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 2021, it was the 186th most commonly prescribed medication in the United States, with more than 2million 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 and Antepsin in Turkey. Sucracell in India.
^
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.
^Si JM, Wang LJ, Chen SJ, Zhao L, Dai N (2003). "Quality of life and cost-effectiveness of combined therapy for reflux esophagitis". Journal of Zhejiang University Science A. 4 (5): 602–6.
doi:
10.1631/jzus.2003.0602.
PMID12958722.
S2CID118845033.
^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.