Interactions between Nalidixic acid and Steglatro
1 drug interaction and 21 additional warnings found for the following 2 drugs:
- nalidixic acid
- Steglatro (ertugliflozin)
Drug interactions
Moderate drug interactions
Moderate:
nalidixic acid ertugliflozin
Applies to: nalidixic acid and Steglatro (ertugliflozin)
Monitor
Quinolone antibiotics may interfere with the therapeutic effects of insulin and other antidiabetic agents. The use of quinolones has been associated with disturbances in blood glucose homeostasis possibly stemming from effects on pancreatic beta cell ATP-sensitive potassium channels that regulate insulin secretion. Both hyperglycemia and hypoglycemia have been reported, usually in diabetic patients receiving concomitant treatment with an oral hypoglycemic agent (e.g., sulfonylurea) or insulin. Although hyperglycemia is significantly more common and infection itself may be an underlying risk factor, hypoglycemia may cause greater morbidity and mortality. An internal safety review conducted by the U.S. Food and Drug Administration (FDA) identified at least 67 reports of severe hypoglycemia associated with quinolone use resulting in coma, death, or permanent and disabling injuries, primarily in elderly and diabetic patients with renal impairment and/or complicated infections. This is in addition to the numerous cases that have been reported for gatifloxacin, which led to its withdrawal from the U.S. market in 2008. Of the five quinolones that the FDA reviewed, levofloxacin had the most cases (44), followed by ciprofloxacin (12), moxifloxacin (9), ofloxacin (2), and gemifloxacin (0). Other quinolones such as nalidixic acid and norfloxacin, as well as some others that have never been marketed or are no longer marketed such as clinafloxacin and temafloxacin, have also been associated with dysglycemia, thus it is generally believed to be a class effect, albeit with varying risks amongst the individual agents. Available data also seem to indicate different time frames for the development of hypo- and hyperglycemia, with the former generally occurring within 1 to 3 days following quinolone initiation and the latter within 4 to 10 days later.
Management
Blood glucose should be closely monitored whenever quinolones are prescribed to diabetic patients, especially if they are elderly, have renal impairment, or are severely ill. Patients should be apprised of the increased risk of dysglycemia and be particularly alert to potential signs and symptoms of hypoglycemia such as headache, dizziness, drowsiness, nervousness, confusion, tremor, hunger, weakness, perspiration, palpitation, and tachycardia. If hypoglycemia occurs, patients should initiate appropriate remedial therapy immediately, discontinue the quinolone, and contact their physician. Alternative antibiotics may need to be considered.
References (42)
- (2002) "Product Information. Cipro (ciprofloxacin)." Bayer
- (2001) "Product Information. Noroxin (norfloxacin)." Merck & Co., Inc
- (2001) "Product Information. Floxin (ofloxacin)." Ortho McNeil Pharmaceutical
- (2001) "Product Information. Levaquin (levofloxacin)." Ortho McNeil Pharmaceutical
- (2001) "Product Information. Raxar (grepafloxacin)." Glaxo Wellcome
- (2001) "Product Information. Trovan (trovafloxacin)." Pfizer U.S. Pharmaceuticals
- Edwards DJ, Bowles SK, Svensson CK, Rybak MJ (1988) "Inhibition of drug metabolism by quinolone antibiotics." Clin Pharmacokinet, 15, p. 194-204
- (2001) "Product Information. Tequin (gatifloxacin)." Bristol-Myers Squibb
