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MyDeficiencies

Oxymorphone

opioid analgesic, full mu-receptor agonist

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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.

Oxymorphone has no classical depletion machinery. The immediate-release label (read through a summarizing tool) describes extensive liver metabolism by reduction and glucuronidation, less than 1% of a dose excreted unchanged in urine, no inhibition of the major CYP enzymes except CYP3A4 at 150 micromolar or above, and no CYP3A4 or CYP2C9 induction in clinical studies with the extended-release product [1]. The words vitamin, calcium, iron, copper, bone, mitochondria, oxidative and microbiome were not found in the label text read [1][2]. Whose data this is matters here (Hard Rule 6): oxymorphone is also a minor CYP2D6 metabolite of oxycodone, present in plasma "only in low concentrations" after oxycodone, with free oxymorphone 0% in urine [3]. Oxycodone studies therefore describe oxycodone, and none of them is carried into this dossier as an oxymorphone finding. Where oxycodone appears, it is named as oxycodone and labeled class extrapolation.

opioid analgesic, full mu-receptor agonist · ATC N02AA11 (WHO ATC/DDD Index [5]) · also sold as Opana (IR) and Opana ER (withdrawn 2017); generics · reviewed 2026-10-07. 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 Oxymorphone 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

Testosterone and the androgen axis: class extrapolation, hormone suppression and not a nutrient deficiency

Yellow — Low

See study details

The oxymorphone label carries the opioid warning for androgen deficiency with extended use and states that opioids inhibit LH, but no study retrieved reports testosterone in oxymorphone users, and the oxycodone cohort results are oxycodone data, not oxymorphone data.

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: PubMed listing "oxymorphone testosterone" returned 2 records (the aromatase paper above and a naltrexone enzyme-kinetics paper), neither with human hormone data [28]. Eight other hormone phrasings were rate-limited or returned 404 (see Sources item 28). In Lamprecht 2018 [15] (mixed opioid users), testosterone in men was associated with BMI but not opioid use on the abstract reconstruction.
  • At-risk subgroups: Not defined for oxymorphone. At class level: men on long-term daily therapy (the label wording is "extended period of time").

Direction

Hormone suppression (endocrine effect). Hard Rule 2: low testosterone is the drug class pharmacologic effect and not a nutrient deficiency. No intake change is implied.

Regulatory status

Section 6.2 postmarketing (Aurolife IR label): "Cases of androgen deficiency have occurred with use of opioids for an extended period of time" [2]. Section 12.2 (Hikma IR label): "Opioids inhibit the secretion of adrenocorticotropic hormone (ACTH), cortisol, and luteinizing hormone (LH)" [1]. One summarizer pass also attributed a hypothalamic-pituitary-gonadal sentence (low libido, erectile dysfunction, infertility) to the label; I did not see that sentence quoted verbatim, so it is not relied on.

Population evidence

None with oxymorphone as the studied drug. Rubinstein 2017 [12]: retrospective cohort of 1,159 men on a single opioid for at least 90 days, hydrocodone as referent; the abstract names fentanyl (OR 25.7), methadone (OR 7.33) and oxycodone (95% CI 1.87 to 5.33; the point estimate was not in the abstract text I read). Oxymorphone is not named in the abstract, and the full text was not opened. Rubinstein 2013 [13]: 81 men, long-acting versus short-acting opioids (74% versus 34% hypogonadal on the abstract reconstruction); hydrocodone and oxycodone named, oxymorphone not. Kafel 2025 [14]: narrative review; prevalence "between 20% and 80%" depending on opioid type, duration, age and threshold; no individual opioids named in the abstract. Daniell 2006 on DHEAS [27]: only indexing metadata was retrievable; no opioid names, no sample size.

Mechanism

Present at class level: LH inhibition per the label [1]; the 2025 review attributes the effect mainly to inhibition of GnRH [14]. An in vitro paper on human placental aromatase tested 20 opiates including oxymorphone [26]; I saw only a PubMed listing quote (agonists including oxymorphone "caused an increase in E(3) formation by 124-160% of control") and could not open the abstract, the enzyme is placental and the concentrations are unknown, so it is not used for grading.

Whose data

Hard Rule 6. Oxymorphone is a minor CYP2D6 metabolite of oxycodone, "present in the plasma only in low concentrations" after oxycodone, with free oxymorphone 0% and conjugated oxymorphone up to 14% in urine [3]. The oxycodone odds ratios in [12] and the oxycodone arm of other studies describe oxycodone exposure. They are not oxymorphone findings and are not carried here.

Class cohort test

CLASS EXTRAPOLATION. Oxymorphone was not confirmed in the cohort of [12], [13], [14] or [15]. Tier C, capped at yellow. The only drug-specific support is the label sentence [1][2], which names "opioids", not oxymorphone.

Counter-evidence held on record

Counter-evidence and confounding Confounding by indication is presumed (Hard Rule 6): chronic pain, obesity, age and comorbidity lower testosterone independently. The largest dataset uses another opioid as the referent, so it would not test any opioid against non-use even if oxymorphone had been included. Framing caution for the consumer surface This is a hormone-axis effect described for long-term opioid use in men, not a nutrient deficiency. Do not suggest zinc, vitamin D or herbal testosterone products from this entry. Evaluation belongs to a prescriber.

Adrenal insufficiency, HPA suppression: class extrapolation, hormone and not a nutrient

Yellow — Low

See study details

The oxymorphone label warns of adrenal insufficiency with opioid use (more often after more than one month) and states that opioids inhibit ACTH and cortisol, but none of the cohorts retrieved names oxymorphone.

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 oxymorphone-specific cortisol, ACTH or stimulation-test study was found. PubMed listings "oxymorphone adrenal cortisol" and "oxymorphone hypothalamic pituitary adrenal" returned 404 (interpreted as no records, not independently confirmed); "oxymorphone adrenal insufficiency" was rate-limited and never read [28].
  • At-risk subgroups: People on opioids for more than one month (label wording) and higher opioid dose (one cross-sectional signal in [15]).

Direction

Hormone suppression (cortisol axis). Hard Rule 2: an endocrine adverse effect, not a nutrient depletion.

