Interactions between Chlorthalidone / reserpine and Corticotropin

The chlorthalidone in chlorthalidone / reserpine has a moderate potential interaction with Abnormal Glucose Tolerance.

Thiazide diuretics may cause hyperglycemia and glycosuria in patients with diabetes. They may also precipitate diabetes in prediabetic patients. These effects are usually reversible following discontinuation of the drugs. Therapy with thiazide diuretics 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 thiazide therapy, and their antidiabetic regimen adjusted accordingly.

Corticotropin 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.

Corticotropin 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 chlorthalidone in chlorthalidone / reserpine has a major potential interaction with Anuria.

The use of thiazide diuretics is contraindicated in patients with anuria.

The chlorthalidone in chlorthalidone / reserpine has a moderate potential interaction with Asthma.

Thiazide diuretics should be used with caution in patients with history of bronchial asthma as sensitivity reactions may occur.

Corticotropin 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 chlorthalidone in chlorthalidone / reserpine has a major potential interaction with Dehydration.

The use of thiazide diuretics is commonly associated with loss of electrolytes, most significantly potassium but also sodium, chloride, bicarbonate, and magnesium. The loss of other electrolytes such as phosphate, bromide and iodide is usually slight. Potassium and magnesium depletion may lead to cardiac arrhythmias and cardiac arrest. Other electrolyte-related complications include metabolic alkalosis and hyponatremia, which are rarely life-threatening. Therapy with thiazide diuretics should be administered cautiously in patients with or predisposed to fluid and electrolyte depletion, including patients with primary or secondary aldosteronism (may have low potassium levels); those with severe or prolonged diarrhea or vomiting; and those with poor nutritional status. Fluid and electrolyte abnormalities should be corrected prior to initiating therapy, and blood pressure as well as serum electrolyte concentrations monitored periodically and maintained at normal ranges during therapy. Patients should be advised to immediately report signs and symptoms of fluid or electrolyte imbalance, including dry mouth, thirst, weakness, lethargy, drowsiness, restlessness, muscle pains or cramps, muscular fatigue, hypotension, oliguria, tachycardia, arrhythmia, or gastrointestinal disturbances such as nausea and vomiting. Digitalized patients and patients with a history of ventricular arrhythmias should be monitored carefully, since development of hypokalemia may be particularly dangerous in these patients. The risk of hypokalemia may be minimized by slow diuresis, a lower thiazide dosage, potassium supplementation, or combined use with a potassium-sparing diuretic.

The reserpine in chlorthalidone / reserpine has a major potential interaction with Depression.

The use of rauwolfia alkaloids is contraindicated in patients with a history of mental depression, especially suicidal tendencies. Rauwolfia alkaloids depletes catecholamine and serotonin stores.

Corticotropin 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 chlorthalidone in chlorthalidone / reserpine has a moderate potential interaction with Diabetes Mellitus.

Thiazide diuretics may cause hyperglycemia and glycosuria in patients with diabetes. They may also precipitate diabetes in prediabetic patients. These effects are usually reversible following discontinuation of the drugs. Therapy with thiazide diuretics 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 thiazide therapy, and their antidiabetic regimen adjusted accordingly.

Corticotropin 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.

The chlorthalidone in chlorthalidone / reserpine has a major potential interaction with Diarrhea.

The use of thiazide diuretics is commonly associated with loss of electrolytes, most significantly potassium but also sodium, chloride, bicarbonate, and magnesium. The loss of other electrolytes such as phosphate, bromide and iodide is usually slight. Potassium and magnesium depletion may lead to cardiac arrhythmias and cardiac arrest. Other electrolyte-related complications include metabolic alkalosis and hyponatremia, which are rarely life-threatening. Therapy with thiazide diuretics should be administered cautiously in patients with or predisposed to fluid and electrolyte depletion, including patients with primary or secondary aldosteronism (may have low potassium levels); those with severe or prolonged diarrhea or vomiting; and those with poor nutritional status. Fluid and electrolyte abnormalities should be corrected prior to initiating therapy, and blood pressure as well as serum electrolyte concentrations monitored periodically and maintained at normal ranges during therapy. Patients should be advised to immediately report signs and symptoms of fluid or electrolyte imbalance, including dry mouth, thirst, weakness, lethargy, drowsiness, restlessness, muscle pains or cramps, muscular fatigue, hypotension, oliguria, tachycardia, arrhythmia, or gastrointestinal disturbances such as nausea and vomiting. Digitalized patients and patients with a history of ventricular arrhythmias should be monitored carefully, since development of hypokalemia may be particularly dangerous in these patients. The risk of hypokalemia may be minimized by slow diuresis, a lower thiazide dosage, potassium supplementation, or combined use with a potassium-sparing diuretic.

