CHAPTER

Beyond Bone: Hormonal Signaling, Immune Regulation, and the Dangers of Excess

Yoon Hang Kim, MD, MPH

Board-Certified in Preventive Medicine

Integrative & Functional Medicine

Introduction: Not Just a Bone Vitamin

Vitamin D is not simply a nutrient that keeps bones strong. It is a hormone-like system that influences calcium balance, skeletal integrity, immune signaling, epithelial-barrier function, and the expression of genes across dozens of tissues through the vitamin D receptor (VDR). Every clinician has patients taking vitamin D. Not every clinician has thought carefully enough about what that means.

A functional-medicine approach to vitamin D should neither dismiss conventional guidance nor treat it as the final word. Instead, it should weave together established physiology, the patient’s phenotype and risk factors, medication and disease context, measured biomarkers, treatment response, and—critically—careful safety monitoring.

This chapter carries a dual message. Vitamin D deficiency matters and should be identified and corrected. But excessive, unmonitored supplementation can kill. Both problems are real. Both are preventable. The clinician’s job is to navigate between them with precision, not enthusiasm.

Why Vitamin D Deserves Its Own Chapter

Vitamin D is a logical follow-up to discussions of B6, general vitamins, and vitamin C because it illustrates a core principle of functional medicine: both low status and excessive supplementation can cause harm. It is the nutrient most likely to be under-dosed in people who need it and over-dosed in people chasing a number they found on social media.

Vitamin D signaling has plausible and increasingly documented roles in immune tolerance, inflammatory regulation, the gut–microbiome interface, and mast-cell biology. For clinicians working with autoimmune disease, chronic inflammation, mast-cell activation, or gut dysfunction, vitamin D is a foundational consideration—but it is not a stand-alone therapy, and the direct clinical evidence for vitamin D as an MCAS treatment remains limited.

Vitamin D Is a Hormone System

Vitamin D3 (cholecalciferol) is synthesized in skin after UVB exposure and is also available from food and supplements. The liver converts it to 25-hydroxyvitamin D, or 25(OH)D, the principal circulating storage form and the standard laboratory marker for vitamin D status.

The kidney and several non-renal tissues can further convert 25(OH)D to 1,25-dihydroxyvitamin D (calcitriol), the active hormonal form. Calcitriol binds the VDR, a nuclear receptor that influences the transcription of genes involved in calcium-phosphate balance, innate immunity, adaptive immune signaling, and epithelial-barrier regulation.

This is why a patient can have a “normal” 25(OH)D value while still requiring broader clinical assessment. Kidney function, inflammation, obesity, malabsorption, medications, calcium intake, magnesium status, PTH physiology, and genetic variation may all influence the biologic response to vitamin D—independent of what the lab report says.

A Functional Interpretation of Vitamin D Levels

The conventional question is often: “Is the level low enough to diagnose deficiency?” A functional question is broader: “Is this person likely to have adequate vitamin D signaling for their skeletal, metabolic, immune, and clinical context—and can we improve that safely?”

There is genuine disagreement about optimal blood levels. Some functional and immune-focused clinicians use a 25(OH)D target of approximately 40–60 ng/mL (100–150 nmol/L), while conventional standards typically use lower thresholds based primarily on skeletal outcomes. The evidence for a universal “optimal” target above the deficiency-prevention range is not definitive, so higher targets should be individualized rather than presented as settled science.

Practical Functional Framework

Important: A laboratory value is not a diagnosis by itself. The appropriate target and dose depend on the individual, not on a social-media “optimal range.”

The “Why” Behind Low Levels

Low vitamin D status is often not simply the result of “not taking enough.” A functional evaluation looks for the contributors that made the level low and that may prevent it from rising appropriately after supplementation.