Regulatory status

Section 5.9: "Cases of adrenal insufficiency have been reported with opioid use, more often following greater than one month of use"; presentation includes nausea, vomiting, anorexia, fatigue, weakness, dizziness and low blood pressure; treatment is corticosteroid replacement and opioid withdrawal [1][2]. Section 12.2: opioids inhibit ACTH, cortisol and LH secretion [1].

Population evidence

None with oxymorphone named. Lamprecht 2018 [15]: cross-sectional, 40 long-term oral or transdermal opioid users versus 25 matched controls; secondary adrenal insufficiency in 22.5% of users versus none of the controls; users with insufficiency had higher morphine-equivalent doses; the only opioid named is morphine, through the dose unit. Gibb 2016 [16]: cross-sectional, 48 chronic pain patients on sustained opioids without recent glucocorticoids; abstract concludes HPA axis suppression occurs in a clinically significant proportion; individual opioids not named; basal cortisol correlated with age (R 0.398) and inversely with BMI (R minus 0.435).

Mechanism

Present as a label statement of opioid-mediated ACTH suppression [1]. Not measured for oxymorphone in any source retrieved.

Class cohort test

CLASS EXTRAPOLATION. Oxymorphone not confirmed in the cohort of [15] or [16]; abstracts do not name the opioids. Tier C, capped at yellow. No oxycodone-specific cortisol data were borrowed.

Counter-evidence held on record

Counter-evidence and confounding Both studies are small cross-sectional designs. Gibb has no opioid-free comparator in the abstract, and obesity and age move cortisol independently. Cohorts were long-term users, so the finding does not describe short courses. Framing caution for the consumer surface This is a symptom-triggered clinical awareness prompt for people on opioids for more than a month. It is not a nutrient claim and does not imply any supplement.

Hyponatremia: dilutional or retention risk, label mechanism sentence only, no oxymorphone-attributed case found

Yellow — Low

See study details

The label states that opioids can reduce diuretic efficacy by inducing antidiuretic hormone release, which makes water retention plausible, but the words hyponatremia and SIADH were not found in the label text read and no oxymorphone case or cohort was found.

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 oxymorphone case report of low sodium turned up in the listings that completed. That is a limited search, not proof of absence.
  • At-risk subgroups: People also taking diuretics or other SIADH-associated drugs, and older adults (the label separately reports about 40% higher oxymorphone exposure in elderly subjects [1]).

Direction

Retention or dilution (excess water relative to sodium). This is not a dietary sodium deficiency. Hard Rule 5: added salt or sodium would be the hazard, not the remedy.

Regulatory status

Section 7: "Opioids can reduce the efficacy of diuretics by inducing the release of antidiuretic hormone" [1]. A word check of the Hikma and Aurolife label text found no hyponatremia, SIADH or sodium adverse-event wording; "sodium" appeared only in page metadata [1][2]. Both pages were summarizer reads and the Aurolife page text stopped inside section 9, so the check covers the sections read, not the whole label.

Population evidence

None for oxymorphone. PubMed listing "oxymorphone hyponatremia OR SIADH" returned 10 records, all general SIADH or hyponatremia papers with no oxymorphone in the retrieved text [28]. Three further phrasings ("oxymorphone sodium SIADH", "oxymorphone electrolyte SIADH case", "oxymorphone hyponatraemia sodium") returned 404 or were rate-limited [28].

Mechanism

Present as a label statement for opioids (ADH release). Magnitude for oxymorphone was not measured in any source retrieved.

Class cohort test

CLASS EXTRAPOLATION. No hyponatremia cohort naming oxymorphone or any other opioid was opened; support is a class-wide label sentence. Tier B or C at most, capped at yellow.

Counter-evidence held on record

Counter-evidence and confounding Confounding by indication is presumed (Hard Rule 6): pain conditions, nausea and co-medications can lower sodium independently, and no retrieved source separates these from oxymorphone. Framing caution for the consumer surface This is a possible water-retention effect, not a sodium shortfall. Supplementing salt would be the hazard. Serum sodium is a monitoring prompt only.

Vitamin D: context flag, reverse direction, confounding by indication

Yellow — Low

See study details

No retrieved study shows oxymorphone lowers 25-hydroxyvitamin D. The observational links run from low vitamin D to opioid use or from treated-population prevalence, which Hard Rules 4 and 6 bar from being filed as a drug effect.

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: PubMed listing "oxymorphone osteoporosis" returned 404 (interpreted as no records); "oxymorphone vitamin D" and "oxymorphone bone density osteoporosis" were rate-limited and not read [28]. No oxymorphone study with measured 25(OH)D was located.
  • At-risk subgroups: Not defined from oxymorphone data.

Direction

Reverse or context only (nutrient status relating to opioid use or response, not the drug lowering the nutrient). Hard Rule 4. Low bone density, if present, would be an outcome and not vitamin D deficiency (Hard Rule 2).

Regulatory status

The words vitamin, calcium, bone and osteoporosis were not found in the label text read [1][2].

Population evidence

Kemeny 2021 [18]: higher prevalence of vitamin D deficiency in patients with opioid use disorder and an inverse dose-dependent association between vitamin D level and self-reported opioid use, plus mouse data that deficient vitamin D signaling amplifies opioid responses; the abstract names no opioid. Frontiers in Nutrition 2024 [19]: NHANES 2001 to 2018, 1,856 long-term prescription opioid users, 67.2% with 25(OH)D below 75 nmol/L and 32.4% below 50 nmol/L; the text names only "narcotic analgesics" and has no opioid-free comparator, so it gives prevalence in a treated population and not a drug effect.

Mechanism

No mechanism by which oxymorphone lowers vitamin D was found. Indirect routes (hypogonadism, reduced sun exposure or activity in chronic pain) are untested hypotheses here.

Class cohort test

CLASS EXTRAPOLATION and context. Oxymorphone not named in [18] or [19]. Tier C, capped at yellow. Confounding by indication is presumed: chronic pain populations may already be low in vitamin D before opioid therapy, and neither source has a before-and-after comparison.

Counter-evidence held on record

Counter-evidence and confounding Low vitamin D may drive pain and opioid use and not the reverse [18]. High prevalence in treated users [19] is a baseline-risk fact, not causal attribution. Framing caution for the consumer surface Do not present this as oxymorphone causing vitamin D deficiency. If vitamin D is checked, the reason is general risk factors, and no dose is recommended here.