- Gajjar DA, LaCreta FP, Kollia GD, et al. (2000) "Effect of multiple-dose gatifloxacin or ciprofloxacin on glucose homeostasis and insulin production in patients with noninsulin-dependent diabetes mellitus maintained with diet and exercise." Pharmacotherapy, 20 (6 Pt 2), s76-86
- Roberge RJ, Kaplan R, Frank R, Fore C (2000) "Glyburide-ciprofloxacin interaction with resistant hypoglycemia." Ann Emerg Med, 36, p. 160-3
- Rubinstein E (2001) "History of quinolones and their side effects." Chemotherapy, 47 Suppl 3, p. 3-8
- Menzies DJ, Dorsainvil PA, Cunha BA, Johnson DH (2002) "Severe and persistent hypoglycemia due to gatifloxacin interaction with oral hypoglycemic agents." Am J Med, 113, p. 232-4
- Baker SE, Hangii MC (2002) "Possible gatifloxacin-induced hypoglycemia." Ann Pharmacother, 36, p. 1722-6
- (2003) "Product Information. Factive (gemifloxacin)." *GeneSoft Inc
- (2003) "Hypoglycemia and hyperglycemia with fluoroquinolones." Med Lett Drugs Ther, 45, p. 64
- Donaldson AR, Vandiver JR, Finch CK (2004) "Possible gatifloxacin-induced hyperglycemia." Ann Pharmacother, 38, p. 602-5
- LeBlanc M, Belanger C, Cossette P (2004) "Severe and resistant hypoglycemia associated with concomitant gatifloxacin and glyburide therapy." Pharmacotherapy, 24, p. 926-31
- Biggs WS (2004) "Hypoglycemia and hyperglycemia associated with gatifloxacin use in elderly patients." J Am Board Fam Pract, 16, p. 455-7
- Gavin JR 3rd, Kubin R, Choudhri S, et al. (2004) "Moxifloxacin and glucose homeostasis: a pooled-analysis of the evidence from clinical and postmarketing studies." Drug Saf, 27, p. 671-86
- Saraya A, Yokokura M, Gonoi T, Seino S (2004) "Effects of fluoroquinolones on insulin secretion and beta-cell ATP-sensitive K(+) channels." Eur J Pharmacol, 497, p. 111-7
- Lin G, Hays DP, Spillane L (2004) "Refractory hypoglycemia from ciprofloxacin and glyburide interaction." J Toxicol Clin Toxicol, 42, p. 295-7
- Friedrich LV, Dougherty R (2004) "Fatal hypoglycemia associated with levofloxacin." Pharmacotherapy, 24, p. 1807-12
- Khovidhunkit W, Sunthornyothin S (2004) "Hypoglycemia, hyperglycemia, and gatifloxacin." Ann Intern Med, 141, p. 969
- Happe MR, Mulhall BP, Maydonovitch CL, Holtzmuller KC (2004) "Gatifloxacin-induced hyperglycemia." Ann Intern Med, 141, p. 968-9
- Greenberg AL, Decerbo M, Fan J (2005) "Gatifloxacin therapy associated with hypoglycemia." Clin Infect Dis, 40, p. 1210-1
- Blommel AL, Lutes RA (2005) "Severe hyperglycemia during renally adjusted gatifloxacin therapy." Ann Pharmacother, 39, p. 1349-52
- Brogan SE, Cahalan MK (2005) "Gatifloxacin as a possible cause of serious postoperative hypoglycemia." Anesth Analg, 101, p. 635-6
- Graumlich JF, Habis S, Avelino RR, et al. (2005) "Hypoglycemia in inpatients after gatifloxacin or levofloxacin therapy: nested case-control study." Pharmacotherapy, 25, p. 1296-302
- Frothingham R (2005) "Glucose homeostasis abnormalities associated with use of gatifloxacin." Clin Infect Dis, 41, p. 1269-76
- Bhasin R, Arce FC, Pasmantier R (2005) "Hypoglycemia associated with the use of gatifloxacin." Am J Med Sci, 330, p. 250-3
- McMorran M, Morrison H, Letourneau G (2006) Gatifloxacin (Tequin): hypoglycemia and hyperglycemia. http://www.hc-sc.gc.ca/dhp-mps/medeff/bulletin/carn-bcei_v13n3_e.html#1
- Park-Wyllie LY, Juurlink DN, Kopp A, et al. (2006) "Outpatient gatifloxacin therapy and dysglycemia in older adults." N Engl J Med, 354, p. 1352-61
- Wang S, Rizvi AA (2006) "Levofloxacin-induced hypoglycemia in a nondiabetic patient." Am J Med Sci, 331, p. 334-5
- Kanbay M, Aydogan T, Bozalan R, et al. (2006) "A rare but serious side effect of levofloxacin: hypoglycemia in a geriatric patient." Diabetes Care, 29, p. 1716-7
- Zvonar R (2006) "Gatifloxacin-induced dysglycemia." Am J Health Syst Pharm, 63, p. 2087-2092
