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MyDeficiencies

Nizatidine

histamine H2 receptor antagonist

Also sold as Axid, Tazac.

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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.

Nizatidine has almost no classical depletion machinery. It is well absorbed (absolute oral bioavailability above 70%), about 60% of an oral dose is excreted unchanged in urine, less than 7% is converted to its principal metabolite, and the label states that it does not inhibit the cytochrome P-450 drug-metabolizing system [1][2][3]. The label summaries retrieved name no vitamin or mineral. The one real mechanism is the one the drug is built to produce, reduced gastric acid, and that is never itself filed as a deficiency. Label pharmacology adds two nizatidine-specific details: pepsin activity was unchanged and betazole-stimulated intrinsic factor secretion rose at 75 to 300 mg [2]. Separately, nizatidine speeds gastric emptying in rats, probably through acetylcholinesterase inhibition [16]. That is a transit effect with no nutrient measurement behind it.

histamine H2 receptor antagonist · ATC A02BA04 (WHO ATC/DDD Index [4]) · also sold as Axid and Tazac [5]; generics (oral capsule and oral solution) · 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 Nizatidine 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

Vitamin B12: absorption, class extrapolation, long-term use

Yellow — Low

See study details

Acid-dependent release of food-bound B12 is a plausible pathway, and H2 blocker use for 2 or more years is modestly associated with a B12 deficiency diagnosis as a class, but no source retrieved studied nizatidine by name.

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 nizatidine B12 measurement was located. A PubMed listing for nizatidine with B12, cobalamin or cyanocobalamin returned one record, the 1988 review [8]. A 2018 Advances in Nutrition review on H2 blockers and B12 names nizatidine once as an example and cites no agent-level data [10].
  • At-risk subgroups: Older adults, continuous users beyond 2 years, people on metformin, vegetarians and vegans (nutrition-status contexts, not nizatidine findings). People with renal impairment have higher nizatidine exposure [1], but no link to B12 was found.

Direction

Depletion (reduced absorption), theoretical for this drug.

Regulatory status

Vitamin B12 is not mentioned in the nizatidine label text retrieved [1][2][3]. Label pharmacology: pepsin activity unchanged and betazole-stimulated intrinsic factor secretion increased at 75 to 300 mg [2].

Population evidence

Lam 2013 [6]: nested case-control, Kaiser Permanente Northern California, 25,956 cases and 184,199 controls, 1997 to 2011. Two or more years of H2 blocker supply: OR 1.25 (95% CI 1.17 to 1.34), with 1,087 cases (4.2%) and 5,897 controls (3.2%) exposed; PPIs for context OR 1.65. H2 blockers were analyzed as one class and the paper does not name individual agents, so nizatidine is not documented in the cohort. Abstract read through OpenAlex and the full article through a summarizing fetch tool.

Mechanism

Present for the class. A 1988 narrative review states that malabsorption of dietary iron and cobalamin appears to result from inhibition of gastric secretions by H2 antagonists [8]. For nizatidine specifically, the label data cut two ways: acid is reduced, but pepsin was unaffected and intrinsic factor secretion rose [2], so the intrinsic factor leg of B12 absorption is not suppressed in the acute pharmacology studies. These were short pharmacology studies and not B12 absorption tests.

Class cohort test

CLASS EXTRAPOLATION. Nizatidine was not named in Lam 2013 [6] and its presence in the cohort cannot be confirmed. It passes at yellow only because the shared mechanism is acid reduction. Capped at yellow. PPI data are not borrowed.

Counter-evidence held on record

Counter-evidence and confounding Confounding by indication is presumed (Hard Rule 6): chronic reflux, older age and metformin co-use carry higher baseline B12 deficiency. The modest odds ratio does not exclude residual confounding. Nizatidine's unchanged pepsin and raised intrinsic factor secretion argue against two of the three usual mechanisms. Framing caution This is a monitoring prompt for long-term users, not a finding that nizatidine causes B12 deficiency. Do not recommend B12 supplementation from this entry.

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

Not graded — disclosed evidence gap

See study details

No nizatidine-specific or defensible class-level evidence on mitochondrial structure, electron transport or biogenesis 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 source was opened to support even a yellow grade, and no circulating consumer claim of nizatidine mitochondrial damage was found (the one claims page found lists six other nutrients [19]). This is a disclosed gap, not a finding of safety. The LiverTox chapter should be re-read when access returns.

