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Interactions between Cafatine and Viloxazine

2 drug interactions and 35 additional warnings found for the following 2 drugs:

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Drug interactions

Moderate drug interactions

Moderate:

ergotamine viloxazine

Applies to: Cafatine (caffeine / ergotamine) and viloxazine
Monitor

Coadministration with inhibitors of CYP450 3A4 may increase the plasma concentrations of ergot derivatives, which are primarily metabolized by the isoenzyme. The interaction has occurred in patients receiving ergotamine or dihydroergotamine with potent CYP450 3A4 inhibitors such as macrolide antibiotics and protease inhibitors. Clinical ergotism has been reported, which can lead to gangrene and myocardial infarction in severe cases. Even small, single doses of ergotamine have resulted in clinically significant interactions, occasionally resulting in surgical amputation or death. No data are available for other, less potent CYP450 3A4 inhibitors.

Management

Caution is advised during concomitant use of ergot derivatives with mild or moderate CYP450 3A4 inhibitors. Patients should be monitored for potential ergot toxicity including peripheral vasospasm, ischemia, thrombosis, tachycardia, and hypertension.

References (25)
  1. Leroy F, Asseman P, Pruvost P, Adnet P, Lacroix D, Thery C (1988) "Dihydroergotamine-erythromycin-induced ergotism." Ann Intern Med, 109, p. 249
  2. Matthews NT, Havill JH (1979) "Ergotism with therapeutic doses of ergotamine tartrate." N Z Med J, 89, p. 476-7
  3. Francis H, Tyndall A, Webb J (1984) "Severe vascular spasm due to erythromycin-ergotamine interaction." Clin Rheumatol, 3, p. 243-6
  4. Hayton AC (1969) "Precipitation of acute ergotism by triacetyloleandomycin." N Z Med J, 69, p. 42
  5. (2002) "Product Information. D.H.E. 45 (dihydroergotamine)." Sandoz Pharmaceuticals Corporation
  6. Ghali R, De Lean J, Douville Y, Noel HP, Labbe R (1993) "Erythromycin-associated ergotamine intoxication: arteriographic and electrophysiologic analysis of a rare cause of severe ischemia of the lower extremities and associated ischemic neuropathy." Ann Vasc Surg, 7, p. 291-6
  7. Horowitz RS, Dart RC, Gomez HF (1996) "Clinical ergotism with lingual ischemia induced by clarithromycin-ergotamine interaction." Arch Intern Med, 156, p. 456-8
  8. (2001) "Product Information. Migranal (dihydroergotamine nasal)." Novartis Pharmaceuticals
  9. Rosenthal E, Sala F, Chichmanian RM, Batt M, Cassuto JP (1999) "Ergotism related to concurrent administration of ergotamine tartrate and indinavir." JAMA, 281, p. 987
  10. Liaudet L, Buclin T, Jaccard C, Eckert P (1999) "Severe ergotism associated with interaction between ritonavir and ergotamine." Br Med J, 318, p. 771
  11. Caballero-Granado FJ, Viciana P, Cordero E, Gomez-Vera MJ, del Nozal M, Lopez-Cortes LF (1997) "Ergotism related to concurrent administration of ergotamine tartrate and ritonavir in an AIDS patient." Antimicrob Agents Chemother, 41, p. 1207
  12. Dresser GK, Spence JD, Bailey DG (2000) "Pharmacokinetic-pharmacodynamic consequences and clinical relevance of cytochrome P450 3A4 inhibition." Clin Pharmacokinet, 38, p. 41-57
  13. Bird PA, Sturgess AD (2000) "Clinical ergotism with severe bilateral upper limb ischaemia precipitated by an erythromycin - ergotamine drug interaction." Aust N Z J Med, 30, p. 635-6
  14. Eadie MJ (2001) "Clinically significant drug interactions with agents specific for migraine attacks." Cns Drugs, 15, p. 105-18
  15. Spiegel M, Schmidauer C, Kampfl A, Sarcletti M, Poewe W (2001) "Cerebral ergotism under treatment with ergotamine and ritonavir." Neurology, 57, p. 743-4
  16. Vila A, Mykietiuk A, Bonvehi P, Temporiti E, Uruena A, Herrera F (2001) "Clinical ergotism induced by ritonavir." Scand J Infect Dis, 33, p. 788-9
  17. Montero A, Giovannoni AG, Tvrde PL (1999) "Leg ischemia in a patient receiving ritonavir and ergotamine." Ann Intern Med, 130, p. 329
  18. Liaudet L (1999) "Severe ergotism associated with interaction between ritonavir and ergotamine." BMJ, 318, p. 771
  19. Mortier E, Pouchet J, Vinceneux P, Lalande M (2001) "Ergotism related to interaction between nelfinavir and ergotamine." Am J Med, 110, p. 594
  20. Blanche P, Rigolet A, Gombert B, Ginsburg C, Salmon D, Sicard D (1999) "Ergotism related to a single dose of ergotamine tartrate in an AIDS patient treated with ritonavir." Postgrad Med J, 75, p. 546-7
  21. Ausband SC, Goodman PE (2001) "An unusual case of clarithromycin associated ergotism." J Emerg Med, 4, p. 411-3
  22. Baldwin ZK, Ceraldi CC (2003) "Ergotism associated with HIV antiviral protease inhibitor therapy." J Vasc Surg, 37, p. 676-8
  23. Tribble MA, Gregg CR, Margolis DM, Amirkhan R, Smith JW (2002) "Fatal ergotism induced by an HIV protease inhibitor." Headache, 42, p. 694-5
  24. (2004) "Product Information. Cafergot (caffeine-ergotamine)." Novartis Pharmaceuticals
  25. Srisuma S, Lavonas EJ, Wananukul W (2014) "Ergotism and factitious hypotension associated with interaction of ergotamine with CYP3A4 inhibitors." Clin Toxicol (Phila), p. 1-4
Moderate:

caffeine viloxazine

Applies to: Cafatine (caffeine / ergotamine) and viloxazine
Monitor

Coadministration with potent CYP450 1A2 inhibitors such as fluvoxamine may increase the plasma concentrations of caffeine in a dose-dependent manner. Caffeine is primarily metabolized by CYP450 1A2 and is considered a probe substrate for the isoenzyme. In 12 healthy volunteers, pretreatment with fluvoxamine for 7 days (10 mg once or twice a day) resulted in a 2-fold increase in the mean 24-hour area under the plasma concentration-time curve (AUC) of a single 100 mg oral dose of caffeine. When the dosage of fluvoxamine was increased (25 mg once or twice a day for 7 days), the mean 24-hour AUC of single-dose caffeine increased 5-fold. The peak plasma concentration (Cmax) of caffeine increased 40% and 141%, respectively, during these treatment phases. Another study found that fluvoxamine (50 mg daily for 4 days, then 100 mg daily for 8 days) decreased the median total clearance of a single 200 mg oral dose of caffeine by 80% and increased the half-life from 5 to 31 hours in eight healthy volunteers.

Management

Caution is advised if caffeine is administered concurrently with potent CYP450 1A2 inhibitors. Dosage adjustment should be considered in patients who experience excessive adverse effects of caffeine such as nausea, vomiting, headache, nervousness, irritability, agitation, restlessness, insomnia, tinnitus, tremors, and tachycardia.

References (3)
  1. Brosen K, Skjelbo E, Rasmussen BB, Poulsen HE, Loft S (1993) "Fluvoxamine is a potent inhibitor of cytochrome P4501A2." Biochem Pharmacol, 45, p. 1211-4
  2. Jeppesen U, Loft S, Poulsen HE, Brosen K (1996) "A fluvoxamine-caffeine interaction study." Pharmacogenetics, 6, p. 213-22
  3. Christensen M, Tybring G, Mihara K, et al. (2002) "Low daily 10-mg and 20-mg doses of fluvoxamine inhibit the metabolism of both caffeine (cytochrome P4501A2) and omeprazole (cytochrome P4502C19)." Clin Pharmacol Ther, 71, p. 141-52