- Zhanel GG, Fontaine S, Adam H, et al. (2006) "A Review of New Fluoroquinolones : Focus on their Use in Respiratory Tract Infections." Treat Respir Med, 5, p. 437-465
- Yip C, Lee AJ (2006) "Gatifloxacin-induced hyperglycemia: a case report and summary of the current literature." Clin Ther, 28, p. 1857-66
- Tomita T, Onishi M, Sato E, Kimura Y, Kihira K (2007) "Gatifloxacin induces augmented insulin release and intracellular insulin." Biol Pharm Bull, 30, p. 644-7
- Kelesidis T, Canseco E (2010) "Quinolone-induced hypoglycemia: a life-threatening but potentially reversible side effect." Am J Med, 123, e5-6
- (2017) "Product Information. Baxdela (delafloxacin)." Melinta Therapeutics, Inc.
- (2021) "Product Information. Ciprofloxacin Hydrochloride (ciprofloxacin)." Aurobindo Pharma USA Inc
- FDA. Food and Drug Admnistration (2023) FDA reinforces safety information about serious low blood sugar levels and mental health side effects with fluoroquinolone antibiotics; requires label changes. https://www.fda.gov/drugs/drug-safety-and-availability/fda-reinforces-safety-information-about
Food/lifestyle interactions
Moderate food/lifestyle interactions
Moderate:
ertugliflozin Food/Lifestyle
Applies to: Steglatro (ertugliflozin)
Generally avoid
Alcohol may cause hypoglycemia or hyperglycemia in patients with diabetes. Hypoglycemia most frequently occurs during acute consumption of alcohol. Even modest amounts can lower blood sugar significantly, especially when the alcohol is ingested on an empty stomach or following exercise. The mechanism involves inhibition of both gluconeogenesis as well as the counter-regulatory response to hypoglycemia. Episodes of hypoglycemia may last for 8 to 12 hours after ethanol ingestion. By contrast, chronic alcohol abuse can cause impaired glucose tolerance and hyperglycemia. Moderate alcohol consumption generally does not affect blood glucose levels in patients with well controlled diabetes. A disulfiram-like reaction (e.g., flushing, headache, and nausea) to alcohol has been reported frequently with the use of chlorpropamide and very rarely with other sulfonylureas.
Management
Patients with diabetes should avoid consuming alcohol if their blood glucose is not well controlled, or if they have hypertriglyceridemia, neuropathy, or pancreatitis. Patients with well controlled diabetes should limit their alcohol intake to one drink daily for women and two drinks daily for men (1 drink = 5 oz wine, 12 oz beer, or 1.5 oz distilled spirits) in conjunction with their normal meal plan. Alcohol should not be consumed on an empty stomach or following exercise.
References (11)
- Jerntorp P, Almer LO (1981) "Chlorpropamide-alcohol flushing in relation to macroangiopathy and peripheral neuropathy in non-insulin dependent diabetes." Acta Med Scand, 656, p. 33-6
- Jerntorp P, Almer LO, Holin H, et al. (1983) "Plasma chlorpropamide: a critical factor in chlorpropamide-alcohol flush." Eur J Clin Pharmacol, 24, p. 237-42
- Barnett AH, Spiliopoulos AJ, Pyke DA, et al. (1983) "Metabolic studies in chlorpropamide-alcohol flush positive and negative type 2 (non-insulin dependent) diabetic patients with and without retinopathy." Diabetologia, 24, p. 213-5
- Hartling SG, Faber OK, Wegmann ML, Wahlin-Boll E, Melander A (1987) "Interaction of ethanol and glipizide in humans." Diabetes Care, 10, p. 683-6
- (2002) "Product Information. Diabinese (chlorpropamide)." Pfizer U.S. Pharmaceuticals
- (2002) "Product Information. Glucotrol (glipizide)." Pfizer U.S. Pharmaceuticals
- "Product Information. Diabeta (glyburide)." Hoechst Marion-Roussel Inc, Kansas City, MO.