What was searched

Web search "nizatidine mitochondrial toxicity OR mitochondrial membrane potential OR oxidative phosphorylation hepatocytes": ten generic drug-induced mitochondrial toxicity reviews, none naming nizatidine in the title. Crossref title search "nizatidine mitochondria ATP cytotoxicity": two USP nizatidine monographs and unrelated mitochondrial papers. PubMed listing "nizatidine AND (mitochondria OR oxidative stress OR antioxidant)": HTTP 429, not read. Label hepatocellular injury [1][2][3] was considered: it is the drug's own toxicity with no stated mechanism and is not evidence of mitochondrial involvement.

Channel outcomes

PubMed listing: 429 rate limit. PubMed and PMC article pages: reCAPTCHA bot-verification. NCBI Bookshelf (LiverTox nizatidine chapter, tried by book ID): reCAPTCHA. livertox.nlm.nih.gov: robots.txt fetch failed. Europe PMC REST: 429. The shared web-search budget was later exhausted. DailyMed and accessdata label text: opened, no mitochondrial content. This is a mixed result: clean zeros on the channels that answered, with tooling-limited access to the primary databases.

Oxidative Stress

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

Oxidative stress: reverse direction, class in vitro only, nizatidine not tested in the source read

Yellow — Low

See study details

Other H2 blockers scavenge radicals in vitro, so a pro-oxidant or antioxidant-depleting effect is not supported; whether nizatidine shares this is unmeasured in any source that could be read.

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 oxidative stress marker (MDA, glutathione, antioxidant enzymes) in nizatidine users or animals was found. The Crossref query on nizatidine with antioxidant, oxidative stress and radical returned only generic oxidative stress textbook chapters.

Direction

Reverse (possibly protective chemistry), not depletion.

Regulatory status

No oxidative-stress statement in the nizatidine label text retrieved [1][2][3].

Population evidence

None in humans. Biedrzycki 2023 [15], read through a summarizing fetch tool: in vitro comparison of ranitidine, cimetidine and famotidine at 1 mM showed 20 to 70% scavenging across superoxide, hydroxyl, nitric oxide, hydrogen peroxide, ABTS and DPPH assays, ranitidine strongest and cimetidine weakest. The paper's systematic review included 8 studies (in vitro and animal) and no human trials. The summary did not mention nizatidine. A 1993 Biochemical Pharmacology paper on H2 antagonist antioxidant properties exists and OpenAlex lists nizatidine as a keyword, but its abstract could not be opened, so none of its findings are used [18].

Mechanism

Radical scavenging by the drug molecule, demonstrated in vitro for other H2 blockers only. Not shown for nizatidine and not shown to change systemic antioxidant capacity in humans.

Class cohort test

CLASS EXTRAPOLATION. Nizatidine was not in the cohort of [15] (ranitidine, cimetidine, famotidine). Grade rests on class chemistry being plausible for a related molecule, with the partial applicability stated. Capped at yellow.

Counter-evidence held on record

Counter-evidence In vitro scavenging at millimolar concentration does not establish an effect at therapeutic plasma levels, and the three tested drugs differed widely from each other, so a result for nizatidine cannot be predicted. Framing caution This is not an antioxidant benefit claim and not an antioxidant depletion claim. Nizatidine should not be described as depleting antioxidants.

Copper and Iron Balance

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

Iron: absorption, class extrapolation, 2 or more years

Yellow — Low

See study details

Non-heme iron absorption depends partly on gastric acid, and long-term H2 blocker use is associated with an iron deficiency diagnosis in class-level datasets that did not name nizatidine.

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: A PubMed listing for nizatidine with iron, ferritin or iron absorption returned three records: the 1988 review [8], an environmental chemistry paper on degrading nizatidine as a contaminant (not a human study), and the 1993 antioxidant paper [18]. None measured iron status in nizatidine users.
  • At-risk subgroups: Menstruating women, people with low dietary iron, people with GI blood loss, concurrent PPI users.

Direction

Depletion (reduced absorption), theoretical for this drug.