Common Contributors

• Limited UVB exposure, higher latitude, winter season, indoor work, clothing practices, sunscreen use, and skin pigmentation.
• Increased adiposity. Higher BMI is associated with lower circulating 25(OH)D and a smaller rise after standard supplementation doses.
• Malabsorptive conditions, bariatric surgery, pancreatic or biliary dysfunction, inflammatory bowel disease, and other gastrointestinal disorders.
• Kidney disease, liver disease, and disorders of calcium or parathyroid physiology.
• Drugs that alter vitamin D metabolism or absorption (including certain anticonvulsants, glucocorticoids, cholestyramine, and some antiretrovirals).
• Dietary patterns low in vitamin-D-containing foods and cofactors relevant to skeletal metabolism.

A level that remains low despite a reasonable dose should prompt a search for absorption issues, adherence problems, product quality concerns, medication effects, obesity-related distribution, or less common metabolic factors—not reflexive dose escalation indefinitely.

Immunity, Gut, and Inflammation

Vitamin D participates in immune homeostasis rather than acting as a simple “immune booster.” VDR signaling can influence innate immune defenses, antigen presentation, T-cell differentiation, and the balance between inflammatory and regulatory immune activity.

In the intestinal tract, vitamin D/VDR signaling is associated with regulation of tight-junction proteins, antimicrobial peptides, mucosal immunity, and host–microbiota interaction. Deficiency is associated with dysbiosis, reduced butyrate-producing organisms, thinner mucus layers, and increased intestinal permeability. These observations are biologically important but do not prove that vitamin D alone reverses complex chronic disease.

For patients with autoimmune disease, chronic inflammatory conditions, or gastrointestinal symptoms, correcting a documented deficiency is reasonable. However, vitamin D should be regarded as a potential foundational factor—not a stand-alone treatment or a substitute for diagnosis, disease-specific treatment, nutrition, sleep, stress regulation, exercise, infection evaluation, and medication management.

MCAS: Promise Without Hype

Vitamin D is commonly included in integrative approaches for mast-cell disorders because mast cells express VDR-related signaling pathways and experimental data suggest that vitamin D can influence mast-cell activation and inflammatory mediator release.

But the clinical evidence requires humility. Available discussions of vitamin D in MCAS largely rely on mechanistic research, related allergic-disease studies, clinical observation, and expert practice patterns. Robust trials demonstrating that vitamin D supplementation reliably improves MCAS are lacking.

For an MCAS patient with documented low vitamin D, repletion may be reasonable as part of a monitored whole-person plan. It should not be promoted as a guaranteed mast-cell stabilizer, and any dose should account for medication sensitivity, excipient intolerance, calcium physiology, renal status, and symptom response.

D3, D2, and Dosing

Vitamin D3 is the form naturally produced in the skin and widely used in supplements. Dosing should start with the clinical objective: prevention, maintenance, treatment of confirmed deficiency, or management of a persistent deficiency in a patient with a known risk factor.

For confirmed deficiency, commonly cited clinical repletion approaches include approximately 50,000 IU weekly or 6,000 IU daily for about 6–8 weeks, followed by an individualized maintenance dose. These are treatment strategies, not default wellness doses for everyone.

People with obesity, malabsorption, or medications that interfere with vitamin D metabolism may need higher doses to achieve a given blood level, but this is an argument for testing and titration—not for permanent, unmonitored high-dose supplementation.

A Sensible Functional-Medicine Dosing Sequence

1. Establish the baseline: 25(OH)D, medication and supplement inventory, sun exposure, diet, symptoms, relevant history, and risk factors.
2. Add context when indicated: calcium, albumin or ionized calcium, phosphorus, magnesium, creatinine/eGFR, and intact PTH. Reserve 1,25-dihydroxyvitamin D for selected clinical questions rather than routine screening.
3. Use the smallest practical dose that achieves the intended clinical target.
4. Recheck 25(OH)D about 8–12 weeks after beginning or materially changing therapy, particularly in patients with obesity, malabsorption, kidney disease, or other factors likely to alter response.
5. Once stable, reassess according to risk and season rather than treating supplementation as a “set it and forget it” intervention.