Food/lifestyle interactions

Moderate food/lifestyle interactions

Moderate:

ergotamine Food/Lifestyle

Applies to: Cafatine (caffeine / ergotamine)
Monitor

Grapefruit or grapefruit juice may increase the plasma concentrations of orally administered drugs that are substrates of the CYP450 3A4 isoenzyme. The proposed mechanism is inhibition of CYP450 3A4-mediated first-pass metabolism in the gut wall by certain compounds present in grapefruit. Because grapefruit juice inhibits primarily intestinal rather than hepatic CYP450 3A4, the magnitude of interaction is greatest for those drugs that undergo significant presystemic metabolism by CYP450 3A4 (i.e., drugs with low oral bioavailability). In general, the effect of grapefruit juice is concentration-, dose- and preparation-dependent, and can vary widely among brands. Certain preparations of grapefruit juice (e.g., high dose, double strength) have sometimes demonstrated potent inhibition of CYP450 3A4, while other preparations (e.g., low dose, single strength) have typically demonstrated moderate inhibition. Pharmacokinetic interactions involving grapefruit juice are also subject to a high degree of interpatient variability, thus the extent to which a given patient may be affected is difficult to predict.

Management

Patients who regularly consume grapefruit or grapefruit juice should be monitored for adverse effects and altered plasma concentrations of drugs that undergo significant presystemic metabolism by CYP450 3A4. Grapefruit and grapefruit juice should be avoided if an interaction is suspected. Orange juice is not expected to interact with these drugs.