Regulatory status

Iron is not mentioned in the nizatidine label text retrieved [1][2][3].

Population evidence

Lam 2017 [7]: community-based case-control, 77,046 incident iron deficiency cases and 389,314 controls, January 1999 to December 2013. H2 blocker use without PPI, 2 or more years: OR 1.58 (95% CI 1.46 to 1.71); risk decreased after stopping. Individual agents are not named in the abstract read through a Kaiser Permanente publication page summary. Taiwan National Health Insurance case-control [9]: 5,326 iron deficiency anemia cases and 21,304 matched controls (2011 to 2018); the combined PPI and H2 blocker group, 2 or more months of continuous use, had aOR 2.36 (95% CI 1.94 to 2.86). H2 blockers were not separated from PPIs in the retrieved text and nizatidine is not mentioned.

Mechanism

Present for the class, unmeasured for nizatidine. The 1988 review lists reduced iron absorption among four categories of H2 antagonist harm [8].

Class cohort test

CLASS EXTRAPOLATION. Nizatidine was not named in Lam 2017 [7] or the Taiwan study [9], and its presence in either cohort is unconfirmed. Capped at yellow. PPI iron data are not borrowed; the Taiwan pooled estimate is shown only to document that no H2-only nizatidine estimate exists.

Counter-evidence held on record

Counter-evidence and confounding An iron deficiency diagnosis triggers GI work-up, and bleeding from the acid disease being treated could cause iron deficiency independent of the drug (confounding by indication). Neither study can separate these. Framing caution Iron deficiency is not anemia, and anemia is not iron deficiency (Hard Rule 2). Iron supplementation is not recommended by this entry, and excess iron carries its own risks.

Copper

Not graded — disclosed evidence gap

See study details

No evidence on nizatidine and copper status, absorption, excretion or chelation 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 for nizatidine, and no circulating copper claim found. This is a disclosed gap, not reassurance, and it is graded separately from Iron (Hard Rule 7). Re-check with PubMed and a copper-specific web search.

What was searched

Crossref title search "nizatidine copper complex": ten records, all USP monographs, drug handbooks, Reactions Weekly, Meyler's Side Effects of Drugs entries, or an unrelated chlorophyllin copper monograph; none a copper study. The nizatidine label text retrieved has no copper statement [1][2][3]. The claims page [19] does not list copper. PubMed listings "nizatidine copper": one returned a 404 (uninterpretable, possibly no records) and a second variant returned 429. Copper-specific web searches were not run before the search budget was exhausted.

Channel outcomes

As in Mitochondrial burden. Tooling-limited for PubMed, and not searched by web search. A Cu(II) chelation study exists for famotidine in the sibling dossier, but that is a different molecule and was not borrowed (Hard Rule 6).

Gut Microbiome Risk

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

Gut microbiome risk: class extrapolation, small effect relative to PPIs

Yellow — Low

See study details

H2 blocker use as a class is associated with small or undetectable microbiome change; nizatidine was not named in either study read, and the one nizatidine-specific microbiome finding runs the other way (bacteria metabolize the drug).

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 randomized trial found no separable H2 blocker microbiome profile [12]. The PubMed listing for nizatidine with microbiota, dysbiosis or C. difficile returned a 429 and was not read; a web search for nizatidine with gut microbiota or 16S returned no nizatidine microbiome study.
  • At-risk subgroups: Not defined. The hemodialysis cohort is heavily confounded.

Direction

Microbiome shift, small, class-level. The separate nizatidine finding is microbiota acting on the drug.

Regulatory status

No microbiome statement in the nizatidine label text retrieved [1][2][3].

Population evidence

Randomized trial [12] (abstract read through an aggregator page): healthy volunteers, 7 days of a PPI (n=23) or an H2 blocker (n=26); H2 blocker versus non-H2 blocker classifier AUROC 0.509 against 0.924 for PPIs, i.e. no discernible H2 blocker signature. The agent was not identified in the retrieved text. Cross-sectional study [13] of 193 hemodialysis patients (32 H2 blocker users, 23 PPI users, 138 controls), 16S sequencing: H2 blocker users had a higher dysbiosis index and enrichment of Prevotella 2, Phascolarctobacterium, Christensenellaceae R-7 group and Eubacterium oxidoreducens group, with no significant alpha-diversity difference; the agents were not named.