Corticotropin 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.

The chlorthalidone in chlorthalidone / reserpine has a major potential interaction with Electrolyte Abnormalities.

The use of thiazide diuretics is commonly associated with loss of electrolytes, most significantly potassium but also sodium, chloride, bicarbonate, and magnesium. The loss of other electrolytes such as phosphate, bromide and iodide is usually slight. Potassium and magnesium depletion may lead to cardiac arrhythmias and cardiac arrest. Other electrolyte-related complications include metabolic alkalosis and hyponatremia, which are rarely life-threatening. Therapy with thiazide diuretics should be administered cautiously in patients with or predisposed to fluid and electrolyte depletion, including patients with primary or secondary aldosteronism (may have low potassium levels); those with severe or prolonged diarrhea or vomiting; and those with poor nutritional status. Fluid and electrolyte abnormalities should be corrected prior to initiating therapy, and blood pressure as well as serum electrolyte concentrations monitored periodically and maintained at normal ranges during therapy. Patients should be advised to immediately report signs and symptoms of fluid or electrolyte imbalance, including dry mouth, thirst, weakness, lethargy, drowsiness, restlessness, muscle pains or cramps, muscular fatigue, hypotension, oliguria, tachycardia, arrhythmia, or gastrointestinal disturbances such as nausea and vomiting. Digitalized patients and patients with a history of ventricular arrhythmias should be monitored carefully, since development of hypokalemia may be particularly dangerous in these patients. The risk of hypokalemia may be minimized by slow diuresis, a lower thiazide dosage, potassium supplementation, or combined use with a potassium-sparing diuretic.

Corticotropin 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 reserpine in chlorthalidone / reserpine has a moderate potential interaction with Fluid Retention.

Peripheral- acting antiadrenergic agents can cause peripheral edema. Therapy with peripheral- acting antiadrenergic agents should be administered cautiously in patients adversely affected by sodium and water retention.

The reserpine in chlorthalidone / reserpine has a moderate potential interaction with Gallstones.

Rauwolfia alkaloids increase gastrointestinal motility and secretion and can precipitate biliary colic in patients with gallstones. Therapy with rauwolfia alkaloids should be administered cautiously in patients with a history of gallstones.

Corticotropin 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 chlorthalidone in chlorthalidone / reserpine has a moderate potential interaction with Gout.

Thiazide diuretics decrease the rate of uric acid excretion. Hyperuricemia occurs frequently but is usually asymptomatic and rarely leads to clinical gout except in patients with a history of gout or chronic renal failure. Therapy with thiazide diuretics should be administered cautiously in such patients.

Corticotropin 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.

Corticotropin 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.

Corticotropin 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 chlorthalidone in chlorthalidone / reserpine has a moderate potential interaction with High Cholesterol.

Thiazide diuretics may increase serum triglyceride and cholesterol levels, primarily LDL and VLDL. Whether these effects are dose-related and sustained during chronic therapy are unknown. Patients with preexisting hyperlipidemia may require closer monitoring during thiazide therapy, and adjustments made accordingly in their lipid-lowering regimen

Corticotropin 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.

Corticotropin 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.

Corticotropin 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.

Corticotropin 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 chlorthalidone in chlorthalidone / reserpine has a major potential interaction with Hyperaldosteronism.

The use of thiazide diuretics is commonly associated with loss of electrolytes, most significantly potassium but also sodium, chloride, bicarbonate, and magnesium. The loss of other electrolytes such as phosphate, bromide and iodide is usually slight. Potassium and magnesium depletion may lead to cardiac arrhythmias and cardiac arrest. Other electrolyte-related complications include metabolic alkalosis and hyponatremia, which are rarely life-threatening. Therapy with thiazide diuretics should be administered cautiously in patients with or predisposed to fluid and electrolyte depletion, including patients with primary or secondary aldosteronism (may have low potassium levels); those with severe or prolonged diarrhea or vomiting; and those with poor nutritional status. Fluid and electrolyte abnormalities should be corrected prior to initiating therapy, and blood pressure as well as serum electrolyte concentrations monitored periodically and maintained at normal ranges during therapy. Patients should be advised to immediately report signs and symptoms of fluid or electrolyte imbalance, including dry mouth, thirst, weakness, lethargy, drowsiness, restlessness, muscle pains or cramps, muscular fatigue, hypotension, oliguria, tachycardia, arrhythmia, or gastrointestinal disturbances such as nausea and vomiting. Digitalized patients and patients with a history of ventricular arrhythmias should be monitored carefully, since development of hypokalemia may be particularly dangerous in these patients. The risk of hypokalemia may be minimized by slow diuresis, a lower thiazide dosage, potassium supplementation, or combined use with a potassium-sparing diuretic.

