Common side effects include constipation.[3] Serious side effects may include bezoar formation and encephalopathy.[6] Use appears to be safe in pregnancy and breastfeeding.[6] How it works is unclear but is believed to involve binding to the ulcer and protecting it from further damage.[3][6]
Sucralfate was approved for medical use in the United States in 1981.[3] It is available as a generic medication.[6][7] In 2022, it was the 214th most commonly prescribed medication in the United States, with more than 1million prescriptions.[8][9]
Stress ulcerprophylaxis—The use of sucralfate rather than H2antagonists for stress ulcer prophylaxis, and measures to prevent aspiration, such as continuous subglottic suctioning, have been shown to reduce the risk of ventilator-associated pneumonia (VAP).[18] Sucralfate is less effective for prophylaxis against gastrointestinal bleeding than either a PPI or H2-blocker. For that reason, it is not commonly used for stress ulcer prophylaxis.
Prevention of stricture formation—Sucralfate has an inhibitory effect on stricture formation in experimental corrosive burns and can be used in the treatment of corrosive esophageal burns to enhance mucosal healing and suppress stricture formation[19]
Grade 1 bleeding experienced immediate relief with sucrasulfate enema for 1 month.
Grade 2 bleeding, sucrasulfate enema] and/or coagulation were effective.
Grade 3 bleeding lasted for 1 year despite frequent transfusions and coagulation.
Grade 2 and 3 rectal bleeding occurred in 8.5% of people. The most significant risk factor was the ICRU-CRBED. Prompt treatment with a combination of sucrasulfate enema and coagulation is effective in controlling Grade 1 and 2 rectal bleeding without the development of fistula or stricture.[21]
Sucralfate suspension is recommended by the US-based National Capital Poison Center (Poison Control) as an intervention for known or suspected button battery ingestions to reduce the risk and severity of injury to the esophagus prior to the battery's endoscopic removal.[22][23]
Protection against ventilator-associated pneumonia - Reductions in gastric acidity and volumes increase bacterial overgrowth and the incidence of ventilator-associated pneumonia. Sucralfate may be considered to have the advantage over H2-blockers and PPIs in this regard because sucralfate does not change the pH of gastric fluid. A majority of meta-analyses found that sucralfate therapy decreased the incidence of ventilator-associated pneumonia compared to H2-antagonists.[10]
Sucralfate is a locally acting substance that in an acidic environment (pH < 4) reacts with hydrochloric acid in the stomach to form a cross-linking, viscous, paste-like material capable of acting as an acid buffer for as long as 6 to 8 hours after a single dose.[29] It also attaches to proteins on the surface of ulcers, such as albumin and fibrinogen, to form stable insoluble complexes. These complexes serve as protective barriers at the ulcer surface, preventing further damage from acid, pepsin, and bile.[29] In addition, sucralfate prevents back diffusion of hydrogen ions, and absorbs both pepsin and bile acids.
Brand names include Carafate in the US, Sucramal in Italy, Sucrafil, Sufrate, Sucralpro, Sucralcoat, Pepsigard, Sucral, Hapifate, Sucralpro tablets and Sucralpro cream in India, Sutra or Musin in parts of South-East Asia, Sulcrate in Canada, Discral (sucralfato) in México, Ulsanic in South Africa and Israel, Andapsin in Sweden, Antepsin in Turkey, Sucracell in India, and Ulsidex in Indonesia
^ abHixson LJ, Kelley CL, Jones WN, Tuohy CD (April 1992). "Current trends in the pharmacotherapy for peptic ulcer disease". Archives of Internal Medicine. 152 (4): 726–32. doi:10.1001/archinte.152.4.726. PMID1558429.
^Hunt RH (August 1991). "Treatment of peptic ulcer disease with sucralfate: a review". The American Journal of Medicine. 91 (2A): 102S –106S. doi:10.1016/0002-9343(91)90459-b. PMID1882894.
^Fashner J, Gitu AC (February 2015). "Diagnosis and Treatment of Peptic Ulcer Disease and H. pylori Infection". American Family Physician. 91 (4): 236–42. PMID25955624.
^Monnig AA, Prittie JE (October 2011). "A review of stress-related mucosal disease". Journal of Veterinary Emergency and Critical Care. 21 (5): 484–95. doi:10.1111/j.1476-4431.2011.00680.x. PMID22316196.
^Safdar N, Crnich CJ, Maki DG (June 2005). "The pathogenesis of ventilator-associated pneumonia: its relevance to developing effective strategies for prevention". Respiratory Care. 50 (6): 725–39, discussion 739–41. PMID15913465.
^Temir ZG, Karkiner A, Karaca I, Ortaç R, Ozdamar A (1 January 2005). "The effectiveness of sucralfate against stricture formation in experimental corrosive esophageal burns". Surgery Today. 35 (8): 617–22. doi:10.1007/s00595-004-3005-0. PMID16034539. S2CID38080924.
^ abSteiner K, Bühring KU, Faro HP, Garbe A, Nowak H (1 January 1982). "Sucralfate: pharmacokinetics, metabolism and selective binding to experimental gastric and duodenal ulcers in animals". Arzneimittel-Forschung. 32 (5): 512–8. PMID6896647.
^ abBrogden RN, Heel RC, Speight TM, Avery GS (March 1984). "Sucralfate. A review of its pharmacodynamic properties and therapeutic use in peptic ulcer disease". Drugs. 27 (3): 194–209. doi:10.2165/00003495-198427030-00002. PMID6368184. S2CID260482050.
