Posaconazole

Limits on what this shows

• Null and lower-risk findings: Prophylaxis vs fluconazole: 30% against 26% is a small excess in a population with high background hypokalemia [3]. Itraconazole's 52% (n = 58) was higher than posaconazole's 30% [3]. Shibata: the abstract now read confirms no correlation between trough concentration and potassium decline or minimum potassium (gamma -0.21, P = 0.32; gamma -0.03, P = 0.88), in conflict with Nguyen's concentration relationship (r = -.39); this is unresolved and means the concentration-response is not consistent across cohorts, although both cohorts show hypokalemia on posaconazole [5][6]. Jensen 2023 [32]: median potassium at supratherapeutic levels 4.0 mmol/L (IQR 3.6 to 4.6), a median fall of 0.3 from baseline 4.3, within the normal range at the median; electrolytes were similar between the 3000 to 4999 and 5000 or more groups. Sci Rep 2024 [12]: tablet and suspension did not differ in hypokalemia (P above 0.05; 7 of 46 against 23 of 98).
• At-risk subgroups: Higher serum concentrations, older age and baseline hypertension (Nguyen [5]); hematology and oncology patients with vomiting, diarrhea or other potassium-wasting drugs such as amphotericin B or diuretics; people on other QT-prolonging drugs; case reports show the syndrome at standard doses.

Direction

Loss / disturbance. Serum potassium falls because of a drug-induced mineralocorticoid-excess state. This is not a dietary shortfall and not an instruction to raise potassium intake: the cause is the drug, the remedy is a prescriber decision (dose or exposure change, switching azole, aldosterone receptor antagonist, potassium and blood pressure management) [1][9]. Hypertension is a feature of the syndrome and a clinical outcome, not a nutrient finding (Hard Rule 2). Low potassium also raises the QT-prolongation concern attached to azoles (nutrient state modifying drug toxicity).

Regulatory status

Tier A. Label 5.4: pseudoaldosteronism, "manifested by the onset of hypertension or worsening of hypertension" with "abnormal laboratory findings (hypokalemia, low serum renin and aldosterone, and elevated 11-deoxycortisol)", reported postmarketing; "Monitor blood pressure and potassium levels and manage as necessary"; management "may include discontinuation of posaconazole, substitution with an appropriate antifungal drug that is not associated with pseudoaldosteronism, or use of aldosterone receptor antagonists". Section 6.2 postmarketing lists "Endocrine Disorders: Pseudoaldosteronism". Label 5.3 directs monitoring and correction of potassium, magnesium and calcium before and during therapy [1][2]. Adverse reaction tables: delayed-release tablet prophylaxis (300 mg daily, n = 210) hypokalemia 22%; oral suspension prophylaxis hypokalemia 30% (n = 605) against fluconazole 26% (n = 539) and itraconazole 52% (n = 58); invasive aspergillosis treatment hypokalemia 28.5% (n = 288) against voriconazole 17.1% (n = 287) [1][2][3].

Population evidence (posaconazole in every cohort)