References (32)
  1. Edgar B, Bailey D, Bergstrand R, et al. (1992) "Acute effects of drinking grapefruit juice on the pharmacokinetics and dynamics on felodipine and its potential clinical relevance." Eur J Clin Pharmacol, 42, p. 313-7
  2. Jonkman JH, Sollie FA, Sauter R, Steinijans VW (1991) "The influence of caffeine on the steady-state pharmacokinetics of theophylline." Clin Pharmacol Ther, 49, p. 248-55
  3. Bailey DG, Arnold JM, Munoz C, Spence JD (1993) "Grapefruit juice--felodipine interaction: mechanism, predictability, and effect of naringin." Clin Pharmacol Ther, 53, p. 637-42
  4. Bailey DG, Arnold JMO, Spence JD (1994) "Grapefruit juice and drugs - how significant is the interaction." Clin Pharmacokinet, 26, p. 91-8
  5. Sigusch H, Hippius M, Henschel L, Kaufmann K, Hoffmann A (1994) "Influence of grapefruit juice on the pharmacokinetics of a slow release nifedipine formulation." Pharmazie, 49, p. 522-4
  6. Bailey DG, Arnold JM, Strong HA, Munoz C, Spence JD (1993) "Effect of grapefruit juice and naringin on nisoldipine pharmacokinetics." Clin Pharmacol Ther, 54, p. 589-94
  7. Yamreudeewong W, Henann NE, Fazio A, Lower DL, Cassidy TG (1995) "Drug-food interactions in clinical practice." J Fam Pract, 40, p. 376-84
  8. (1995) "Grapefruit juice interactions with drugs." Med Lett Drugs Ther, 37, p. 73-4
  9. Hukkinen SK, Varhe A, Olkkola KT, Neuvonen PJ (1995) "Plasma concentrations of triazolam are increased by concomitant ingestion of grapefruit juice." Clin Pharmacol Ther, 58, p. 127-31
  10. Min DI, Ku YM, Geraets DR, Lee HC (1996) "Effect of grapefruit juice on the pharmacokinetics and pharmacodynamics of quinidine in healthy volunteers." J Clin Pharmacol, 36, p. 469-76
  11. Majeed A, Kareem A (1996) "Effect of grapefruit juice on cyclosporine pharmacokinetics." Pediatr Nephrol, 10, p. 395
  12. Clifford CP, Adams DA, Murray S, Taylor GW, Wilkins MR, Boobis AR, Davies DS (1996) "Pharmacokinetic and cardiac effects of terfenadine after inhibition of its metabolism by grapefruit juice." Br J Clin Pharmacol, 42, p662
  13. Josefsson M, Zackrisson AL, Ahlner J (1996) "Effect of grapefruit juice on the pharmacokinetics of amlodipine in healthy volunteers." Eur J Clin Pharmacol, 51, p. 189-93
  14. Kantola T, Kivisto KT, Neuvonen PJ (1998) "Grapefruit juice greatly increases serum concentrations of lovastatin and lovastatin acid." Clin Pharmacol Ther, 63, p. 397-402
  15. Ozdemir M, Aktan Y, Boydag BS, Cingi MI, Musmul A (1998) "Interaction between grapefruit juice and diazepam in humans." Eur J Drug Metab Pharmacokinet, 23, p. 55-9
  16. Bailey DG, Malcolm J, Arnold O, Spence JD (1998) "Grapefruit juice-drug interactions." Br J Clin Pharmacol, 46, p. 101-10
  17. Bailey DG, Kreeft JH, Munoz C, Freeman DJ, Bend JR (1998) "Grapefruit juice felodipine interaction: Effect of naringin and 6',7'-dihydroxybergamottin in humans." Clin Pharmacol Ther, 64, p. 248-56
  18. Garg SK, Kumar N, Bhargava VK, Prabhakar SK (1998) "Effect of grapefruit juice on carbamazepine bioavailability in patients with epilepsy." Clin Pharmacol Ther, 64, p. 286-8
  19. Lilja JJ, Kivisto KT, Neuvonen PJ (1998) "Grapefruit juice-simvastatin interaction: Effect on serum concentrations of simvastatin, simvastatin acid, and HMG-CoA reductase inhibitors." Clin Pharmacol Ther, 64, p. 477-83
  20. Fuhr U, Maier-Bruggemann A, Blume H, et al. (1998) "Grapefruit juice increases oral nimodipine bioavailability." Int J Clin Pharmacol Ther, 36, p. 126-32
  21. Lilja JJ, Kivisto KT, Neuvonen PJ (1999) "Grapefruit juice increases serum concentrations of atorvastatin and has no effect on pravastatin." Clin Pharmacol Ther, 66, p. 118-27
  22. Eagling VA, Profit L, Back DJ (1999) "Inhibition of the CYP3A4-mediated metabolism and P-glycoprotein-mediated transport of the HIV-I protease inhibitor saquinavir by grapefruit juice components." Br J Clin Pharmacol, 48, p. 543-52
  23. Damkier P, Hansen LL, Brosen K (1999) "Effect of diclofenac, disulfiram, itraconazole, grapefruit juice and erythromycin on the pharmacokinetics of quinidine." Br J Clin Pharmacol, 48, p. 829-38
  24. Lee AJ, Chan WK, Harralson AF, Buffum J, Bui BCC (1999) "The effects of grapefruit juice on sertraline metabolism: An in vitro and in vivo study." Clin Ther, 21, p. 1890-9
  25. Dresser GK, Spence JD, Bailey DG (2000) "Pharmacokinetic-pharmacodynamic consequences and clinical relevance of cytochrome P450 3A4 inhibition." Clin Pharmacokinet, 38, p. 41-57
  26. Gunston GD, Mehta U (2000) "Potentially serious drug interactions with grapefruit juice." S Afr Med J, 90, p. 41
  27. Takanaga H, Ohnishi A, Maatsuo H, et al. (2000) "Pharmacokinetic analysis of felodipine-grapefruit juice interaction based on an irreversible enzyme inhibition model." Br J Clin Pharmacol, 49, p. 49-58
  28. Libersa CC, Brique SA, Motte KB, et al. (2000) "Dramatic inhibition of amiodarone metabolism induced by grapefruit juice." Br J Clin Pharmacol, 49, p. 373-8
  29. Bailey DG, Dresser GR, Kreeft JH, Munoz C, Freeman DJ, Bend JR (2000) "Grapefruit-felodipine interaction: Effect of unprocessed fruit and probable active ingredients." Clin Pharmacol Ther, 68, p. 468-77
  30. Zaidenstein R, Soback S, Gips M, Avni B, Dishi V, Weissgarten Y, Golik A, Scapa E (2001) "Effect of grapefruit juice on the pharmacokinetics of losartan and its active metabolite E3174 in healthy volunteers." Ther Drug Monit, 23, p. 369-73
  31. Sato J, Nakata H, Owada E, Kikuta T, Umetsu M, Ito K (1993) "Influence of usual intake of dietary caffeine on single-dose kinetics of theophylline in healthy human subjects." Eur J Clin Pharmacol, 44, p. 295-8
  32. Flanagan D (2005) "Understanding the grapefruit-drug interaction." Gen Dent, 53, 282-5; quiz 286
Moderate:

ergotamine Nicotine

Applies to: Cafatine (caffeine / ergotamine)
Monitor

Nicotine may cause vasoconstriction in some patients and potentiate the ischemic response to ergot alkaloids.

