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Durabac (acetaminophen / caffeine / phenyltoloxamine / salicylamide) Disease Interactions

There are 22 disease interactions with Durabac (acetaminophen / caffeine / phenyltoloxamine / salicylamide):

Major

Acetaminophen (Includes Durabac) ↔ Alcoholism

Severe Potential Hazard, High plausibility

Applies to: Alcoholism

Chronic alcohol abusers may be at increased risk of hepatotoxicity during treatment with acetaminophen (APAP). Severe liver injury, including cases of acute liver failure resulting in liver transplant and death, has been reported in patients using acetaminophen. Therapy with acetaminophen should be administered cautiously, if at all, in patients who consume three or more alcoholic drinks a day. In general, patients should avoid drinking alcohol while taking acetaminophen-containing medications. Patients should be warned not to exceed the maximum recommended total daily dosage of acetaminophen (4 g/day in adults and children 12 years of age or older), and to read all prescription and over-the-counter medication labels to ensure they are not taking multiple acetaminophen-containing products, or check with a healthcare professional if they are unsure. They should also be advised to seek medical attention if they experience signs and symptoms of liver injury such as fever, rash, anorexia, nausea, vomiting, fatigue, right upper quadrant pain, dark urine, and jaundice.

References

  1. Whitcomb DC, Block GD "Association of acetaminopphen hepatotoxicity with fasting and ethanol use." JAMA 272 (1994): 1845-50
  2. Zimmerman HJ, Maddrey WC "Acetaminophen (paracetamol) hepatotoxicity with regular intake of alcohol: analysis of instances of therapeutic misadventure." Hepatology 22 (1995): 767-73
  3. Bonkovsky HL "Acetaminophen hepatotoxicity, fasting, and ethanol." JAMA 274 (1995): 301
  4. Kaysen GA, Pond SM, Roper MH, Menke DJ, Marrama MA "Combined hepatic and renal injury in alcoholics during therapeutic use of acetaminophen." Arch Intern Med 145 (1985): 2019-23
  5. Nelson EB, Temple AR "Acetaminophen hepatotoxicity, fasting, and ethanol." JAMA 274 (1995): 301
  6. O'Dell JR, Zetterman RK, Burnett DA "Centrilobular hepatic fibrosis following acetaminophen-induced hepatic necrosis in an alcoholic." JAMA 255 (1986): 2636-7
  7. Kartsonis A, Reddy KR, Schiff ER "Alcohol, acetaminophen, and hepatic necrosis." Ann Intern Med 105 (1986): 138-9
  8. Seeff LB, Cuccherini BA, Zimmerman HJ, Adler E, Benjamin SB "Acetaminophen hepatotoxicity in alcoholics." Ann Intern Med 104 (1986): 399-404
  9. "Product Information. Tylenol (acetaminophen)." McNeil Pharmaceutical, Raritan, NJ.
  10. Prescott LF, Critchley JA "Drug interactions affecting analgesic toxicity." Am J Med 75 (1983): 113-6
  11. McClain CJ, Kromhout JP, Peterson FJ, Holtzman JL "Potentiation of acetaminophen hepatotoxicity by alcohol." JAMA 244 (1980): 251-3
View all 11 references
Major

Acetaminophen (Includes Durabac) ↔ Liver Disease

Severe Potential Hazard, High plausibility

Applies to: Liver Disease

Acetaminophen is primarily metabolized in the liver to inactive forms. However, small quantities are converted by minor pathways to metabolites that can cause hepatotoxicity or methemoglobinemia. Patients with hepatic impairment may be at increased risk of toxicity due to increased minor metabolic pathway activity. Likewise, chronic or overuse of acetaminophen can saturate the primary hepatic enzymes and lead to increased metabolism by minor pathways. Severe liver injury, including cases of acute liver failure resulting in liver transplant and death, has been reported in patients using acetaminophen. Therapy with acetaminophen should be administered cautiously in patients with hepatic insufficiency. Clinical monitoring of hepatic function is recommended. Instruct patients to avoid drinking alcohol while taking acetaminophen-containing medications. Patients should be warned not to exceed the maximum recommended total daily dosage of acetaminophen (4 g/day in adults and children 12 years of age or older), and to read all prescription and over-the-counter medication labels to ensure they are not taking multiple acetaminophen-containing products, or check with a healthcare professional if they are unsure.

References

  1. Gillette JR "An integrated approach to the study of chemically reactive metabolites of acetaminophen." Arch Intern Med 141 (1981): 375-9
  2. "Product Information. Tylenol (acetaminophen)." McNeil Pharmaceutical, Raritan, NJ.
  3. Arnman R, Olsson R "Elimination of paracetamol in chronic liver disease." Acta Hepatogastroenterol (Stuttg) 25 (1978): 283-6
  4. Forrest JA, Adriaenssens P, Finlayson ND, Prescott LF "Paracetamol metabolism in chronic liver disease." Eur J Clin Pharmacol 15 (1979): 427-31
  5. Clements JA, Critchley JA, Prescott LF "The role of sulphate conjugation in the metabolism and disposition of oral and intravenous paracetamol in man." Br J Clin Pharmacol 18 (1984): 481-5
  6. Venkataramanan R, Kalp K, Rabinovitch M, et al "Conjugative drug metabolism in liver transplant patients." Transplant Proc 21 (1989): 2455
View all 6 references
Major

