Can you take Byvalson with Cosyntropin?

Cosyntropin has a moderate potential interaction with Abnormal Glucose Tolerance.

Adrenocorticotropic agents may impair glucose tolerance and cause hyperglycemia. Therapy with these agents should be administered cautiously in patients with diabetes mellitus, glucose intolerance, or a predisposition to hyperglycemia. Patients with diabetes mellitus should be monitored more closely during adrenocorticotropic therapy, and their antidiabetic regimen adjusted accordingly.

Cosyntropin has a major potential interaction with Adrenal Insufficiency.

The use of adrenocorticotropic agents is contraindicated in patients with primary adrenocortical insufficiency because of the lack of adrenal responsiveness.

The nebivolol in Byvalson has a major potential interaction with Allergies.

The use of beta-adrenergic receptor blocking agents (aka beta-blockers) in patients with a history of allergic reactions or anaphylaxis may be associated with heightened reactivity to culprit allergens. The frequency and/or severity of attacks may be increased during beta-blocker therapy. In addition, these patients may be refractory to the usual doses of epinephrine used to treat acute hypersensitivity reactions and may require a beta-agonist such as isoproterenol.

The valsartan in Byvalson has a major potential interaction with Angioedema.

The use of these agents is contraindicated in patients with a history of angioedema related to previous angiotensin-converting enzyme (ACE) inhibitor or angiotensin II receptor blocker (ARB) therapy or in patients with hereditary angioedema. Patients with a history of angioedema unrelated to these agents may be at increased risk of angioedema while receiving angiotensin II receptor (AR) antagonists. Patients should be advised to immediately report any signs or symptoms suggestive of angioedema (swelling of face, extremities, eyes, lips, or tongue, or difficulty swallowing or breathing) and to stop taking the medication until otherwise directed by their physician. Emergency therapy and/or measures to prevent airway obstruction are required for angioedema involving the tongue, glottis, or larynx. Treatment with angiotensin II receptor (AR) antagonists should be discontinued permanently if angioedema develops in association with therapy.

The nebivolol in Byvalson has a moderate potential interaction with Asthma.

Patients with bronchospastic disease, should, in general, not receive beta blockers, including cardioselective beta-blockers. Because of the relative beta-1 selectivity, cardioselective beta-blockers may be used in patients with bronchospastic disease who do not respond to, or cannot tolerate, other antihypertensive treatment. Because beta-1 selectivity is not absolute, the lowest possible dose of these agents should be used. Consider administering in smaller doses to avoid the higher plasma levels associated with the longer dosing intervals. If dosage must be increased, dividing the dose should be considered to achieve lower peak blood levels. It is recommended to have bronchodilators, including beta-2 agonists, readily available or administered concomitantly if necessary.

The valsartan in Byvalson has a moderate potential interaction with Biliary Obstruction.

Valsartan is primarily eliminated by biliary excretion, and a minority is excreted in the urine. Dosage adjustments are not necessary in patients with renal impairment unless they are also volume-depleted, in which case therapy should be initiated under medical supervision. Likewise, patients with mild to moderate hepatic impairment or biliary obstruction generally do not require a dosage adjustment. The manufacturer recommends administering valsartan therapy with caution in patients with impaired renal and/or liver function, particularly if these conditions are severe.

The nebivolol in Byvalson has a major potential interaction with Cardiogenic Shock.

The use of beta-adrenergic receptor blocking agents (aka beta-blockers) is contraindicated in patients with hypotension or cardiogenic shock. Due to their negative inotropic and chronotropic effects on the heart, the use of beta-blockers is likely to further depress cardiac output and blood pressure, which can be detrimental in these patients.

The nebivolol in Byvalson has a moderate potential interaction with Cerebrovascular Insufficiency.

Beta-adrenergic blocking agents (beta-blockers), should be used with caution in patients with cerebrovascular insufficiency because of their potential effects relative to blood pressure and pulse. If signs or symptoms suggesting reduced cerebral blood flow are observed, consideration should be given to discontinuing these agents.

Cosyntropin has a moderate potential interaction with Cirrhosis.

Adrenocorticotropic agents may have enhanced effects in patients with cirrhosis. Dosage adjustments may be necessary in these patients.