Management

Caution may be advisable when ergot alkaloids are used in combination with nicotine products. Patients should be advised to seek immediate medical attention if they experience potential symptoms of ischemia such as coldness, pallor, cyanosis, numbness, tingling, or pain in the extremities; muscle weakness; severe or worsening headache; visual disturbances; severe abdominal pain; chest pain; and shortness of breath.

References (4)
  1. (2001) "Product Information. Migranal (dihydroergotamine nasal)." Novartis Pharmaceuticals
  2. (2004) "Product Information. Cafergot (caffeine-ergotamine)." Novartis Pharmaceuticals
  3. Cerner Multum, Inc. "UK Summary of Product Characteristics."
  4. Cerner Multum, Inc. "Australian Product Information."

Minor food/lifestyle interactions

Minor:

caffeine Food/Lifestyle

Applies to: Cafatine (caffeine / ergotamine)

The effect of grapefruit juice on the pharmacologic activity of caffeine is controversial. One report suggests that grapefruit juice increases the effect of caffeine. The proposed mechanism is inhibition of cytochrome P-450 metabolism of caffeine. However, a well-conducted pharmacokinetic/pharmacodynamic study did not demonstrate this effect. The clinical significance of this potential interaction is unknown.

References (2)
  1. (1995) "Grapefruit juice interactions with drugs." Med Lett Drugs Ther, 37, p. 73-4
  2. Maish WA, Hampton EM, Whitsett TL, Shepard JD, Lovallo WR (1996) "Influence of grapefruit juice on caffeine pharmacokinetics and pharmacodynamics." Pharmacotherapy, 16, p. 1046-52

Disease interactions

32 potential interactions Applies to: 21 conditions, including High Blood Pressure, Depression, GERD, Bipolar Disorder, and Heart Attack.

Angina

Moderate:

Cafatine

The caffeine in Cafatine has a moderate potential interaction with Angina.

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.

Bipolar Disorder

Moderate:

viloxazine

Viloxazine has a moderate potential interaction with Bipolar Disorder.

All antidepressants may occasionally cause mania or hypomania, particularly in patients with bipolar disorder. Therapy with antidepressants should be administered cautiously in patients with a history of mania/hypomania.

Depression

Major:

Cafatine

The caffeine in Cafatine has a major potential interaction with Depression.

The use of CNS stimulants can cause psychotic symptoms, suicidal ideation, and aggression, and can exacerbate symptoms of behavior disturbance and thought disorder; CNS stimulants may induce a manic or mixed episode in patients with bipolar disorder. Psychiatric symptoms have been reported in patients with and without history of psychiatric disorders. All patients (particularly those with psychotic or bipolar disorders) should be monitored closely, especially 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. Prior to initiating therapy, all patients should be screened for risk factors for developing a manic episode (e.g., comorbid or history of depressive symptoms or family history of suicide, bipolar disease, or depression). If any psychiatric symptoms emerge or are exacerbated, treatment suspension should be considered. Some CNS stimulants are contraindicated in patients with marked agitation or anxiety.

Major:

viloxazine

Viloxazine has a major potential interaction with Depression.

Patients being treated with viloxazine should be monitored for clinical worsening and emergence of suicidal thoughts and behaviors. In clinical trials, higher rates of suicidal thoughts and behavior were reported in patients with attention deficit hyperactivity disorder (ADHD) receiving this drug than placebo. Prior to initiating treatment, patients should be screened for a personal or family history of suicide, bipolar disorder, and depression.

GERD

Moderate:

Cafatine

The caffeine in Cafatine has a moderate potential interaction with GERD.

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.

Heart Attack

Moderate:

Cafatine

The caffeine in Cafatine has a moderate potential interaction with Heart Attack.

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.

Heart Disease

Major:

Cafatine

The caffeine in Cafatine has a major potential interaction with Heart Disease.

Many CNS stimulants are 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 patients with structural cardiac abnormalities or other serious cardiac disease who are treated with CNS stimulants at the recommended dosages for attention deficit hyperactivity disorder; use of these agents should be avoided in patients with known structural cardiac abnormalities, cardiomyopathy, serious cardiac arrhythmia, coronary artery disease, or other serious cardiac disease. 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.

High Blood Pressure

Major:

Cafatine

The ergotamine in Cafatine has a major potential interaction with High Blood Pressure.

