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MyDeficiencies

Sucralfate

mucosal protectant, sucrose octasulfate aluminum complex

Also sold as Carafate.

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Findings for this medication

Research about this medication, graded for how strongly each finding can be attributed to it. Nothing here describes your own levels.

Sucralfate has almost no classical depletion machinery. The retrieved label sections say it is "only minimally absorbed," acts locally rather than systemically, and that the small absorbed amount of sulfated disaccharide is excreted mainly in urine. No metabolism or CYP statement appeared in the sections retrieved, and the label does not mention phosphate, vitamins, minerals or any other nutrient [1][2]. The one mechanism present is luminal: sucralfate forms an ulcer-adherent complex, adsorbs bile salts, and binds co-administered drugs in the gut, which the label manages with a 2-hour separation [1][2][1][2]. That is a timing interaction, not a depletion, and it runs in the direction of drug to drug.

mucosal protectant, sucrose octasulfate aluminum complex · ATC A02BX02 (WHO ATC/DDD Index [3]) · also sold as Carafate; many generics · reviewed 2026-10-04. This describes research about the medication. It does not say anything about your own levels or health.

How to read the evidence grades

These colours describe how strongly a finding can be attributed to the medication in the research. They are not a severity score and they say nothing about your own health.

Grades describe how strongly a finding can be attributed to Sucralfate in the research — not how common it is, how serious it would be, and not anything about you personally.

Red — Severe
Two or more independent Tier A sources, this drug in the cohort, the nutrient directly measured, consistent direction, clinically meaningful magnitude, a named mechanism, no substantial contradicting Tier A evidence.
Orange — Moderate
At least one Tier A source with this drug in the cohort showing a real but bounded deficit: an exposure window, a subgroup, low frequency, or a functional rather than circulating deficit.
Yellow — Low
Mechanistic plausibility only (Tier B), or class extrapolation (Tier C) with no drug-specific human status data; also used for context flags and interactions running the other direction.
Not graded — disclosed evidence gap
Nothing has been measured here, so this finding cannot be graded. That does not establish either safety or harm, and it is not the same as a White result.Source definition: Not gradeable under the rules above because nothing has been measured. Published as a documented gap, never as reassurance that there is no effect.

What the research found

Aluminum retention: excess exposure bounded to renal impairment, dialysis and prolonged courses

Orange — Moderate

See study details

Sucralfate delivers a small absorbed aluminum load that raises plasma and urine aluminum, and where kidney excretion is impaired the label warns it can accumulate. This is an excess risk, not a deficiency.

Full detail and limits

What the grade means here: At least one Tier A source with this drug in the cohort showing a real but bounded deficit: an exposure window, a subgroup, low frequency, or a functional rather than circulating deficit. Orange

Limits on what this shows

  • Null findings and tissue data: Rat study [11]: 8 weeks of sucralfate raised bone aluminum without a serum change, so serum aluminum may under-read tissue uptake. No retrieved human study measured an aluminum-related clinical outcome in sucralfate users. A narrative review states accumulation and toxicity "have been reported" in compromised renal function [10] (Tier C narrative, not stratified; case reports not opened).
  • At-risk subgroups: Chronic renal failure, dialysis, and by the label's own wording any renal impairment; prolonged or maintenance courses; elderly patients (the Moore cohort was elderly [6], but no age-specific risk was shown).

Regulatory status

Label warning: "Patients with chronic renal failure or those receiving dialysis have impaired excretion of absorbed aluminum... Aluminum accumulation and toxicity (aluminum osteodystrophy, osteomalacia, encephalopathy) have been described in patients with renal impairment" [1]. The Carafate label retrieved carries the same renal and aluminum warning in summary [2].

Population evidence

All abstract-level, sucralfate in the cohort. Allain 1990 [4]: 25 healthy subjects, 4 g daily for 21 days, significant rises in plasma and urine aluminum that decreased rapidly after stopping. Burgess 1992 [5]: 6 patients with chronic renal failure, significant elevations of serum aluminum, caution advised for prolonged use. Moore 1995 [6]: crossover, 20 elderly volunteers, plasma aluminum significantly higher on sucralfate than on ranitidine alone. Mistry 1991 [7]: 10 dyspeptic patients, significant plasma aluminum rise during 6 weeks of treatment. Schutze 1995 [8]: serum aluminum almost doubled in both effervescent and standard formulation groups. Haram 1987 [9]: 11 subjects, measurable absorbed aluminum in urine. Numeric effect sizes were not captured in the abstract text retrieved.

Mechanism

Present. The drug is an aluminum salt of sucrose octasulfate, a small fraction of the aluminum is absorbed, and the kidney clears it; renal failure removes that route [1][4][5].

Counter-evidence held on record

Counter-evidence and confounding Healthy volunteers showed rises that fell quickly after the drug was stopped [4], and none of the retrieved studies tied the rise to toxicity. Patients with renal failure already carry aluminum from other sources, such as aluminum-containing phosphate binders and antacids, which this review cannot separate. Osteomalacia and encephalopathy are outcomes, not nutrient deficiencies (Hard Rule 2); aluminum itself was the measured parameter here. Framing caution This is an excess or retention risk. Nothing here suggests increasing intake of any nutrient, and no supplement is recommended. The hazard is cumulative aluminum exposure in impaired excretion. Decisions about prolonged use in kidney disease belong to the prescriber.

Phosphate: luminal binding shown in hyperphosphatemic kidney failure; no sucralfate hypophosphatemia located

Yellow — Low

See study details

Sucralfate lowers serum phosphate in patients whose phosphate is high from kidney failure, similar to aluminum hydroxide. No retrieved human source reports sucralfate causing low phosphate in people with normal phosphate.