- Skillman TG, Feldman JM (1981) "The pharmacology of sulfonylureas." Am J Med, 70, p. 361-72
- (2002) "Position Statement: evidence-based nutrition principles and recommendations for the treatment and prevention of diabetes related complications. American Diabetes Association." Diabetes Care, 25(Suppl 1), S50-S60
- Cerner Multum, Inc. "UK Summary of Product Characteristics."
- (2026) "Product Information. Awiqli FlexTouch (insulin icodec)." Novo Nordisk Pharmaceuticals Inc
Moderate:
nalidixic acid multivitamins with minerals
Applies to: nalidixic acid
Adjust dosing interval
Oral preparations that contain magnesium, aluminum, or calcium may significantly decrease the gastrointestinal absorption of nalidixic acid. Absorption may also be reduced by sucralfate, which contains aluminum, as well as other polyvalent cations such as iron and zinc. The mechanism is chelation of nalidixic acid by polyvalent cations, forming a complex that is poorly absorbed from the gastrointestinal tract.
Management
When coadministration cannot be avoided, nalidixic acid should be dosed at least 2 hours before or 2 hours after polyvalent cation-containing products to minimize the potential for interaction.
References (1)
- "Product Information. Neggram (nalidixic acid)." Sanofi Winthrop Pharmaceuticals
Moderate:
nalidixic acid Caffeine
Applies to: nalidixic acid
Monitor
Coadministration with certain quinolones may increase the plasma concentrations and pharmacologic effects of caffeine due to inhibition of the CYP450 1A2 metabolism of caffeine. Quinolones that may inhibit CYP450 1A2 include ciprofloxacin, enoxacin, grepafloxacin, nalidixic acid, norfloxacin, pipemidic acid, and pefloxacin (not all commercially available). In healthy volunteers, enoxacin (100 to 400 mg twice daily) increased systemic exposure (AUC) of caffeine by 2- to 5-fold and reduced its clearance by approximately 80%. Pipemidic acid (400 to 800 mg twice daily) increased AUC of caffeine by 2- to 3-fold and reduced its clearance by approximately 60%. Ciprofloxacin (250 to 750 mg twice daily) increased AUC and elimination half-life of caffeine by 50% to over 100%, and reduced its clearance by 30% to 50%. Norfloxacin 400 mg twice daily increased caffeine AUC by 16%, while 800 mg twice daily increased caffeine AUC by 52% and reduced its clearance by 35%. Pefloxacin (400 mg twice daily) has been shown to reduce caffeine clearance by 47%.
Management
Patients using caffeine-containing products should be advised that increased adverse effects such as headache, tremor, restlessness, nervousness, insomnia, tachycardia, and blood pressure increases may occur during coadministration with quinolones that inhibit CYP450 1A2. Caffeine intake should be limited when taking high dosages of these quinolones. If an interaction is suspected, other quinolones such as gatifloxacin, gemifloxacin, levofloxacin, lomefloxacin, moxifloxacin, and ofloxacin may be considered, since they are generally believed to have little or no effect on CYP450 1A2 or have been shown not to interact with caffeine.
References (17)
- Polk RE (1989) "Drug-drug interactions with ciprofloxacin and other fluoroquinolones." Am J Med, 87, s76-81
- Healy DP, Polk RE, Kanawati L, Rock DT, Mooney ML (1989) "Interaction between oral ciprofloxacin and caffeine in normal volunteers." Antimicrob Agents Chemother, 33, p. 474-8
- Harder S, Fuhr U, Staib AH, Wolf T (1989) "Ciprofloxacin-caffeine: a drug interaction established using in vivo and in vitro investigations." Am J Med, 87, p. 89-91
- Carbo ML, Segura J, De la Torre R, et al. (1989) "Effect of quinolones on caffeine disposition." Clin Pharmacol Ther, 45, p. 234-40
- (1993) "Product Information. Penetrax (enoxacin)." Rhone-Poulenc Rorer, Collegeville, PA.