Antihistamines (Includes Durabac) ↔ Anticholinergic Effects

Severe Potential Hazard, High plausibility

Applies to: Gastrointestinal Obstruction, Glaucoma/Intraocular Hypertension, Urinary Retention

Antihistamines often have anticholinergic activity, to which elderly patients are particularly sensitive. Therapy with antihistamines should be administered cautiously, if at all, in patients with preexisting conditions that are likely to be exacerbated by anticholinergic activity, such as urinary retention or obstruction; angle-closure glaucoma, untreated intraocular hypertension, or uncontrolled primary open-angle glaucoma; and gastrointestinal obstructive disorders. Conventional, first-generation antihistamines such as the ethanolamines (bromodiphenhydramine, carbinoxamine, clemastine, dimenhydrinate, diphenhydramine, doxylamine, phenyltoloxamine) tend to exhibit substantial anticholinergic effects. In contrast, the newer, relatively nonsedating antihistamines (e.g., cetirizine, fexofenadine, loratadine) reportedly have low to minimal anticholinergic activity at normally recommended dosages and may be appropriate alternatives.

References

  1. "Product Information. Tavist (clemastine)." Sandoz Pharmaceuticals Corporation, East Hanover, NJ.
  2. "Product Information. Optimine (azatadine)." Schering Laboratories, Kenilworth, NJ.
  3. "Product Information. Periactin (cyproheptadine)." Merck & Co, Inc, West Point, PA.
  4. "Product Information. Temaril (trimeprazine)" Allergan Inc, Irvine, CA.
  5. "Product Information. Marezine (cyclizine)." Glaxo Wellcome, Research Triangle Park, NC.
  6. "Product Information. Drixoral (dextromethorphan)." Schering-Plough, Liberty Corner, NJ.
  7. "Product Information. Semprex-D (acrivastine-pseudoephedrine)." Endo Laboratories LLC, Chadds Ford, PA.
  8. "Product Information. Poly-Histine-D (pyrilamine)." Bock Pharmaceutical Company, St. Louis, MO.
  9. Watemberg NM, Roth KS, Alehan FK, Epstein CE "Central anticholinergic syndrome on therapeutic doses of cyproheptadine." Pediatrics 103 (1999): 158-60
  10. "Product Information. Benadryl (diphenhydramine)." Parke-Davis, Morris Plains, NJ.
  11. "Product Information. Zyrtec (cetirizine)." Pfizer US Pharmaceuticals, New York, NY.
  12. "Product Information. Phenergan (promethazine)." Wyeth-Ayerst Laboratories, Philadelphia, PA.
  13. "Product Information. Dramamine (dimenhydrinate)" Pharmacia and Upjohn, Kalamazoo, MI.
  14. "Product Information. Dimetane (brompheniramine)." Wyeth-Ayerst Laboratories, Philadelphia, PA.
  15. "Product Information. Chlortrimeton (chlorpheniramine)." Schering-Plough, Liberty Corner, NJ.
  16. "Product Information. Tacaryl (methdilazine)." Westwood Squibb Pharmaceutical Corporation, Buffalo, NY.
  17. Schuller DE, Turkewitz D "Adverse effects of antihistamines." Postgrad Med 79 (1986): 75-86
  18. "Product Information. Vistaril (hydroxyzine)." Pfizer US Pharmaceuticals, New York, NY.
  19. DiPiro JT, Talbert RL, Yee GC, Matzke GR, Wells BG, Posey LM "Pharmacotherapy: A Pathophysiologic Approach 4th" Stamford, CT: Appleton & Lange (1999):
  20. "Product Information. Antivert (meclizine)." Roerig Division, New York, NY.
View all 20 references
Major

Antihistamines (Includes Durabac) ↔ Asthma/Copd

Severe Potential Hazard, Moderate plausibility

Applies to: Asthma, Chronic Obstructive Pulmonary Disease

It has been suggested that the anticholinergic effect of antihistamines may reduce the volume and cause thickening of bronchial secretions, resulting in obstruction of respiratory tract. Some manufacturers and clinicians recommend that therapy with antihistamines be administered cautiously in patients with asthma or chronic obstructive pulmonary disease.

References

  1. "Product Information. Temaril (trimeprazine)" Allergan Inc, Irvine, CA.
  2. "Product Information. Tavist (clemastine)." Sandoz Pharmaceuticals Corporation, East Hanover, NJ.
  3. "Product Information. Periactin (cyproheptadine)." Merck & Co, Inc, West Point, PA.
  4. "Product Information. Drixoral (dextromethorphan)." Schering-Plough, Liberty Corner, NJ.
  5. "Product Information. Benadryl (diphenhydramine)." Parke-Davis, Morris Plains, NJ.
  6. "Product Information. Marezine (cyclizine)." Glaxo Wellcome, Research Triangle Park, NC.
  7. "Product Information. Dramamine (dimenhydrinate)" Pharmacia and Upjohn, Kalamazoo, MI.
  8. Maddox DE, Reed CE "Clinical pharmacodynamics of antihistamines." Ann Allergy 59 (1987): 43-8
  9. "Product Information. Semprex-D (acrivastine-pseudoephedrine)." Endo Laboratories LLC, Chadds Ford, PA.
  10. "Product Information. Vistaril (hydroxyzine)." Pfizer US Pharmaceuticals, New York, NY.
  11. "Product Information. Poly-Histine-D (pyrilamine)." Bock Pharmaceutical Company, St. Louis, MO.
  12. "Product Information. Dimetane (brompheniramine)." Wyeth-Ayerst Laboratories, Philadelphia, PA.
  13. "Product Information. Tacaryl (methdilazine)." Westwood Squibb Pharmaceutical Corporation, Buffalo, NY.
  14. "Product Information. Phenergan (promethazine)." Wyeth-Ayerst Laboratories, Philadelphia, PA.
  15. "Product Information. Chlortrimeton (chlorpheniramine)." Schering-Plough, Liberty Corner, NJ.
  16. "Product Information. Optimine (azatadine)." Schering Laboratories, Kenilworth, NJ.
  17. "Product Information. Antivert (meclizine)." Roerig Division, New York, NY.
View all 17 references
Major