The Cofactor Conversation

Magnesium is relevant because it participates in vitamin D metabolism and broader calcium–PTH physiology. Low magnesium intake or magnesium depletion can be a reasonable consideration in patients who respond poorly to repletion, have dietary risk factors, use medications that affect magnesium balance, or have compatible clinical findings.

Vitamin K2 is frequently paired with vitamin D in functional practice based on its role in activating vitamin-K-dependent proteins involved in calcium handling. This is a biologically plausible pairing, but the evidence does not establish that every person who takes vitamin D requires K2, nor does it justify overselling K2 as protection from vitamin D toxicity.

Calcium is not automatically a required companion to vitamin D. Patients should consider total dietary and supplemental calcium, kidney-stone history, hypercalcemia risk, bone density, dietary pattern, and the reason vitamin D is being used before adding calcium supplements.

When Vitamin D Becomes Dangerous: Toxicity, ICU Admissions, and Death

This is the section that matters most. Vitamin D is fat-soluble, which means it accumulates in adipose tissue. Unlike water-soluble vitamins, excess doses are not simply excreted. When intake exceeds the body’s capacity to regulate it, 25(OH)D levels climb into a range that overwhelms normal calcium-handling physiology, producing hypercalcemia—a potentially lethal condition.

Toxicity is uncommon when dosing is thoughtful and monitored. But “uncommon” is not the same as “impossible,” and the published literature contains case after case of patients who landed in the ICU—or the morgue—because they or their clinicians treated vitamin D as if it were harmless at any dose.

What Vitamin D Toxicity Looks Like Clinically

The primary danger of vitamin D excess is hypercalcemia. The symptoms are nonspecific early on, which makes the diagnosis easy to miss until it becomes a crisis:

• Nausea, vomiting, constipation, abdominal pain, anorexia
• Profound thirst, polyuria, and dehydration
• Confusion, lethargy, altered mental status, obtundation
• Muscle weakness, fatigue
• Shortened QT interval and cardiac arrhythmia risk
• Acute kidney injury, nephrocalcinosis, kidney stones
• In severe or prolonged cases: renal failure requiring dialysis, cardiac complications, and death

A vitamin D level is only part of the safety picture. For suspected toxicity, evaluation commonly includes total and/or ionized calcium, PTH, 25(OH)D, phosphorus, creatinine/eGFR, and—when clinically appropriate—1,25-dihydroxyvitamin D and urinary calcium evaluation.

Published Cases of Vitamin D Toxicity Requiring Hospitalization and ICU Care

The following cases are drawn from the peer-reviewed literature. They are not theoretical warnings. These are real patients who were harmed by vitamin D—sometimes by their own choices, sometimes by clinician errors, sometimes by product failures. Every clinician who prescribes or recommends vitamin D should know these stories.

Case 1: The Man Who Took 200,000 IU Daily—and Arrived Obtunded

A 64-year-old man with a history of COPD and alcohol use presented to an emergency department with profoundly altered mental status. He was obtunded on arrival and unable to provide any history. After stabilization and workup, his team discovered that he had misunderstood his medication instructions and had been consuming four vitamin D 50,000 IU tablets daily—200,000 IU per day—for an extended period.

His labs revealed symptomatic hypercalcemia (serum calcium 12.8 mg/dL, ionized calcium 6.3) with suppressed PTH and markedly elevated 25(OH)D (>150 ng/mL), consistent with exogenous vitamin D toxicity. He also had notable hypophosphatemia (2.2 mg/dL), a known but sometimes overlooked paradox in vitamin D toxicity that can misdirect the workup. Initial volume expansion with 3 L of normal saline did not improve his mentation; calcitonin was added on hospital day 2 and zoledronic acid on hospital day 3 before his hypercalcemia and cognition improved.