The nebivolol in Byvalson has a moderate potential interaction with COPD.

Patients with bronchospastic disease, should, in general, not receive beta blockers, including cardioselective beta-blockers. Because of the relative beta-1 selectivity, cardioselective beta-blockers may be used in patients with bronchospastic disease who do not respond to, or cannot tolerate, other antihypertensive treatment. Because beta-1 selectivity is not absolute, the lowest possible dose of these agents should be used. Consider administering in smaller doses to avoid the higher plasma levels associated with the longer dosing intervals. If dosage must be increased, dividing the dose should be considered to achieve lower peak blood levels. It is recommended to have bronchodilators, including beta-2 agonists, readily available or administered concomitantly if necessary.

The valsartan in Byvalson has a major potential interaction with Dehydration.

Angiotensin II receptor (AR) antagonists can cause symptomatic hypotension in patients with an activated renin-angiotensin system, such as volume- and/or sodium-depleted patients. Therapy with AR antagonists should be administered cautiously in such patients and in those predisposed to hypovolemic or hyponatremic states (e.g., patients on diuretic therapy, especially if high doses were used or if recently instituted; those on dietary salt restriction; renal dialysis patients). Volume and/or sodium depletion should be corrected prior to initiating therapy with AR antagonists, and the patient should be hemodynamically stable. Ideally, patients at risk for excessive hypotension should initiate AR antagonist therapy under close medical supervision, preferably with a lower dose, and followed closely for the first 2 weeks of treatment and whenever the dosage of AR antagonist or diuretic is increased.

Cosyntropin has a moderate potential interaction with Depression.

Adrenocorticotropic agents may aggravate the symptoms of psychosis and emotional instability. Patients with these conditions should be monitored for increased or worsened symptoms during adrenocorticotropic therapy.

The nebivolol in Byvalson has a major potential interaction with Diabetes Mellitus.

Beta-adrenergic receptor blocking agents (aka beta-blockers) may mask symptoms of hypoglycemia such as tremors, tachycardia and blood pressure changes. In addition, the nonselective beta-blockers (e.g., propranolol, pindolol, timolol) may inhibit catecholamine-mediated glycogenolysis, thereby potentiating insulin-induced hypoglycemia and delaying the recovery of normal blood glucose levels. Since cardioselectivity is not absolute, larger doses of beta-1 selective agents may demonstrate these effects as well. Therapy with beta-blockers should be administered cautiously in patients with diabetes or predisposed to spontaneous hypoglycemia.

The valsartan in Byvalson has a major potential interaction with Diabetes Mellitus.

The coadministration of some angiotensin II receptor blocker agents with aliskiren is contraindicated in patients with diabetes.

Cosyntropin has a moderate potential interaction with Diabetes Mellitus.

Adrenocorticotropic agents may impair glucose tolerance and cause hyperglycemia. Therapy with these agents should be administered cautiously in patients with diabetes mellitus, glucose intolerance, or a predisposition to hyperglycemia. Patients with diabetes mellitus should be monitored more closely during adrenocorticotropic therapy, and their antidiabetic regimen adjusted accordingly.

Cosyntropin has a major potential interaction with Diverticulitis.

Adrenocorticotropic agents may cause gastrointestinal perforation and hemorrhage, usually when given in high dosages or for prolonged periods. They may also mask symptoms of complications such as peritonitis or intraabdominal sepsis. Therapy with adrenocorticotropic agents should be administered cautiously in patients with diverticulitis, nonspecific ulcerative colitis (if there is a probability of impending perforation, abscess, or other pyogenic infection), or recent intestinal anastomoses.

Cosyntropin has a major potential interaction with Fluid Retention.

Adrenocorticotropic agents may cause hypernatremia, hypokalemia, fluid retention, and elevation in blood pressure. Therapy with these agents, particularly if intended for longer than brief periods, should be administered cautiously in patients with preexisting fluid retention or conditions that may be aggravated by these effects. Dietary sodium restriction and potassium supplementation may be advisable. The manufacturers consider the use of adrenocorticotropic agents to be contraindicated in patients with congestive heart failure or uncontrolled hypertension.

The nebivolol in Byvalson has a moderate potential interaction with Glaucoma/Intraocular Hypertension.