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: class extrapolation from other opioids in cell and animal models, mixed direction

Yellow — Low

See study details

Cell-culture work on six other opioids shows reduced viability in mitochondrial-activity assays, and an oxycodone rat model shows the opposite (protection), but oxymorphone was not tested in any source retrieved.

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 study measured mitochondrial function in people taking oxymorphone. PubMed listings "oxymorphone mitochondrial toxicity" returned 404; five other mitochondria phrasings were rate-limited and not read [28].
  • At-risk subgroups: Not defined.

Direction

Mixed and model-dependent: adverse in cultured cells for several opioids, protective in an oxycodone ischemia-reperfusion model. Not a nutrient entry.

Regulatory status

The word mitochondria was not found in the label text read [1][2].

Population evidence

Nylander 2024 [23]: six opioids (methadone, morphine, oxycodone, hydromorphone, ketobemidone, fentanyl) in primary cortical neurons, SH-SY5Y cells and two NG108-15 cell types; MTT assay (mitochondrial activity) and LDH leakage; all reduced viability, methadone most toxic, then fentanyl, morphine minimal; concentrations not captured; oxymorphone not tested. Jiang 2025 [24]: oxycodone only, rat ischemia-reperfusion and H9c2 cells; reduced LDH release and ROS and stabilized mitochondrial membrane potential via AMPK, SIRT1 and PGC-1 alpha. These are oxycodone and other-opioid data, not oxymorphone data (Hard Rule 6).

Mechanism

Named only for oxycodone in the protective setting (AMPK pathway) [24]. None for oxymorphone.

Class cohort test

CLASS EXTRAPOLATION. Oxymorphone not in the cohort of [23] or [24]. Tier C, capped at yellow.

Counter-evidence held on record

Counter-evidence and confounding Culture concentrations are unlikely to match clinical plasma levels (oxymorphone binds plasma protein only 10 to 12% and has about 10% oral bioavailability [1]), MTT is a surrogate, and the toxic and protective findings cannot be reconciled without dose data. Framing caution for the consumer surface Preclinical signal for other opioids only. Not a statement that oxymorphone damages mitochondria and not a reason to take mitochondrial supplements.

Oxidative Stress

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

Oxidative stress: class extrapolation from other opioids, mixed and reverse direction

Yellow — Low

See study details

Mouse macrophage work found opioids other than oxymorphone enhanced reactive oxygen output, while an oxycodone rat model found lower ROS, and no human redox marker data exist for oxymorphone.

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 glutathione, malondialdehyde or antioxidant-enzyme data in people taking oxymorphone. PubMed listings "oxymorphone oxidative stress" and "oxymorphone antioxidant glutathione" returned 404; "oxymorphone reactive oxygen species" was rate-limited and not read [28].
  • At-risk subgroups: Not defined.

Direction

Mixed. Pro-oxidant in mouse macrophages (morphine, fentanyl, methadone, oxycodone, buprenorphine); reverse (lower ROS) in oxycodone ischemia-reperfusion [24].

Regulatory status

The words oxidative and antioxidant were not found in the label text read [1][2].

Population evidence

Kozlowski 2017 [25]: murine macrophages, oxycodone and buprenorphine tested alongside previously studied opioids; chemiluminescence and colorimetric assays; opioids enhanced reactive oxygen intermediates and gave mixed nitric oxide results, adjuvants (amitriptyline most) lowered them; oxymorphone not named. Jiang 2025 [24]: oxycodone lowered ROS in a rat heart model. Neither study is a human study and neither includes oxymorphone.

Mechanism

Not established for oxymorphone. Protective route named for oxycodone only (AMPK linked) [24].

Class cohort test

CLASS EXTRAPOLATION. Oxymorphone not in the cohort of [24] or [25]. Tier C, capped at yellow.

Counter-evidence held on record

Counter-evidence and confounding Macrophage assays from injected mice and ischemia models are not comparable with each other or with oral therapeutic exposure. Both entries were read as OpenAlex reconstructions of abstracts, not full text. Framing caution for the consumer surface Mixed preclinical data for other opioids. Not an oxidative-stress deficiency claim and not a reason for antioxidant supplements.

Copper and Iron Balance

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

Copper: class extrapolation from heroin, methadone and morphine-rat data, possible retention direction, not depletion

Yellow — Low

See study details

No study measured copper in people taking oxymorphone. Human reports in heroin users and methadone maintenance and a morphine rat study point toward higher copper, not lower.

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: PubMed listing "oxymorphone trace element" returned 4 records, all synthetic chemistry, receptor-binding or analytic methods papers with iron or manganese appearing as reagents and none reporting copper in people [28]. "Oxymorphone copper" and "oxymorphone iron OR ferritin OR copper" were rate-limited and not read [28].
  • At-risk subgroups: Not defined for oxymorphone.

Direction

Possible retention or elevation (higher plasma and red-cell copper in heroin users, reduced copper elimination under methadone, higher serum copper in morphine-dependent rats). Not a copper shortfall. Hard Rule 5: if real, the risk is excess, and copper supplementation would be the hazard, not the remedy.

Regulatory status

Copper not found in the label text read [1][2].

Population evidence

Ciubotariu 2015 [20], a narrative review opened through a summarizing tool: "low zinc plasma is accompanied by low intraerythrocytic zinc and by increased plasma and intraerythrocytic copper" in heroin addicts (cites Ruiz Martinez 1990) and "copper elimination is slightly, but significantly decreased" during methadone detoxification (cites Iyengar 1994). Primary papers not opened; sizes and effect estimates not captured. The text names morphine; oxymorphone, oxycodone and hydrocodone are not mentioned. Yousofvand 2014 [21]: 24 male Wistar rats, morphine injected twice daily for 30 days; serum copper and zinc significantly higher and manganese significantly lower than controls (p below 0.05; values not in the abstract).

Mechanism

Not established. The review links the findings to opioid-associated zinc imbalance; no mechanism for oxymorphone and copper was found.

Class cohort test

CLASS EXTRAPOLATION. Oxymorphone was NOT in the cohort of [20] or [21]: heroin users, methadone patients and morphine-treated rats. Tier C, capped at yellow. No oxycodone data were borrowed.