Full detail and limits

What the grade means here: Mechanistic plausibility only (Tier B), or class extrapolation (Tier C) with no drug-specific human status data; also used for context flags and interactions running the other direction. Yellow

Limits on what this shows

  • Null findings: Quimby 2016 [15]: in normal cats and cats with chronic kidney disease, sucralfate did not change fecal phosphorus significantly; the study was stopped for lack of efficacy and side effects. Animal, Tier B, and a species mismatch with human data.
  • At-risk subgroups: Not defined for low phosphate. The measured effect is in hyperphosphatemic dialysis and uremic patients, where lowering is the intended effect of off-label use and not a deficiency.

Regulatory status

Phosphate is not mentioned in the label sections retrieved [1][2]. Sucralfate is not labeled as a phosphate binder.

Population evidence

Roxe 1989 [12]: crossover, 21 hemodialysis patients, sucralfate an "effective, albeit expensive, alternative to aluminum hydroxide" for hyperphosphatemia. Leung 1983 [13]: 3-week comparison in uremia, serum phosphate decrease comparable with aluminum hydroxide. Marks 1991 review [14]: sucralfate reduces hyperphosphataemia in chronic uremia "albeit at the risk of raised blood aluminium levels." Sucralfate was in all cohorts; abstract level only. A PubMed search for sucralfate with hypophosphatemia or osteomalacia returned general hypophosphatemia literature with no record naming sucralfate.

Mechanism

Plausible, not directly tested in the retrieved abstracts: aluminum-based luminal phosphate binding, by analogy with the aluminum hydroxide comparator in [13].

Counter-evidence held on record

Counter-evidence and confounding Lowering phosphate from a high baseline is not a nutrient deficiency (Hard Rules 2 and 5), and the cat data found no binding. The kidney-failure effect cannot be extended to people with normal kidneys and normal phosphate. Framing caution Context flag only. Not a hypophosphatemia claim, and no phosphate supplement is recommended. The finding matters to clinicians managing phosphate and binders in kidney disease.

Drug-binding interactions (levothyroxine, fluoroquinolones): timing, not depletion

Yellow — Low

See study details

Sucralfate binds co-administered drugs in the gut and lowers their absorption. This is a drug-to-drug timing interaction, filed here as a context flag and not as a nutrient depletion (Hard Rule 4).

Full detail and limits

What the grade means here: Mechanistic plausibility only (Tier B), or class extrapolation (Tier C) with no drug-specific human status data; also used for context flags and interactions running the other direction. Yellow

Regulatory status

Label section 7 lists l-thyroxine and fluoroquinolone antibiotics among drugs with reduced bioavailability, and states that dosing the other drug 2 hours before sucralfate eliminated the interaction [1][2]. The mechanism is described as nonsystemic binding in the gut (RxList text, Tier D) [28].

Population evidence

Sherman 1994 [16]: sucralfate 1 g reduced peak levothyroxine absorption to 225 micrograms (95% CI 151 to 299) versus 796 micrograms without it, and separating the doses by 8 hours restored absorption (abstract text via summarizing fetch tool; sample size and units not captured). Lehto 1994 [17]: crossover in 8 volunteers, lomefloxacin AUC 0 to 24 hours reduced by 51% with sucralfate. Lomaestro 1995 [18] review: sucralfate and magnesium-aluminum antacids had the greatest effect on quinolone bioavailability.

Mechanism

Luminal adsorption or chelation. Named in the label as binding in the GI tract.

Class cohort test

CLASS EXTRAPOLATION across the affected fluoroquinolone class: sucralfate was in the cohort of [17], but only lomefloxacin was the studied quinolone in the primary study retrieved. The label extends the warning to the class; capped at yellow. For levothyroxine, sucralfate was in the cohort [16], but a 2017 review calls the sucralfate-levothyroxine evidence "not well founded or contradictory" in some settings [19].

Counter-evidence held on record

Counter-evidence The levothyroxine interaction is contested in the review literature [19]. The 8-hour separation in [16] is longer than the label's 2-hour rule for other drugs, so the interval is drug-specific and belongs to the prescriber or pharmacist. Framing caution A timing interaction, not a deficiency. It does not imply that any supplement be added. No dose is recommended.

Fat-soluble vitamins (A, D, E, K): label bile-salt adsorption, plausibility only

Yellow — Low

See study details

The label states sucralfate adsorbs bile salts, which is a plausible route to reduced fat-soluble vitamin absorption, but no study retrieved measured any fat-soluble vitamin in sucralfate users.

Full detail and limits

What the grade means here: Mechanistic plausibility only (Tier B), or class extrapolation (Tier C) with no drug-specific human status data; also used for context flags and interactions running the other direction. Yellow

Limits on what this shows

  • Null findings: No sucralfate vitamin deficiency report was found in the retrieved listings.

Regulatory status

The label states sucralfate "adsorbs bile salts" and does not mention vitamins [1][2].

Population evidence

None. A PubMed search for sucralfate with vitamin returned 38 results (first 10 read): none reported vitamin absorption or status in sucralfate users. A 1984 vitamin A cytoprotection trial (Patty, PMID 6397969, abstract seen in the listing only) concerns ulcer healing, not absorption and is not used as nutrient evidence.

Mechanism

Plausible by the label's bile-salt adsorption, not demonstrated for vitamins. This is a Tier B mechanism statement for the drug, and the sole basis for the yellow grade.

Counter-evidence held on record

Counter-evidence Adsorbing bile salts in the lumen does not show reduced vitamin uptake; sucralfate acts mainly at the ulcer site. This entry rests on mechanism alone and could be re-graded ungraded if a reviewer holds that a label mechanism line is not enough. Framing caution Theoretical only. Not a deficiency claim and not a reason to supplement any vitamin.