Systemic beta-adrenergic receptor blocking agents (aka beta-blockers) may lower intraocular pressure. Therefore, patients with glaucoma or intraocular hypertension may require adjustments in their ophthalmic regimen following a dosing change or discontinuation of beta-blocker therapy.

Cosyntropin has a moderate potential interaction with Glaucoma/Intraocular Hypertension.

Prolonged use of adrenocorticotropic agents may cause elevated intraocular pressure and glaucoma with possible damage to the optic nerves. Long-term therapy with these agents should be administered cautiously in patients with preexisting glaucoma (particularly open-angle glaucoma) or increased intraocular pressure.

The nebivolol in Byvalson has a major potential interaction with Heart Block.

The use of beta-adrenergic receptor blocking agents (aka beta-blockers) is contraindicated in patients with sinus bradyarrhythmia or heart block greater than the first degree (unless a functioning pacemaker is present). Due to their negative inotropic and chronotropic effects on the heart, the use of beta-blockers is likely to exacerbate these conditions.

The nebivolol in Byvalson has a major potential interaction with Heart Failure.

Beta-adrenergic receptor blocking agents (aka beta-blockers) in general should not be used in patients with overt congestive heart failure (CHF). Sympathetic stimulation may be important in maintaining the hemodynamic function in these patients, thus beta-blockade can worsen the heart failure. However, therapy with beta-blockers may be beneficial and can be administered cautiously in some CHF patients provided they are well compensated and receiving digitalis, diuretics, an ACE inhibitor, and/or nitrates. Carvedilol, specifically, is indicated for use with these agents in the treatment of mild to severe heart failure of ischemic or cardiomyopathic origin. There is also increasing evidence that the addition of a beta-blocker to standard therapy can improve morbidity and mortality in patients with advanced heart failure, although it is uncertain whether effectiveness varies significantly with the different agents. Data from one meta-analysis study suggest a greater reduction of mortality risk for nonselective beta-blockers than for beta-1 selective agents.

Cosyntropin has a major potential interaction with Heart Failure.

Adrenocorticotropic agents may cause hypernatremia, hypokalemia, fluid retention, and elevation in blood pressure. Therapy with these agents, particularly if intended for longer than brief periods, should be administered cautiously in patients with preexisting fluid retention or conditions that may be aggravated by these effects. Dietary sodium restriction and potassium supplementation may be advisable. The manufacturers consider the use of adrenocorticotropic agents to be contraindicated in patients with congestive heart failure or uncontrolled hypertension.

The valsartan in Byvalson has a moderate potential interaction with Heart Failure.

Angiotensin II receptor (AR) antagonists can cause renal impairment in patients whose renal function depends on the activity of the renin-angiotensin-aldosterone system. In addition, symptomatic hypotension can occur in susceptible individuals, which may compromise renal and myocardial perfusion. In patients with severe congestive heart failure (CHF), treatment with AR antagonists has been associated with oliguria and/or progressive azotemia and, rarely, renal failure, myocardial ischemia, and death. Therapy with AR antagonists should be initiated cautiously in patients with severe CHF, especially when accompanied by volume and/or sodium depletion. In patients who experience a decline in renal function, discontinuation of AR antagonist therapy is usually not required provided there is symptomatic improvement of the heart failure and renal deterioration is well-tolerated. Transient hypotension is also not a contraindication to further treatment with AR antagonists, since therapy can usually be reinstated without difficulty after blood pressure stabilizes.

The valsartan in Byvalson has a major potential interaction with Hemodialysis.

Angiotensin II receptor (AR) antagonists can cause symptomatic hypotension in patients with an activated renin-angiotensin system, such as volume- and/or sodium-depleted patients. Therapy with AR antagonists should be administered cautiously in such patients and in those predisposed to hypovolemic or hyponatremic states (e.g., patients on diuretic therapy, especially if high doses were used or if recently instituted; those on dietary salt restriction; renal dialysis patients). Volume and/or sodium depletion should be corrected prior to initiating therapy with AR antagonists, and the patient should be hemodynamically stable. Ideally, patients at risk for excessive hypotension should initiate AR antagonist therapy under close medical supervision, preferably with a lower dose, and followed closely for the first 2 weeks of treatment and whenever the dosage of AR antagonist or diuretic is increased.