- Mahr G, Sorgel F, Granneman GR, et al. (1992) "Effects of temafloxacin and ciprofloxacin on the pharmacokinetics of caffeine." Clin Pharmacokinet, 22, p. 90-7
- (2002) "Product Information. Cipro (ciprofloxacin)." Bayer
- (2001) "Product Information. Noroxin (norfloxacin)." Merck & Co., Inc
- Staib AH, Stille W, Dietlein G, et al. (1987) "Interaction between quinolones and caffeine." Drugs, 34 Suppl 1, p. 170-4
- Stille W, Harder S, Micke S, et al. (1987) "Decrease of caffeine elimination in man during co-administration of 4-quinolones." J Antimicrob Chemother, 20, p. 729-34
- Harder S, Staib AH, Beer C, Papenburg A, Stille W, Shah PM (1988) "4-Quinolones inhibit biotransformation of caffeine." Eur J Clin Pharmacol, 35, p. 651-6
- Nicolau DP, Nightingale CH, Tessier PR, et al. (1995) "The effect of fleroxacin and ciprofloxacin on the pharmacokinetics of multiple dose caffeine." Drugs, 49 Suppl 2, p. 357-9
- (2001) "Product Information. Raxar (grepafloxacin)." Glaxo Wellcome
- Carrillo JA, Benitez J (2000) "Clinically significant pharmacokinetic interactions between dietary caffeine and medications." Clin Pharmacokinet, 39, p. 127-53
- Fuhr U, Wolff T, Harder S, Schymanski P, Staib AH (1990) "Quinolone inhibition of cytochrome P-450 dependent caffeine metabolism in human liver microsomes." Drug Metab Dispos, 18, p. 1005-10
- Kinzig-Schippers M, Fuhr U, Zaigler M, et al. (1999) "Interaction of pefloxacin and enoxacin with the human cytochrome P450 enzyme CYP1A2." Clin Pharmacol Ther, 65, p. 262-74
- Healy DP, Schoenle JR, Stotka J, Polk RE (1991) "Lack of interaction between lomefloxacin and caffeine in normal volunteers." Antimicrob Agents Chemother, 35, p. 660-4
Disease interactions
18 potential interactions Applies to: 15 conditions, including Rheumatoid Arthritis, Peripheral Neuropathy, Diarrhea, Hypotension, and Myasthenia Gravis.
Central Nervous System Disorders
Major:
nalidixic acid
Nalidixic acid has a major potential interaction with Central Nervous System Disorders.
Quinolones may cause CNS stimulation manifested as tremors, agitation, restlessness, anxiety, confusion, hallucinations, paranoia, insomnia, toxic psychosis, and/or seizures. Benign intracranial hypertension has also been reported. Therapy with quinolones should be administered cautiously in patients with or predisposed to seizures or other CNS abnormalities. In addition, these patients should be advised to avoid the consumption of caffeine-containing products during therapy with some quinolones, most notably ciprofloxacin, enoxacin, and cinoxacin, since these agents can substantially reduce the clearance of caffeine and other methylxanthines, potentially resulting in severe CNS reactions.
Dehydration
Moderate:
nalidixic acid
Nalidixic acid has a moderate potential interaction with Dehydration.
Crystalluria has been reported rarely during quinolone therapy. Although it is not expected to occur under normal circumstances with usual recommended dosages, patients who are dehydrated (e.g., due to severe diarrhea or vomiting) may be at increased risk and should be encouraged to consume additional amounts of liquid or given intravenous fluid to ensure an adequate urinary output. Alkalinity of the urine should be avoided, since it may also increase the risk of crystalluria. Renal function tests should be performed periodically during prolonged therapy (> 2 weeks).