Source: Nguyen T, Joe D, Shah AD. Forget the phosphorus: A case of hypervitaminosis D-induced symptomatic hypercalcemia. Clin Nephrol Case Stud. 2021;9:1–3. DOI: 10.5414/CNCS110414

Lesson: A patient’s understanding of dosing instructions cannot be assumed. This patient consumed 200,000 IU daily—many multiples of any recognized maintenance or treatment dose—because he misunderstood how to take his tablets. A single medication-reconciliation check could have caught the error before it produced obtundation and a hospital admission.

Case 2: A 72-Year-Old Woman with Severe Supplement-Driven Hypercalcemia

A 72-year-old woman with hypertension and arthritis presented with an albumin-corrected serum calcium of 14.4 mg/dL (normal: 8.5–10.5). Her workup showed a PTH of 6 pg/mL (suppressed), calcitriol at 949 pg/mL (markedly elevated), and a 25(OH)D above the measurable range at >154 ng/mL. Her creatinine had risen from a baseline of 0.93 to 1.47 mg/dL, indicating acute kidney injury.

The cause was prolonged, unsupervised use of over-the-counter vitamin D supplements. She required hospitalization with IV fluids, subcutaneous calcitonin, and IV pamidronate. Her calcium normalized by hospital day 4 and her mental status cleared, but the episode underscored a critical problem: the months-long half-life of vitamin D means toxicity does not resolve when you stop taking it—it persists for weeks to months.

Source: Krinsky D, Mazori A (Icahn School of Medicine at Mount Sinai). A Case of Severe Hypercalcemia Secondary to Supplement-Associated Vitamin D Toxicity. Endocr Pract. 2026;32(4 Suppl):S153 (abstract). DOI: 10.1016/j.eprac.2026.01.365

Lesson: Over-the-counter availability does not mean over-the-counter safety at any dose. This patient had no clinician monitoring her levels. The fat-soluble pharmacokinetics of vitamin D mean that by the time symptoms appear, the body has already accumulated a dangerous reservoir.

Case 3: Three Family Members Hospitalized from Contaminated Cooking Oil

In a case reported from the Postgraduate Institute of Medical Education and Research in Chandigarh, India (2025), three adults from the same household presented within three days of each other with severe hypercalcemia and acute kidney injury. None of them were taking any vitamin D supplements.

The index case, a 26-year-old man, arrived with persistent vomiting, confusion (GCS of 12), polyuria, and reduced urine output. His younger brother presented with abdominal pain and vomiting. Their father reported progressive fatigue and appetite loss. All three had conjunctival injection, a clinical sign associated with hypercalcemia-induced vascular changes.

Laboratory findings were dramatic. The index case had a serum calcium of 17.3 mg/dL, a 25(OH)D of 988 ng/mL, a PTH of 1.2 pg/mL (profoundly suppressed), and a creatinine of 4.9 mg/dL. His brother had a 25(OH)D of 976 ng/mL. Their father’s level was 886 ng/mL. All three had acute kidney injury, and the index case required hemodialysis.

The source was eventually identified: a locally sourced, unpackaged cooking oil that the family had been using as their sole cooking medium for two months. Mass spectrometry analysis confirmed vitamin D3 contamination at 1,286 μg/mL, an enormously toxic concentration from unregulated fortification. Two additional family members and several neighbors who consumed the same oil also developed hypercalcemia.

All three hospitalized patients were treated with IV hydration, calcitonin, and denosumab (bisphosphonates were avoided due to renal dysfunction). The index case required two sessions of hemodialysis. All recovered fully, but their 25(OH)D levels remained elevated and only approached the upper limit of normal after four months—a stark illustration of how long fat-soluble vitamin D persists in the body even after the source is removed.