Cosyntropin has a major potential interaction with Herpetic Keratitis.

Adrenocorticotropic agents should be used cautiously, if at all, in patients with ocular herpes simplex because of the risk of corneal perforation. The manufacturers consider their use to be contraindicated in such setting.

Cosyntropin has a major potential interaction with High Blood Pressure.

Adrenocorticotropic agents may cause hypernatremia, hypokalemia, fluid retention, and elevation in blood pressure. Therapy with these agents, particularly if intended for longer than brief periods, should be administered cautiously in patients with preexisting fluid retention or conditions that may be aggravated by these effects. Dietary sodium restriction and potassium supplementation may be advisable. The manufacturers consider the use of adrenocorticotropic agents to be contraindicated in patients with congestive heart failure or uncontrolled hypertension.

The nebivolol in Byvalson has a moderate potential interaction with High Cholesterol.

Beta-adrenergic receptor blocking agents (aka beta-blockers) may alter serum lipid profiles. Increases in serum VLDL and LDL cholesterol and triglycerides, as well as decreases in HDL cholesterol, have been reported with some beta-blockers. Patients with preexisting hyperlipidemia may require closer monitoring during beta-blocker therapy, and adjustments made accordingly in their lipid-lowering regimen.

Cosyntropin has a major potential interaction with History, Peptic Ulcer.

Adrenocorticotropic agents may cause peptic ulcer disease and gastrointestinal (GI) hemorrhage, usually when given in high dosages or for prolonged periods. Delayed healing of peptic ulcers has also been reported. Therapy with adrenocorticotropic agents, if necessary, should be administered cautiously in patients with active or latent peptic ulcers or other risk factors for GI bleeding. The manufacturers consider their use to be contraindicated in such setting.

Cosyntropin has a moderate potential interaction with History, Thrombotic/Thromboembolic Disorder.

Adrenocorticotropic agents may increase blood coagulability and have rarely been associated with the development of intravascular thrombosis, thromboembolism, and thrombophlebitis. These agents should be used cautiously in patients with thrombotic or thromboembolic disorders.

Cosyntropin has a major potential interaction with History, Tuberculosis.

In patients with latent tuberculosis or tuberculin reactivity, the use of pharmacologic dosages of adrenocorticotropic agents may cause a reactivation of the disease. Close monitoring for signs and symptoms of tuberculosis is recommended if adrenocorticotropic therapy is administered to these patients. During prolonged use, tuberculosis chemoprophylaxis may be considered.

Cosyntropin has a major potential interaction with Hyperadrenocorticism.

The use of adrenocorticotropic agents is contraindicated in patients with adrenocortical hyperfunction. These agents stimulate the release of cortisol and aldosterone and may aggravate symptoms of hyperadrenocorticism.

The valsartan in Byvalson has a moderate potential interaction with Hyperkalemia.

Drugs that inhibit the renin-angiotensin, such as angiotensin II receptor antagonist system can cause hyperkalemia. Concomitant use of these agents with drugs that increase potassium levels may increase the risk of hyperkalemia. Use caution when using these agents together and monitor serum potassium periodically.

Cosyntropin has a major potential interaction with Hypernatremia.

Adrenocorticotropic agents may cause hypernatremia, hypokalemia, hypocalcemia, and fluid retention. Therapy with these agents, particularly if intended for longer than brief periods, should be administered cautiously in patients with preexisting electrolyte disturbances. Caution is also advised when treating patients with seizure disorders, since electrolyte disturbances may trigger seizure activity.

The nebivolol in Byvalson has a moderate potential interaction with Hyperthyroidism.

When beta-adrenergic receptor blocking agents (aka beta-blockers) are used to alleviate symptoms of hyperthyroidism such as tachycardia, anxiety, tremor and heat intolerance, abrupt withdrawal can exacerbate thyrotoxicosis or precipitate a thyroid storm. To minimize this risk, cessation of beta-blocker therapy, when necessary, should occur gradually with incrementally reduced dosages over a period of 1 to 2 weeks. Patients should be advised not to discontinue treatment without first consulting with the physician. Close monitoring is recommended during and after therapy withdrawal.