Counter-evidence held on record

Counter-evidence and confounding Confounding by population is presumed (Hard Rule 6): illicit drug use, hepatitis, diet and addiction treatment alter copper independently, and plasma copper rises with inflammation. The human findings are small, older and read only through a secondary review. Extrapolation to prescribed oral oxymorphone for pain is unsupported. Framing caution for the consumer surface Not a copper deficiency claim and not a reason to take copper or zinc. The direction suggested is excess, so supplementation is the hazard. Context flag only.

Iron: class extrapolation from morphine in rat neurons, cellular redistribution only, no systemic iron measure

Yellow — Low

See study details

Morphine shifted iron between compartments in rat cortical neurons, but no opioid study opened measured serum iron, ferritin or hemoglobin, and oxymorphone was not tested.

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 oxymorphone anemia listing returned only injection-associated microangiopathy and sickle cell records [11]. The oxymorphone trace element listing returned only chemistry papers [28]. No ferritin, serum iron or hemoglobin study in oxymorphone users was found.
  • At-risk subgroups: None identified.

Direction

Intracellular iron redistribution (endolysosomal iron down, cytoplasmic labile iron up) in cultured neurons. Not iron deficiency and not an iron-status finding (Hard Rule 2). Independent of the Copper entry.

Regulatory status

Iron not found in the label text read [1][2]. The adverse-reaction table summarized did not list anemia.

Population evidence

Nash 2019 [22]: rat cortical neurons in vitro and in vivo; morphine increased cytoplasmic labile iron as endolysosomal iron fell, preceding ferritin heavy chain upregulation; chelating endolysosomal iron blocked the effect and iron overloading mimicked it; morphine only, abstract read through a summarizing tool. No human data.

Mechanism

Named for morphine in neurons (endolysosomal iron release). Not shown for oxymorphone.

Class cohort test

CLASS EXTRAPOLATION. Oxymorphone not in the cohort of [22] (morphine only). Tier C, capped at yellow. The hemolysis reports under Oxygen delivery are not iron data.

Counter-evidence held on record

Counter-evidence and confounding Neuronal iron handling in a model of neurocognitive disease does not map onto systemic iron status. Confounding by indication (blood loss, diet, inflammation) would dominate any human comparison. Framing caution for the consumer surface A cell-level finding for a different opioid. It does not indicate iron deficiency or any need for iron.

Gut Microbiome Risk

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

Gut microbiome risk: class extrapolation from one human opioid cohort, no oxymorphone microbiome study

Yellow — Low

See study details

A cirrhosis cohort found altered gut bacteria in chronic opioid users, but the opioids were not named, and no microbiome study of oxymorphone in any species turned up.

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: PubMed listings "oxymorphone gut microbiome" and "oxymorphone dysbiosis microbiota" returned 404 (interpreted as no records, not confirmed) [28]. Rodent microbiome studies of oxycodone and morphine exist in the sibling dossier set; I did not open them, they do not test oxymorphone, and they are not borrowed.
  • At-risk subgroups: Not defined for oxymorphone. The one human cohort is people with cirrhosis.

Direction

Composition change (neither depletion nor excess of a nutrient). No nutrient shortfall is shown to follow from it.

Regulatory status

No microbiome wording found in the label text read. Constipation is a labeled adverse reaction: 4% on oxymorphone versus 1% on placebo in the adverse-reaction table as summarized (two independent summarizer reads agreed) [1][2]. Constipation is the drug effect on motility and is context here, not microbiome evidence.

Population evidence

Acharya 2017 [17]: prospective cohort of 200 hospitalized patients with cirrhosis, plus 72 chronic opioid users matched to 72 non-users by age and MELD score; stool sequencing showed dysbiosis in opioid users with reduced Bacteroidaceae and higher pathways for aromatic amino acid and endotoxin production, with higher IL-6 and IL-17; all-cause readmission 69% versus 48%. The abstract does not name individual opioids.

Mechanism

Plausible, not demonstrated for oxymorphone: slower transit and constipation could change the gut environment.

Class cohort test

CLASS EXTRAPOLATION. Oxymorphone not named in [17]. Tier C, capped at yellow.

Counter-evidence held on record

Counter-evidence and confounding The cirrhosis population limits generalizability, and diet, laxatives, lactulose, rifaximin and disease severity are plausible confounders of any stool comparison. Framing caution for the consumer surface This is not a claim of dysbiosis in people taking oxymorphone and not a reason for probiotics or supplements.

Oxygen and ATP Output

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

Oxygen delivery/utilization: oxymorphone-specific case series of hemolytic anemia after injecting crushed extended-release tablets, outcome only

Yellow — Low

See study details

Fifteen Tennessee cases and several single reports link intravenous injection of dissolved Opana ER tablets to thrombotic microangiopathy with hemolytic anemia, but a mechanistic study attributed it to the tablet excipient and not to oxymorphone, and no hemoglobin or oxygen-carrying nutrient was measured in oral 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: PubMed listing "oxymorphone anemia" returned 10 records: the injection-associated microangiopathy reports above, one sickle cell vaso-occlusive crisis review, and nothing on hemoglobin or red-cell indices in people taking oxymorphone as prescribed [11]. No methemoglobinemia report was seen.
  • At-risk subgroups: People who crush and inject extended-release tablets. Not applicable to oral use as prescribed.

Direction

Outcome (microangiopathic hemolytic anemia, low platelets, kidney injury) in a misuse route. Hard Rule 2: anemia is not iron deficiency, and this is not an oxygen-delivery nutrient finding. Opioid respiratory slowing, the class pharmacology, is likewise not an oxygen-delivery deficiency and is not graded.

Regulatory status

Anemia was not listed in the IR adverse-reaction table summarized; the words thrombotic microangiopathy, hemolysis and methemoglobin were not found in the IR label text read [1][2]. The extended-release label (Amneal) was not opened: the fetch was refused with a 429 [4]. Opana ER was withdrawn from the US market in 2017 on FDA request (Wikipedia, used for this fact only) [6].