Diabetes Mellitus
Moderate:
nalidixic acid
Nalidixic acid has a moderate potential interaction with Diabetes Mellitus.
The use of certain quinolones has been associated with disturbances in blood glucose homeostasis possibly stemming from effects on pancreatic beta cell ATP-sensitive potassium channels that regulate insulin secretion. Hypoglycemia and, less frequently, hyperglycemia have been reported, although the latter may also occur due to infection alone. Hypoglycemia has usually occurred in patients with diabetes receiving concomitant oral hypoglycemic agents and/or insulin. Administration of ciprofloxacin, levofloxacin, norfloxacin, and especially gatifloxacin in patients treated with sulfonylureas or other oral hypoglycemic agents has resulted in severe, refractory hypoglycemia and hypoglycemic coma. Elderly patients and patients with reduced renal function are particularly susceptible. Blood glucose should be monitored more closely whenever quinolones are prescribed to patients with diabetes. Gatifloxacin has been known to cause hypoglycemic episodes generally within the first 3 days of therapy and sometimes even after the first dose, while hyperglycemia usually occurs 4 to 10 days after initiation of therapy. Patients should be counseled to recognize symptoms of hypoglycemia such as headache, dizziness, drowsiness, nausea, tremor, weakness, hunger, excessive perspiration, and palpitations. If hypo- or hyperglycemia occur during quinolone therapy, patients should initiate appropriate remedial therapy immediately, discontinue the antibiotic, and contact their physician.
Diarrhea
Moderate:
nalidixic acid
Nalidixic acid has a moderate potential interaction with Diarrhea.
Crystalluria has been reported rarely during quinolone therapy. Although it is not expected to occur under normal circumstances with usual recommended dosages, patients who are dehydrated (e.g., due to severe diarrhea or vomiting) may be at increased risk and should be encouraged to consume additional amounts of liquid or given intravenous fluid to ensure an adequate urinary output. Alkalinity of the urine should be avoided, since it may also increase the risk of crystalluria. Renal function tests should be performed periodically during prolonged therapy (> 2 weeks).
Hypotension
Moderate:
Steglatro
The ertugliflozin in Steglatro has a moderate potential interaction with Hypotension.
Sodium-glucose cotransporter 2 (SGLT2) inhibitors cause intravascular volume contraction which may lead to symptomatic hypotension after treatment initiation, especially in older adult patients, patients with impaired renal function, patients with low systolic blood pressure, or those using diuretics. Volume status should be assessed and corrected before starting treatment and patients should be monitored during therapy.
Infection
Moderate:
Steglatro
The ertugliflozin in Steglatro has a moderate potential interaction with Infection.
Sodium-glucose cotransporter 2 (SGLT2) inhibitors increase the risk of genital mycotic infections. Care should be exercised when using an SGLT2 inhibitor in patients who have a history of chronic or recurrent genital mycotic infections or who are uncircumcised as these patients are more likely to develop genital mycotic infections. Patients should be monitored and treated appropriately.
Liver Disease
Major:
nalidixic acid
Nalidixic acid has a major potential interaction with Liver Disease.
Nalidixic acid is primarily metabolized by the liver and may accumulate in patients with impaired hepatic function. Therapy with nalidixic acid should be administered cautiously in patients with liver disease.
Major:
Steglatro
The ertugliflozin in Steglatro has a major potential interaction with Liver Disease.
Sodium-glucose cotransporter 2 (SGLT2) inhibitors ertugliflozin and canagliflozin are not recommended for use in patients with severe hepatic impairment due to lack of clinical data. Sotagliflozin is not recommended for use in patients with moderate to severe hepatic impairment. Dapagliflozin has not been studied in patients with severe hepatic impairment and caution is recommended. The manufacturer's product labeling should be consulted for specific dosing of SGLT2 inhibitors in patients with hepatic impairment.
Myasthenia Gravis
Major:
nalidixic acid
Nalidixic acid has a major potential interaction with Myasthenia Gravis.