Cosyntropin has a major potential interaction with Hypocalcemia.

Adrenocorticotropic agents may cause hypernatremia, hypokalemia, hypocalcemia, and fluid retention. Therapy with these agents, particularly if intended for longer than brief periods, should be administered cautiously in patients with preexisting electrolyte disturbances. Caution is also advised when treating patients with seizure disorders, since electrolyte disturbances may trigger seizure activity.

Cosyntropin has a major potential interaction with Hypokalemia.

Adrenocorticotropic agents may cause hypernatremia, hypokalemia, hypocalcemia, and fluid retention. Therapy with these agents, particularly if intended for longer than brief periods, should be administered cautiously in patients with preexisting electrolyte disturbances. Caution is also advised when treating patients with seizure disorders, since electrolyte disturbances may trigger seizure activity.

The valsartan in Byvalson has a major potential interaction with Hyponatremia.

Angiotensin II receptor (AR) antagonists can cause symptomatic hypotension in patients with an activated renin-angiotensin system, such as volume- and/or sodium-depleted patients. Therapy with AR antagonists should be administered cautiously in such patients and in those predisposed to hypovolemic or hyponatremic states (e.g., patients on diuretic therapy, especially if high doses were used or if recently instituted; those on dietary salt restriction; renal dialysis patients). Volume and/or sodium depletion should be corrected prior to initiating therapy with AR antagonists, and the patient should be hemodynamically stable. Ideally, patients at risk for excessive hypotension should initiate AR antagonist therapy under close medical supervision, preferably with a lower dose, and followed closely for the first 2 weeks of treatment and whenever the dosage of AR antagonist or diuretic is increased.

The nebivolol in Byvalson has a major potential interaction with Hypotension.

The use of beta-adrenergic receptor blocking agents (aka beta-blockers) is contraindicated in patients with hypotension or cardiogenic shock. Due to their negative inotropic and chronotropic effects on the heart, the use of beta-blockers is likely to further depress cardiac output and blood pressure, which can be detrimental in these patients.

Cosyntropin has a major potential interaction with Infection.

The immunosuppressant and anti-inflammatory effects of adrenocorticotropic agents, particularly in higher dosages, may decrease host resistance to infectious agents, decrease the ability to localize infections, and mask the symptoms of infection. Secondary infections may be more likely to develop. In general, adrenocorticotropic agents should not be used in patients with active infections, especially systemic fungal infections, unless they are medically necessary and effective antimicrobial therapy or other appropriate treatment has been instituted. For patients who have received prolonged adrenocorticotropic therapy who develop a severe or life-threatening infection, supplemental doses of rapid-acting corticosteroids may be required, since these patients may have hypothalamic-pituitary insufficiency.

Cosyntropin has a major potential interaction with Intestinal Anastomoses.

Adrenocorticotropic agents may cause gastrointestinal perforation and hemorrhage, usually when given in high dosages or for prolonged periods. They may also mask symptoms of complications such as peritonitis or intraabdominal sepsis. Therapy with adrenocorticotropic agents should be administered cautiously in patients with diverticulitis, nonspecific ulcerative colitis (if there is a probability of impending perforation, abscess, or other pyogenic infection), or recent intestinal anastomoses.

The nebivolol in Byvalson has a major potential interaction with Ischemic Heart Disease.

Heightened sensitivity to catecholamines may occur after prolonged use of beta-adrenergic receptor blocking agents (aka beta-blockers). Exacerbation of angina, myocardial infarction and ventricular arrhythmias have been reported in patients with coronary artery disease following abrupt withdrawal of therapy. Cessation of beta-blocker therapy, whenever necessary, should occur gradually with incrementally reduced dosages over a period of 1 to 2 weeks in patients with coronary insufficiency. Patients should be advised not to discontinue treatment without first consulting with the physician. In patients who experience an exacerbation of angina following discontinuation of beta-blocker therapy, the medication should generally be reinstituted, at least temporarily, along with other clinically appropriate measures.

The nebivolol in Byvalson has a major potential interaction with Liver Disease.

