strength Side Effects
Please note - some side effects for Excedrin Back & Body Extra Strength may not be reported. Always consult your doctor or healthcare specialist for medical advice. You may also report side effects to the FDA.
Side Effects of Excedrin Back & Body Extra Strength - for the Consumer
Excedrin Back & Body Extra Strength
All medicines may cause side effects, but many people have no, or minor, side effects. Check with your doctor if any of these most COMMON side effects persist or become bothersome when using Excedrin Back & Body Extra Strength:
Seek medical attention right away if any of these SEVERE side effects occur when using Excedrin Back & Body Extra Strength:
Heartburn; nausea; upset stomach.
Severe allergic reactions (rash; hives; itching; difficulty breathing; tightness in the chest; swelling of the mouth, face, lips, or tongue); black or bloody stools; confusion; dark urine or pale stools; diarrhea; dizziness; drowsiness; hearing loss; ringing in the ears; severe stomach pain; unusual fatigue; vomiting; yellowing of the skin or eyes.
This is not a complete list of all side effects that may occur. If you have questions about side effects, contact your health care provider. Call your doctor for medical advice about side effects. To report side effects to the appropriate agency, please read the Guide to Reporting Problems to FDA.Top
Side Effects by Body System - for Healthcare Professionals
Applies to: oral tablet
Cardiovascular side effects of aspirin have included salicylate- induced variant angina, ventricular ectopy, conduction abnormalities, and hypotension, particularly during salicylate toxicity. In addition, at least one case of fluid retention simulating acute congestive heart failure has been reported during aspirin therapy.
Cardiovascular side effects including two cases of hypotension have been reported following the administration of acetaminophen.
A 29- year- old female with a history of migraine developed chest pain, tachycardia and orthopnea following aspirin consumption at doses of 1500 mg per day for several days. After discontinuation of aspirin therapy, the patient's symptoms promptly resolved. The patient consented to a pharmacological challenge test which once again triggered the symptoms.
Two cases hypotension have been reported following the administration of acetaminophen. Both patients experienced significant decreases in blood pressure. One of the two patients required pressor agents to maintain adequate mean arterial pressures. Neither episode was associated with symptoms of anaphylaxis. Neither patient was rechallenged after resolution of the initial episode.
Dermatologic side effects of aspirin have included Stevens-Johnson syndrome and a lichenoid eruption.
Dermatologic side effects including erythematous skin rashes associated with acetaminophen have been reported, but are rare. Acetaminophen associated bullous erythema and purpura fulminans have been reported. One case of toxic epidermal necrolysis associated with acetaminophen administered to a pediatric patient has been reported.
Endocrine side effects of aspirin have included hypoglycemia (which has been reported in children) and hyperglycemia.
Gastrointestinal side effects of aspirin have included epigastric distress (in as many as 83% of patients treated with regular aspirin), abdominal discomfort or pain, endoscopically identifiable gastric mucosal lesions, nausea, and vomiting. More serious gastrointestinal effects include hemorrhage, peptic ulcers, perforation, and esophageal ulcerations.
Gastrointestinal side effects of acetaminophen are rare except in alcoholics and after overdose. Cases of acute pancreatitis have been reported rarely.
Endoscopically identifiable gastric mucosal lesions occur in most patients who receive a single dose of aspirin. Clinically evident gastrointestinal bleeding has been reported in as many as 3% of treated elderly patients. Anorectal ulceration and rectal stenosis have been reported in patients who abuse aspirin- containing rectal suppositories. One case- controlled study has suggested that an association between aspirin (and other NSAID) consumption and appendicitis may exist.
One study has suggested that acetaminophen may precipitate acute biliary pain and cholestasis. The mechanism of this effect may be related to inhibition of prostaglandin and alterations in the regulation of the sphincter of Oddi.
In general, acetaminophen is well- tolerated when administered in therapeutic doses.
Hematologic side effects of aspirin have included increased blood fibrinolytic activity. In addition, hypoprothrombinemia, thrombocytopenia, thrombocyturia, megaloblastic anemia, and pancytopenia have been reported rarely. Aplastic anemia and eosinophilia have also been reported.
Hematologic side effects including rare cases of thrombocytopenia associated with acetaminophen have been reported. Acute thrombocytopenia has also been reported as having been caused by sensitivity to acetaminophen glucuronide, the major metabolite of acetaminophen. Methemoglobinemia with resulting cyanosis has also been observed in the setting of acute overdose.
Alcoholic patients may develop hepatotoxicity after even modest doses of acetaminophen. In healthy patients, approximately 15 grams of acetaminophen is necessary to deplete liver glutathione stores by 70% in a 70 kg person. However, hepatotoxicity has been reported following smaller doses. Glutathione concentrations may be repleted by the antidote N-acetylcysteine. One case report has suggested that hypothermia may also be beneficial in decreasing liver damage during overdose.
In a recent retrospective study of 306 patients admitted for acetaminophen overdose, 6.9% had severe liver injury but all recovered. None of the 306 patients died.
A 19-year-old female developed hepatotoxicity, reactive plasmacytosis and agranulocytosis followed by a leukemoid reaction after acute acetaminophen toxicity.