Cns Stimulants (Includes Durabac) ↔ Cardiac Disease

Severe Potential Hazard, Moderate plausibility

Applies to: Hypertension, Hyperthyroidism, Heart Disease, Pheochromocytoma, Peripheral Arterial Disease

The use of CNS stimulants is contraindicated in patients with significant cardiovascular impairment such as uncompensated heart failure, severe coronary disease, severe hypertension (including that associated with hyperthyroidism or pheochromocytoma), cardiac structural abnormalities, serious arrhythmias, etc. Sudden death has been reported in adults and children taking CNS stimulant treatment. Additionally, stroke, myocardial infarction, chest pain, syncope, arrhythmias and other symptoms have been reported in adults under treatment. A careful assessment of the cardiovascular status should be done in patients being considered for treatment. This includes family history, physical exam and further cardiac evaluation (EKG and echocardiogram). Patients who develop symptoms should have a detailed cardiac evaluation and if needed, treatment should be suspended.

References

  1. "Product Information. Dopram (doxapram)." West-Ward Pharmaceutical Corporation, Eatontown, NJ.
Major

Cns Stimulants (Includes Durabac) ↔ Hypertension

Severe Potential Hazard, Moderate plausibility

Applies to: Hypertension

CNS stimulant medications have shown to increase blood pressure and their use is contraindicated in patients with severe hypertension. Caution should be used when administering to patients with preexisting high blood pressure and other cardiovascular conditions. All patients under treatment should be regularly monitored for changes in blood pressure and heart rate.

References

  1. "Product Information. Dopram (doxapram)." West-Ward Pharmaceutical Corporation, Eatontown, NJ.
Major

Cns Stimulants (Includes Durabac) ↔ Liver Disease

Severe Potential Hazard, Moderate plausibility

Applies to: Liver Disease

In general, CNS stimulants are extensively metabolized by the liver. Their plasma clearance may be decreased and their half-life prolonged in patients with impaired hepatic function. Therapy with CNS stimulants should be administered cautiously in patients with moderate to severe liver disease, and the dosage should be adjusted accordingly. Additionally, postmarketing reports have shown that atomoxetine can cause severe liver injury. Laboratory testing should be done at the first sign or symptom of liver dysfunction (jaundice, dark urine, upper quadrant tenderness) and treatment should be discontinued in patients with evidence of liver injury.

References

  1. "Product Information. Provigil (modafinil)." Cephalon, Inc, West Chester, PA.
Major

Methylxanthines (Includes Durabac) ↔ Pud

Severe Potential Hazard, High plausibility

Applies to: Peptic Ulcer

Methylxanthines are known to stimulate peptic acid secretion. Therapy with products containing methylxanthines should be administered with extreme caution in patients with active peptic ulcer disease. Some manufacturers consider their use to be contraindicated under such circumstance.

References

  1. "Product Information. Theo-Dur (theophylline)." Schering Laboratories, Kenilworth, NJ.
  2. Stoller JL "Oesophageal ulceration and theophylline." Lancet 2 (1985): 328-9
  3. Alterman P, Spiegel D, Feldman J, Yaretzky A "Histamine h2-receptor antagonists and chronic theophylline toxicity." Am Fam Physician 54 (1996): 1473
  4. "Product Information. Lufyllin (dyphylline)" Wallace Laboratories, Cranbury, NJ.
View all 4 references
Major

Salicylates (Includes Durabac) ↔ Gi Toxicity

Severe Potential Hazard, High plausibility

Applies to: Duodenitis/Gastritis, Gastrointestinal Hemorrhage, Gastrointestinal Perforation, History - Peptic Ulcer, Peptic Ulcer, Alcoholism, Colitis/Enteritis (Noninfectious), Colonic Ulceration