Corticotropin 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 chlorthalidone in chlorthalidone / reserpine has a moderate potential interaction with Hyperparathyroidism.

Urinary calcium excretion is decreased by thiazide diuretics during chronic administration. Pathologic changes in the parathyroid gland with hypercalcemia and hypophosphatemia have been reported during prolonged therapy. However, the common complications of hyperparathyroidism such as renal lithiasis, bone resorption, and peptic ulceration have not been seen. Clinicians should be cognizant of these effects when prescribing or administering thiazide therapy to patients with hyperparathyroidism. These drugs should be discontinued before carrying out tests for parathyroid function.

Corticotropin 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.

The chlorthalidone in chlorthalidone / reserpine has a major potential interaction with Hypokalemia.

The use of thiazide diuretics is commonly associated with loss of electrolytes, most significantly potassium but also sodium, chloride, bicarbonate, and magnesium. The loss of other electrolytes such as phosphate, bromide and iodide is usually slight. Potassium and magnesium depletion may lead to cardiac arrhythmias and cardiac arrest. Other electrolyte-related complications include metabolic alkalosis and hyponatremia, which are rarely life-threatening. Therapy with thiazide diuretics should be administered cautiously in patients with or predisposed to fluid and electrolyte depletion, including patients with primary or secondary aldosteronism (may have low potassium levels); those with severe or prolonged diarrhea or vomiting; and those with poor nutritional status. Fluid and electrolyte abnormalities should be corrected prior to initiating therapy, and blood pressure as well as serum electrolyte concentrations monitored periodically and maintained at normal ranges during therapy. Patients should be advised to immediately report signs and symptoms of fluid or electrolyte imbalance, including dry mouth, thirst, weakness, lethargy, drowsiness, restlessness, muscle pains or cramps, muscular fatigue, hypotension, oliguria, tachycardia, arrhythmia, or gastrointestinal disturbances such as nausea and vomiting. Digitalized patients and patients with a history of ventricular arrhythmias should be monitored carefully, since development of hypokalemia may be particularly dangerous in these patients. The risk of hypokalemia may be minimized by slow diuresis, a lower thiazide dosage, potassium supplementation, or combined use with a potassium-sparing diuretic.

Corticotropin 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 chlorthalidone in chlorthalidone / reserpine has a major potential interaction with Hyponatremia.

The use of thiazide diuretics is commonly associated with loss of electrolytes, most significantly potassium but also sodium, chloride, bicarbonate, and magnesium. The loss of other electrolytes such as phosphate, bromide and iodide is usually slight. Potassium and magnesium depletion may lead to cardiac arrhythmias and cardiac arrest. Other electrolyte-related complications include metabolic alkalosis and hyponatremia, which are rarely life-threatening. Therapy with thiazide diuretics should be administered cautiously in patients with or predisposed to fluid and electrolyte depletion, including patients with primary or secondary aldosteronism (may have low potassium levels); those with severe or prolonged diarrhea or vomiting; and those with poor nutritional status. Fluid and electrolyte abnormalities should be corrected prior to initiating therapy, and blood pressure as well as serum electrolyte concentrations monitored periodically and maintained at normal ranges during therapy. Patients should be advised to immediately report signs and symptoms of fluid or electrolyte imbalance, including dry mouth, thirst, weakness, lethargy, drowsiness, restlessness, muscle pains or cramps, muscular fatigue, hypotension, oliguria, tachycardia, arrhythmia, or gastrointestinal disturbances such as nausea and vomiting. Digitalized patients and patients with a history of ventricular arrhythmias should be monitored carefully, since development of hypokalemia may be particularly dangerous in these patients. The risk of hypokalemia may be minimized by slow diuresis, a lower thiazide dosage, potassium supplementation, or combined use with a potassium-sparing diuretic.

Corticotropin 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.

The reserpine in chlorthalidone / reserpine has a major potential interaction with Inflammatory Bowel Disease.

The use of rauwolfia alkaloids is contraindicated in patients with active peptic ulcer or ulcerative colitis. Since rauwolfia alkaloids increase gastrointestinal motility and secretion, these conditions may be aggravated. Therapy with rauwolfia alkaloids should be administered cautiously in patients with a history of peptic ulcer or ulcerative colitis because of the risk of reactivation.

Corticotropin 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 chlorthalidone in chlorthalidone / reserpine has a major potential interaction with Liver Disease.