Population evidence, this drug in cohort

MMWR 2013 [7]: 15 cases of TTP-like illness reported by the end of October 2012 in a rural county in northeast Tennessee, all in people who dissolved and injected tablets; 14 of 15 injected reformulated Opana ER; 12 of 15 had hepatitis C or anti-HCV; 7 of 15 were also treated for sepsis; none fatal. Blood 2016 to 2017 [8]: three patients with microangiopathic hemolytic anemia, thrombocytopenia and acute kidney injury after injection, plus a guinea pig model; the high-molecular-weight polyethylene oxide excipient alone produced comparable findings, and the authors attributed the syndrome to the excipient and not to oxymorphone. Gandhi and colleagues [9]: single case, 25-year-old man with polysubstance use who injected oxymorphone (Opana) two weeks before presentation; hemolytic anemia, thrombocytopenia and kidney injury; improved after dialysis, steroids and plasmapheresis. Am J Kidney Dis 2014 [10]: three biopsy-confirmed cases, poor kidney recovery (listing quote only). Five further records in the PubMed listings are titles only [10][11].

Mechanism

Named in [8]: excipient (high-molecular-weight polyethylene oxide) toxicity after injection of a tablet designed to resist crushing. Not an effect of oral oxymorphone and not a red-cell or iron mechanism.

Whose data

Oxymorphone product and oxymorphone in the cohort, so these reports are Tier B for this drug (case reports and series). They do not support any effect on oxygen delivery from oral therapeutic use. The one oxycodone hemolysis case report in the sibling dossier is oxycodone data and is not used.

Counter-evidence held on record

Counter-evidence and confounding The cases carry heavy confounding (hepatitis C, sepsis, polysubstance use), and the one mechanistic study points to the excipient and route [8]. Case series cannot give a rate. Framing caution for the consumer surface Not a consumer deficiency claim and not a reason to take iron or other supplements. Injecting dissolved tablets is a safety matter for a clinician.

ATP production

Not graded — disclosed evidence gap

See study details

No study measured cellular ATP or oxidative phosphorylation output with oxymorphone exposure, and no class-level source opened did either.

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 of an ATP effect from oxymorphone or any opioid in the sources opened, and no circulating consumer claim for opioids and ATP was found (the claim audit itself could not be run). The result is mixed: a clean zero in the records that opened, plus tooling limits (five mitochondria listings never read, 404 responses not independently confirmed as zero hits). A re-check is recommended. Not a finding of safety. Membrane-potential and MTT surrogates are carried only under Mitochondrial burden.

What was searched

PubMed listing "oxymorphone ATP oxygen consumption" (404, interpreted as no records). The mitochondria listings "oxymorphone mitochondria", "oxymorphone mitochondrial", "oxymorphone mitochondria respiration", "oxymorphone mitochondrial membrane potential" and "oxymorphone mitochondria oxidative" were each rate-limited (429) and never read; "oxymorphone mitochondrial toxicity" returned 404. WebSearch was refused (shared budget exhausted). Opened and checked for ATP, oxygen consumption or respiration: Jiang 2025 [24] (oxycodone; ROS, LDH, membrane potential, AMPK; the reconstruction states no ATP measurement) and Nylander 2024 [23] (six other opioids; MTT and LDH only; oxymorphone not tested).

Channel outcomes

DailyMed label pages: opened, no ATP or energy-metabolism content. OpenAlex single-record lookups: worked. OpenAlex search, Crossref search and PubMed listings: intermittently 429 across the session. PubMed article pages, Europe PMC, Semantic Scholar and Unpaywall: not tried through this route, per the environment note.

Counter-evidence held on record

Counter-evidence and confounding Not applicable: nothing to counter. The adjacent mitochondrial and oxidative entries rest on other opioids and are not evidence about ATP. Framing caution for the consumer surface No statement about energy production should be made for oxymorphone from this dossier.

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.

  • Constipation as a nutrient problem (fiber, fluid or mineral depletion)

    Where it comes from: The batch brief lists constipation among the nutrient angles for this drug. Origin on a consumer page not traced.

    Why it fails: Constipation is a labeled adverse reaction (4% on oxymorphone versus 1% on placebo in the adverse-reaction table as summarized) and the drug effect on gut motility [1][2]. It is an outcome, not a nutrient measurement, so Hard Rule 2 bars filing it as a deficiency. No source retrieved shows a nutrient fall caused by oxymorphone constipation. It is carried only as context in the Gut microbiome entry.

  • Calcium deficiency and bone density loss (vitamin D and calcium depletion)

    Where it comes from: The batch candidate rationale for this drug reads "chronic-use hypogonadism and bone density effects relevant to vitamin D and calcium". Origin on a consumer page not traced.

    Why it fails: Bone density and fracture are outcomes, and no calcium, 25(OH)D or bone density measurement in oxymorphone users was found; the label text read contains no vitamin, calcium, bone or osteoporosis wording [1][2]. PubMed "oxymorphone osteoporosis" returned 404, and the vitamin D and bone density listings were rate-limited [28]. Any bone effect would be an outcome of a hormone effect (see the Testosterone entry), not a calcium or vitamin D depletion, and without a measured nutrient the claim is unfalsifiable (Hard Rule 3). The vitamin D context flag is a separate yellow entry.

How the body handles this medication

Metabolism and enzymes
Highly metabolized in the liver by reduction or conjugation with glucuronic acid; major metabolites are oxymorphone-3-glucuronide and 6-hydroxy-oxymorphone (active and inactive products). In vitro, no inhibition of the major CYP isoforms; CYP3A4 inhibition only at 150 micromolar or above. Clinical studies with the ER product showed no induction of CYP3A4 or CYP2C9.[1] Hikma IR label sec 12.3, summarizer read
Relationship to oxycodone
Oxymorphone is formed from oxycodone by CYP2D6 and is present in plasma only in low concentrations after oxycodone; urinary free oxymorphone 0%, conjugated oxymorphone up to 14% of an oxycodone dose. This dossier concerns oxymorphone given as the drug, and oxycodone findings are not oxymorphone findings.[3] Roxicodone label sec 12.3 (oxycodone label, relationship only)
Absorption and food
Absolute oral bioavailability about 10%; dose proportional over 5 to 20 mg; steady state after 3 days. Food raised Cmax and AUC by about 38%; the label advises dosing at least 1 hour before or 2 hours after eating. This is a food effect on the drug, a timing interaction and not a depletion. No named absorption transporter appears in the text read.[1] sec 12.3
Elimination
Less than 1% excreted unchanged in urine; 33 to 38% as oxymorphone-3-glucuronide. Half-life about 9 to 11 hours after a single oral dose. Plasma protein binding 10 to 12%.[1] sec 12.3
Hepatic, renal impairment and age
Bioavailability rose 1.6-fold (mild), 3.7-fold (moderate) and 12.2-fold (severe) in hepatic impairment; renal impairment raised it by 26%, 57% and 65% (mild, moderate, severe); elderly subjects had about 40% higher plasma levels. Alcohol raised Cmax by 70% on average (up to 270% in individuals) with 40% ethanol.[1] sec 12.3
Renal water handling, minerals, interactions
The label states opioids can reduce diuretic efficacy by inducing antidiuretic hormone release, the only renal water-handling statement found. Section 7 also lists CNS depressants, serotonergic drugs, MAOIs, mixed agonist-antagonist opioids, muscle relaxants, anticholinergics and cimetidine. No vitamin, mineral, antacid or chelation interaction appears in the text read.[1][2] sec 7, word check