Read at label-table, abstract or listing level. 1. Label prophylaxis studies [2][3]: active-comparator tables above; the sources do not report a mean potassium change. 2. Maertens 2021 [7]: phase 3 randomised, double-blind, double-dummy, non-inferiority trial at 91 sites in 26 countries, 575 randomised (posaconazole 288, voriconazole 287); treatment-related adverse events 30% against 40% (difference -10.2%, 95% CI -17.9 to -2.4); the abstract names hypokalaemia among the most common treatment-related events on posaconazole; the label table drawn from this design gives 28.5% against 17.1% [2]. 3. Nguyen 2020 [5] (full text read through a summarizing tool after repair): single-centre retrospective cohort of 69 outpatients on posaconazole for at least 7 days, 16 (23.2%) with pseudohyperaldosteronism (defined as a systolic rise of at least 10 mm Hg and/or a potassium fall of at least 0.5 mmol/L from the last pre-dose value, with raised 11-deoxycortisol, undetectable aldosterone and low to low-normal renin, no other cause); the comparison group was 53 contemporaneous posaconazole-treated patients without the syndrome, not a no-drug group; median time to diagnosis 46 days (range 14 to 96); absolute potassium values were not reported; calcineurin inhibitors were used by 13% of affected against 45% of unaffected patients (P =.02), which the authors think may have masked hypokalemia; median serum posaconazole 3.0 against 1.2 micrograms/mL (P at most.0001); level against change in serum potassium r = -.39 (P =.006), against change in systolic pressure r =.37 (P =.01), against serum 11-deoxycortisol r =.69 (P below.0001); affected patients were older (61.1 against 44.7 years) and more often hypertensive at baseline (68.8% against 32.1%). 4. Shibata 2026 [6][20][28]: single-centre study of 24 hematology patients on oral posaconazole (Aichi Medical University Hospital) with trough concentrations by HPLC and potassium followed 60 days; hypokalemia defined as potassium below 3.0 mEq/L with a fall of at least 10.0% from baseline, in 41.7% (10 of 24). The abstract (read in a PubMed record after repair) reports no significant correlation of trough concentration with the rate of potassium decline (gamma -0.21, P = 0.32) or with minimum potassium (gamma -0.03, P = 0.88), and similar median troughs with and without hypokalemia (2.5 against 2.4 micrograms/mL); the authors conclude posaconazole may cause hypokalemia regardless of trough concentration. 5. Nakano 2026 [8]: systematic review and meta-analysis of randomised trials; posaconazole against voriconazole risk ratio for hypokalaemia 10.41 (95% CI 2.00 to 54.27, I2 = 0%); the number of trials and patients is not in the abstract read, and this analysis probably overlaps the Maertens trial, so it is not counted as independent. The same paper's FAERS analysis (Tier C): 29.8% (95% CI 22.1 to 38.4) of posaconazole-associated pseudoaldosteronism reports also named hypokalaemia. 5b. Yang 2024 [12] (full text read through a summarizing tool after repair): single-centre retrospective cohort of 144 inpatients with invasive fungal infection (tablet 46, suspension 98); hypokalemia (CTCAE v5.0) in 30 of 144 (20.8%), 7 on tablets and 23 on suspension (percentages 15.2% and 23.5% are computed here from the counts; the paper reports only the total percentage); no significant group difference; no potassium values and no comparator. 5c. Jensen 2023 [32] (full text read through a summarizing tool): Mayo Clinic retrospective review of 90 patients with posaconazole levels of at least 3000 ng/mL (80 at 3000 to 4999, 10 at 5000 or more); median potassium 4.3 mmol/L (IQR 3.9 to 4.5, n = 76) at baseline and 4.0 (IQR 3.6 to 4.6, n = 85) at the supratherapeutic level, no P value, no hypokalemia count; no pseudohyperaldosteronism was identified, but aldosterone and renin were ordered in only 4 patients. 6. Davis 2020 [9][19]: 20 consecutive adults with posaconazole-induced pseudohyperaldosteronism from the same centre as Nguyen (not independent); 17 (85%) had therapy changed (dose reduction 11, discontinuation 3, switch 2, spironolactone 1) and 9 of 17 improved, with a mean potassium rise of 0.22 mmol/L and systolic fall of 7.1 mmHg. Case-level (Tier B) [10][11][27]: apparent mineralocorticoid excess with resolution on withdrawal (Thompson 2017); two patients on tablets for over 30 days with mean systolic rise 59 mmHg, alkalosis and levels 4.3 to 4.6 micrograms/mL (Crossref conference abstract); further case reports and letters listed by PubMed, including refractory hypokalemia at low dose, hypokalemia in a hemodialysis patient and severe hypokalemia with blastomycosis.

Independence of the Tier A sources

Counted as independent for the red grade: the label prophylaxis and treatment trials (different programs, different comparators); Maertens 2021 (a separate randomised trial); Nguyen 2020 (one academic center, potassium measured against drug level); Shibata 2026 (a different research group, 24 patients, direct potassium); Yang 2024 (a Chinese hospital cohort, CTCAE hypokalemia 20.8%). Jensen 2023 (a Mayo Clinic cohort, median potassium 4.3 to 4.0) is consistent in direction but reports no hypokalemia count and is supporting only. Not counted as independent: Davis 2020 (same center as Nguyen), Nakano 2026 (secondary analysis likely overlapping Maertens), FAERS (reports, not incidence).

Mechanism

Named and demonstrated. Thompson 2017 [10] (abstract reconstructed from OpenAlex): a patient with apparent mineralocorticoid excess on posaconazole; "Clinical and laboratory investigation confirmed 11beta-hydroxysteroid dehydrogenase inhibition"; withholding therapy resolved all clinical and laboratory abnormalities and restarting at a lower dose did not recur. Nguyen 2020 [5]: the rise in 11-deoxycortisol with drug level (r =.69) fits steroidogenic enzyme blockade. PubMed listing summaries [11] describe other work: posaconazole mainly inhibiting CYP11B1 (Beck 2020), human 11-beta-HSD2 strongly inhibited with rodent and zebrafish enzymes weakly inhibited (Inderbinen 2021), and two case reports in which one resolved after a switch to isavuconazole and another after dose reduction, with different proposed enzymes. The exact enzyme (11-beta-HSD2 against CYP11B1) is not settled in the sources read; either route produces mineralocorticoid-receptor activation with low renin and aldosterone, as the label states.