Source: Jha V, Rouniyar R, Rao SD, Dua A, Bhadada SK. An Outbreak of Vitamin D Toxicity in a Family: Report of 3 Cases From Unregulated Fortification. JCEM Case Reports. 2025;3(12):luaf230. DOI: 10.1210/jcemcr/luaf230

Lesson: Vitamin D toxicity does not always come from supplements. Unregulated fortification, compounding errors, and contaminated food products are real and underappreciated dangers. When multiple patients from the same household present with unexplained hypercalcemia, a shared dietary or environmental source should be investigated immediately.

Case 4: A 17-Year-Old Adolescent—594 ng/mL from Milkshakes

A 17-year-old male presented with abdominal pain, knee pain, and loss of appetite. His serum calcium was 15.5 mg/dL. History revealed that he had been drinking homemade milkshakes supplemented with vitamin D3—approximately 14,045 IU per 16-ounce serving—daily for about a year, and had doubled his intake to 32 ounces daily for the 10 days before presentation.

His 25(OH)D was 594 ng/mL and his 1,25-dihydroxyvitamin D was 101 pg/mL. He had a corrected calcium of 13.2 mg/dL with suppressed PTH, and his ECG showed a shortened QT interval. Because he was hemodynamically stable with only moderate hypercalcemia, his team deliberately did not use calcitonin, steroids, or bisphosphonates. He was managed with IV fluids at twice maintenance for six days and a short course of IV furosemide, alongside a low-calcium diet. His symptoms resolved within a day, calcium normalized within a month, and his 25(OH)D took roughly six months to fall back into range.

Source: Gordon L, Zipursky R, Cheung CC, Pillai SS. Vitamin D Intoxication in an Adolescent due to Over-Supplementation: A Case Report and Review of Literature. AACE Endocrinol Diabetes. 2026;13(1):93–97. Online October 15, 2025. DOI: 10.1016/j.aed.2025.10.008. PMC12866089.

Lesson: Young patients, fitness enthusiasts, and health-conscious consumers are increasingly at risk because they view vitamin D as an unconditionally positive supplement. The cumulative dose over months or years—not just the daily number—is what creates the danger.

Case 5: A 53-Year-Old Given 2,000 Times His Prescribed Dose

A 53-year-old man with diabetes, hypertension, and chronic kidney disease was hospitalized for worsening renal function, pruritus, muscle weakness, and weight loss. Investigation revealed a compounding pharmacy error: his prescribed vitamin D dose had been miscalculated, and the preparation he received contained approximately 2,000 times the intended amount of cholecalciferol.

The result was severe hypervitaminosis D with worsening renal function and hypercalcemia superimposed on his pre-existing chronic kidney disease. With treatment his condition improved, but follow-up testing months later still showed renal dysfunction (creatinine 2.40 mg/dL) and elevated ionized calcium. Because he had baseline CKD, the report does not establish full renal recovery or that all residual impairment was newly caused by the overdose—but it does illustrate how a compounding error can drive serious, incompletely reversible harm in a vulnerable patient.

Source: Marins TA et al. Vitamin D intoxication: case report. Einstein (São Paulo). 2014;12(2):242–244. DOI: 10.1590/S1679-45082014RC2860. PMC4891171.

Lesson: Compounding errors are a known and recurring source of vitamin D toxicity. When prescribing vitamin D from a compounding pharmacy, verify the concentration independently and consider lot-specific testing for high-potency preparations.

Case 6: A 3-Year-Old Child After Accidental Ingestion of 800,000 IU

A 3-year-old child was brought to medical attention after accidentally ingesting approximately 800,000 IU of cholecalciferol. The child remained clinically asymptomatic throughout, with only mild, intermittent hypercalcemia that peaked at 11.26 mg/dL; the 25(OH)D level peaked at 880 ng/mL on day 5. Management included IV saline, oral prednisolone, calcium restriction, and IV furosemide added on hospital day 3. No dialysis or ICU-level intervention was required.

This case illustrates that while children can sometimes tolerate acute single large doses better than chronic overexposure, any accidental ingestion of concentrated vitamin D demands immediate medical evaluation. The outcome was favorable here, but outcomes are not uniformly benign—especially in children with smaller body mass and faster metabolism.