The use of ergot alkaloids is contraindicated in patients with conditions predisposing them to vasospastic reactions, including, ischemic heart disease (angina, history of myocardial infarction, silent ischemia), peripheral vascular disease, sepsis, shock, vascular surgery, uncontrolled hypertension, and severely impaired hepatic or renal function. The vasoconstriction produced be ergot alkaloids may exacerbate these conditions. Ergot alkaloids may cause vasospastic reactions other than coronary artery vasospasm such as peripheral vascular reactions, and colonic ischemia, causing muscle pains, numbness, coldness, pallor, and cyanosis of the digits. In patients with compromised circulation, persistent vasospasm may result in gangrene or death. Nitroprusside and heparin have been used to treat ergotamine- induced severe vasoconstriction.

Major:

Cafatine

The caffeine in Cafatine has a major potential interaction with High Blood Pressure.

CNS stimulants increase blood pressure and heart rate; the use of some agents may be contraindicated in patients with severe/uncontrolled hypertension. Caution should be used when administering to patients with preexisting high blood pressure (even mild hypertension) and other cardiovascular conditions. All patients under treatment should be regularly monitored for potential tachycardia and hypertension.

Major:

Cafatine

The caffeine in Cafatine has a major potential interaction with High Blood Pressure.

Many CNS stimulants are 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 patients with structural cardiac abnormalities or other serious cardiac disease who are treated with CNS stimulants at the recommended dosages for attention deficit hyperactivity disorder; use of these agents should be avoided in patients with known structural cardiac abnormalities, cardiomyopathy, serious cardiac arrhythmia, coronary artery disease, or other serious cardiac disease. 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.

Moderate:

Cafatine

The caffeine in Cafatine has a moderate potential interaction with High Blood Pressure.

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.

Hyperthyroidism

Major:

Cafatine

The caffeine in Cafatine has a major potential interaction with Hyperthyroidism.

Many CNS stimulants are 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 patients with structural cardiac abnormalities or other serious cardiac disease who are treated with CNS stimulants at the recommended dosages for attention deficit hyperactivity disorder; use of these agents should be avoided in patients with known structural cardiac abnormalities, cardiomyopathy, serious cardiac arrhythmia, coronary artery disease, or other serious cardiac disease. 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.

Moderate:

Cafatine

The caffeine in Cafatine has a moderate potential interaction with Hyperthyroidism.

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.

Ischemic Heart Disease

Major:

Cafatine

The ergotamine in Cafatine has a major potential interaction with Ischemic Heart Disease.

The use of ergot alkaloids is contraindicated in patients with conditions predisposing them to vasospastic reactions, including, ischemic heart disease (angina, history of myocardial infarction, silent ischemia), peripheral vascular disease, sepsis, shock, vascular surgery, uncontrolled hypertension, and severely impaired hepatic or renal function. The vasoconstriction produced be ergot alkaloids may exacerbate these conditions. Ergot alkaloids may cause vasospastic reactions other than coronary artery vasospasm such as peripheral vascular reactions, and colonic ischemia, causing muscle pains, numbness, coldness, pallor, and cyanosis of the digits. In patients with compromised circulation, persistent vasospasm may result in gangrene or death. Nitroprusside and heparin have been used to treat ergotamine- induced severe vasoconstriction.

Liver Disease

Major:

Cafatine

The ergotamine in Cafatine has a major potential interaction with Liver Disease.

The use of ergot alkaloids is contraindicated in patients with conditions predisposing them to vasospastic reactions, including, ischemic heart disease (angina, history of myocardial infarction, silent ischemia), peripheral vascular disease, sepsis, shock, vascular surgery, uncontrolled hypertension, and severely impaired hepatic or renal function. The vasoconstriction produced be ergot alkaloids may exacerbate these conditions. Ergot alkaloids may cause vasospastic reactions other than coronary artery vasospasm such as peripheral vascular reactions, and colonic ischemia, causing muscle pains, numbness, coldness, pallor, and cyanosis of the digits. In patients with compromised circulation, persistent vasospasm may result in gangrene or death. Nitroprusside and heparin have been used to treat ergotamine- induced severe vasoconstriction.