Counter-evidence held on record

Counter-evidence and confounding No placebo or no-treatment comparison for potassium was found in any source opened. The only placebo-controlled posaconazole trial located, STOP-CHAGAS [33] (120 asymptomatic Chagas carriers; posaconazole 400 mg twice daily n = 30 against placebo n = 30, plus benznidazole arms; JACC 2017), reports in the accessible abstract and summaries no potassium or hypokalemia data (serious adverse events occurred only in benznidazole arms); its full text was blocked (publisher robots restriction), so whether potassium was recorded there is unknown. The comparators that do exist are active: fluconazole (26% against 30%), itraconazole (52%, itself a pseudoaldosteronism-causing azole) and voriconazole (17.1%, an azole with labeled hypokalemia, so the contrast likely understates a no-drug difference). Nguyen's comparison group were other posaconazole recipients. Only one source reports a potassium change from baseline in absolute terms (Jensen: median 0.3 mmol/L lower, unpaired medians, no P value), and Davis reports a mean rise of 0.22 mmol/L after intervention, so the average effect size is small to moderate while the tail (potassium below 3.0 in about 42% of 24) is large. The meta-analytic risk ratio of 10.41 sits far from the label ratio of about 1.7 (28.5 against 17.1), so the trials entering that analysis are unknown and heterogeneity is likely despite I2 = 0%. Confounding by indication was weighed (Hard Rule 6): hematology and transplant patients lose potassium to chemotherapy, vomiting, diarrhea and amphotericin B, and fluconazole prophylaxis alone shows 26%. It is argued down by the double-blind voriconazole comparison (28.5% against 17.1%), the meta-analytic risk ratio 10.41 (wide interval, 2.00 to 54.27), the concentration-response in Nguyen, positive dechallenge in case reports and a demonstrated enzyme mechanism. Hypokalemia definitions differ across sources (below 3.0 mEq/L plus a 10% fall in Shibata; CTCAE v5.0 in Yang; a fall of 0.5 mmol/L or a systolic rise in Nguyen; unstated in label tables). Calcineurin inhibitors (hyperkalemic) were more common in Nguyen's unaffected group and may have masked hypokalemia. Full texts of Shibata, Maertens and Nakano were not read. Why red is retained after scrutiny The red criteria are met as written: at least two independent Tier A sources with posaconazole in the cohort and potassium directly measured (Nguyen 2020, Shibata 2026, Yang 2024, plus the label and Maertens trial tables); a consistent direction (lower potassium) in every source that reports one; clinically meaningful size (hypokalemia in 20.8% to 41.7% in cohorts, 28.5% against 17.1% for voriconazole in a double-blind trial); a named mechanism (11-beta-HSD2 or CYP11B1 inhibition with demonstrated enzyme inhibition and positive dechallenge in cases); and no Tier A source showing the opposite direction. The inconsistent concentration-response (Nguyen against Shibata) and the small median fall in Jensen limit how the effect is described, not whether it occurs. The absence of a no-drug control is a stated limitation on the size of the average effect; attribution rests on the active-comparator trial, mechanism and dechallenge rather than on a placebo contrast. Framing caution Monitoring prompt, not a deficiency claim and not a reason to take potassium. This is a drug-induced loss with hypertension as part of the syndrome. Potassium, magnesium, blood pressure and drug-level questions belong with the prescriber. Supplementing potassium without clinical direction is not advised.

Limits on what this shows

• Null findings: Fluconazole 16% and itraconazole 19% against posaconazole 18% in the same prophylaxis table [3].
• At-risk subgroups: Patients with vomiting or diarrhea or on other potassium- or magnesium-wasting drugs (context only; no source read ties these to posaconazole magnesium).

Direction

Possible loss (disturbance), unproven. Not a dietary deficiency claim; low magnesium is also a QT-risk modifier for the drug.