Zinc

Not graded — disclosed evidence gap

See study details

No evidence was found that sucralfate changes zinc absorption or status.

Full detail and limits

What the grade means here: Nothing has been measured here, so this finding cannot be graded. That does not establish either safety or harm, and it is not the same as a White result. Ungraded

Limits on what this shows

  • Why no grade: Dual condition met: no Tier B or C sucralfate-zinc evidence and no sucralfate-specific circulating zinc claim located. Not a finding of safety.

What was searched

Pass 1: the two trace-element listings used for Copper, plus the 1992 quinolone interaction review (Brouwers, PMID 1524699) seen in the iron listing. Pass 2: PubMed listing "sucralfate zinc", read in full (6 records): four quinolone interaction reviews (PMIDs 1763542, 12089990, 7669261 [18], 1524699) list zinc salts, iron and sucralfate as separate agents that each reduce quinolone absorption, which is a nutrient-to-drug timing direction (Hard Rule 4) and not a sucralfate effect on zinc; PMID 1791051 (a gastric cytoprotection review) lists zinc sulphate as a cytoprotective drug alongside sucralfate; PMID 30038513 is a topical product. None measured zinc status, absorption or excretion in sucralfate users. Label: no zinc mention [1][2].

Channel outcomes

Three distinct PubMed listings returned content across two passes. Likely genuine gap, depth limited by tooling.

Vitamin B12

Not graded — disclosed evidence gap

See study details

No evidence was found for sucralfate and B12 status, and the PPI and H2 blocker B12 findings were not extended to it.

Full detail and limits

What the grade means here: Nothing has been measured here, so this finding cannot be graded. That does not establish either safety or harm, and it is not the same as a White result. Ungraded

Limits on what this shows

  • Why no grade: Dual condition met: no Tier B or C sucralfate B12 evidence and no circulating claim naming sucralfate for B12 was located. The B12 pathway for PPIs and H2 blockers depends on acid suppression, which is not an established action of sucralfate (see the B011 PPI and H2 blocker dossiers). Not a finding of safety.

What was searched

Pass 1: PubMed listing "sucralfate vitamin" (38 results, first 10 read): none concerned B12. Pass 2: PubMed listing "sucralfate cobalamin OR vitamin B12" (10 records, all general B12 literature from 1950 to 2022, none mentioning sucralfate). A consumer interaction page lists vitamin B12 among "most frequently checked" supplement interactions with sucralfate without a claim, mechanism or severity [26]. The Mayo Clinic FAQ on heartburn medicines and B12 names H2 blockers and PPIs and does not name sucralfate [27].

Channel outcomes

Two distinct PubMed listings returned content across two passes. Partly tooling-limited, leaning toward a genuine gap.

The five body-system areas

Each finding is counted once, in a single area. Where a study is mentioned in a second area it is context only.

Mitochondrial Burden

Each finding below is counted once, in this area only.

Mitochondrial burden: one in vitro gastric-cell finding of mixed direction, no oral, in vivo or human measurement

Yellow — Low

See study details

In one study of cultured gastric mucosal cells challenged with indomethacin, sucralfate accentuated the indomethacin-induced fall in mitochondrial function while reducing LDH release. No mitochondrial measurement of sucralfate alone, after oral dosing, or in people was located. This is a drug effect signal, not a nutrient deficiency (Hard Rule 2).

Full detail and limits

What the grade means here: Mechanistic plausibility only (Tier B), or class extrapolation (Tier C) with no drug-specific human status data; also used for context flags and interactions running the other direction. Yellow

Limits on what this shows

  • Null findings: The same study found sucralfate protective in vivo and protective on LDH release in vitro [30]. Other records in the "sucralfate mitochondrial" PubMed listing (PMIDs 40488849, 31955823, 20858483) used sucralfate only as a comparator or formulation component and were not used as evidence.
  • At-risk subgroups: Not defined.
  • Access caveat: Three renderings of this abstract by the summarizing fetch tool disagreed on which drug worsened mitochondrial function (one OpenAlex-derived rendering attributed it to cimetidine). Two PubMed renderings, including a request for the exact abstract field text, attribute it to sucralfate, and that wording is relied on here. Full text could not be opened (Wiley returned 403; Crossref disallowed by robots.txt). Re-check against the full text before any promotion.

Regulatory status

No mitochondrial statement in the label sections retrieved [1][2].

Population evidence

None in humans. Goineau 2017 [30] (Tier B, in vitro plus rat; sucralfate was a tested drug): rats given sucralfate 300 mg/kg orally before indomethacin 30 mg/kg had fewer gastric ulcers (-50%, P < 0.05) and shorter lesions (-62%, P < 0.05). In the in vitro arm, gastric mucosal cells were incubated with sucralfate (3 and 5 mg/mL) before indomethacin (3.8 mM) and LDH release and mitochondrial function were measured. Sucralfate inhibited LDH release, but the abstract states "sucralfate accentuated the indomethacin-induced decrease in mitochondrial function." Rebamipide and cimetidine instead improved mitochondrial function in the same assay. Abstract level only; the cell line and the mitochondrial assay are not named in the abstract text read.

Mechanism

Not established. The reported effect is an interaction with an indomethacin insult in cultured cells at 3 to 5 mg/mL, not an effect of sucralfate alone, and the abstract names no mechanism. The readout is "mitochondrial function," not ATP content, so it is not carried into the ATP production entry.