Moderate:

Cafatine

The caffeine in Cafatine has a moderate potential interaction with 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 in certain agents. Additionally, postmarketing reports have shown that atomoxetine can cause severe liver injury; laboratory testing should be done at the first sign/symptom of liver dysfunction (jaundice, dark urine, upper quadrant tenderness) and treatment should be discontinued in patients with evidence of liver injury.

Moderate:

viloxazine

Viloxazine has a moderate potential interaction with Liver Disease.

The effect of hepatic impairment on the pharmacokinetics of viloxazine is unknown.

Mania

Moderate:

viloxazine

Viloxazine has a moderate potential interaction with Mania.

All antidepressants may occasionally cause mania or hypomania, particularly in patients with bipolar disorder. Therapy with antidepressants should be administered cautiously in patients with a history of mania/hypomania.

Peptic Ulcer

Major:

Cafatine

The caffeine in Cafatine has a major potential interaction with 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.

Peripheral Arterial Disease

Major:

Cafatine

The ergotamine in Cafatine has a major potential interaction with Peripheral Arterial Disease.

The use of ergot alkaloids is contraindicated in patients with conditions predisposing them to vasospastic reactions, including, ischemic heart disease (angina, history of myocardial infarction, silent ischemia), peripheral vascular disease, sepsis, shock, vascular surgery, uncontrolled hypertension, and severely impaired hepatic or renal function. The vasoconstriction produced be ergot alkaloids may exacerbate these conditions. Ergot alkaloids may cause vasospastic reactions other than coronary artery vasospasm such as peripheral vascular reactions, and colonic ischemia, causing muscle pains, numbness, coldness, pallor, and cyanosis of the digits. In patients with compromised circulation, persistent vasospasm may result in gangrene or death. Nitroprusside and heparin have been used to treat ergotamine- induced severe vasoconstriction.

Major:

Cafatine

The caffeine in Cafatine has a major potential interaction with Peripheral Arterial Disease.

Many CNS stimulants are 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 patients with structural cardiac abnormalities or other serious cardiac disease who are treated with CNS stimulants at the recommended dosages for attention deficit hyperactivity disorder; use of these agents should be avoided in patients with known structural cardiac abnormalities, cardiomyopathy, serious cardiac arrhythmia, coronary artery disease, or other serious cardiac disease. 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.

Pheochromocytoma

Major:

Cafatine

The caffeine in Cafatine has a major potential interaction with Pheochromocytoma.

Many CNS stimulants are 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 patients with structural cardiac abnormalities or other serious cardiac disease who are treated with CNS stimulants at the recommended dosages for attention deficit hyperactivity disorder; use of these agents should be avoided in patients with known structural cardiac abnormalities, cardiomyopathy, serious cardiac arrhythmia, coronary artery disease, or other serious cardiac disease. 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.

Post MI Syndrome

Moderate:

Cafatine

The caffeine in Cafatine has a moderate potential interaction with Post MI Syndrome.

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.

Psychosis

Major:

Cafatine

The caffeine in Cafatine has a major potential interaction with Psychosis.

The use of CNS stimulants can cause psychotic symptoms, suicidal ideation, and aggression, and can exacerbate symptoms of behavior disturbance and thought disorder; CNS stimulants may induce a manic or mixed episode in patients with bipolar disorder. Psychiatric symptoms have been reported in patients with and without history of psychiatric disorders. All patients (particularly those with psychotic or bipolar disorders) should be monitored closely, especially 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. Prior to initiating therapy, all patients should be screened for risk factors for developing a manic episode (e.g., comorbid or history of depressive symptoms or family history of suicide, bipolar disease, or depression). If any psychiatric symptoms emerge or are exacerbated, treatment suspension should be considered. Some CNS stimulants are contraindicated in patients with marked agitation or anxiety.

Renal Dysfunction

Major:

Cafatine

The ergotamine in Cafatine has a major potential interaction with Renal Dysfunction.

The use of ergot alkaloids is contraindicated in patients with conditions predisposing them to vasospastic reactions, including, ischemic heart disease (angina, history of myocardial infarction, silent ischemia), peripheral vascular disease, sepsis, shock, vascular surgery, uncontrolled hypertension, and severely impaired hepatic or renal function. The vasoconstriction produced be ergot alkaloids may exacerbate these conditions. Ergot alkaloids may cause vasospastic reactions other than coronary artery vasospasm such as peripheral vascular reactions, and colonic ischemia, causing muscle pains, numbness, coldness, pallor, and cyanosis of the digits. In patients with compromised circulation, persistent vasospasm may result in gangrene or death. Nitroprusside and heparin have been used to treat ergotamine- induced severe vasoconstriction.