Mechanism

Plausible but small for the class: less gastric acid may let more oral and upper-GI bacteria survive transit. Not demonstrated for nizatidine. In the other direction, Basit 2002 [14] (abstract read through an aggregator page): in vitro, nizatidine and ranitidine were degraded by colonic bacteria (virtually no nizatidine remaining after 12 hours) while cimetidine and famotidine were stable. This is the microbiota affecting the drug (Hard Rule 4) and says nothing about nizatidine changing the microbiome. Because most of an oral dose is absorbed and excreted in urine [1][3], how much nizatidine reaches the colon is an open question (inference).

Class cohort test

CLASS EXTRAPOLATION. Nizatidine was not named in [12] or [13] and its presence is unconfirmed. Capped at yellow. The Dutch three-cohort PPI microbiome study and other PPI data were not borrowed.

Counter-evidence held on record

Counter-evidence The strongest class-level data point toward no detectable effect, and the dialysis taxa differences may reflect kidney disease, diet and other medications. Framing caution This entry is not a claim of dysbiosis, and PPI microbiome findings do not apply to nizatidine.

Oxygen and ATP Output

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

Oxygen delivery/utilization: label anemia signal and one aplastic anemia case, a hematologic toxicity outcome and not a nutrient finding

Yellow — Low

See study details

The label records anemia more often with nizatidine than placebo and one fatal aplastic anemia case is published, but no hemoglobin, hematocrit or oxygenation measurement in nizatidine users was found and the mechanism is not named.

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 oxygen-carrying or hemoglobin series for nizatidine users was located. A web search for nizatidine with hemolytic anemia, pancytopenia, aplastic anemia or methemoglobinemia returned only the case above. The PubMed listing for nizatidine with anemia, hemoglobin or hemolytic returned a 429 and was not read.
  • At-risk subgroups: Dialysis and severe renal impairment (one case; label dose-reduction group). Not defined beyond that.

Direction

Neutral for nutrients. This is a drug adverse event (blood-cell toxicity). It is not a depletion, and it is kept apart from the Iron and B12 entries (Hard Rule 2).

Regulatory status

Labeled: anemia reported significantly more frequently with nizatidine than placebo (0.2% versus 0%), rare thrombocytopenic purpura, fatal thrombocytopenia in a patient given nizatidine and another H2 blocker, and eosinophilia in the adverse event listing [1][2][3].

Population evidence

Case report [17], read at abstract level through a summarizing fetch tool: a 55-year-old woman with end-stage diabetic nephropathy, on hemodialysis for 2 years, developed fever and severe pancytopenia 12 days after starting nizatidine (previously on lansoprazole). Drug-induced aplastic anemia was diagnosed and she died on hospital day 23 from generalized fungal infections. Dose, blood counts, bone marrow findings and withdrawal or rechallenge were not available in the abstract. Tier B, nizatidine-specific. Narrative review [8]: 85 reported H2 antagonist cytopenia cases, 75 (88%) with cimetidine; that review is Tier C for nizatidine.

Mechanism

Not named. The label states nizatidine is excreted mainly by the kidney and half-life reaches 3.5 to 11 hours in renal impairment [1][2], and the case occurred in renal failure, but the summarized abstract does not discuss accumulation. Linking the two would be inference.

Counter-evidence held on record

Counter-evidence Anemia at 0.2% versus 0% is a very small absolute difference of unknown clinical size, and a single case cannot establish causation. Anemia is an outcome (Hard Rule 2). Nothing here shows reduced oxygen delivery was measured. Framing caution Do not present this as a nutrient depletion or as impaired oxygen-carrying capacity. It is a rare blood-cell adverse event that belongs with the label, not with a supplement prompt.

ATP production

Not graded — disclosed evidence gap

See study details

No evidence on nizatidine 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 claim. Not a finding of safety. Kept independent of Mitochondrial burden and Oxygen delivery/utilization (Hard Rule 7). This is largely the same gap as Mitochondrial burden viewed twice (see Overlap map).