Counter-evidence held on record

Counter-evidence Sucralfate is minimally absorbed [1][2], so direct 3 to 5 mg/mL exposure of cells applies at most to the gut lumen and ulcer surface, not to systemic tissue. The in vivo arm of the same study showed protection, and the single study is a one-off model comparison that has not been replicated in the retrieved literature. Framing caution Not a claim that sucralfate damages mitochondria in people, and not a deficiency claim. No supplement, including CoQ10, is recommended.

Oxidative Stress

Each finding below is counted once, in this area only.

Oxidative stress: reverse direction, rat colon data, no human measurement

Yellow — Low

See study details

In rats, sucralfate applied as enemas lowered markers of tissue oxidative damage. No study found sucralfate lowering antioxidant capacity.

Full detail and limits

What the grade means here: Mechanistic plausibility only (Tier B), or class extrapolation (Tier C) with no drug-specific human status data; also used for context flags and interactions running the other direction. Yellow

Limits on what this shows

  • Null findings: No depleting or pro-oxidant sucralfate finding was located.

Regulatory status

No oxidative-stress statement in the label sections retrieved [1][2].

Population evidence

None in humans. Sato 2021 [20]: 36 male Wistar rats, daily saline or sucralfate enemas (1 to 2 g/kg/day) for 2 to 4 weeks into colonic segments without fecal stream; sucralfate reduced inflammation and oxidative stress. Zanesco 2025 [21]: 48 rats, sucralfate enemas 2 g/kg, with or without N-acetylcysteine; sucralfate alone reduced colonic inflammation and tissue myeloperoxidase and malondialdehyde and increased antioxidant enzymes (Tier B, abstract level).

Mechanism

Topical mucosal protection in an injured colon model. Not shown to alter systemic antioxidant status after oral dosing.

Counter-evidence held on record

Counter-evidence Rectal dosing at 1 to 2 g/kg in a diversion-colitis model is not oral human exposure. Both studies use the same experimental model, so they are one line of evidence (see Overlap map). Framing caution Not an antioxidant benefit claim and not a deficiency claim. Sucralfate should not be described as depleting antioxidants.

Copper and Iron Balance

Copper and iron are assessed separately. Nothing here is counted twice.

Copper

Not graded — disclosed evidence gap

See study details

No evidence was found that sucralfate changes copper absorption, status or excretion.

Full detail and limits

What the grade means here: Nothing has been measured here, so this finding cannot be graded. That does not establish either safety or harm, and it is not the same as a White result. Ungraded

Limits on what this shows

  • Why no grade: Dual condition met: no Tier B or C evidence, and no circulating copper claim for sucralfate was located. Kept independent of Iron and Zinc (Hard Rule 7). Not a finding of safety.

What was searched

Pass 1: PubMed listings "sucralfate copper zinc" (records were copper and zinc literature with no sucralfate content) and "sucralfate trace elements absorption" (10 records, none about sucralfate). Pass 2: PubMed listing "sucralfate copper", read in full (4 records): PMID 30038513 and PMID 18342112 are topical dermo-cosmetic or dermatitis products containing copper and zinc salts; PMID 7692970 mentions copper only as protection against protein oxidation; PMID 11119069 describes trace metals in hemodialysis patients without analyzing sucralfate. None measured copper status, absorption, ceruloplasmin or excretion in sucralfate users. Label sections retrieved: no copper mention [1][2].

Channel outcomes

Four distinct listings returned content across two passes (all PubMed, 10-record relevance-ranked pages). Direct database hosts blocked by policy and WebSearch exhausted. Conclusion leans toward a genuine gap, with depth limited by tooling (first page of each listing only, abstract-level text via a summarizing fetch tool).

Iron

Not graded — disclosed evidence gap

See study details

No evidence was found that sucralfate lowers iron absorption or iron stores, and the acid-suppression iron findings for PPIs and H2 blockers were not extended to it.

Full detail, limits and 1 references

What the grade means here: Nothing has been measured here, so this finding cannot be graded. That does not establish either safety or harm, and it is not the same as a White result. Ungraded

Limits on what this shows

  • Why no grade: Dual condition met: no readable Tier B or C evidence and no sucralfate-specific circulating iron claim located. Sucralfate is not an antisecretory drug, so PPI and H2 blocker iron data (B011 siblings) are not borrowed. Not a finding of safety.

What was searched

Pass 1: PubMed listings "sucralfate iron absorption" (7 records: levothyroxine and quinolone interaction reviews where iron is a co-interacting agent, a CKD phosphate binder review, and a 1986 iron deficiency review in the elderly, Freedman, PMID 3081556, whose two summaries disagreed about whether it implicates sucralfate; not opened and not used) and "sucralfate anemia hemoglobin" (6 records, all unrelated). Pass 2: "sucralfate iron" (PMID 28153426 [19], a levothyroxine absorption review, and PMID 31463226, a radiation proctitis management paper listing iron and sucralfate as separate therapies; no primary sucralfate-iron study); "sucralfate iron deficiency OR serum iron OR ferritin" (10 records, none studying sucralfate); "sucralfate aluminium hydroxide iron absorption OR ferrous" (10 records on iron formulations, none testing sucralfate or antacids). Label: no iron mention [1][2].

Channel outcomes

Five distinct PubMed listings returned content across two passes. A sixth listing ("sucralfate anemia") returned HTTP 429 in pass 2 and was not retried, per the fetch tool instruction. Other channels as above. Partly tooling-limited, leaning toward a genuine gap.

Gut Microbiome Risk

Each finding below is counted once, in this area only.

Gut microbiome risk: mouse data only, effects reported as limited

Yellow — Low

See study details

Mouse studies in an H. pylori model found limited effects of sucralfate on infection-related microbiota disorders. No human sucralfate microbiome study was located.