Metabolism of nebivolol is decreased in patients with moderate hepatic impairment. d-Nebivolol peak plasma concentration increased 3-fold, exposure (AUC) increased 10-fold, and the apparent clearance decreased by 86% in patients with moderate hepatic impairment (Child-Pugh Class B). Patients with liver disease may be at greater risk for adverse effects from nebivolol due to decreased drug clearance. Therapy with nebivolol should be administered cautiously in patients with liver disease. Dosage adjustments may be necessary. No formal studies have been performed in patients with severe hepatic impairment and nebivolol should be contraindicated for these patients.

The valsartan in Byvalson has a moderate potential interaction with Liver Disease.

Valsartan is primarily eliminated by biliary excretion, and a minority is excreted in the urine. Dosage adjustments are not necessary in patients with renal impairment unless they are also volume-depleted, in which case therapy should be initiated under medical supervision. Likewise, patients with mild to moderate hepatic impairment or biliary obstruction generally do not require a dosage adjustment. The manufacturer recommends administering valsartan therapy with caution in patients with impaired renal and/or liver function, particularly if these conditions are severe.

The nebivolol in Byvalson has a moderate potential interaction with Myasthenia Gravis.

Beta-adrenergic receptor blocking agents (aka beta-blockers) may potentiate muscle weakness consistent with certain myasthenic symptoms such as diplopia, ptosis, and generalized weakness. Several beta-blockers have been associated rarely with aggravation of muscle weakness in patients with preexisting myasthenia gravis or myasthenic symptoms. Use cautiously in patients with myasthenia gravis.

Cosyntropin has a moderate potential interaction with Myasthenia Gravis.

While corticotropin has been used effectively in severe, refractory myasthenia gravis to increase muscle strength, it should nevertheless be administered with extreme caution in such setting. Patients must be treated in an intensive care unit and receive respiratory support, since muscle strength will markedly decrease initially. Improvement usually occurs several days after the first or second course of treatment. Similar responses might be expected of other adrenocorticotropic agents, although their use in myasthenia gravis has not been studied extensively.

Cosyntropin has a moderate potential interaction with Myoneural Disorder.

Toxic myopathy may occur with the prolonged use of adrenocorticotropic agents, often in patients with disorders of neuromuscular transmission such as myasthenia gravis or in patients receiving neuromuscular blocking agents. Steroid myopathy is generalized and sometimes accompanied by respiratory weakness and dyspnea. In some cases, it has resulted in quadraparesis. Elevations of creatine kinase may also occur, albeit infrequently. After withdrawal of ACTH therapy, recovery may be slow and incomplete. Therapy with adrenocorticotropic agents should be administered cautiously in patients with preexisting myopathy or myoneural disorders, since these conditions may confound the diagnosis of steroid-induced myopathy. The presence of a normal serum CK level, minimal or no changes of myopathy on EMG, and type 2 muscle fiber atrophy on biopsy are helpful in suggesting steroid-induced weakness. If steroid myopathy is suspected, a dosage reduction or discontinuation of adrenocorticotropic therapy should be considered.

Cosyntropin has a moderate potential interaction with Myopathy.

Toxic myopathy may occur with the prolonged use of adrenocorticotropic agents, often in patients with disorders of neuromuscular transmission such as myasthenia gravis or in patients receiving neuromuscular blocking agents. Steroid myopathy is generalized and sometimes accompanied by respiratory weakness and dyspnea. In some cases, it has resulted in quadraparesis. Elevations of creatine kinase may also occur, albeit infrequently. After withdrawal of ACTH therapy, recovery may be slow and incomplete. Therapy with adrenocorticotropic agents should be administered cautiously in patients with preexisting myopathy or myoneural disorders, since these conditions may confound the diagnosis of steroid-induced myopathy. The presence of a normal serum CK level, minimal or no changes of myopathy on EMG, and type 2 muscle fiber atrophy on biopsy are helpful in suggesting steroid-induced weakness. If steroid myopathy is suspected, a dosage reduction or discontinuation of adrenocorticotropic therapy should be considered.

Cosyntropin has a major potential interaction with Osteoporosis.