Moderate:

Cafatine

The caffeine in Cafatine has a moderate potential interaction with 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 in certain agents.

Moderate:

viloxazine

Viloxazine has a moderate potential interaction with Renal Dysfunction.

The exposure of viloxazine increases in patients with renal impairment. Dose reduction is recommended in patients with severe renal impairment (estimated glomerular filtration rate less than 30 mL/min/1.73 m3).

Seizures

Moderate:

Cafatine

The caffeine in Cafatine has a moderate potential interaction with 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 history of seizures, with prior electroencephalogram (EEG) abnormalities without seizures, and very rarely, without history of seizures and no prior EEG evidence of seizures. Therapy with CNS stimulants should be used with caution in patients with or predisposed to seizures. If seizures occur, therapy should be discontinued.

Sepsis

Major:

Cafatine

The ergotamine in Cafatine has a major potential interaction with Sepsis.

The use of ergot alkaloids is contraindicated in patients with conditions predisposing them to vasospastic reactions, including, ischemic heart disease (angina, history of myocardial infarction, silent ischemia), peripheral vascular disease, sepsis, shock, vascular surgery, uncontrolled hypertension, and severely impaired hepatic or renal function. The vasoconstriction produced be ergot alkaloids may exacerbate these conditions. Ergot alkaloids may cause vasospastic reactions other than coronary artery vasospasm such as peripheral vascular reactions, and colonic ischemia, causing muscle pains, numbness, coldness, pallor, and cyanosis of the digits. In patients with compromised circulation, persistent vasospasm may result in gangrene or death. Nitroprusside and heparin have been used to treat ergotamine- induced severe vasoconstriction.

Shock

Major:

Cafatine

The ergotamine in Cafatine has a major potential interaction with Shock.

The use of ergot alkaloids is contraindicated in patients with conditions predisposing them to vasospastic reactions, including, ischemic heart disease (angina, history of myocardial infarction, silent ischemia), peripheral vascular disease, sepsis, shock, vascular surgery, uncontrolled hypertension, and severely impaired hepatic or renal function. The vasoconstriction produced be ergot alkaloids may exacerbate these conditions. Ergot alkaloids may cause vasospastic reactions other than coronary artery vasospasm such as peripheral vascular reactions, and colonic ischemia, causing muscle pains, numbness, coldness, pallor, and cyanosis of the digits. In patients with compromised circulation, persistent vasospasm may result in gangrene or death. Nitroprusside and heparin have been used to treat ergotamine- induced severe vasoconstriction.

Tachyarrhythmia

Major:

Cafatine

The ergotamine in Cafatine has a major potential interaction with Tachyarrhythmia.

The amine ergot alkaloids, ergonovine and methylergonovine, can cause serious cardiovascular complications because of their vasospastic effects. Hypertension (more often with ergonovine) has been most commonly reported, particularly when administered IV undiluted or at an excessive rate or when used in conjunction with regional anesthesia or vasoconstrictors. Headaches, seizures, cerebrovascular accidents and death have been associated with the hypertensive episodes. Other, less common adverse effects include acute myocardial infarction, transient chest pains, thrombophlebitis, tachycardia and palpitations. Therapy with ergot alkaloids should generally be avoided, except under special circumstances, in patients with chronic hypertension, preeclampsia or eclampsia, cardiovascular disease, cerebrovascular disease, or peripheral vascular disease. Caution is advised when these agents are administered to patients with venoatrial shunts, mitral valve stenosis, or sepsis. Close monitoring of cardiovascular status is highly recommended during therapy.

Moderate:

Cafatine

The caffeine in Cafatine has a moderate potential interaction with Tachyarrhythmia.

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.

More resources

Cafatine

A total of 442 drugs are known to interact with Cafatine.

viloxazine

A total of 293 drugs are known to interact with viloxazine.

Drug Interaction Classification

These classifications are only a guideline. The relevance of a particular drug interaction to a specific individual is difficult to determine. Always consult your healthcare provider before starting or stopping any medication.
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 interaction information available.

Further information

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