Salicylates, particularly aspirin, can cause dose-related gastrointestinal bleeding and mucosal damage, which may occur independently of each other. Occult, often asymptomatic GI blood loss is quite common with usual dosages of aspirin and stems from the drug's local effect on the GI mucosa. During chronic therapy, this type of bleeding may occasionally produce iron deficiency anemia. In contrast, major upper GI bleeding rarely occurs except in patients with active peptic ulcers or recent GI bleeding. However, these patients generally do not experience greater occult blood loss than healthy patients following small doses of aspirin. Mucosal damage associated with the use of salicylates may lead to development of peptic ulcers with or without bleeding, reactivation of latent ulcers, and ulcer perforation. Therapy with salicylates and related agents such as salicylamide should be considered and administered cautiously in patients with a history of GI disease or alcoholism, particularly if they are elderly and/or debilitated, since such patients may be more susceptible to the GI toxicity of these drugs and seem to tolerate ulceration and bleeding less well than other individuals. Extreme caution and thorough assessment of risks and benefits are warranted in patients with active or recent GI bleeding or lesions. Whenever possible, especially if prolonged use is anticipated, treatment with non-ulcerogenic agents should be attempted first. If salicylates are used, close monitoring for toxicity is recommended. Some adverse GI effects may be minimized by administration with high dosages of antacids, use of enteric-coated or extended-release formulations, and/or concurrent use of a histamine H2-receptor antagonist or a cytoprotective agent such as misoprostol. Patients with active peptic ulceration or GI bleeding treated with salicylates should generally be administered a concomitant anti-ulcer regimen.

References

  1. Lanas A, Serrano P, Bajador E, Esteva F, Benito R, Sainz R "Evidence of aspirin use in both upper and lower gastrointestinal perforation." Gastroenterology 112 (1997): 683-9
  2. Savon JJ, Allen ML, Dimarino AJ, Hermann GA, Krum RP "Gastrointestinal blood loss with low dose (325 mg) plain and enteric-coated aspirin administration." Am J Gastroenterol 90 (1995): 581-5
  3. "Product Information. Salflex (salsalate)." Carnrick Laboratories Inc, Cedar Knolls, NJ.
  4. American Medical Association, Division of Drugs and Toxicology "Drug evaluations annual 1994." Chicago, IL: American Medical Association; (1994):
  5. Stalnikowiczdarvasi R "Gastrointestinal bleeding during low-dose aspirin administration for prevention of arterial occlusive events: a critical analysis." J Clin Gastroenterol 21 (1995): 13-6
  6. Marks RD "Aspirin use and fecal occult blood testing." Am J Med 100 (1996): 596-7
  7. Mehta S, Dasarathy S, Tandon RK, Mathur M, Malaviya AN "A prospective randomized study of the injurious effects of aspirin and naproxen on the gastroduodenal mucosa in patients with rheumatoid arthritis." Am J Gastroenterol 87 (1992): 996-1000
  8. Naschitz JE, Yeshurun D, Odeh M, Bassan H, Rosner I, Stermer E, Levy N "Overt gastrointestinal bleeding in the course of chronic low-dose aspirin administration for secondary prevention of arterial occlusive disease." Am J Gastroenterol 85 (1990): 408-11
  9. Bergmann JF, Chassany O, Geneve J, Abiteboul M, Caulin C, Segrestaa JM "Endoscopic evaluation of the effect of ketoprofen, ibuprofen and aspirin on the gastroduodenal mucosa." Eur J Clin Pharmacol 42 (1992): 685-8
  10. Weil J, Colinjones D, Langman M, Lawson D, Logan R, Murphy M, Rawlins M, Vessey M, Wainwright P "Prophylactic aspirin and risk of peptic ulcer bleeding." BMJ 310 (1995): 827-30
  11. "Product Information. Ecotrin (aspirin)." SmithKline Beecham, Philadelphia, PA.
  12. Graham DY, Smith JL "Aspirin and the stomach." Ann Intern Med 104 (1986): 390-8
  13. Roderick PJ, Wilkes HC, Meade TW "The gastrointestinal toxicity of aspirin: an overview of randomised controlled trials." Br J Clin Pharmacol 35 (1993): 219-26
  14. Wilcox CM, Shalek KA, Cotsonis G "Striking prevalence of over-the-counter nonsteroidal anti- inflammatory drug use in patients with upper gastrointestinal hemorrhage." Arch Intern Med 154 (1994): 42-6
  15. Prichard PJ, Kitchingman GK, Walt RP, Daneshmend TK, Hawkey CJ "Human gastric mucosal bleeding induced by low dose aspirin, but not warfarin." BMJ 298 (1989): 493-6
  16. Silagy CA, McNeil JJ, Donnan GA, Tonkin AM, Worsam B, Campion K "Adverse effects of low-dose aspirin in a healthy elderly population." Clin Pharmacol Ther 54 (1993): 84-9
  17. Sabesin SM, Boyce HW Jr, King CE, Mann JA, Ruoff G, Wall E "Comparative evaluation of gastrointestinal intolerance produced by plain and tri-buffered aspirin tablets." Am J Gastroenterol 83 (1988): 1220-5
  18. Greenberg PD, Cello JP, Rockey DC "Asymptomatic chronic gastrointestinal blood loss in patients taking aspirin or warfarin for cardiovascular disease." Am J Med 100 (1996): 598-604
  19. Levy M, Miller DR, Kaufman DW, Siskind V, Schwingl P, Rosenberg L, Strom B, Shapiro S "Major upper gastrointestinal tract bleeding. Relation to the use of aspirin and other nonnarcotic analgesics." Arch Intern Med 148 (1988): 281-5
View all 19 references
Major

Salicylates (Includes Durabac) ↔ Reye's Syndrome

Severe Potential Hazard, Moderate plausibility

Applies to: Varicella-Zoster, Influenza

The use of salicylates, primarily aspirin, in children with varicella infections or influenza-like illnesses has been associated with an increased risk of Reye's syndrome. Although a causal relationship has not been established, the majority of evidence to date seems to support the association. Most authorities, including the American Academy of Pediatrics Committee on Infectious Diseases, recommend avoiding the use of salicylates in children and teenagers with known or suspected varicella or influenza and during presumed outbreaks of influenza. If antipyretic or analgesic therapy is indicated under these circumstances, acetaminophen may be an appropriate alternative. The same precautions should also be observed with related agents such as salicylamide or diflunisal because of their structural and pharmacological similarities to salicylate.