What was searched

The same web search and Crossref queries as Mitochondrial burden, which included oxidative phosphorylation, mitochondrial membrane potential, ATP and cytotoxicity terms. No nizatidine result. No circulating "low energy" claim for nizatidine was found on the claims page [19].

Channel outcomes

Same as Mitochondrial burden. Clean zeros on answering channels, tooling-limited for PubMed and NCBI.

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.

  • Calcium deficiency and bone loss

    Where it comes from: Tier D claims page [19], which rates calcium "Insignificant Depletion" and cites Recker 1985 and Bo-Linn 1984 (not opened).

    Why it fails: NHANES 1999 to 2006 analysis of 4,232 adults aged 60 and over, 169 H2 blocker users; the exposure definition names cimetidine, ranitidine, famotidine and nizatidine. No association of long-term H2 blocker use with lumbar spine BMD (adjusted beta 0.0182, 95% CI -0.0050 to 0.0413) and no serum calcium difference (9.50 versus 9.51 mg/dL, P=0.78) [11]. Limits: H2 blockers were pooled, the nizatidine share is not stated, absorption was not measured, and the design is cross-sectional. Fracture and BMD are outcomes, not calcium deficiency. The label has no calcium statement.

  • Folic acid (provisional, tooling-limited)

    Where it comes from: Tier D claims page [19], "Insignificant Depletion", citing Russell 1988 and Termanini 1998 (not opened).

    Why it fails: No nizatidine folate measurement was found, the label is silent, and the cited papers could not be read, so they were not used. A pH-dependent absorption mechanism is conceivable, so this is not a mechanistic rule-out and is not graded white on the merits. Held out of publication as a deficiency claim pending a re-check that could convert it to yellow.

  • Zinc (provisional, tooling-limited)

    Where it comes from: Tier D claims page [19], "Insignificant Depletion", citing Sturniolo 1991 (not opened).

    Why it fails: No nizatidine zinc measurement was found and the cited study was not opened. Held, not rebutted, for the same reason as folic acid.

  • Chromium (provisional, tooling-limited)

    Where it comes from: Tier D claims page [19], rated "Insufficient Evidence" by the page itself, citing the Food and Nutrition Board 2002 (not opened).

    Why it fails: The page's own rating concedes the absence of evidence. No nizatidine chromium data were found and the cited source was not opened. Held, not rebutted.

  • "Vitamin B12 moderate depletion" as stated

    Where it comes from: Tier D claims page [19] (rating "Moderate Depletion" with eight citations, none opened).

    Why it fails: The wording overstates the evidence. The relationship is carried here as yellow class extrapolation with confounding shown; no study measured B12 in nizatidine users. Included so readers see the difference between the circulating rating and the graded entry.

How the body handles this medication

Metabolism and enzymes
Less than 7% of an oral dose is metabolized to N2-monodesmethylnizatidine, an active H2 antagonist; the N2-oxide (under 5%) and S-oxide (under 6%) are minor. The label states nizatidine does not inhibit the cytochrome P-450 system. No enzyme induction is described, and no CYP isoform is named.[1][2] DailyMed labels, clinical pharmacology and drug interactions
Elimination
More than 90% of an oral dose is excreted in urine within 12 hours; about 60% is unchanged drug. Half-life 1 to 2 hours, plasma clearance 40 to 60 L/h.[1][3] (labels read through a summarizing fetch tool)
Absorption and distribution
Absolute oral bioavailability exceeds 70%; peak 0.5 to 3 hours. Food raises AUC and Cmax by about 10%. About 35% protein-bound, mainly to alpha-1 acid glycoprotein; volume of distribution 0.8 to 1.5 L/kg. No absorption transporter is named in the label sections retrieved.[1][3]
Renal and hepatic handling
Moderate to severe renal impairment prolongs half-life to 3.5 to 11 hours and dose reduction is required. Uncomplicated hepatic dysfunction with normal renal function left disposition similar to normal. Hepatocellular injury with raised liver enzymes is a labeled adverse reaction, with marked elevations above 500 IU/L and one above 2,000 IU/L, reversible on discontinuation.[1][2][3] (numeric detail from [3])
Gastric acid, pepsin, intrinsic factor
Inhibits nocturnal acid secretion for up to 12 hours and food, caffeine, betazole and pentagastrin-stimulated secretion. At 75 to 300 mg it did not affect pepsin activity and increased betazole-stimulated intrinsic factor secretion; no effect on basal serum gastrin.[2] pharmacodynamics section
Antacid, drug and laboratory interactions
Aluminum and magnesium hydroxide antacids with simethicone decrease nizatidine absorption by about 10% (a mineral acting on the drug, a timing matter and not a depletion). Aspirin at 3,900 mg daily raised serum salicylate with nizatidine 150 mg twice daily. False-positive urobilinogen on Multistix may occur. No interaction seen with theophylline, chlordiazepoxide, lorazepam, lidocaine, phenytoin or warfarin.[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.