Adrenocorticotropic agents inhibit the absorption of intestinal calcium and increase urinary excretion of calcium, which can result in bone resorption and bone loss during prolonged therapy. In addition, bone matrix may be affected by the protein-catabolic effects of these agents, especially when given in high dosages or for prolonged periods, leading to aseptic necrosis and fractures. Long-term or high-dose adrenocorticotropic therapy should be administered cautiously and only if necessary in patients with or at risk for osteoporosis. The manufacturers consider the use of adrenocorticotropic agents to be contraindicated in such setting.

Cosyntropin has a major potential interaction with Peptic Ulcer.

Adrenocorticotropic agents may cause peptic ulcer disease and gastrointestinal (GI) hemorrhage, usually when given in high dosages or for prolonged periods. Delayed healing of peptic ulcers has also been reported. Therapy with adrenocorticotropic agents, if necessary, should be administered cautiously in patients with active or latent peptic ulcers or other risk factors for GI bleeding. The manufacturers consider their use to be contraindicated in such setting.

The nebivolol in Byvalson has a major potential interaction with Peripheral Arterial Disease.

Due to their negative inotropic and chronotropic effects on the heart, beta-adrenergic receptor blocking agents (aka beta-blockers) reduce cardiac output and may precipitate or aggravate symptoms of arterial insufficiency in patients with peripheral vascular disease. In addition, the nonselective beta-blockers (e.g., propranolol, pindolol, timolol) may attenuate catecholamine-mediated vasodilation during exercise by blocking beta-2 receptors in peripheral vessels. Therapy with beta-blockers should be administered cautiously in patients with peripheral vascular disease. Close monitoring for progression of arterial obstruction is advised.

The nebivolol in Byvalson has a moderate potential interaction with Pheochromocytoma.

Administration of beta-blockers alone in the setting of pheochromocytoma has been associated with a paradoxical increase in blood pressure due to the attenuation of beta receptor-mediated vasodilatation in skeletal muscle. In patients with pheochromocytoma, an alpha-blocking agent should be initiated prior to the use of any beta-blocking agent. Caution should be taken in the administration of these agents to patients suspected of having pheochromocytoma.

The nebivolol in Byvalson has a moderate potential interaction with Psoriasis.

The use of beta-blockers in psoriatic patients should be carefully weighed since the use of these agents may cause an aggravation in psoriasis.

Cosyntropin has a moderate potential interaction with Psychosis.

Adrenocorticotropic agents may aggravate the symptoms of psychosis and emotional instability. Patients with these conditions should be monitored for increased or worsened symptoms during adrenocorticotropic therapy.

Cosyntropin has a major potential interaction with Renal Dysfunction.

Adrenocorticotropic agents may cause hypernatremia, hypokalemia, fluid retention, and elevation in blood pressure. Therapy with these agents, particularly if intended for longer than brief periods, should be administered cautiously in patients with preexisting fluid retention or conditions that may be aggravated by these effects. Dietary sodium restriction and potassium supplementation may be advisable. The manufacturers consider the use of adrenocorticotropic agents to be contraindicated in patients with congestive heart failure or uncontrolled hypertension.

The nebivolol in Byvalson has a moderate potential interaction with Renal Dysfunction.

Renal clearance of nebivolol is decreased in patients with severe renal impairment. The apparent clearance of nebivolol was unchanged following a single 5 mg dose of nebivolol in patients with mild renal impairment (CrCl 50 to 80 mL/min, n =7), and it was reduced negligibly in patients with moderate (CrCl 30 to 50 mL/min, n =9), but clearance was reduced by 53% in patients with severe renal impairment (CrCl<30 mL/min, n =5). Patients with severe renal impairment may be at greater risk for adverse effects from nebivolol due to decreased drug clearance. Therapy with nebivolol should be administered cautiously in patients with severe renal impairment. Dosage adjustments may be necessary. No studies have been conducted in patients on dialysis

The valsartan in Byvalson has a moderate potential interaction with Renal Dysfunction.

Changes in renal function including acute renal failure can be caused by drugs that inhibit the renin-angiotensin system and by diuretics. Patients whose renal function may depend in part on the activity of the renin-angiotensin system (e.g., patients with renal artery stenosis, chronic kidney disease, severe congestive heart failure, or volume depletion) may be at particular risk of developing acute renal failure with these agents. Monitor renal function periodically in these patients. Consider withholding or discontinuing therapy in patients who develop a clinically significant decrease in renal function with these agents.