Full detail and limits

What the grade means here: Mechanistic plausibility only (Tier B), or class extrapolation (Tier C) with no drug-specific human status data; also used for context flags and interactions running the other direction. Yellow

Limits on what this shows

  • Null findings: The one study that addressed microbiota directly called sucralfate effects limited [22].
  • At-risk subgroups: Not defined.

Regulatory status

No microbiome statement in the label sections retrieved. The label lists constipation (2%) and bezoars, which alter transit [1][2].

Population evidence

None in humans. Liu 2019 [22]: C57BL/6J mice, sucralfate lowered H. pylori positivity (50% versus 91.67% in untreated infected controls) and the authors state its effects on H. pylori-induced gastrointestinal microbiota disorders are "limited." Teng 2020 [23]: sucralfate added to triple therapy in H. pylori mice improved eradication; the flora comparison was against another treatment arm, so sucralfate alone was not isolated (abstract level). Cheng 2024 [24]: sucralfate was used to induce constipation in mice; reported microbiota shifts compare a probiotic with constipated controls and do not isolate a sucralfate effect, so it is context only.

Mechanism

Plausible but small: constipation and mucosal coating could alter transit and the niche. Not demonstrated for human oral sucralfate.

Counter-evidence held on record

Counter-evidence All data are mouse and indirect. The strongest data point toward a limited effect. PPI and H2 blocker microbiome findings in the B011 siblings are not borrowed, because those drugs suppress acid and sucralfate does not. Framing caution Not a claim of dysbiosis in people. Do not extend PPI microbiome findings to sucralfate.

Oxygen and ATP Output

Oxygen delivery and ATP production are assessed separately. Nothing here is counted twice.

Oxygen delivery/utilization

Not graded — disclosed evidence gap

See study details

No evidence was found that sucralfate reduces hemoglobin, red-cell mass or tissue oxygen delivery.

Full detail and limits

What the grade means here: Nothing has been measured here, so this finding cannot be graded. That does not establish either safety or harm, and it is not the same as a White result. Ungraded

Limits on what this shows

  • Why no grade: Dual condition met: no Tier B or C evidence, and no circulating claim about oxygen-carrying capacity for sucralfate was found. Anemia is an outcome, not a nutrient (Hard Rule 2). Kept independent of ATP production (Hard Rule 7).

What was searched

Pass 1: PubMed listing "sucralfate anemia hemoglobin": 6 records, none reporting sucralfate lowering hemoglobin or causing anemia (the retrieved summary concluded none implicates sucralfate). Related phosphate and ATP literature in the listings concerns hypophosphatemia in general and was not tied to sucralfate. Pass 2: the iron-status listings above (none studying sucralfate) bear on the iron route to oxygen delivery. Three further hemoglobin or hematologic phrasings ("sucralfate hemoglobin", "sucralfate anemia", "sucralfate hematologic OR leukopenia OR thrombocytopenia OR hemoglobin") each returned HTTP 429 and were not read.

Channel outcomes

One hemoglobin-specific phrasing returned content in total; three more were rate limited. This entry is more tooling-limited than the others and should be re-checked first when full database access is available.

ATP production

Not graded — disclosed evidence gap

See study details

No evidence on sucralfate and cellular ATP synthesis or energy output was retrieved.

Full detail and limits

What the grade means here: Nothing has been measured here, so this finding cannot be graded. That does not establish either safety or harm, and it is not the same as a White result. Ungraded

Limits on what this shows

  • Why no grade: Dual condition met: no Tier B or C evidence and no circulating "low energy" claim specific to sucralfate found. Not a finding of safety.

What was searched

Pass 1: the "sucralfate mitochondria" listing, plus a title-restricted ATP and energy phrasing that was rate limited and not read. Pass 2: PubMed listing "sucralfate energy metabolism" read in full: PMID 3060617 (1988) is a general narrative that mentions "energy (ATP) metabolism" among NSAID mechanisms without measuring it in sucralfate-treated subjects; PMID 7667394 (1995) reports that sucralfate "failed to influence H. pylori F1-ATPase", a bacterial enzyme, so it does not bear on host ATP production (abstract-level summary only, not used as evidence); other records use sucralfate only as a comparator. Listings "sucralfate ATP" and "sucralfate oxygen consumption OR adenosine triphosphate OR respiration" returned HTTP 429 and were not read. The mitochondrial-function readout in Goineau 2017 [30] is not an ATP measurement and is not used here; the phosphate entry was not used as ATP evidence.

Channel outcomes

Two distinct listings returned content; two were rate limited. Tooling-limited, with a likely thin literature.

Claims checked and not supported

These circulate online for this medication. They are listed here only so they can be answered, never as findings, and they are not graded.

A claim with no supporting evidence is not necessarily disproven. Where evidence actually argues against a claim, that is stated below.

  • No sucralfate-specific depletion claim located

    Where it comes from: Checked: drugs.com monograph [25], drugs.com interaction listing [26], RxList Carafate page [28], Mayo Clinic FAQ [27]. Antidote Research, Healthline and WebMD sucralfate pages returned 404. The Drugs.com side-effects page [29] did not mention hypophosphatemia, vitamin deficiency or reduced vitamin or mineral absorption.

    Why it fails: None of the pages opened claimed that sucralfate depletes a nutrient. The RxList text describes binding to co-administered drugs only [28]. The audit was limited by WebSearch exhaustion and by 404s on retailer pages, so a claim may circulate elsewhere. Not a finding that none exists.

  • Supplement interaction list (CoQ10, fish oil, iron, B12, vitamin C, vitamins D2 and D3)

    Where it comes from: Drugs.com interaction page for sucralfate, "most frequently checked" supplement list [26] (Tier D).