  • Lab / long-term use

    Vitamin B12 status

    Worth considering serum B12, with methylmalonic acid or homocysteine if borderline, for people on continuous therapy beyond about 2 years, especially older adults and people also on metformin. This is a monitoring prompt, not a finding of nizatidine-caused deficiency.

  • Lab / symptoms

    Iron indices

    Complete blood count and ferritin if fatigue, pallor or heavy menstrual loss, or if on long-term therapy with other risk factors. New iron deficiency in an adult warrants evaluation for GI blood loss rather than assumption of a drug cause.

  • Hematology / early therapy

    Blood counts after starting

    Fever, infection, bruising or bleeding soon after starting should prompt a complete blood count, particularly in renal failure or dialysis. The published aplastic anemia case authors wrote that careful observation is required after starting an H2 antagonist in hemodialysis patients [17]. This is a drug safety prompt, not a nutrient one.

  • Renal / liver

    Kidney and liver function

    Dose reduction is a label matter in moderate to severe renal insufficiency (half-life 3.5 to 11 hours) [1][2]. Hepatocellular injury with raised ALT, AST or alkaline phosphatase is labeled and was reversible on stopping [1][3].

  • Timing / laboratory

    Supplements, antacids, tests

    Aluminum or magnesium hydroxide antacids with simethicone lower nizatidine absorption by about 10%; the label does not require a separation interval [1]. No mineral or vitamin timing interaction is listed. Nizatidine can cause false-positive urobilinogen on Multistix [1]. No supplement dose appears anywhere in this dossier, so no upper-limit comparison was needed.

  • Special populations

    Pregnancy, pediatrics, older adults

    No adequate well-controlled pregnancy studies; about 0.1% of an oral dose appears in breast milk; pediatric safety and effectiveness not established; of 955 trial patients, 337 (35.3%) were 65 or older with no overall safety difference [2]. No nutrient-specific consideration was found for these groups.

Overlap map, to prevent double counting

  • Vitamin B12

    Shares evidence with: Iron

    Note: Same mechanism (acid reduction impairing micronutrient absorption), the same research group and database (Kaiser Permanente Northern California, [6] and [7]), and the same 1988 review [8]. One mechanism and one data source, not two independent confirmations.

  • Iron; Vitamin B12

    Shares evidence with: Oxygen delivery/utilization

    Note: Any hemoglobin effect from nutrient malabsorption would run through these two entries. The Oxygen delivery entry rests on different sources (label adverse events and a case report [17]) and describes marrow toxicity, not nutrient loss. The 1988 review [8] is cited in three entries for different statements.

  • Oxygen delivery/utilization

    Shares evidence with: Fails verification: calcium

    Note: No shared source. The NHANES cohort [11] is used only for the calcium rebuttal.

  • Oxidative stress

    Shares evidence with: Mitochondrial burden; ATP production (ungraded)

    Note: No shared evidence. In vitro scavenging by other H2 blockers [15] says nothing about mitochondria or ATP and is not used for either.

  • Mitochondrial burden

    Shares evidence with: ATP production

    Note: Both ungraded for the same reason, with identical searches and the same blocked databases. One gap viewed twice.

  • Copper

    Shares evidence with: Iron

    Note: No shared source. Graded separately per Hard Rule 7; copper has no evidence at all.

  • Gut microbiome risk

    Shares evidence with: Vitamin B12; Iron

    Note: No shared source. A microbiome shift is a hypothetical modifier of absorption and is not claimed. The nizatidine bacterial-metabolism finding [14] is microbiota acting on the drug and is used for neither nutrient.