Regulatory status

Tier A. Label 5.3 names magnesium among electrolytes to monitor and correct [1]. Tables: tablet prophylaxis (n = 210) hypomagnesemia 10%; oral suspension prophylaxis 18% (n = 605) against fluconazole 16% (n = 539) and itraconazole 19% (n = 58); invasive aspergillosis 10.1% against voriconazole 6.3% (n = 288 and 287) [1][2][3].

Population evidence

Label tables only (above). Case report: Burston 2018 [15], "Posaconazole and isavuconazole induced hypomagnesaemia", Med Mycol Case Rep (abstract field empty in OpenAlex and in the PubMed record; the free PMC full text, PMC6258827, was requested after repair and returned a bot-verification page, so magnesium values and dosing remain unread). A PubMed listing for hypomagnesemia and hypokalemia in hematologic prophylaxis [21] returned 15 records, none a posaconazole cohort with magnesium reported.

Mechanism

None named in the sources read. Physiologically, potassium loss and gastrointestinal loss can accompany low magnesium, but no source read ties posaconazole to magnesium handling.

Counter-evidence held on record

Counter-evidence and confounding Adverse reaction tables in cancer and transplant patients carry high background hypomagnesemia, and the label gives neither a placebo nor a laboratory definition. The 10.1% against 6.3% difference against voriconazole has no confidence interval in the label text read. Framing caution Monitoring prompt only. Not a magnesium deficiency claim and not a reason to take magnesium; electrolyte correction is a prescriber decision.

Limits on what this shows

• Null findings: Itraconazole hypertension 5% (n = 58) was below posaconazole's 18% [3]; fluconazole 16%.
• At-risk subgroups: People with hypertension at baseline, older people, high posaconazole concentrations [5].

Direction

Retention-type clinical syndrome. Hypertension and edema are outcomes (Hard Rule 2); sodium was not reported in any source read. Dietary sodium advice is a clinical decision, not a depletion or supplementation claim.

Regulatory status

Tier A. Tablet prophylaxis (n = 210): peripheral edema 16%, hypertension 11%. Suspension prophylaxis: hypertension 18% against fluconazole 16% and itraconazole 5%; leg edema 15% against 12% and 19%. Invasive aspergillosis: peripheral edema 11.1% against voriconazole 8.4% [1][2][3].

Population evidence

Label tables above; Nguyen 2020 [5] (hypertension at baseline 68.8% in the affected group; systolic pressure change r =.37 with drug level); Davis 2020 [9] (mean systolic fall 7.1 mmHg after intervention); case reports [10][27].

Mechanism

Mineralocorticoid-receptor activation with low renin and aldosterone (label 5.4) [1]; see the potassium entry.

Counter-evidence held on record

Counter-evidence and confounding Cancer, transplant and critical-illness populations have many causes of edema and hypertension (steroids, fluids, calcineurin inhibitors). The label gives no sodium values. Framing caution Clinical outcome entry. Not a sodium deficiency or excess claim; report new swelling or high blood pressure to the prescriber.

Limits on what this shows

• Null findings: None sought beyond the label; no controlled trial of adrenal function on posaconazole alone was found.
• At-risk subgroups: People on corticosteroids, higher drug concentrations, older age.

Direction

Steroid-pathway enzyme inhibition. Not a deficiency of any nutrient (Hard Rule 2).

Regulatory status

Tier A. Label section 6.1: "Endocrine disorders: adrenal insufficiency" among reactions in under 5% of treated patients; 5.4 raised 11-deoxycortisol [1][2].

Population evidence

Nguyen 2020 [5]: serum 11-deoxycortisol correlated with posaconazole level (r =.69, P below.0001), n = 69. Nakano 2026 [8] (Tier C for this question): FAERS signal for pseudoaldosteronism with posaconazole and itraconazole. Case (Tier B) [18]: 74-year-old man on 300 mg daily, early-morning cortisol 2.4 micrograms/dL, ACTH 101.7 pg/mL, peak stimulated cortisol 8.6 micrograms/dL, hypokalemia, normal blood pressure; improved after stopping (PubMed listing summary of PMID 41212062, abstract level).

Mechanism

Inhibition of steroid-pathway enzymes; PubMed listing summaries describe posaconazole mainly inhibiting CYP11B1 [11]. A corticosteroid interaction was not read for posaconazole in this review.

Counter-evidence held on record

Counter-evidence and confounding Fungal disease itself can affect the adrenal glands, and single cases cannot separate drug from disease. Framing caution Hormone and drug-interaction effect for the prescriber; not a nutrient entry and not a reason to supplement anything.