References

  1. Belay ED, Bresee JS, Holman RC, Khan AS, Shahriari A, Schonberger LB "Reye's syndrome in the United States from 1981 through 1997." N Engl J Med 340 (1999): 1377-82
  2. "Product Information. Salflex (salsalate)." Carnrick Laboratories Inc, Cedar Knolls, NJ.
  3. "Product Information. Ecotrin (aspirin)." SmithKline Beecham, Philadelphia, PA.
  4. "Product Information. Rexolate (sodium thiosalicylate)" Hyrex Pharmaceuticals, Memphis, TN.
  5. American Academy of Pediatrics. Committee on Infectious Diseases; Peter G, ed. "Red BooK: Report of the Committee on Infectious Diseases. 24th" Grove Village, IL: American Academy of Pediatrics (1997):
  6. Hasking GJ, Duggan JM "Encephalopathy from bismuth subsalicylate." Med J Aust 2 (1982): 167
  7. Epidemiology Office, Divisiion of Viral and Rickettsial Diseasses, Center for Infectious Diseases, Centers for Disease Control. "Leads from the MMWR. Reye syndrome surveillance--United States, 1987 and 1988." JAMA 261 (1989): 3520,
  8. Behrman R, Kliegman R, Arvin A, Nelson W, eds. "Nelson Textbook of Pediatrics. 15th ed." Philadelphia, PA: W.B. Saunders Company (1996):
  9. "Product Information. Pepto-Bismol (bismuth subsalicylate)." Procter and Gamble Pharmaceuticals, Cincinnati, OH.
View all 9 references
Moderate

Acetaminophen (Includes Durabac) ↔ Pku

Moderate Potential Hazard, High plausibility

Applies to: Phenylketonuria

Several oral acetaminophen and acetaminophen-combination products, particularly flavored chewable tablets, contain the artificial sweetener, aspartame (NutraSweet). Aspartame is converted to phenylalanine in the gastrointestinal tract following ingestion. Chewable and effervescent formulations of acetaminophen products may also contain phenylalanine. The aspartame/phenylalanine content should be considered when these products are used in patients who must restrict their intake of phenylalanine (i.e. phenylketonurics).

References

  1. "Product Information. Tylenol (acetaminophen)." McNeil Pharmaceutical, Raritan, NJ.
Moderate

Antihistamines (Includes Durabac) ↔ Cardiovascular

Moderate Potential Hazard, Moderate plausibility

Applies to: Cardiovascular Disease, Hyperthyroidism, Hypotension

Antihistamines may infrequently cause cardiovascular adverse effects related to their anticholinergic and local anesthetic (quinidine-like) activities. Tachycardia, palpitation, ECG changes, arrhythmias, hypotension, and hypertension have been reported. Although these effects are uncommon and usually limited to overdosage situations, the manufacturers and some clinicians recommend that therapy with antihistamines be administered cautiously in patients with cardiovascular disease, hypertension, and/or hyperthyroidism.

References

  1. "Product Information. Dimetane (brompheniramine)." Wyeth-Ayerst Laboratories, Philadelphia, PA.
  2. "Product Information. Chlortrimeton (chlorpheniramine)." Schering-Plough, Liberty Corner, NJ.
  3. "Product Information. Optimine (azatadine)." Schering Laboratories, Kenilworth, NJ.
  4. "Product Information. Antivert (meclizine)." Roerig Division, New York, NY.
  5. "Product Information. Tavist (clemastine)." Sandoz Pharmaceuticals Corporation, East Hanover, NJ.
  6. "Product Information. Benadryl (diphenhydramine)." Parke-Davis, Morris Plains, NJ.
  7. "Product Information. Periactin (cyproheptadine)." Merck & Co, Inc, West Point, PA.
  8. "Product Information. Drixoral (dextromethorphan)." Schering-Plough, Liberty Corner, NJ.
  9. "Product Information. Zyrtec (cetirizine)." Pfizer US Pharmaceuticals, New York, NY.
  10. "Product Information. Dramamine (dimenhydrinate)" Pharmacia and Upjohn, Kalamazoo, MI.
  11. Smith SJ "Cardiovascular toxicity of antihistamines." Otolaryngol Head Neck Surg 111 Suppl (1994): 348-54
  12. Schuller DE, Turkewitz D "Adverse effects of antihistamines." Postgrad Med 79 (1986): 75-86
  13. "Product Information. Poly-Histine-D (pyrilamine)." Bock Pharmaceutical Company, St. Louis, MO.
  14. "Product Information. Vistaril (hydroxyzine)." Pfizer US Pharmaceuticals, New York, NY.
  15. Woosley RL "Cardiac actions of antihistamines." Annu Rev Pharmacol Toxicol 36 (1996): 233-52
View all 15 references
Moderate

Antihistamines (Includes Durabac) ↔ Renal/Liver Disease

Moderate Potential Hazard, High plausibility

Applies to: Liver Disease, Renal Dysfunction

Limited pharmacokinetic data are available for the older, first-generation antihistamines. Many appear to be primarily metabolized by the liver, and both parent drugs and metabolites are excreted in the urine. Patients with renal and/or liver disease may be at greater risk for adverse effects from antihistamines due to drug and metabolite accumulation. Therapy with antihistamines should be administered cautiously in such patients. Lower initial dosages may be appropriate.