Hepatic side effects of aspirin have included hepatotoxicity and cholestatic hepatitis.
Hepatic side effects of acetaminophen including severe and sometimes fatal dose dependent hepatitis have been reported in alcoholic patients. Hepatotoxicity has been increased during fasting. Several cases of hepatotoxicity from chronic acetaminophen therapy at therapeutic doses have also been reported despite a lack of risk factors for toxicity.
Hypersensitivity side effects of aspirin have included bronchospasm, rhinitis, conjunctivitis, urticaria, angioedema, and anaphylaxis. Approximately 10% to 30% of asthmatics are aspirin- sensitive (with the clinical triad of aspirin sensitivity, bronchial asthma, and nasal polyps).
Hypersensitivity side effects including anaphylaxis and fixed drug eruptions have been reported rarely in association with acetaminophen use.
The mechanism of aspirin- induced hypersensitivity may be related to an up- regulation of the 5- lipoxygenase pathway of arachidonic acid metabolism with a resulting increase in the products of 5- lipoxygenase (such as leukotrienes).
Metabolic side effects of aspirin have included dehydration and hyperkalemia. Respiratory alkalosis and metabolic acidosis, particularly during salicylate toxicity, have been reported. A case of hypoglycemia has been reported in a patient on hemodialysis. Salicylates have also been reported to displace triiodothyronine (T3) and thyroxine (T4) from protein binding sites. The initial effect is an increase in serum free T4 concentrations.
Metabolic side effects including metabolic acidosis have been reported following a massive overdose of acetaminophen.
In the case of metabolic acidosis, causality is uncertain as more than one drug was ingested. The case of metabolic acidosis followed the ingestion of 75 grams of acetaminophen, 1.95 grams of aspirin, and a small amount of a liquid household cleaner. The patient also had a history of seizures which the authors reported may have contributed to an increased lactate level indicative of metabolic acidosis.
Musculoskeletal side effects of aspirin have included rhabdomyolysis.
Central nervous system side effects of aspirin have included agitation, cerebral edema, coma, confusion, dizziness, headache, cranial hemorrhage, lethargy and seizures. Tinnitus and subjective hearing loss (or both) may occur. Some investigators have reported that modest doses may result in decreased frequency selectivity and may therefore impair hearing performance, particularly in the setting of background noise.
Some investigators have suggested that tinnitus may be a less reliable indicator of salicylate toxicity than previously believed. Patients with high frequency hearing loss may have difficulty perceiving tinnitus. In a study of rheumatoid arthritis patients, those with tinnitus had no greater salicylate levels than those without tinnitus. Elderly patients may be less likely to perceive tinnitus than younger patients.
Ocular side effects of aspirin have included cases of localized periorbital edema.
Oncologic side effects of aspirin have included reports of pancreatic cancer. Several epidemiologic studies have suggested that chronic aspirin use may decrease the risk of large bowel neoplasms. However, other studies have not found such a beneficial effect.
Reye's syndrome, following use of aspirin, typically involves vomiting, neurologic dysfunction, and hepatic dysfunction during or shortly after an acute viral infection.
Other side effects of aspirin have included Reye's syndrome with use in children with an acute viral illness. Reye's syndrome has also been reported even more rarely in adults.
The mechanism of an aspirin- induced decrease in renal function may be related to inhibition of renal prostaglandin synthesis with consequent decreases in renal blood flow. Vasodilating renal prostaglandins may be particularly important in patients who exhibit arterial underfilling (i.e., heart failure, cirrhosis). The administration of high doses of NSAIDs to such patients has produced acute renal failure in rare instances.
Acute tubular necrosis usually occurs in conjunction with liver failure, but has been observed as an isolated finding in rare cases. A possible increase in the risk of renal cell carcinoma has been associated with chronic acetaminophen use as well.
One case-control study of patients with end-stage renal disease suggested that long term consumption of acetaminophen may significantly increase the risk of end-stage renal disease particularly in patients taking more than two pills per day.
However, a recent cohort study of analgesia use of initially healthy men concluded that moderate use of analgesics including acetaminophen was not associated with increased risk of renal disease.
Renal side effects of aspirin have included reduction in glomerular filtration rate (particularly in patients who are sodium restricted or who exhibit diminished effective arterial blood volume, such as patients with advanced heart failure or cirrhosis), interstitial nephritis, papillary necrosis, elevations in serum creatinine, elevations in blood urea nitrogen, proteinuria, hematuria, and renal failure.
Renal side effects of acetaminophen are rare and have included acute renal failure, acute tubular necrosis, and interstitial nephritis. Adverse renal effects are most often observed after overdose, after chronic abuse (often with multiple analgesics), or in association with acetaminophen- related hepatotoxicity.
Aspirin desensitization has been used to decrease disease activity and reduce the need for systemic corticosteroids in patients with aspirin- exacerbated respiratory disease.
Respiratory side effects of aspirin have included hyperpnea, pulmonary edema, and tachypnea.
Respiratory side effects including a case of acetaminophen- induced eosinophilic pneumonia have been reported.
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