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 / men on long-term use

    Morning total testosterone

    Worth considering for men on daily opioid therapy beyond about 3 months who report low libido, erectile dysfunction, fatigue or low mood, drawn in the morning as in the class cohorts [12][13] and repeated if low. This is a hormone-axis prompt drawn from class evidence and the label [2], not an oxymorphone finding and not a nutrient finding.

  • Symptoms / use beyond a month

    Adrenal insufficiency awareness

    Persistent nausea, vomiting, anorexia, fatigue, weakness, dizziness or low blood pressure on opioids beyond a month warrants a morning cortisol discussion with a prescriber, as the label notes [1][2].

  • Lab / conditional

    Serum sodium

    Only if confusion, nausea or new weakness occur, or if a diuretic or another SIADH-linked drug is co-prescribed [1]. A low result is a water-balance question, not a prompt to add salt.

  • Context

    Vitamin D and bone

    No oxymorphone-specific reason to test was found. Testing follows general risk factors (age, sun exposure, bone history) rather than oxymorphone use. No dose is recommended here.

  • Timing interaction (food affects the drug)

    Food and alcohol

    A meal raised oxymorphone exposure by about 38%, and the label advises dosing at least 1 hour before or 2 hours after eating [1]. Alcohol raised Cmax by 70% on average (up to 270% in individuals) [1]. These are drug-exposure interactions with no nutrient implication. No vitamin or mineral separation interval is listed in the text read.

  • Special populations

    Hepatic, renal impairment and age

    Exposure rises 1.6-fold (mild), 3.7-fold (moderate) and 12.2-fold (severe) in hepatic impairment, by 26% to 65% in renal impairment, and about 40% in the elderly [1]. Dose rules are label matters for the prescriber; I did not retrieve the label's dosing or contraindication sections.

  • Safety / misuse route

    Injection of crushed tablets

    Hemolysis, low platelets and kidney injury after injecting dissolved extended-release tablets are documented [7][8][9][10]. Fever, pallor, dark urine or reduced urine output after injection need urgent clinical evaluation, not nutrient testing.

Overlap map, to prevent double counting

  • Testosterone and the androgen axis

    Shares evidence with: Adrenal insufficiency

    Note: Both rest on the same label sentence (section 12.2: opioids inhibit ACTH, cortisol and LH) and the same central opioid mechanism. They are two hormone axes, not independent confirmations of one another. Neither has oxymorphone in a retrieved cohort.

  • Testosterone; Adrenal insufficiency

    Shares evidence with: Vitamin D (context); Fails verification: calcium and bone

    Note: Any bone claim would be a downstream outcome of the hormone effects, not a separate vitamin D or calcium finding. No shared study.

  • Adrenal insufficiency

    Shares evidence with: Hyponatremia

    Note: Both are hormone-mediated and could share a clinical presentation (nausea, weakness), but the evidence is separate: cohorts [15][16] versus one label ADH sentence in section 7 [1].

  • Mitochondrial burden

    Shares evidence with: Oxidative stress; ATP production (ungraded)

    Note: Jiang 2025 [24] (oxycodone) supports both the mitochondrial and oxidative entries, as the reverse-direction finding in each. Count as one source, not two. Nylander 2024 [23] is mitochondrial only. ATP is ungraded; [23] and [24] were opened for it and contain no ATP measurement.

  • Oxygen delivery/utilization

    Shares evidence with: Iron

    Note: The Opana ER hemolysis reports [7][8][9] are the only anemia evidence and are not iron data. The oxygen entry is an outcome entry; iron remains a separate class-extrapolation entry (Hard Rule 7).

  • Copper

    Shares evidence with: Iron

    Note: No shared source. [20] and [21] report copper (and zinc, manganese) and [22] reports iron in neurons. Separate entries per Hard Rule 7. All three come from heroin, methadone or morphine populations, so they share the same class-extrapolation limit.

  • Gut microbiome risk

    Shares evidence with: Fails verification: constipation

    Note: The label constipation figure is cited in both as context. No independent microbiome evidence comes from it.

  • Testosterone; Adrenal insufficiency; Vitamin D

    Shares evidence with: Oxycodone sibling dossier

    Note: The oxycodone dossier covers the same label sentences for oxycodone. Its findings are oxycodone data, were not carried over, and every cited paper here was re-opened for this dossier and cohort-checked for oxymorphone.