Patients with severe liver disease or cirrhosis are very susceptible to thiazide-induced hypokalemic hypochloremic alkalosis. Blood ammonia concentrations may be further increased in patients with previously elevated concentrations. Hepatic encephalopathy and death have occurred secondary to the electrolyte alterations accompanying diuretic use. Therapy with thiazide diuretics should be administered cautiously in patients with impaired hepatic function or progressive liver disease, and discontinued promptly if signs of impending hepatic coma appear (e.g., tremors, confusion, and increased jaundice).

The chlorthalidone in chlorthalidone / reserpine has a major potential interaction with Lupus Erythematosus.

The use of thiazide diuretics has been reported to possibly exacerbate or activate systemic lupus erythematosus. Reported cases have generally been associated with chlorothiazide and hydrochlorothiazide. Therapy with thiazide diuretics should be administered cautiously in patients with a history or risk of SLE.

The chlorthalidone in chlorthalidone / reserpine has a major potential interaction with Magnesium Imbalance.

The use of thiazide diuretics is commonly associated with loss of electrolytes, most significantly potassium but also sodium, chloride, bicarbonate, and magnesium. The loss of other electrolytes such as phosphate, bromide and iodide is usually slight. Potassium and magnesium depletion may lead to cardiac arrhythmias and cardiac arrest. Other electrolyte-related complications include metabolic alkalosis and hyponatremia, which are rarely life-threatening. Therapy with thiazide diuretics should be administered cautiously in patients with or predisposed to fluid and electrolyte depletion, including patients with primary or secondary aldosteronism (may have low potassium levels); those with severe or prolonged diarrhea or vomiting; and those with poor nutritional status. Fluid and electrolyte abnormalities should be corrected prior to initiating therapy, and blood pressure as well as serum electrolyte concentrations monitored periodically and maintained at normal ranges during therapy. Patients should be advised to immediately report signs and symptoms of fluid or electrolyte imbalance, including dry mouth, thirst, weakness, lethargy, drowsiness, restlessness, muscle pains or cramps, muscular fatigue, hypotension, oliguria, tachycardia, arrhythmia, or gastrointestinal disturbances such as nausea and vomiting. Digitalized patients and patients with a history of ventricular arrhythmias should be monitored carefully, since development of hypokalemia may be particularly dangerous in these patients. The risk of hypokalemia may be minimized by slow diuresis, a lower thiazide dosage, potassium supplementation, or combined use with a potassium-sparing diuretic.

The chlorthalidone in chlorthalidone / reserpine has a major potential interaction with Malnourishment.

The use of thiazide diuretics is commonly associated with loss of electrolytes, most significantly potassium but also sodium, chloride, bicarbonate, and magnesium. The loss of other electrolytes such as phosphate, bromide and iodide is usually slight. Potassium and magnesium depletion may lead to cardiac arrhythmias and cardiac arrest. Other electrolyte-related complications include metabolic alkalosis and hyponatremia, which are rarely life-threatening. Therapy with thiazide diuretics should be administered cautiously in patients with or predisposed to fluid and electrolyte depletion, including patients with primary or secondary aldosteronism (may have low potassium levels); those with severe or prolonged diarrhea or vomiting; and those with poor nutritional status. Fluid and electrolyte abnormalities should be corrected prior to initiating therapy, and blood pressure as well as serum electrolyte concentrations monitored periodically and maintained at normal ranges during therapy. Patients should be advised to immediately report signs and symptoms of fluid or electrolyte imbalance, including dry mouth, thirst, weakness, lethargy, drowsiness, restlessness, muscle pains or cramps, muscular fatigue, hypotension, oliguria, tachycardia, arrhythmia, or gastrointestinal disturbances such as nausea and vomiting. Digitalized patients and patients with a history of ventricular arrhythmias should be monitored carefully, since development of hypokalemia may be particularly dangerous in these patients. The risk of hypokalemia may be minimized by slow diuresis, a lower thiazide dosage, potassium supplementation, or combined use with a potassium-sparing diuretic.

Corticotropin 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.

Corticotropin 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.

Corticotropin 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.

Corticotropin 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.

The reserpine in chlorthalidone / reserpine has a major potential interaction with Peptic Ulcer.

The use of rauwolfia alkaloids is contraindicated in patients with active peptic ulcer or ulcerative colitis. Since rauwolfia alkaloids increase gastrointestinal motility and secretion, these conditions may be aggravated. Therapy with rauwolfia alkaloids should be administered cautiously in patients with a history of peptic ulcer or ulcerative colitis because of the risk of reactivation.

Corticotropin 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.

Corticotropin 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.