    Why it fails: A list of frequently searched supplements, not a depletion claim: no mechanism, direction or severity was displayed. B12, iron and vitamin D are covered above as ungraded or yellow entries; no evidence was found for CoQ10, fish oil or vitamin C. Not graded.

  • Acid-suppression nutrient claims (B12, iron, magnesium, calcium) carried over from PPIs and H2 blockers

    Where it comes from: Neighboring consumer literature: the Mayo FAQ names only H2 blockers and PPIs [27]. No page naming sucralfate for these nutrients was found.

    Why it fails: Not a located claim, listed as a boundary for readers who meet the class claims. The retrieved label describes local action and an ulcer-adherent complex, not antisecretory action [1][2]; no PPI or H2 blocker cohort studied sucralfate. The class data are not borrowed.

How the body handles this medication

Absorption and local action
"Only minimally absorbed from the gastrointestinal tract"; effect is "local, rather than systemic." The retrieved label sections give no percentage absorbed, so the 3 to 5% figure supplied with the request was not confirmed here.[1][2] DailyMed labels, clinical pharmacology (text via summarizing fetch tool)
Metabolism and enzymes
No metabolism, CYP substrate, inhibition or induction statement appeared in the sections retrieved. Not recorded as absent from the full label, only as not found in the text retrieved.[1][2]
Elimination and aluminum
Absorbed sulfated disaccharide is excreted primarily in urine. The label warns that chronic renal failure or dialysis impairs excretion of absorbed aluminum. Plasma and urine aluminum rise on treatment in volunteers and patients [4][5][6][7][9].[1][2] label; [4]-[9] studies
Mechanism in the gut lumen
Forms an ulcer-adherent complex that protects against acid, pepsin and bile salts; inhibits pepsin activity in gastric juice by 32%; adsorbs bile salts; about 14 to 16 mEq acid-neutralizing capacity per 1 g dose.[1][2]
Drug, food and antacid interactions
Reduced bioavailability named for cimetidine, digoxin, fluoroquinolone antibiotics, ketoconazole, l-thyroxine, phenytoin, quinidine, ranitidine, tetracycline and theophylline; warfarin cases also noted. Dosing the other drug 2 hours before sucralfate eliminated the interaction. A 30-minute antacid interval appears on a consumer drug monograph (Tier D, [25]) and was not captured from the label text retrieved. RxList text (Tier D) says the mechanism is nonsystemic binding in the gut.[1][2] sec 7; [25] Tier D for the antacid interval; [28] Tier D for the mechanism text
Adverse reactions, special populations
Constipation 2%; any adverse effect 129 of over 2,700 patients (4.7%). Bezoars and aspiration reports. Pregnancy: use only if clearly needed. Pediatric safety and effectiveness not established.[1][2]

What the research says is worth watching

General information from the medication label and the studies above. It is not personal medical advice, and any change belongs with your prescriber.

  • Timing / interactions

    Separate other drugs from sucralfate

    The label says dosing the other drug 2 hours before sucralfate eliminated the interaction for drugs including levothyroxine, fluoroquinolones, tetracycline, digoxin, phenytoin and others [1][2]. One levothyroxine study found an 8-hour separation restored absorption [16]. A consumer monograph advises 30 minutes around antacids [25]. Intervals are for the prescriber or pharmacist to set.

  • Renal / aluminum

    Kidney function and prolonged use

    In chronic renal failure or dialysis, the label warns of aluminum accumulation and toxicity [1]. Serum aluminum is the parameter measured in the retrieved studies [5]; whether and when to check it is a prescriber decision. Avoid adding other aluminum exposure without review.

  • Lab / kidney disease

    Serum phosphate

    Relevant where phosphate is managed in kidney failure, since sucralfate lowered phosphate in hemodialysis and uremic patients [12][13]. No routine phosphate monitoring is supported for people with normal kidneys.

  • Not supported

    Routine vitamin, iron, copper, zinc or B12 testing

    No sucralfate-specific evidence was found to justify routine testing of these. Test only on clinical grounds.

  • Adverse reactions

    Constipation, bezoar, swallowing

    Constipation 2%, bezoars reported, and caution is advised with impaired swallowing [1][2]. Constipation can reduce appetite and intake in some patients, but that was not studied here.

  • Special populations

    Pregnancy, pediatrics, renal impairment

    Pregnancy: use only if clearly needed. Pediatric safety and effectiveness not established. Renal impairment is the documented sensitivity group for aluminum [1][2]. No supplement dose appears in this dossier, so no upper-limit comparison was needed.

Overlap map, to prevent double counting

  • Aluminum retention

    Shares evidence with: Phosphate

    Note: Both rest on aluminum chemistry. The phosphate-lowering studies in kidney failure [12][13] and the reviews [10][14] are the same literature that raises the aluminum concern. Treat as one mechanism, not two independent confirmations.

  • Phosphate

    Shares evidence with: Drug-binding interactions; Fat-soluble vitamins

    Note: All three rest on one luminal-binding mechanism (adsorption or complexation in the gut), supported by the same label statements [1][2]. Different endpoints, one mechanism.

  • Fat-soluble vitamins

    Shares evidence with: Drug-binding interactions

    Note: The vitamin entry rests solely on the label bile-salt adsorption line and has no independent data. It is not extra confirmation of binding.

  • Oxidative stress

    Shares evidence with: None (within entry: [20] and [21])

    Note: Both rat studies use the same experimental model (colonic segments without fecal stream, sucralfate enemas). One line of evidence.

  • Gut microbiome risk

    Shares evidence with: None

    Note: [22] and [23] are both H. pylori mouse studies with overlapping author lists (Liu, Teng); treat as one line of evidence.

