Presence of Gastric Malignancy: In adults, symptomatic response to therapy with DEXILANT does not preclude the presence of gastric malignancy. Consider additional follow-up and diagnostic testing in adult patients who have a suboptimal response or an early symptomatic relapse after completing treatment with a PPI. In older patients, also consider an endoscopy.
Acute Interstitial Nephritis: Acute interstitial nephritis has been observed in patients taking PPIs including lansoprazole. Acute interstitial nephritis may occur at any point during PPI therapy and is generally attributed to an idiopathic hypersensitivity reaction. Discontinue DEXILANT if acute interstitial nephritis develops (see Contraindications).
Cyanocobalamin (Vitamin B-12) Deficiency: Daily treatment with any acid-suppressing medications over a long period of time (e.g., longer than 3 years) may lead to malabsorption of cyanocobalamin (vitamin B-12) caused by hypo- or achlorhydria. Rare reports of cyanocobalamin deficiency occurring with acid-suppressing therapy have been reported in the literature. This diagnosis should be considered if clinical symptoms consistent with cyanocobalamin deficiency are obsereved in patients treated with DEXILANT.
Clostridium difficile-Associated Diarrhea: Published observational studies suggest that PPI therapy like DEXILANT may be associated with an increased risk of Clostridium difficile associated diarrhea, especially in hospitalized patients. This diagnosis should be considered for diarrhea that does not improve (see Adverse Reactions).
Patients should use the lowest dose and shortest duration of PPI therapy appropriate to the condition being treated.
Bone Fracture: Several published observational studies suggest that proton pump inhibitor (PPI) therapy may be associated with an increased risk for osteoporosis-related fractures of the hip, wrist or spine. The risk of fracture was increased in patients who received high-dose, defined as multiple daily doses, and long-term PPI therapy (a year or longer). Patients should use the lowest dose and shortest duration of PPI therapy appropriate to the conditions being treated.
Patients at risk for osteoporosis-related fractures should be managed according to established treatment guidelines (see Dosage & Administration and Adverse Reactions).
Hypomagnesemia: Hypomagnesemia, symptomatic and asymptomatic, has been reported rarely in patients treated with PPIs for at least three months, in most cases after a year of therapy. Serious adverse events include tetany, arrhythmias, and seizures. In most patients, treatment of hypomagnesemia required magnesium replacement and discontinuation of the PPI.
For patients expected to be on prolonged treatment or who take PPIs with medications such as digoxin or drugs that may cause hypomagnesemia (e.g., diuretics), health care professionals may consider monitoring magnesium levels prior to initiation of PPI treatment and periodically (see Adverse Reactions).
Interactions with Investigations for Neuroendocrine Tumors: Serum chromogranin A (CgA) levels increase secondary to drug-induced decreases in gastric acidity. The increased CgA level may cause false positive results in diagnostic investigations for neuroendocrine tumors. Healthcare providers should temporarily stop dexlansoprazole treatment at least 14 days before assessing CgA levels and consider repeating the test if initial CgA levels are high. If serial tests are performed (e.g. for monitoring), the same commercial laboratory should be used for testing, as reference ranges between tests may vary (see Pharmacology under Actions and Interactions).
Interaction with Methotrexate: Literature suggests that concomitant use of PPIs with methotrexate (primarily at high dose) may elevate and prolong serum levels of methotrexate and/or its metabolite, possibly leading to methotrexate toxicities. In high-dose methotrexate administration, a temporary withdrawal of the PPI may be considered in some patients (see Interactions).
Cutaneous and Systemic Lupus Erythematosus: Cutaneous lupus erythematosus (CLE) and systemic lupus erythematosus (SLE) have been reported in patients taking PPIs, including lansoprazole. These events have occurred as both new onset and an exacerbation of existing autoimmune disease. The majority of PPI-induced lupus erythematosus cases were CLE.
The most common form of CLE reported in patients treated with PPIs was subacute CLE (SCLE) and occurred within weeks to years after continuous drug therapy in patients ranging from infants to the elderly. Generally, histological findings were observed without organ involvement.
Systemic lupus erythematosus (SLE) is less commonly reported than CLE in patients receiving PPIs. PPI associated SLE is usually milder than non-drug induced SLE. Onset of SLE typically occurred within days to years after initiating treatment primarily in patients ranging from young adults to the elderly. The majority of patients presented with rash; however, arthralgia and cytopenia were also reported.
Avoid administration of PPIs for longer than medically indicated. If signs or symptoms consistent with CLE or SLE are noted in patients receiving DEXILANT, discontinue the drug and refer the patient to the appropriate specialist for evaluation. Most patients improve with discontinuation of the PPI alone in 4 to 12 weeks.
Serological testing (e.g., ANA) may be positive and elevated serological test results may take longer to resolve than clinical manifestations.
Hepatic Impairment: No dosage adjustment for DEXILANT is necessary for patients with mild hepatic impairment (Child-Pugh Class A).
In a study of patients with moderate hepatic impairment (Child-Pugh Class B) who received a single 60 mg DEXILANT, there was a significant increase in systemic exposure of dexlansoprazole compared to healthy subjects with normal hepatic function (see Pharmacology under Actions). Therefore, for patients with moderate hepatic impairment (Child-Pugh Class B), dosage reduction is recommended for the healing of EE (see Dosage & Administration).
No studies have been conducted in patients with severe hepatic impairment (Child-Pugh Class C); the use of DEXILANT is not recommended for these patients (see Dosage & Administration).
Use in Children: The safety and effectiveness of DEXILANT have been established in pediatric patients 12 to 17 years of age for the healing of all grades of EE. The safety and effectiveness of DEXILANT ahave been established in pediatric patients 12 to 17 years of age for the maintenance of healed EE and relief of heartburn, and treatment of heartburn associated with symptomatic non-erosive GERD.
Use of DEXILANT in this age group is supported by evidence from adequate and well-controlled studies of DEXILANT in adults with additional safety, efficacy and pharmacokinetic data in pediatric patients 12 to 17 years of age (see Pharmacology under Actions, Dosage & Administration and Adverse Reactions).
The adverse reaction profile in patients 12 to 17 years of age was similar to adults.
The safety and effectiveness of DEXILANT have not been established in pediatric patients less than 12 years of age.
The use of DEXILANT is not recommended for symptomatic non-erosive GERD in pediatric patients less than 1 year of age because studies in this class of drugs have not demonstrated efficacy.
Use in Elderly: Of the total number of patients (n=4548) in clinical studies of DEXILANT, 11% of patients were aged 65 years and over, while 2% were 75 years and over. No overall differences in safety or effectiveness were observed between these patients and younger patients, and other reported clinical experience has not identified significant differences in responses between geriatric and younger patients, but greater sensitivity of some older individuals cannot be ruled out (see Pharmacology under Actions).