References

  1. Paton DM, Webster DR "Clinical pharmacokinetics of H1-receptor antagonists (the antihistamines)." Clin Pharmacokinet 10 (1985): 477-97
  2. Blyden GT, Greenblatt DJ, Scavone JM, Shader RI "Pharmacokinetics of diphenhydramine and a demethylated metabolite following intravenous and oral administration." J Clin Pharmacol 26 (1986): 529-33
  3. Meredith CG, Christian CD Jr, Johnson RF, Madhavan SV, Schenker S "Diphenhydramine disposition in chronic liver disease." Clin Pharmacol Ther 35 (1984): 474-9
  4. Rumore MM "Clinical pharmacokinetics of chlorpheniramine." Drug Intell Clin Pharm 18 (1984): 701-7
  5. Bruce RB, Turnbull LB, Newman JH, Pitts JE "Metabolism of brompheniramine." J Med Chem 11 (1968): 1031-4
  6. Simons FE, Frith EM, Simons KJ "The pharmacokinetics and antihistaminic effects of brompheniramine." J Allergy Clin Immunol 70 (1982): 458-64
  7. Glazko AJ, Dill WA, Young RM, Smith TC, Ogilvie RI "Metabolic disposition of diphenhydramine." Clin Pharmacol Ther 16 (1974): 1066-76
  8. Albert KS, Hallmark MR, Sakmar E, Weidler DJ, Wagner JG "Pharmacokinetics of diphenhydramine in man." J Pharmacokinet Biopharm 3 (1975): 159-70
  9. Simons KJ, Simons FE, Luciuk GH, Frith EM "Urinary excretion of chlorpheniramine and its metabolites in children." J Pharm Sci 73 (1984): 595-9
  10. Simons FE, Simons KJ, Frith EM "The pharmacokinetics and antihistaminic of the H1 receptor antagonist hydroxyzine." J Allergy Clin Immunol 73 (1984): 69-75
  11. Simons FE, Watson WT, Chen XY, Minuk GY, Simons KJ "The pharmacokinetics and pharmacodynamics of hydroxyzine in patients with primary biliary cirrhosis." J Clin Pharmacol 29 (1989): 809-15
  12. Hintze KL, Wold JS, Fischer LJ "Disposition of cyproheptadine in rats, mice, and humans and identification of a stable epoxide metabolite." Drug Metab Dispos 3 (1975): 1-9
  13. Huang SM, Athanikar NK, Sridhar K, Huang YC, Chiou WL "Pharmacokinetics of chlorpheniramine after intravenous and oral administration in normal adults." Eur J Clin Pharmacol 22 (1982): 359-65
  14. Porter CC, Arison BH, Gruber VF, Titus DC, Vandenheuvel WJ "Human metabolism of cyproheptadine." Drug Metab Dispos 3 (1975): 189-97
  15. Maddox DE, Reed CE "Clinical pharmacodynamics of antihistamines." Ann Allergy 59 (1987): 43-8
View all 15 references
Moderate

Caffeine (Includes Durabac) ↔ Cardiotoxicity

Moderate Potential Hazard, Moderate plausibility

Applies to: Tachyarrhythmia, Myocardial Infarction, Post MI Syndrome, Hypertension, Hyperthyroidism, Angina Pectoris

Like other methylxanthines, caffeine at high dosages may be associated with positive inotropic and chronotropic effects on the heart. Caffeine may also produce an increase in systemic vascular resistance, resulting in elevation of blood pressure. Therapy with products containing caffeine should be administered cautiously in patients with severe cardiac disease, hypertension, hyperthyroidism, or acute myocardial injury. Some clinicians recommend avoiding caffeine in patients with symptomatic cardiac arrhythmias and/or palpitations and during the first several days to weeks after an acute myocardial infarction.

References

  1. "Multum Information Services, Inc. Expert Review Panel"
Moderate

Cns Stimulants (Includes Durabac) ↔ Psychiatric Disorders

Moderate Potential Hazard, Moderate plausibility

Applies to: Psychosis, Depression

The use of CNS stimulants can cause psychotic or maniac symptoms, suicidal ideation, aggression and can exacerbate symptoms of behavior disturbance and thought disorder. Psychiatric symptoms have been reported in patients with and without history of psychiatric disorders, and all patients should be monitored closely, specially during treatment initiation and at times of dose changes. Extreme caution should be exercised when CNS stimulants are given to patients with a history of psychosis, depression, mania, or bipolar disorder. All patients receiving treatment should be screened for bipolar disease prior to initiation. If any psychiatric symptoms emerge or are exacerbated, treatment suspension should be considered. CNS stimulants are contraindicated in patients with marked agitation or anxiety.