Limits on what this shows

• Null findings: No difference between formulations in safety [12]; voriconazole and fluconazole were not cytotoxic in the cell panel [13].
• At-risk subgroups: Serious underlying disease, higher exposure (800 mg daily suspension), hypoalbuminemia, renal replacement therapy, longer courses.

Direction

Drug toxicity (outcome). Not a nutrient entry (Hard Rule 2).

Regulatory status

Tier A. Label 5.5: hepatic reactions (mild to moderate ALT, AST, alkaline phosphatase, total bilirubin elevations and/or clinical hepatitis) reversible on discontinuation; "more severe hepatic reactions including cholestasis or hepatic failure including deaths" in patients with serious underlying conditions, "primarily in subjects receiving the Noxafil oral suspension 800 mg daily"; "Liver tests should be evaluated at the start of and during the course of posaconazole therapy" [1][3]. Invasive aspergillosis trial: ALT increased 14.6% against 12.9% and AST 13.2% against 12.5% for voriconazole [2]. Prophylaxis suspension studies: grade 3 to 4 ALT shift 47 of 271 (17%) against 39 of 272 (14%) for fluconazole in one study [2].

Population evidence

Maertens 2021 [7]: raised AST or ALT among the most common treatment-related events on posaconazole, with fewer treatment-related events overall than voriconazole (30% against 40%). Sci Rep 2024 [12]: retrospective cohort of 144 (tablet 46, suspension 98); risk factors for liver dysfunction were renal replacement therapy (OR 10.071, P = 0.006), hypoalbuminemia (OR 6.646, P = 0.002) and posaconazole duration (OR 1.119, P = 0.002); tablets and suspension did not differ.

Mechanism

Not established for patients. In HepG2 and HepaRG cells posaconazole was cytotoxic and lowered cellular ATP, an in vitro mitochondrial signal (see the mitochondrial and ATP entries) [13].

Counter-evidence held on record

Counter-evidence and confounding Hematologic malignancy, transplant medicines and co-administered azoles carry their own liver risk. Framing caution Drug toxicity entry. Liver tests are a prescriber and pharmacist check; no nutrient is the remedy.

Limits on what this shows

• Null findings: Antacids and H2 blockers (non-cimetidine) had no clinically relevant effect on the suspension; the tablet showed none with antacid, ranitidine or esomeprazole [1][2].
• At-risk subgroups: People unable to eat (mucositis, nausea) taking the suspension; people on acid suppressors taking the suspension; tube-fed patients.

Direction

Diet or acid to drug. Filed as timing interactions under Hard Rule 4. Nothing here says posaconazole lowers a nutrient.

Regulatory status

Tier A. Suspension: give "during or immediately (i.e., within 20 minutes) following a full meal"; if a full meal is not possible, "with a liquid nutritional supplement or an acidic carbonated beverage"; avoid cimetidine or esomeprazole [2]. Delayed-release tablets: "Administer with or without food"; "Swallow tablets whole. Do not divide, crush, or chew"; suspension and tablets are not substitutable [1].

Population evidence

Healthy-volunteer crossover data in the label [3]: suspension 200 mg AUC 4,179 (fasted), 10,753 (nonfat meal), 15,059 (high-fat, 54 g fat) ng.hr/mL; 400 mg with a liquid nutritional supplement (14 g fat) 11,295 against 5,258 fasted; relative to fasted, AUC rose 382% when dosed during a high-fat meal and 387% 20 minutes after, but only 111% when dosed 5 minutes before; ginger ale raised AUC 70% (Cmax 92%); esomeprazole lowered AUC 30%; metoclopramide lowered AUC 19%; nasogastric tube administration lowered Cmax 19% and AUC 23%, and substantially in 5 subjects (Cmax -27% to -53%, AUC -33% to -51%). Tablets: high-fat meal Cmax +16%, AUC +51% (ratio 1.51, CI 1.33 to 1.72; 14 fasted, 16 fed); antacid, ranitidine and esomeprazole no clinically relevant change [1].

Mechanism

The label describes the suspension's dependence on food and gastric acid and the tablet's lack of dependence on gastric pH; the formulation basis was not read [1][3].

Counter-evidence held on record

Counter-evidence and confounding These are single-dose volunteer studies. Consumer pages differ: Drugs.com states the manufacturer recommends the tablet with food, whereas the current label read says with or without food [30][1]. Framing caution Timing and administration entry. Follow the dispensing label for the product in hand; do not change meal patterns or acid suppressors without the prescriber or pharmacist.