  • Iron; Copper; Zinc

    Shares evidence with: Each other (ungraded)

    Note: All three share the same two trace-element search listings and the same null outcome. One gap viewed three times, graded separately per Hard Rule 7 for iron and copper.

  • Oxygen delivery/utilization

    Shares evidence with: Iron; Vitamin B12 (ungraded)

    Note: Any hemoglobin effect would run through the iron or B12 entries, and both are ungraded. The anemia listing is used for both Iron and Oxygen delivery; one search, not two.

  • Mitochondrial burden (yellow)

    Shares evidence with: ATP production (ungraded)

    Note: Mitochondrial burden rests on [30] alone. ATP production shares the same "sucralfate mitochondrial" and energy-metabolism search listings but [30] is not used as ATP evidence because its readout is mitochondrial function, not ATP content. Kept independent per Hard Rule 7 and the skill's category rules.

All references used above
  1. Sucralfate tablets, prescribing information (DailyMed, Zydus Lifesciences). — Regulatory label (Tier A). Revision 03/2024. Indications, warnings (aluminum, chronic renal failure, dialysis, aspiration), section 7 interactions with the 2-hour instruction, clinical pharmacology, adverse reactions. Text read through a summarizing fetch tool; the two summaries of this page differed on whether section 12.3 was present, and only the clinical pharmacology wording was relied on.
  2. CARAFATE (sucralfate) tablet, DailyMed label, Allergan. — Regulatory label (Tier A). Revision May 2024. Section 7 list, minimal absorption statement, renal and aluminum warnings, adverse reaction frequencies (4.7% of over 2,700), pediatric use. Read through a summarizing fetch tool; no percentage absorbed was returned.
  3. WHO Collaborating Centre, ATC/DDD Index: sucralfate, A02BX02, DDD 4 g oral. — Reference index. Opened via summarizing fetch tool.
  4. Allain P, Mauras Y, Krari N, Duchier J, Cournot A, Larcheveque J. Plasma and urine aluminium concentrations in healthy subjects after administration of sucralfate. Br J Clin Pharmacol 1990. — Healthy volunteers, 25 subjects, 4 g daily for 21 days. PMID 2328192. Abstract level.Abstract text seen inside a PubMed search listing, summarized by the fetch tool; article page and full text not opened.
  5. Burgess E, Muruve D, Audette R. Aluminum absorption and excretion following sucralfate therapy in chronic renal insufficiency. Am J Med 1992. — 6 patients with chronic renal failure. PMID 1580293. Abstract level.Abstract text via PubMed listing and summarizing fetch tool; full text not opened.
  6. Moore JG, Coburn JW, Sanders MC, McSorley DJ, Sirgo MA. Effects of sucralfate and ranitidine on aluminum concentrations in elderly volunteers. Pharmacotherapy 1995. — Crossover, 20 elderly subjects; active comparator ranitidine. PMID 8602382. Abstract level.Abstract text via PubMed listing and summarizing fetch tool; full text not opened. Ranitidine is the comparator, not a non-use control.
  7. Mistry P, Varghese Z, Pounder RE. Plasma aluminium concentration and 24-hour urinary aluminium excretion before, during and after treatment with sucralfate. Aliment Pharmacol Ther 1991. — 10 dyspeptic patients, 6-week treatment. PMID 1793786. Abstract level.Abstract text via PubMed listing and summarizing fetch tool; full text not opened.
  8. Schutze K, Hentschel E, Happonen P, Akkila J. Sucralfate effervescent tablet: treatment of peptic ulcer disease and change in serum aluminium concentration. Hepato-Gastroenterology 1995. — Clinical trial comparing formulations. PMID 7590572. Abstract level.Abstract text via PubMed listing and summarizing fetch tool; sample size not captured; full text not opened.
  9. Haram EM, Weberg R, Berstad A. Urinary excretion of aluminium after ingestion of sucralfate and an aluminium-containing antacid in man. Scand J Gastroenterol 1987. — 11 subjects. PMID 3629187. Abstract level.Abstract text via PubMed listing and summarizing fetch tool; full text not opened.
  10. Hemstreet BA. Use of sucralfate in renal failure. Ann Pharmacother 2001. — Narrative review (Tier C for effect sizes). PMID 11261535.Abstract text via PubMed listing and summarizing fetch tool; underlying case reports not opened.
  11. Burnatowska-Hledin MA, Mayor GH. The effects of sucralfate ingestion on serum and specific tissue aluminum concentration in normal rats. J Toxicol Clin Toxicol 1984. — Rat study (Tier B), 8 weeks. PMID 6548526. Abstract level.Abstract text via PubMed listing and summarizing fetch tool; full text not opened.
  12. Roxe DM, Mistovich M, Barch DH. Phosphate-binding effects of sucralfate in patients with chronic renal failure. Am J Kidney Dis 1989. — Crossover, 21 hemodialysis patients. PMID 2919600. Abstract level.Abstract text via PubMed listing and summarizing fetch tool; full text not opened. Active comparator aluminum hydroxide.
  13. Leung AC, Henderson IS, Halls DJ, Dobbie JW. Aluminium hydroxide versus sucralfate as a phosphate binder in uraemia. Br Med J 1983. — 3-week comparison in uremia; sample size not captured. PMID 6404468. Abstract level.Abstract text via PubMed listing and summarizing fetch tool; full text not opened. Active comparator study; does not test sucralfate against non-use.
  14. Marks IN. Sucralfate: safety and side effects. Scand J Gastroenterol Suppl 1991. — Narrative review. PMID 1957123.Abstract text via PubMed listing and summarizing fetch tool; full text not opened.