References

  1. "Product Information. Provigil (modafinil)." Cephalon, Inc, West Chester, PA.
Moderate

Cns Stimulants (Includes Durabac) ↔ Renal Dysfunction

Moderate Potential Hazard, Moderate plausibility

Applies to: Renal Dysfunction

Overall CNS stimulants should be administered with caution in patients with significantly impaired renal function as the reduction in the rate of elimination may alter the therapeutic response. The dosage should be adjusted accordingly.

References

  1. "Product Information. Provigil (modafinil)." Cephalon, Inc, West Chester, PA.
Moderate

Cns Stimulants (Includes Durabac) ↔ Seizure Disorders

Moderate Potential Hazard, Moderate plausibility

Applies to: Seizures

Due to general central nervous system stimulation, therapy with CNS stimulant drugs may cause seizures. These drugs may lower the convulsive threshold in patients with prior history of seizures or EEG abnormalities, and very rarely in patients with no previous history of seizures. Therapy with CNS stimulants should be used with caution in patients with or predisposed to seizures. If seizures appear, therapy should be discontinued.

References

  1. American Medical Association, Division of Drugs and Toxicology "Drug evaluations annual 1994." Chicago, IL: American Medical Association; (1994):
Moderate

Methylxanthines (Includes Durabac) ↔ Gerd

Moderate Potential Hazard, High plausibility

Applies to: Gastroesophageal Reflux Disease

Methylxanthines increase gastric acidity and may also relax lower esophageal sphincter, which can lead to gastric reflux into the esophagus. Therapy with products containing methylxanthines should be administered cautiously in patients with significant gastroesophageal reflux.

References

  1. American Medical Association, Division of Drugs and Toxicology "Drug evaluations annual 1994." Chicago, IL: American Medical Association; (1994):
  2. Stoller JL "Oesophageal ulceration and theophylline." Lancet 2 (1985): 328-9
  3. Alterman P, Spiegel D, Feldman J, Yaretzky A "Histamine h2-receptor antagonists and chronic theophylline toxicity." Am Fam Physician 54 (1996): 1473
  4. "Product Information. Lufyllin (dyphylline)" Wallace Laboratories, Cranbury, NJ.
View all 4 references
Moderate

Salicylates (Includes Durabac) ↔ Anemia

Moderate Potential Hazard, Moderate plausibility

Applies to: Anemia

Occult, often asymptomatic GI blood loss occurs quite frequently with the use of normal dosages of aspirin and stems from the drug's local effect on the GI mucosa. During chronic therapy, this type of bleeding may occasionally produce iron deficiency anemia. Other salicylates reportedly cause little or no GI blood loss at usual dosages, but may do so at high dosages. Prolonged therapy with salicylates, particularly aspirin, should be administered cautiously in patients with or predisposed to anemia. Periodic monitoring of hematocrit is recommended. The same precautions should also be observed with the use of related agents such as salicylamide because of their structural and pharmacological similarities to salicylate.

References

  1. Naschitz JE, Yeshurun D, Odeh M, Bassan H, Rosner I, Stermer E, Levy N "Overt gastrointestinal bleeding in the course of chronic low-dose aspirin administration for secondary prevention of arterial occlusive disease." Am J Gastroenterol 85 (1990): 408-11
  2. Savon JJ, Allen ML, Dimarino AJ, Hermann GA, Krum RP "Gastrointestinal blood loss with low dose (325 mg) plain and enteric-coated aspirin administration." Am J Gastroenterol 90 (1995): 581-5
  3. "Product Information. Salflex (salsalate)." Carnrick Laboratories Inc, Cedar Knolls, NJ.
  4. Stalnikowiczdarvasi R "Gastrointestinal bleeding during low-dose aspirin administration for prevention of arterial occlusive events: a critical analysis." J Clin Gastroenterol 21 (1995): 13-6
  5. Marks RD "Aspirin use and fecal occult blood testing." Am J Med 100 (1996): 596-7
  6. "Product Information. Ecotrin (aspirin)." SmithKline Beecham, Philadelphia, PA.
  7. Prichard PJ, Kitchingman GK, Walt RP, Daneshmend TK, Hawkey CJ "Human gastric mucosal bleeding induced by low dose aspirin, but not warfarin." BMJ 298 (1989): 493-6
  8. Greenberg PD, Cello JP, Rockey DC "Asymptomatic chronic gastrointestinal blood loss in patients taking aspirin or warfarin for cardiovascular disease." Am J Med 100 (1996): 598-604
View all 8 references
Moderate

Salicylates (Includes Durabac) ↔ Coagulation

Moderate Potential Hazard, Moderate plausibility

Applies to: Bleeding, Coagulation Defect, Thrombocytopathy, Thrombocytopenia, Vitamin K Deficiency

All salicylates can interfere with the action of vitamin K and induce a dose-dependent alteration in hepatic synthesis of coagulation factors VII, IX and X. At usual recommended dosages, a slight increase in prothrombin time (PT) may occur. Therapy with salicylates, especially if given in high dosages, should be administered cautiously in patients with significant active bleeding or a hemorrhagic diathesis, including hemostatic and/or coagulation defects associated with hemophilia, vitamin K deficiency, hypoprothombinemia, thrombocytopenia, thrombocytopathy, or severe hepatic impairment. The same precaution should also be observed with the use of related agents such as salicylamide because of their structural and pharmacological similarities to salicylate.