Fluoroquinolones have neuromuscular blocking activity and may exacerbate muscle weakness in persons with myasthenia gravis. Postmarketing serious adverse events, including deaths and requirement for ventilatory support, have been associated with fluoroquinolones use in persons with myasthenia gravis. Fluoroquinolones should be avoided in patients with history of myasthenia gravis.
Noninfectious Colitis
Major:
nalidixic acid
Nalidixic acid has a major potential interaction with Noninfectious Colitis.
Clostridioides difficile-associated diarrhea (CDAD), formerly pseudomembranous colitis, has been reported with almost all antibacterial drugs and may range from mild diarrhea to fatal colitis. The most common culprits include clindamycin and lincomycin. Antibacterial therapy alters the normal flora of the colon, leading to overgrowth of C difficile, whose toxins A and B contribute to CDAD development. Morbidity and mortality are increased with hypertoxin-producing strains of C difficile; these infections can be resistant to antimicrobial therapy and may require colectomy. CDAD must be considered in all patients who present with diarrhea after antibacterial use. Since CDAD has been reported to occur more than 2 months after antibacterial use, careful medical history is necessary. Therapy with broad-spectrum antibacterials and other agents with significant antibacterial activity should be administered cautiously in patients with history of gastrointestinal disease, particularly colitis; pseudomembranous colitis (generally characterized by severe, persistent diarrhea and severe abdominal cramps, and sometimes associated with the passage of blood and mucus), if it occurs, may be more severe in these patients and may be associated with flares in underlying disease activity. Antibacterial drugs not directed against C difficile may need to be stopped if CDAD is suspected or confirmed. Appropriate fluid and electrolyte management, protein supplementation, antibacterial treatment of C difficile, and surgical evaluation should be started as clinically indicated.
Organ Transplant
Major:
nalidixic acid
Nalidixic acid has a major potential interaction with Organ Transplant.
Tendonitis and ruptures of the shoulder, hand, and Achilles tendons have been reported in patients receiving quinolones, both during and after treatment. Avoid the use of these agents in patients who have a history of tendon disorders or have experienced tendinitis or tendon rupture. Therapy with quinolones should be administered cautiously in patients with patients with kidney, heart, and lung transplant, since it may delay the recognition or confound the diagnosis of a quinolone-induced musculoskeletal effect. Factors that may independently increase the risk of tendon rupture include strenuous physical activity, renal failure, and previous tendon disorders such as rheumatoid arthritis. It is recommended to discontinue these agents if, at any time during therapy, pain, inflammation or rupture of a tendon develops and institute appropriate treatment.
Peripheral Neuropathy
Major:
nalidixic acid
Nalidixic acid has a major potential interaction with Peripheral Neuropathy.
The use of quinolones has been associated with an increased risk of peripheral neuropathy. Monitor closely and discontinue their use in patients experiencing symptoms of peripheral neuropathy. It is recommended to avoid these agents in patients who have previously experienced peripheral neuropathy.
Renal Dysfunction
Major:
nalidixic acid
Nalidixic acid has a major potential interaction with Renal Dysfunction.
Tendonitis and ruptures of the shoulder, hand, and Achilles tendons have been reported in patients receiving quinolones, both during and after treatment. Avoid the use of these agents in patients who have a history of tendon disorders or have experienced tendinitis or tendon rupture. Therapy with quinolones should be administered cautiously in patients with patients with kidney, heart, and lung transplant, since it may delay the recognition or confound the diagnosis of a quinolone-induced musculoskeletal effect. Factors that may independently increase the risk of tendon rupture include strenuous physical activity, renal failure, and previous tendon disorders such as rheumatoid arthritis. It is recommended to discontinue these agents if, at any time during therapy, pain, inflammation or rupture of a tendon develops and institute appropriate treatment.
Major:
Steglatro
The ertugliflozin in Steglatro has a major potential interaction with Renal Dysfunction.