  15. Quimby J, Lappin M. Evaluating sucralfate as a phosphate binder in normal cats and cats with chronic kidney disease. J Am Anim Hosp Assoc 2016. — Animal study (Tier B). PMID 26606202. Abstract level.Abstract text via PubMed listing and summarizing fetch tool; full text not opened. Cat data; species mismatch.
  16. Sherman SI, Tielens ET, Ladenson PW. Sucralfate causes malabsorption of L-thyroxine. Am J Med 1994. — PMID 8017451. Peak absorption 225 micrograms (95% CI 151 to 299) with sucralfate versus 796 micrograms without; 8-hour separation restored absorption, as summarized.Abstract text via PubMed listing and summarizing fetch tool; sample size and units not captured; full text not opened.
  17. Lehto P, Kivisto KT. Different effects of products containing metal ions on the absorption of lomefloxacin. Clin Pharmacol Ther 1994. — Crossover, 8 volunteers; lomefloxacin AUC 0 to 24 h reduced 51% with sucralfate. PMID 7955811.Abstract text via PubMed listing and summarizing fetch tool; full text not opened. Lomefloxacin only; other quinolones are class extrapolation.
  18. Lomaestro BM, Bailie GR. Absorption interactions with fluoroquinolones. 1995 update. Drug Saf 1995. — Narrative review (Tier C, not stratified). PMID 7669261.Abstract text via PubMed listing and summarizing fetch tool; full text not opened.
  19. Skelin M, Lucijanic T, Amidzic Klaric D, et al. Factors affecting gastrointestinal absorption of levothyroxine: a review. Clin Ther 2017. — Narrative review (Tier C). PMID 28153426. Calls sucralfate-levothyroxine evidence not well founded or contradictory in the context quoted.Abstract text via PubMed listing and summarizing fetch tool; full text not opened.
  20. Sato DT, Campos FG, Kotze PG, et al. Sucralfate enemas reduce the oxidative tissue damage and preserves the contents of E-cadherin and beta-catenin in colonic mucosa without fecal stream. Acta Cir Bras 2021. — Animal study (Tier B), 36 male Wistar rats. PMID 34852133. Abstract level.Abstract text via PubMed listing and summarizing fetch tool; full text not opened.
  21. Zanesco MC, Yoshitani MM, Fagundes FL, et al. Enemas with sucralfate and N-acetylcysteine can reduce inflammation and oxidative stress in colonic mucosa without fecal stream. Acta Cir Bras 2025. — Animal study (Tier B), 48 rats. PMID 40834221. Abstract level.Abstract text via PubMed listing and summarizing fetch tool; full text not opened.
  22. Liu Y, Teng GG, Wang WH, et al. Protective effects of sucralfate on gastric mucosal injury induced by Helicobacter pylori and its effects on gastrointestinal flora in mice. Zhonghua Yi Xue Za Zhi 2019. — Animal study (Tier B), C57BL/6J mice. PMID 31154720. Abstract level.Abstract text via PubMed listing and summarizing fetch tool; full text not opened.
  23. Teng G, Liu Y, Wu T, et al. Efficacy of sucralfate-combined quadruple therapy on gastric mucosal injury induced by Helicobacter pylori and its effect on gastrointestinal flora. Biomed Res Int 2020. — Animal study (Tier B), combination regimen. PMID 32934960. Abstract level.Abstract text via PubMed listing and summarizing fetch tool; full text not opened. Sucralfate not isolated from the regimen.
  24. Cheng S, Cui H, Zhang J, et al. Probiotic potential of Lacticaseibacillus rhamnosus VHProbi M15 on sucralfate-induced constipation in mice. Sci Rep 2024. — Mouse model (n=64) using sucralfate to induce constipation. PMID 38212429. Abstract level.Abstract text via PubMed listing and summarizing fetch tool; full text not opened. Context only; does not isolate a sucralfate microbiome effect.
  25. Drugs.com. Sucralfate monograph for consumers. — Tier D. Used only for the antacid timing interval and as a circulating-claim origin check; no depletion claim found.Read through a summarizing fetch tool.
  26. Drugs.com. Sucralfate drug interactions page. — Tier D. "Most frequently checked" supplement list only; no claims, mechanisms or severities displayed.Read through a summarizing fetch tool.
  27. Mayo Clinic. Heartburn medicines and B-12 deficiency (patient FAQ). — Tier D. Names H2 blockers and PPIs; does not name sucralfate. Used only as a circulating-claim origin check.Read through a summarizing fetch tool.
  28. RxList. Carafate drug page. — Tier D. States the interaction mechanism is nonsystemic binding in the gut; no nutrient or hypophosphatemia claim.Read through a summarizing fetch tool.
  29. Drugs.com. Sucralfate side effects page. — Tier D. Used only as a circulating-claim origin check; the summary stated no mention of hypophosphatemia, vitamin deficiency or reduced vitamin or mineral absorption.Read through a summarizing fetch tool.
  30. Goineau S, Castagne V. Complementarity of in vitro and in vivo models for the evaluation of gastro-protective effects of pharmacological substances. Fundam Clin Pharmacol 2017. — Tier B (rat in vivo plus in vitro gastric mucosal cells; sucralfate a tested drug alongside rebamipide and cimetidine). PMID 27739140; DOI 10.1111/fcp.12248. Sucralfate 300 mg/kg oral in rats; 3 and 5 mg/mL in cells; sucralfate accentuated the indomethacin-induced decrease in mitochondrial function.Abstract text via PubMed listing (format=pubmed) and summarizing fetch tool; renderings of this abstract disagreed across fetches (see the Mitochondrial burden access caveat); Wiley full text returned 403 and Crossref was disallowed by robots.txt, so full text not opened.