All references used above
  1. Oxymorphone hydrochloride tablets, prescribing information (Hikma Pharmaceuticals USA), DailyMed, SPL published Dec 22, 2025. — Regulatory label (Tier A), immediate-release tablet. Source of sections 5.9, 5.10, 6 (adverse-reaction table), 7, 12.1, 12.2 and 12.3 facts (bioavailability, food effect, metabolism, CYP statements, excretion, hepatic and renal impairment, alcohol).Read through a summarizing fetch tool at offsets 30,000, 88,000 and 100,000 of about 108,600 characters; statements are the summarizer's quotes, not a verbatim full reading. The first pass on the drugInfo page stopped before section 12, which is why this display endpoint was used. Absence of a word in a summary is not proof of absence in the label.
  2. Oxymorphone hydrochloride tablets, prescribing information (Aurolife Pharma), DailyMed, label revision shown as June 29, 2026. — Regulatory label (Tier A), immediate-release tablet. Source of section 5.9, 5.10, 6.2 (androgen deficiency postmarketing sentence), 7 (interaction list) and the word check.Summarizer read; the page text (about 110,300 characters) did not reach section 12, so no pharmacokinetic statement is taken from this label. Word check covers the sections read only.
  3. ROXICODONE (oxycodone hydrochloride) tablets, prescribing information (SpecGx LLC), DailyMed, section 12.3. — Regulatory label (Tier A) for OXYCODONE, used only to document that oxymorphone is an oxycodone metabolite for Hard Rule 6: "The metabolism of oxycodone to oxymorphone is catalyzed by CYP2D6"; "Oxymorphone is present in the plasma only in low concentrations"; urinary free oxymorphone 0%, conjugated oxymorphone up to 14%.Summarizer read at offset 90,000. Not a source of any oxymorphone finding.
  4. DailyMed SPL index for oxymorphone (service API). — Used to identify oxymorphone labels and forms (14 entries: IR tablets, ER tablets, Opana, Opana ER). Not used for any clinical claim.The DailyMed search.cfm page returned 429 and the tool asked not to retry it; the extended-release Amneal label (setid 3f4e703a-e398-42fd-8759-e398c79955f1) was refused with a 429 and not read.
  5. WHO Collaborating Centre, ATC/DDD Index: oxymorphone, N02AA11. — Reference index. Oxymorphone is listed under N02AA11; DDD and administration route fields are blank. Read via summarizing fetch.
  6. Wikipedia, Oxymorphone. — Encyclopedia page (not graded evidence; Tier D for any clinical claim). Used only for brand names (Numorphan, Opana) and the 2017 FDA-requested withdrawal of Opana ER. Its metabolism summary names CYP3A4, which the label text I read does not support, and was not used.
  7. Thrombotic thrombocytopenic purpura (TTP)-like illness associated with intravenous Opana ER abuse, Tennessee, 2012. MMWR Morb Mortal Wkly Rep 2013. PMID 23302815. — Public-health case series, 15 cases (Tier B for oxymorphone). No abstract in OpenAlex; case details are from the OpenAlex record as summarized by the fetch tool and a PubMed listing quote. Full text not opened.
  8. A mechanistic investigation of thrombotic microangiopathy associated with IV abuse of Opana ER. Blood (OpenAlex year 2016, PubMed listing year 2017). PMID 27864296, DOI 10.1182/blood-2016-08-736579. — 3 patients plus guinea pig model (Tier B for oxymorphone product). Abstract read as an OpenAlex reconstruction via summarizing tool; full text not opened. Authors attributed the syndrome to the polyethylene oxide excipient.
  9. Gandhi A, Ullah S, Kotadia S, Nasser S. Oxymorphone induced thrombotic microangiopathy mimicking atypical haemolytic uremic syndrome. J Ayub Med Coll Abbottabad (OpenAlex year 2019; PubMed listing year 2017). PMID 28718268. — Single case report (Tier B). Abstract via OpenAlex reconstruction; full text not opened.
  10. PubMed listing "Opana ER injection hemolytic" (4 records). — Listing summary only: Thrombotic microangiopathy and acute kidney injury associated with intravenous abuse of an oral extended-release formulation of oxymorphone hydrochloride, Am J Kidney Dis 2014 (PMID 24529995, 3 cases, partial kidney recovery); Lebanese Medical Journal 2016 case (PMID 27169165). Records not opened beyond the listing quote.Listing summary via fetch tool; abstracts not opened.
  11. PubMed listing "oxymorphone anemia" (10 records). — Listing summary only. Records: the three above plus PMIDs 28607779, 29998206, 26437280, 24369032 (injection-associated microangiopathy, titles and one quote only) and 25288149 (sickle cell vaso-occlusive crisis review). Not opened.Listing summary via fetch tool; abstracts not opened.
  12. Rubinstein AL, Carpenter DM. Association between commonly prescribed opioids and androgen deficiency in men: a retrospective cohort analysis. Pain Med 2017. PMID 27516365, DOI 10.1093/pm/pnw182. — Retrospective cohort, 1,159 men. Abstract via OpenAlex reconstruction; full text not opened.Oxymorphone not named in the abstract (fentanyl, methadone, oxycodone, hydrocodone named): not confirmed in cohort, Tier C for this drug.
  13. Rubinstein AL, Carpenter DM, Minkoff JR. Hypogonadism in men with chronic pain linked to the use of long-acting rather than short-acting opioids. Clin J Pain 2013. PMID 24384986, DOI 10.1097/AJP.0b013e31827c7b5d. — Retrospective cohort, 81 men, same health system as the 2017 paper. Abstract via OpenAlex reconstruction.Hydrocodone and oxycodone named; oxymorphone not named: Tier C for this drug.
  14. Kafel H, Braga-Basaria M, Basaria S. Opioid-induced androgen deficiency in men: prevalence, pathophysiology, and efficacy of testosterone therapy. Andrology 2025. PMID 39982737, DOI 10.1111/andr.70013. — Narrative review. Abstract via OpenAlex reconstruction.No individual opioids named in the abstract; oxymorphone not confirmed (Tier C).
  15. Lamprecht A, Sorbello J, Jang C, Torpy DJ, Inder WJ. Secondary adrenal insufficiency and pituitary dysfunction in oral/transdermal opioid users with non-cancer pain. Eur J Endocrinol 2018. PMID 30324794, DOI 10.1530/eje-18-0530. — Cross-sectional, 40 users and 25 controls. Abstract via OpenAlex reconstruction.Only morphine named (through morphine-equivalent dose): oxymorphone not confirmed (Tier C).