The glucose lowering effects of sodium-glucose cotransporter 2 (SGLT2) inhibitors are decreased in patients with worsening renal function. Additionally, patients with impaired renal function (estimated GFR less than 60 mL/min/1.73 m2), older adult patients, and patients on loop diuretics may be more likely to experience adverse reactions related to volume depletion such as hypotension and acute kidney injury during therapy. Renal function should be evaluated prior to treatment initiation and monitored regularly in at-risk patients. Volume status should be assessed and volume depletion corrected before initiating therapy. The use of SGLT2 inhibitors in patients undergoing dialysis is either contraindicated or not recommended. The manufacturer product information should be consulted for contraindications and indication specific renal dosing.
Moderate:
Steglatro
The ertugliflozin in Steglatro has a moderate potential interaction with Renal Dysfunction.
Sodium-glucose cotransporter 2 (SGLT2) inhibitors cause intravascular volume contraction which may lead to symptomatic hypotension after treatment initiation, especially in older adult patients, patients with impaired renal function, patients with low systolic blood pressure, or those using diuretics. Volume status should be assessed and corrected before starting treatment and patients should be monitored during therapy.
Rheumatoid Arthritis
Major:
nalidixic acid
Nalidixic acid has a major potential interaction with Rheumatoid Arthritis.
Tendonitis and ruptures of the shoulder, hand, and Achilles tendons have been reported in patients receiving quinolones, both during and after treatment. Avoid the use of these agents in patients who have a history of tendon disorders or have experienced tendinitis or tendon rupture. Therapy with quinolones should be administered cautiously in patients with patients with kidney, heart, and lung transplant, since it may delay the recognition or confound the diagnosis of a quinolone-induced musculoskeletal effect. Factors that may independently increase the risk of tendon rupture include strenuous physical activity, renal failure, and previous tendon disorders such as rheumatoid arthritis. It is recommended to discontinue these agents if, at any time during therapy, pain, inflammation or rupture of a tendon develops and institute appropriate treatment.
Tendonitis
Major:
nalidixic acid
Nalidixic acid has a major potential interaction with Tendonitis.
Tendonitis and ruptures of the shoulder, hand, and Achilles tendons have been reported in patients receiving quinolones, both during and after treatment. Avoid the use of these agents in patients who have a history of tendon disorders or have experienced tendinitis or tendon rupture. Therapy with quinolones should be administered cautiously in patients with patients with kidney, heart, and lung transplant, since it may delay the recognition or confound the diagnosis of a quinolone-induced musculoskeletal effect. Factors that may independently increase the risk of tendon rupture include strenuous physical activity, renal failure, and previous tendon disorders such as rheumatoid arthritis. It is recommended to discontinue these agents if, at any time during therapy, pain, inflammation or rupture of a tendon develops and institute appropriate treatment.
Vomiting
Moderate:
nalidixic acid
Nalidixic acid has a moderate potential interaction with Vomiting.
Crystalluria has been reported rarely during quinolone therapy. Although it is not expected to occur under normal circumstances with usual recommended dosages, patients who are dehydrated (e.g., due to severe diarrhea or vomiting) may be at increased risk and should be encouraged to consume additional amounts of liquid or given intravenous fluid to ensure an adequate urinary output. Alkalinity of the urine should be avoided, since it may also increase the risk of crystalluria. Renal function tests should be performed periodically during prolonged therapy (> 2 weeks).
More resources
nalidixic acid
A total of 320 drugs are known to interact with nalidixic acid.
- Nalidixic acid is in the following drug classes: quinolones and Fluoroquinolones, urinary anti-infectives.
- Nalidixic acid is used to treat the following conditions:
Steglatro
A total of 413 drugs are known to interact with Steglatro.
- Steglatro is in the drug class SGLT-2 inhibitors.
- Steglatro is used to treat Type 2 Diabetes.
Drug Interaction Classification
| Highly clinically significant. Avoid combinations; the risk of the interaction outweighs the benefit. | |
| Moderately clinically significant. Usually avoid combinations; use it only under special circumstances. | |
| 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. | |
| No interaction information available. |
Further information
Always consult your healthcare provider to ensure the information displayed on this page applies to your personal circumstances.