Gaviscon-2 Side Effects
Generic Name: alginic acid / aluminum hydroxide / magnesium trisilicate
Note: This page contains information about the side effects of alginic acid / aluminum hydroxide / magnesium trisilicate. Some of the dosage forms included on this document may not apply to the brand name Gaviscon-2.
Not all side effects for Gaviscon-2 may be reported. You should always consult a doctor or healthcare professional for medical advice. Side effects can be reported to the FDA here.
Applies to alginic acid / aluminum hydroxide / magnesium trisilicate: oral tablet chewable
Gastrointestinal side effects have been reported the most frequently. These have included constipation (secondary to aluminum hydroxide therapy) and diarrhea (secondary to magnesium trisilicate therapy). These agents are combined so lower doses may be used and the constipating and diarrheal effects may be balanced out. However, diarrhea tends to be the dominating effect, regardless of the ratio. Rarely, gastrointestinal obstruction has occurred with the use of aluminum hydroxide.
Sources of aluminum in patients with renal failure have included water used for dialysate solution, in addition to aluminum hydroxide. Adverse effects of aluminum accumulation in these patients has led to monitoring of water source aluminum content by dialysis units and periodic measurements of serum aluminum in patients undergoing chronic dialysis.
High aluminum concentrations in patients are generally also associated with high daily dosage. One study suggested that increased aluminum concentrations in uremic patients was most significant with daily doses greater than 3 grams of aluminum hydroxide. Age of the patient has also been directly correlated with aluminum concentrations, with younger age groups perhaps demonstrating higher concentrations.
Concurrent administration of aluminum hydroxide with citrate containing products has been associated with unusually high serum concentrations of aluminum and, especially in cases of renal failure, severe toxicity. It was speculated that citrate increases aluminum's solubility and absorption.
Aluminum concentrations during aluminum hydroxide therapy have also been correlated with body iron stores. One study demonstrated a negative correlation between serum aluminum concentrations and serum ferritin levels. It was postulated that high serum ferritin and high transferritin saturation might hamper gut absorption of aluminum.
During long-term use, aluminum has been shown to deposit in bone, joints, and the brain of patients who accumulate aluminum.
Signs and symptoms of hypermagnesemia may include hypotension, nausea, vomiting, EKG changes, respiratory depression, loss of deep tendon reflex, dilated pupils, altered mental status, and coma.
Although the majority of aluminum ingested is eliminated by the gastrointestinal tract, absorption of aluminum and increases in serum concentrations have been demonstrated. Accumulation of aluminum and resulting toxicity is confined to patients with renal dysfunction and impaired elimination of aluminum.
Magnesium may be systemically absorbed following administration of magnesium trisilicate. In patients with normal renal function, increased magnesium elimination in the urine occurs and no significant changes in serum magnesium levels would be expected. However, magnesium may accumulate in patients with renal insufficiency.
Metabolic side effects have included hypophosphatemia with the use of aluminum hydroxide. In patients on long-term aluminum hydroxide therapy, especially in association with poor diets, hypophosphatemia may result in muscle weakness, rhabdomyolysis, hemolysis, and encephalopathy.
Aluminum hydroxide complexes with phosphate in the gut to form insoluble aluminum phosphate, thus inhibiting the absorption of dietary phosphate. Aluminum hydroxide is commonly used in patients with renal dysfunction to regulate the accumulation of phosphate due to decreased elimination.
Hypophosphatemia is thought to stimulate the conversion of calcifediol (25-hydroxy vitamin D3) to calcitriol (1,25-dihydroxy vitamin D3), a potent stimulator of calcium and phosphorus intestinal absorption and osteoclastic resorption. Hypercalciuria is generally associated with hypophosphatemia.
Musculoskeletal side effects have included osteomalacia, due to aluminum hydroxide, which may occur by two different mechanisms. Osteomalacia may occur due to hypophosphatemia or due to aluminum accumulation in bone. Osteomalacia due to hypophosphatemia is often accompanied by malaise, bone pain, muscular weakness, and bone fractures. Osteomalacia due to aluminum deposition may present in a similar fashion and occurs predominately in patients with chronic renal failure. Aluminum deposits typically can be observed on bone biopsy.
Aluminum hydroxide associated hypophosphatemia, if severe and chronic, results in decreased bone mineralization and potentially osteomalacia. Hypophosphatemia is also thought to stimulate the conversion of calcifediol (25-hydroxy vitamin D3) to calcitriol (1,25-dihydroxy vitamin D3), a potent stimulator of osteoclastic resorption, contributing to osteomalacia. These patients generally require phosphorus replacement therapy. Symptoms of osteomalacia may take several weeks to resolve.
Osteomalacia due to aluminum deposition in bone is generally only seen in patients with chronic renal failure. Bone formation slows in response to aluminum bone deposits. Aluminum may also deposit in joint tissue, resulting in arthropathy and hydrarthrosis.
Nervous system side effects have included encephalopathy which has occasionally been reported in patients with renal failure on long-term therapy with aluminum hydroxide. When available, basal and/or deferoxamine stimulated aluminum serum levels reveal high concentrations.
Encephalopathy associated with aluminum accumulation is generally characterized by speech disorders, dysarthria, dyspraxia, dysphasia, tremor, myoclonus, seizures, coma, and death. EEG of patients with aluminum encephalopathy has shown paroxysmal slowing, and diffuse rhythmical bursts of delta activity.
The interval between commencement of aluminum hydroxide therapy and development of encephalopathy in eight reported cases ranged from three weeks to three months. In two of these patients, aluminum serum concentrations ranged from 871 to 2267 mcg/L. These patients were also on sodium citrate therapy which enhances GI aluminum absorption. Most chronic dialysis patients develop aluminum encephalopathy slowly over many years.
Renal side effects have rarely included formation of renal calculi, most probably due to hypercalciuria, with the use of aluminum hydroxide.
Antacids may interfere with drug therapies because of their effect on gastric pH, adsorption or binding to drugs, and changes in urinary pH.
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