  • All entries

    Shares evidence with: Label sources [1][2][3]

    Note: The labels supply the pharmacokinetic and adverse event facts and the "no nutrient mentioned" statements across entries. This is one regulatory source family, not independent confirmation.

All references used above
  1. Nizatidine capsules, prescribing information (DailyMed, Actavis Pharma label). — Regulatory label (Tier A). Revision shown as Rev. A 6/2022. Source of bioavailability, metabolism, excretion, food and antacid effects, aspirin interaction, urobilinogen interference, anemia and hepatocellular injury statements. Read through a summarizing fetch tool, not as raw text.
  2. Nizatidine capsules, prescribing information (DailyMed, Dr. Reddy's Laboratories label). — Regulatory label (Tier A). Revised 12/2018. Source of pharmacodynamics (pepsin, intrinsic factor, gastrin), interaction list, renal warning, geriatric, pediatric, pregnancy and nursing sections, and hematologic and hepatic adverse reactions. Read through a summarizing fetch tool.
  3. AXID (nizatidine) oral solution, FDA label (NDA 21-494, 2005). — Regulatory label (Tier A). Pharmacokinetics, anemia 0.2% versus 0%, eosinophilia, thrombocytopenia, and liver enzyme elevations above 500 IU/L with one above 2,000 IU/L. No nutrient mention reported. Read through a summarizing fetch tool.
  4. WHO Collaborating Centre, ATC/DDD Index: nizatidine, A02BA04, DDD 0.3 g, oral and parenteral. — Reference index.
  5. Wikipedia, Nizatidine. — Used only for brand names (Axid, Tazac). Not evidence for any grade.
  6. Lam JR, et al. Proton pump inhibitor and histamine 2 receptor antagonist use and vitamin B12 deficiency. JAMA 2013 (authors beyond the first not captured in retrieval; first author as given in the sibling famotidine dossier, not independently confirmed). — Nested case-control, 25,956 cases and 184,199 controls, Kaiser Permanente Northern California. DOI 10.1001/jama.2013.280490. Abstract reconstructed from OpenAlex; article text through a summarizing fetch tool.H2 blockers pooled; individual agents not named or reported. Nizatidine not documented in the cohort. Tier C for nizatidine.
  7. Proton pump inhibitor and histamine-2 receptor antagonist use and iron deficiency. Gastroenterology (OpenAlex year 2016). — Community-based case-control, 77,046 cases and 389,314 controls, 1999 to 2013. DOI 10.1053/j.gastro.2016.11.023. Abstract read through the Kaiser Permanente publication page summary; OpenAlex metadata had no abstract text.H2 blockers pooled; individual agents not named in the abstract. Nizatidine not documented in the cohort. Tier C for nizatidine.
  8. Aymard JP, Aymard B, Netter P, Bannwarth B, Tréchot P, Streiff F. Haematological adverse effects of histamine H2-receptor antagonists. Med Toxicol Adverse Drug Exp 1988;3(6):430-448. — Narrative review; 85 cytopenia cases, 75 (88%) with cimetidine. DOI 10.1007/BF03259895; PMID 2905759. Nizatidine appears in the review's history of H2 antagonists; the abstract was not available and the page was read through a summarizing fetch tool.Narrative class review without drug-level stratification for nizatidine. Tier C.
  9. Is use of a long-term proton pump inhibitor or histamine-2 receptor antagonist a risk factor for iron-deficiency anaemia in Taiwan? A neglected clinical drug-drug interaction. Fam Pract 2023;42(2):cmad090. — Retrospective matched case-control, Taiwan National Health Insurance Research Database 2011 to 2018, 5,326 cases and 21,304 controls. Authors not captured. Read through a summarizing fetch tool.Combined PPI and H2 blocker estimate; nizatidine not mentioned. Tier C.
  10. Miller JW. Proton pump inhibitors, H2-receptor antagonists, metformin, and vitamin B-12 deficiency: clinical implications. Adv Nutr 2018. — Narrative review. Names nizatidine once, in a list of H2 blockers; cites no agent-level data. Read through a summarizing fetch tool.No nizatidine data. Tier C context only.