Limits on what this shows

• Null findings: Diarrhea was identical to voriconazole (18.1%) [2].
• At-risk subgroups: Patients receiving chemotherapy, conditioning regimens or other emetogenic drugs.

Direction

Context flag (mechanism H, changed intake and loss). Not a drug-specific nutrient finding.

Regulatory status

Tier A. Tablet prophylaxis (n = 210): diarrhea 29%, nausea 27%, vomiting 13%, abdominal pain 11%, constipation 10%. Aspergillosis trial: nausea 22.6% against 17.8%, vomiting 18.1% against 13.6%, diarrhea 18.1% against 18.1% (voriconazole) [1][2].

Population evidence

Label tables only. No study read ties these symptoms to a measured nutrient change on posaconazole.

Mechanism

Direct gastrointestinal effects of the drug; in the aspergillosis trial the nausea and vomiting excess over voriconazole is a few percentage points.

Counter-evidence held on record

Counter-evidence and confounding Chemotherapy and graft-versus-host disease produce the same symptoms in the same patients, so the label percentages cannot be attributed to posaconazole alone. Framing caution Context entry; no intake advice implied. Persistent vomiting or diarrhea should be reported to the care team.

Limits on what this shows

• Null findings: Vitamin D and PTH were normal in the case, which argues against a vitamin D or PTH cause [16]. No cohort measured calcium on posaconazole.
• At-risk subgroups: Patients on retinoid therapy for acute promyelocytic leukemia.

Direction

Excess (hypercalcemia) from a drug-drug interaction. Tretinoin is a retinoid medicine here, not a dietary vitamin A exposure. No supplementation implication in either direction.

Regulatory status

Tier A (monitoring statement only). Label 5.3 lists calcium among electrolytes to monitor [1]. No hypercalcemia statement was found in the label text read.

Population evidence

Tier B. Case report, one 49-year-old woman with acute promyelocytic leukemia [16]: serum calcium rose from 10.3 to 11.1 mg/dL after posaconazole was started with ATRA; 25-hydroxyvitamin D 21.9 ng/mL and PTH 17.8 pg/mL were in range; calcium normalised after both drugs were stopped; the authors call it the first report of this combination (PubMed listing summary, abstract level).

Mechanism

Proposed by the authors as an interaction; the posaconazole enzyme mechanism for retinoic acid was not read.

Counter-evidence held on record

Counter-evidence and confounding A single case; the leukemia and its treatment can also alter calcium. Framing caution Drug-interaction entry for prescribers. Not a calcium, vitamin D or vitamin A deficiency claim.

Limits on what this shows

• Why no grade: Dual condition met: no Tier B or C source for a posaconazole effect on vitamin D or bone, and no circulating claim found. Fracture or low bone density, if ever reported, would be an outcome and not a vitamin D deficiency (Hard Rule 2). A disclosed gap, not a finding of safety.

What was searched

PubMed "posaconazole AND (vitamin D OR osteoporosis OR bone mineral OR calcitriol OR CYP24A1)" (3 records, read through a summarizing tool) [26]: an allergic bronchopulmonary aspergillosis review in children mentioning posaconazole and vitamin D as separate options; a pharmacogenetic study of 636 samples across azoles in which vitamin D-related gene variants (VDR Cdx2, CYP27B1 -1260, GC 1296) predicted posaconazole concentrations above 700 ng/mL, a direction of gene to drug level and not a vitamin D status measurement [17]; and the ATRA hypercalcemia case already carried in the calcium entry, where vitamin D 21.9 ng/mL and PTH 17.8 pg/mL were in range [16]. Labels and consumer pages read make no vitamin D or bone statement [1][2][29][30][31].

Channel outcomes

Original pass: one PubMed query. Repair pass: "posaconazole vitamin D" (3 records, same three), "posaconazole hypercalcemia" (3 records: the ATRA case already carried, a fluconazole-ATRA case, and a pediatric leukemia malignant hypercalcemia case where posaconazole was incidental), "posaconazole bone" (168 hits, first 10 read: guidelines, reviews and bone infection or drug penetration; none on bone density), and "posaconazole bone mineral density" (2 records: a 2007 drug-approvals note and a voriconazole periostitis review naming posaconazole only as an alternative). "posaconazole osteoporosis" returned a fetch error twice and was replaced by the bone mineral density phrasing. Crossref and OpenAlex were not queried for this topic, and the other 158 'posaconazole bone' hits were not read. Open-web search was unavailable. Partly tooling-limited; the absence of a primary study in the records read is a literature gap as far as read.