  16. Gibb FW, Stewart A, Walker BR, Strachan MWJ. Adrenal insufficiency in patients on long-term opioid analgesia. Clin Endocrinol 2016. PMID 27260138, DOI 10.1111/cen.13125. — Cross-sectional, 48 patients. Abstract via OpenAlex reconstruction (partial).Opioids not named in the abstract: oxymorphone not confirmed (Tier C).
  17. Acharya C, Betrapally NS, Gillevet PM, et al. Chronic opioid use is associated with altered gut microbiota and predicts readmissions in patients with cirrhosis. Aliment Pharmacol Ther (OpenAlex year 2016). PMID 27868217, DOI 10.1111/apt.13858. — Prospective cohort, 200 inpatients plus 72 matched pairs with cirrhosis. Abstract via OpenAlex reconstruction.Individual opioids not named: oxymorphone not confirmed (Tier C). Cirrhosis population.
  18. Kemeny LV, Robinson KC, Hermann AL, et al. Vitamin D deficiency exacerbates UV/endorphin and opioid addiction. Sci Adv 2021. PMID 34117054, DOI 10.1126/sciadv.abe4577. — Human opioid use disorder association plus mouse models. Abstract via OpenAlex reconstruction.No opioid named; direction check only (vitamin D to opioid response). Tier C.
  19. Associations of vitamin D status with all-cause and cause-specific mortality in long-term prescription opioid users. Front Nutr 2024. DOI 10.3389/fnut.2024.1422084. — NHANES 2001 to 2018, 1,856 long-term prescription opioid users; 67.2% with 25(OH)D below 75 nmol/L, 32.4% below 50 nmol/L. Read via summarizing fetch of the full-text page.Individual opioids not named, no opioid-free comparator: prevalence only, Tier C.
  20. Ciubotariu D, Ghiciuc CM, Lupusoru CE. Zinc involvement in opioid addiction and analgesia: should zinc supplementation be recommended for opioid-treated persons? Subst Abuse Treat Prev Policy 2015. — Narrative review of human, animal and in vitro studies. Read via summarizing fetch of the full-text page; the copper statements cite Ruiz Martinez 1990 and Iyengar 1994, neither opened.Names morphine; oxymorphone, oxycodone and hydrocodone not mentioned. Class extrapolation, Tier C. The text has no iron statement for opioid users.
  21. Yousofvand N, Ghowsi M, Pourmotabbed A. The effect of morphine dependency on serum levels of trace elements (copper, zinc and manganese) in male rats. Armaghane Danesh 2014;19(3):195-203. — Experimental study, 24 male Wistar rats. Abstract page read via summarizing fetch.Morphine only: oxymorphone excluded from cohort (Tier C).
  22. Nash B, et al. Morphine-induced modulation of endolysosomal iron mediates upregulation of ferritin heavy chain in cortical neurons. eNeuro 2019;6(4). — Rat cortical neurons in vitro and in vivo. Abstract page read via summarizing fetch.Morphine only: oxymorphone excluded from cohort (Tier C).
  23. Nylander E, Stam F, Katila L, et al. Revisiting opioid toxicity: cellular effects of six commonly used opioids. Scand J Pain 2024. PMID 39636779, DOI 10.1515/sjpain-2024-0038. — In vitro, four cell cultures. Abstract via OpenAlex reconstruction.Opioids tested: methadone, morphine, oxycodone, hydromorphone, ketobemidone, fentanyl. Oxymorphone not tested (Tier C).
  24. Jiang Y, He H, Jia X. Protective role of oxycodone in myocardial oxidative stress and mitochondrial dysfunction induced by ischemia-reperfusion. J Biochem Mol Toxicol 2025. PMID 39865943, DOI 10.1002/jbt.70151. — Rat model and H9c2 cells. Abstract via OpenAlex reconstruction; no ATP measurement reported.OXYCODONE data, not oxymorphone data (Hard Rule 6). Tier C for this drug.
  25. Kozlowski M, et al. The impact of advanced opioid drugs and analgesic adjuvants on murine macrophage oxygen burst. Folia Med Cracov (OpenAlex year 2019). PMID 29121034. — Murine macrophage study. Abstract via OpenAlex reconstruction.Opioids named: morphine, fentanyl, methadone, oxycodone, buprenorphine. Oxymorphone not named (Tier C).
  26. Zharikova OL, et al. The effect of opiates on the activity of human placental aromatase/CYP19. Biochem Pharmacol (OpenAlex year 2006; PubMed listing year 2007). PMID 17118343, DOI 10.1016/j.bcp.2006.08.019. — In vitro enzyme study naming oxymorphone among the opiates tested. Seen only as a PubMed listing quote and OpenAlex metadata; abstract text not retrievable and not opened.Not opened. Not used for grading: placental enzyme, concentrations unknown.
  27. Daniell HW, et al. DHEAS deficiency during consumption of sustained-action prescribed opioids. J Pain 2006. DOI 10.1016/j.jpain.2006.04.011. — Crossref title search and OpenAlex DOI lookup returned metadata only.No abstract, no opioid names, no sample size retrievable. Not used for any claim.
  28. Search log: PubMed listing queries run for this review (all with format=pubmed). — Completed with results: oxymorphone testosterone (2 records, neither human hormone data); oxymorphone anemia (10); Opana ER injection hemolytic (4); oxymorphone trace element (4, chemistry); oxymorphone hyponatremia OR SIADH (10, none oxymorphone). Returned 404, interpreted as no matching records but not independently confirmed: oxymorphone adrenal cortisol; oxymorphone sodium SIADH; oxymorphone gut microbiome; oxymorphone oxidative stress; oxymorphone osteoporosis; oxymorphone electrolyte SIADH case; oxymorphone ATP oxygen consumption; oxymorphone dysbiosis microbiota; oxymorphone antioxidant glutathione; oxymorphone mitochondrial toxicity; oxymorphone hypothalamic pituitary adrenal; oxymorphone sex hormones opioid users. Rate-limited (429) and never read: oxymorphone hypogonadism; oxymorphone thrombotic microangiopathy; oxymorphone adrenal insufficiency; oxymorphone hyponatremia (twice); oxymorphone hyponatraemia sodium; oxymorphone mitochondria; oxymorphone mitochondrial; oxymorphone mitochondria respiration; oxymorphone mitochondrial membrane potential; oxymorphone mitochondria oxidative; oxymorphone vitamin D; oxymorphone bone density osteoporosis; oxymorphone iron OR ferritin OR copper; oxymorphone copper; oxymorphone endocrine OR androgen; oxymorphone androgen deficiency; oxymorphone reactive oxygen species; oxymorphone hormone; oxymorphone luteinizing hormone prolactin; oxymorphone opioid endocrinopathy; oxymorphone hypogonadism men.Listing pages were read through a summarizing fetch tool. The 404 interpretation is an assumption; the 429 queries are unresolved gaps.