The valsartan in Byvalson has a moderate potential interaction with Renal Dysfunction.

Valsartan is primarily eliminated by biliary excretion, and a minority is excreted in the urine. Dosage adjustments are not necessary in patients with renal impairment unless they are also volume-depleted, in which case therapy should be initiated under medical supervision. Likewise, patients with mild to moderate hepatic impairment or biliary obstruction generally do not require a dosage adjustment. The manufacturer recommends administering valsartan therapy with caution in patients with impaired renal and/or liver function, particularly if these conditions are severe.

Cosyntropin has a major potential interaction with Seizures.

Adrenocorticotropic agents may cause hypernatremia, hypokalemia, hypocalcemia, and fluid retention. Therapy with these agents, particularly if intended for longer than brief periods, should be administered cautiously in patients with preexisting electrolyte disturbances. Caution is also advised when treating patients with seizure disorders, since electrolyte disturbances may trigger seizure activity.

The nebivolol in Byvalson has a major potential interaction with Sinus Node Dysfunction.

The use of beta-adrenergic receptor blocking agents (aka beta-blockers) is contraindicated in patients with sinus bradyarrhythmia or heart block greater than the first degree (unless a functioning pacemaker is present). Due to their negative inotropic and chronotropic effects on the heart, the use of beta-blockers is likely to exacerbate these conditions.

Cosyntropin has a major potential interaction with Systemic Sclerosis.

The use of adrenocorticotropic agents is contraindicated in patients with scleroderma. Adrenocorticotropic agents may precipitate renal crisis with malignant hypertension in these patients, possibly via steroid-induced increases in renin substrate and angiotensin II levels and decreases in vasodilator prostaglandin production. Renal failure may ensue. If treatment is required for inflammatory myositis or pericarditis, glucocorticoids are preferable because of their more predictable pharmacologic effect. However, glucocorticoids should also be avoided in the long-term treatment of patients with scleroderma for similar reasons.

The nebivolol in Byvalson has a moderate potential interaction with Tachyarrhythmia.

Beta-adrenergic blockade in patients with Wolff-Parkinson-White syndrome and tachycardia has been associated with severe bradycardia requiring treatment with a pacemaker. In one case, this result was reported after an initial dose of 5 mg propranolol. The use of beta-adrenergic receptor blocking agents (aka beta-blockers) should be administered cautiously in these patients.

Cosyntropin has a moderate potential interaction with Thrombotic/Thromboembolic Disorder.

Adrenocorticotropic agents may increase blood coagulability and have rarely been associated with the development of intravascular thrombosis, thromboembolism, and thrombophlebitis. These agents should be used cautiously in patients with thrombotic or thromboembolic disorders.

Cosyntropin has a major potential interaction with Tuberculosis, Latent.

In patients with latent tuberculosis or tuberculin reactivity, the use of pharmacologic dosages of adrenocorticotropic agents may cause a reactivation of the disease. Close monitoring for signs and symptoms of tuberculosis is recommended if adrenocorticotropic therapy is administered to these patients. During prolonged use, tuberculosis chemoprophylaxis may be considered.

Cosyntropin has a major potential interaction with Ulcerative Colitis.

Adrenocorticotropic agents may cause gastrointestinal perforation and hemorrhage, usually when given in high dosages or for prolonged periods. They may also mask symptoms of complications such as peritonitis or intraabdominal sepsis. Therapy with adrenocorticotropic agents should be administered cautiously in patients with diverticulitis, nonspecific ulcerative colitis (if there is a probability of impending perforation, abscess, or other pyogenic infection), or recent intestinal anastomoses.

Cosyntropin has a moderate potential interaction with Underactive Thyroid.

Adrenocorticotropic agents may have enhanced effects in patients with hypothyroidism. Dosage adjustments may be necessary in these patients.

Cosyntropin has a major potential interaction with Vaccination.

The administration of live or live, attenuated vaccines is contraindicated in patients receiving large or immunosuppressive doses of adrenocorticotropic agents. Inactivated viral or bacterial vaccines should be used with caution, since their administration may pose a risk of neurological complications in these patients. Additionally, a diminished or inadequate serum antibody response may be anticipated.