References

  1. Fausa O "Salicylate-induced hypoprothrombinemia: a report of four cases." Acta Med Scand 188 (1970): 403-8
  2. "Product Information. Pepto-Bismol (bismuth subsalicylate)." Procter and Gamble Pharmaceuticals, Cincinnati, OH.
  3. "Product Information. Salflex (salsalate)." Carnrick Laboratories Inc, Cedar Knolls, NJ.
  4. American Medical Association, Division of Drugs and Toxicology "Drug evaluations annual 1994." Chicago, IL: American Medical Association; (1994):
  5. Barrow MV, Quick DT, Cunningham RW "Salicylate hypoprothrombinemia in rheumatoid arthritis with liver disease. Report of two cases." Arch Intern Med 120 (1967): 620-4
View all 5 references
Moderate

Salicylates (Includes Durabac) ↔ G-6-Pd Deficiency

Moderate Potential Hazard, Low plausibility

Applies to: G-6-PD Deficiency

Salicylates, particularly aspirin, may cause or aggravate hemolysis in patients with pyruvate kinase or glucose-6-phosphate dehydrogenase (G-6-PD) deficiency. However, this effect has not been clearly established. Until more data are available, therapy with salicylates should be administered cautiously in patients with G-6-PD deficiency. The same precaution should also be observed with the use of related agents such as salicylamide because of their structural and pharmacological similarities to salicylate.

References

  1. "Product Information. Ecotrin (aspirin)." SmithKline Beecham, Philadelphia, PA.
  2. "Product Information. Rexolate (sodium thiosalicylate)" Hyrex Pharmaceuticals, Memphis, TN.
  3. "Product Information. Salflex (salsalate)." Carnrick Laboratories Inc, Cedar Knolls, NJ.
Moderate

Salicylates (Includes Durabac) ↔ Hepatotoxicity

Moderate Potential Hazard, Moderate plausibility

Applies to: Liver Disease

The use of salicylates has occasionally been associated with acute, reversible hepatotoxicity, primarily manifested as elevations of serum transaminases, alkaline phosphatase and/or, rarely, bilirubin. Hepatic injury consistent with chronic active hepatitis has also been reported in a few patients, which resulted rarely in encephalopathy or death. Salicylate-induced hepatotoxicity appears to be dependent on serum salicylate concentration (> 25 mg/dL) and has occurred most frequently in patients with juvenile arthritis, active systemic lupus erythematosus, rheumatic fever, or preexisting hepatic impairment. Therapy with salicylates, particularly when given in high dosages, should be administered cautiously in these patients, and periodic monitoring of liver function is recommended. The same precautions should also be observed with the use of related agents such as salicylamide because of their structural and pharmacological similarities to salicylate. A dosage reduction may be necessary if liver function abnormalities develop and serum salicylate concentration exceeds 25 mg/dL, although serum transaminase elevations may sometimes be transient and return to pretreatment values despite continued therapy without dosage adjustment.

References

  1. Wolfe JD, Metzger AL, Goldstein RC "Aspirin hepatitis." Ann Intern Med 80 (1974): 74-6
  2. "Product Information. Rexolate (sodium thiosalicylate)" Hyrex Pharmaceuticals, Memphis, TN.
  3. "Product Information. Salflex (salsalate)." Carnrick Laboratories Inc, Cedar Knolls, NJ.
  4. American Medical Association, Division of Drugs and Toxicology "Drug evaluations annual 1994." Chicago, IL: American Medical Association; (1994):
  5. Patel DK, Hesse A, Ogunbona A, Notarianni LJ, Bennett PN "Metabolism of aspirin after therapeutic and toxic doses." Hum Exp Toxicol 9 (1990): 131-6
  6. Jorup-Ronstrom C, Beermann B, Wahlin-Boll E, Melander A, Britton S "Reduction of paracetamol and aspirin metabolism during viral hepatitis." Clin Pharmacokinet 11 (1986): 250-6
  7. Seaman WE, Ishak KG, Plotz PH "Aspirin-induced hepatotoxicity in patients with systemic lupus erythematosus." Ann Intern Med 80 (1974): 1-8
  8. Sbarbaro JA, Bennett RM "Aspirin hepatotoxicity and disseminated intravascular coagulation." Ann Intern Med 86 (1977): 183-5
View all 8 references

Durabac (acetaminophen / caffeine / phenyltoloxamine / salicylamide) drug Interactions

There are 959 drug interactions with Durabac (acetaminophen / caffeine / phenyltoloxamine / salicylamide)

Durabac (acetaminophen / caffeine / phenyltoloxamine / salicylamide) alcohol/food Interactions

There are 6 alcohol/food interactions with Durabac (acetaminophen / caffeine / phenyltoloxamine / salicylamide)

Drug Interaction Classification

The classifications below are a general guideline only. It is difficult to determine the relevance of a particular drug interaction to any individual given the large number of variables.
Major Highly clinically significant. Avoid combinations; the risk of the interaction outweighs the benefit.
Moderate Moderately clinically significant. Usually avoid combinations; use it only under special circumstances.
Minor Minimally clinically significant. Minimize risk; assess risk and consider an alternative drug, take steps to circumvent the interaction risk and/or institute a monitoring plan.
Unknown No information available.

Do not stop taking any medications without consulting your healthcare provider.

Further information

Always consult your healthcare provider to ensure the information displayed on this page applies to your personal circumstances.

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