  11. Gao S, et al. NHANES cross-sectional analysis of PPI and H2 receptor antagonist use and bone mineral density. Front Med 2021 (full title and authors not captured in this retrieval). — NHANES 1999 to 2006 cross-sectional, 4,232 participants aged 60 and over, 169 H2 blocker users. The exposure definition names cimetidine, ranitidine, famotidine and nizatidine. DOI 10.3389/fmed.2021.725359. Read through a summarizing fetch tool.Nizatidine named as an included type but pooled; the number of nizatidine users is not stated.
  12. Zhu J, Sun C, Li M, Hu G, Zhao X-M, Chen W-H. Compared to histamine-2 receptor antagonist, proton pump inhibitor induces stronger oral-to-gut microbial transmission and gut microbiome alterations: a randomised controlled trial. Gut 2023;72(7):1087-1097. — RCT, healthy volunteers, 7 days; PPI n=23, H2 blocker n=26.Read through an aggregator summary, not the journal page. H2 blocker agent not specified in the retrieved text. Tier C.
  13. Anti-acid drug treatment induces changes in the gut microbiome composition of hemodialysis patients. Microorganisms 2021;9(2):286. — Cross-sectional, 193 patients (32 H2 blocker users), 16S sequencing. Read through a summarizing fetch tool.Specific H2 blockers not named. Tier C.
  14. Basit AW, Newton JM, Lacey LF. Susceptibility of the H2-receptor antagonists cimetidine, famotidine and nizatidine to metabolism by the gastrointestinal microflora. Int J Pharm 2002. — In vitro colonic bacteria incubation; nizatidine and ranitidine degraded, cimetidine and famotidine stable. Abstract read through an Academia.edu page summary; full text not opened.Direction is microbiota acting on the drug. Tier B, nizatidine-specific, but not a drug effect on the microbiome.
  15. Biedrzycki G, Wolszczak-Biedrzycka B, Dorf J, Michalak D, Zendzian-Piotrowska M, Zalewska A, Maciejczyk M. Antioxidant and anti-glycation potential of H2 receptor antagonists: in vitro studies and a systematic literature review. Pharmaceuticals 2023;16(9):1273. — In vitro comparison of ranitidine, cimetidine and famotidine plus a systematic review of 8 studies. Read through a summarizing fetch tool.Nizatidine not tested and not mentioned in the summary read. Tier C for nizatidine.
  16. Kaneko H, Mitsuma T, Uchida K, Nagai H, Harada M, Kotera H. Nizatidine accelerates gastric emptying of a solid meal in rats. Dig Dis Sci 1995. — Animal study, male Wistar rats; dose-dependent acceleration at 1 to 30 mg/kg; nizatidine and N-desmethyl nizatidine stimulated emptying while nizatidine S-oxide, cimetidine and famotidine did not; mechanism proposed as direct and/or indirect (acetylcholinesterase inhibition) cholinergic. Abstract level via a summarizing fetch tool.Tier B, nizatidine-specific, but a transit effect with no nutrient measurement. Used only as context in the headline.
  17. Nakano et al. Aplastic anemia associated with initiation of nizatidine therapy in a hemodialysis patient. Clin Exp Nephrol 2004 (journal and year as given by the page summary). — Case report, one patient. PMID 15235935 as listed in search results. Abstract level via a summarizing fetch tool; dose, counts and marrow findings not available.
  18. van Zyl JM, Kriegler A, van der Walt BJ. Anti-oxidant properties of H2-receptor antagonists. Effects on myeloperoxidase-catalysed reactions and hydroxyl radical generation in a ferrous-hydrogen peroxide system. Biochem Pharmacol 1993;45(12):2389-2397. — DOI 10.1016/0006-2952(93)90218-L; PMID 8101078. Bibliographic metadata only, from OpenAlex and Crossref; OpenAlex lists nizatidine as a keyword.Not opened: abstract unavailable (PubMed bot-verification; OpenAlex and Crossref have no abstract). No finding from this paper is used for any grade.
  19. HelloPharmacist. Nizatidine nutrient depletions (nutrient depletion checker page). — Tier D. Used only as a circulating-claim origin (calcium, folic acid, iron, zinc, vitamin B12, chromium); its cited references were not opened. Read through a summarizing fetch tool.