Aluminium Hydroxide

Aluminium hydroxide is a nonsystemic antacid that neutralises gastric acid and binds dietary phosphate in the gut. It relieves dyspepsia quickly and is used as a phosphate binder, but aluminium accumulation in kidney impairment limits its long-term use.

Classification. Antacid; aluminium-based phosphate binder.

Mechanism. Reacts with hydrochloric acid to form aluminium chloride and water, raising gastric pH. In the intestine, aluminium binds phosphate to form insoluble aluminium phosphate, reducing phosphate absorption. It also inhibits pepsin and binds bile acids.

Pharmacodynamics. Onset within minutes; duration about 30 minutes when fasting and up to 3 hours when taken 1 hour after a meal. Slower and weaker neutralisation than magnesium or calcium salts.

Pharmacokinetics. A small fraction of aluminium is absorbed and normally excreted by the kidneys; the rest leaves in faeces. Citrate greatly increases aluminium absorption.

Accumulation. In kidney impairment, absorbed aluminium accumulates in bone, brain and blood, causing osteomalacia, encephalopathy and microcytic anaemia.

Adult oral doses unless stated. Products vary in aluminium hydroxide content, so dose by milligrams and check the product strength.

Dyspepsia and heartburn.

• Aluminium hydroxide 500 mg to 1 g orally, taken 1 hour after meals and at bedtime, or when symptoms occur.

• Usual maximum about 4 g daily; review if used for over 2 weeks.

• It is most often combined with magnesium hydroxide to balance constipation against diarrhoea.

Hyperphosphataemia in chronic kidney disease, short-term.

• 300 to 600 mg orally three times daily with meals, adjusted to serum phosphate.

• Limit to about 4 weeks because of aluminium toxicity.

• Calcium-based or nonmetal binders are preferred for long-term use.

• Where those are unavailable or unaffordable, aluminium may be used for short courses with serum aluminium monitoring.

Paediatric hyperphosphataemia. 50 to 150 mg/kg daily in divided doses with meals, short-term only, under specialist supervision.

Paediatric dyspepsia. Rarely needed; use product-specific age dosing for children over 6 years.

Contraindications. Hypophosphataemia; porphyria; intestinal obstruction. Avoid regular use in severe kidney impairment except for short-term phosphate binding.

Common adverse effects. Constipation, nausea, chalky taste and faecal impaction, particularly in older adults and with opioid use.

Serious adverse effects.

• Hypophosphataemia with prolonged use in normal kidney function, causing weakness, anorexia and osteomalacia.

• Aluminium toxicity in kidney impairment or with prolonged high doses: encephalopathy, osteomalacia, proximal myopathy and microcytic anaemia.

• Intestinal obstruction or bezoar formation.

Major interactions. Aluminium chelates or adsorbs many drugs; separate dosing.

• Tetracyclines, fluoroquinolones and oral iron: give the other drug 2 hours before or 4 to 6 hours after the antacid.

• Integrase inhibitors (dolutegravir, raltegravir, bictegravir): give the antiretroviral 2 hours before or 6 hours after.

• Levothyroxine and bisphosphonates: separate by at least 4 hours and 2 hours respectively.

• Digoxin, ketoconazole, itraconazole, mycophenolate, penicillamine and chloroquine: reduced absorption; separate by 2 to 4 hours.

• Enteric-coated tablets may dissolve early in raised gastric pH.

• Citrate, including calcium citrate and effervescent preparations, increases aluminium absorption; avoid together.

Special groups.

• Pregnancy: minimal absorption; occasional use at usual doses is acceptable. Avoid prolonged high doses.

• Breastfeeding: compatible.

• Children: use only with clear indication; infants and children with kidney disease are at highest risk of aluminium toxicity.

• Older adults: constipation and impaction risk; monitor bowel habit.

• Kidney impairment: avoid regular antacid use when eGFR is under 30 mL/min/1.73 m2; restrict phosphate-binding courses and monitor aluminium.

• Liver impairment: no dose change; constipation may precipitate hepatic encephalopathy, so pair with a laxative.

• Regional: aluminium-based phosphate binders remain in use where alternatives are scarce; set a clear end date.

Formulations. Oral suspension, chewable tablets and capsules of varying strength; frequently combined with magnesium hydroxide, with or without simeticone or alginate.

Administration.

• Dyspepsia: take 1 hour after meals and at bedtime for the longest neutralising effect. Shake suspensions well; chew tablets thoroughly before swallowing.

• Phosphate binding: take with or immediately before meals.

• Do not give with citrate-containing drinks or medicines.

Baseline. Phosphate, calcium and kidney function before phosphate-binding or regular use.

Monitoring.

• Phosphate and calcium every 1 to 3 months during regular use.

• Serum aluminium in kidney impairment on prolonged therapy, at baseline and then about every 3 months.

• Bowel habit, particularly in older adults and in liver disease.

Therapeutic drug monitoring. Not applicable; serum aluminium is a toxicity measure, not a therapeutic target.

Stopping. Stop if phosphate falls under the reference range, aluminium rises or encephalopathy or bone pain develops. Antacid use for over 2 weeks needs assessment for an underlying cause.

Referral and escalation. Endoscopy for persistent dyspepsia or alarm features. Nephrology input for suspected aluminium toxicity; desferrioxamine chelation is a specialist decision.