The chlorthalidone in chlorthalidone / reserpine has a major potential interaction with Renal Dysfunction.

Thiazide diuretics may be ineffective when the glomerular filtration rate is low (GFR < 25 mL/min) because they are not expected to be filtered into the renal tubule, their site of action. In addition, thiazide diuretics decrease the GFR and may precipitate azotemia in renal disease. Cumulative effects may also develop because most of these drugs are excreted unchanged in the urine by glomerular filtration and active tubular secretion. Therapy with thiazide diuretics should be administered cautiously at reduced dosages in patients with renal impairment. If renal function becomes progressively worse, as indicated by rising BUN or serum creatinine levels, an interruption or discontinuation of thiazide therapy should be considered.

Corticotropin 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 reserpine in chlorthalidone / reserpine has a moderate potential interaction with Renal Dysfunction.

In general, lowering the blood pressure may cause some decrease in renal function. Therefore, rauwolfia alkaloids should be used with caution in patients with renal impairment, since these patients may adjust poorly to the hypotensive effects of these agents.

Corticotropin 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.

Corticotropin 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.

Corticotropin 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.

The chlorthalidone in chlorthalidone / reserpine has a moderate potential interaction with Thyroid Disease.

Thiazide diuretics may decrease serum PBI (protein-bound iodine) levels without associated thyroid disturbance. Clinicians should be cognizant of this effect when prescribing or administering thiazide therapy to patients with thyroid disorders.

Corticotropin 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.

Corticotropin 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.

Corticotropin 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.

Corticotropin 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.

The chlorthalidone in chlorthalidone / reserpine has a major potential interaction with Ventricular Arrhythmia.

The use of thiazide diuretics is commonly associated with loss of electrolytes, most significantly potassium but also sodium, chloride, bicarbonate, and magnesium. The loss of other electrolytes such as phosphate, bromide and iodide is usually slight. Potassium and magnesium depletion may lead to cardiac arrhythmias and cardiac arrest. Other electrolyte-related complications include metabolic alkalosis and hyponatremia, which are rarely life-threatening. Therapy with thiazide diuretics should be administered cautiously in patients with or predisposed to fluid and electrolyte depletion, including patients with primary or secondary aldosteronism (may have low potassium levels); those with severe or prolonged diarrhea or vomiting; and those with poor nutritional status. Fluid and electrolyte abnormalities should be corrected prior to initiating therapy, and blood pressure as well as serum electrolyte concentrations monitored periodically and maintained at normal ranges during therapy. Patients should be advised to immediately report signs and symptoms of fluid or electrolyte imbalance, including dry mouth, thirst, weakness, lethargy, drowsiness, restlessness, muscle pains or cramps, muscular fatigue, hypotension, oliguria, tachycardia, arrhythmia, or gastrointestinal disturbances such as nausea and vomiting. Digitalized patients and patients with a history of ventricular arrhythmias should be monitored carefully, since development of hypokalemia may be particularly dangerous in these patients. The risk of hypokalemia may be minimized by slow diuresis, a lower thiazide dosage, potassium supplementation, or combined use with a potassium-sparing diuretic.

The chlorthalidone in chlorthalidone / reserpine has a major potential interaction with Vomiting.

The use of thiazide diuretics is commonly associated with loss of electrolytes, most significantly potassium but also sodium, chloride, bicarbonate, and magnesium. The loss of other electrolytes such as phosphate, bromide and iodide is usually slight. Potassium and magnesium depletion may lead to cardiac arrhythmias and cardiac arrest. Other electrolyte-related complications include metabolic alkalosis and hyponatremia, which are rarely life-threatening. Therapy with thiazide diuretics should be administered cautiously in patients with or predisposed to fluid and electrolyte depletion, including patients with primary or secondary aldosteronism (may have low potassium levels); those with severe or prolonged diarrhea or vomiting; and those with poor nutritional status. Fluid and electrolyte abnormalities should be corrected prior to initiating therapy, and blood pressure as well as serum electrolyte concentrations monitored periodically and maintained at normal ranges during therapy. Patients should be advised to immediately report signs and symptoms of fluid or electrolyte imbalance, including dry mouth, thirst, weakness, lethargy, drowsiness, restlessness, muscle pains or cramps, muscular fatigue, hypotension, oliguria, tachycardia, arrhythmia, or gastrointestinal disturbances such as nausea and vomiting. Digitalized patients and patients with a history of ventricular arrhythmias should be monitored carefully, since development of hypokalemia may be particularly dangerous in these patients. The risk of hypokalemia may be minimized by slow diuresis, a lower thiazide dosage, potassium supplementation, or combined use with a potassium-sparing diuretic.