Source: Kasiri H, Farzaneh AH, Khosravi N. A 3-Year-Old Child With Incidental High-Dose Vitamin D Intoxication: A Case Report and Literature Review. Case Rep Endocrinol. 2025;2025:6614996. DOI: 10.1155/crie/6614996.

Summary of Published Toxicity Cases

Systematic Evidence: Even “Moderate” Doses Carry Risk

The cases above are extreme, but they are not the whole story. The more common and easily overlooked risk is modest harm at doses many people consider routine. A 2023 systematic review and meta-analysis of 22 randomized controlled trials (12,952 participants) examining daily vitamin D supplementation at 3,200–4,000 IU found that even at these commonly used doses, there were statistically significant increases in the risk of hypercalcemia (relative risk 2.21, 95% CI 1.26–3.87), falls (RR 1.25), and hospitalization (RR 1.16). The vitamin-D-induced frequency of hypercalcemia in this dose range was approximately 4 per 1,000 individuals. This does not mean severe overdose, dialysis, or ICU admission are common at 3,200–4,000 IU—the case reports and the meta-analysis describe different points on the risk spectrum—but it does show that measurable harm begins well below the megadose range.

This is not a dose range that most clinicians would consider “high.” Many functional-medicine practitioners routinely recommend 4,000–5,000 IU daily. The meta-analysis does not prove that these doses are uniformly dangerous, but it does prove that they are not uniformly safe either—and that the assumption of harmlessness is not supported by the aggregate evidence.

Source: Zittermann A, Trummer C, Theiler-Schwetz V, Pilz S. Long-term supplementation with 3200 to 4000 IU of vitamin D daily and adverse events: a systematic review and meta-analysis of randomized controlled trials. Eur J Nutr. 2023;62(4):1833–1844. DOI: 10.1007/s00394-023-03124-w.

Who Should Not Self-Direct High-Dose Vitamin D

Patients should avoid self-directed high-dose vitamin D supplementation if they have any of the following:

• Known hypercalcemia or a history of hypercalcemic episodes
• Current or prior kidney stones (calcium-containing)
• Significant kidney disease (CKD stage 3b or worse)
• Sarcoidosis or another granulomatous disorder (these convert 25(OH)D to calcitriol autonomously)
• Primary hyperparathyroidism
• Any unexplained elevation in serum calcium
• Use of thiazide diuretics (which reduce renal calcium excretion and can compound hypercalcemia risk)

In any of these settings, vitamin D dosing should be individualized under direct clinician supervision with appropriate monitoring of calcium, PTH, renal function, and 25(OH)D levels.

Genetics and Personalization

Genetic variants in pathways involving vitamin D binding and metabolism—including genes such as GC, CYP2R1, CYP27B1, CYP24A1, and VDR—may contribute to differences in vitamin D status or biologic response.

This science is interesting, but most patients do not need genetic testing before vitamin D treatment. In current practice, measured 25(OH)D response, safety markers, symptoms, absorption risk, body composition, and clinical context are usually more actionable than consumer genetic reports. CYP24A1 loss-of-function variants deserve special mention, as they can impair vitamin D catabolism and predispose to toxicity at doses that would be safe for most people.

A Practical Takeaway

The goal is not to chase the highest vitamin D number or to accept the lowest acceptable laboratory cutoff without thought. The goal is to identify deficiency when it matters, understand why it exists, correct it safely, monitor the response, and integrate vitamin D into a broader plan for bone health, immune regulation, metabolic health, gastrointestinal function, and long-term resilience.

Vitamin D can be an important foundational intervention, particularly when deficiency or high-risk physiology is present. But it works best when treated as one measurable part of a personalized clinical strategy—not as a cure-all and not as an invitation for unsupervised megadosing.

The cases in this chapter are real. People have ended up in intensive care units, on dialysis, with permanent kidney damage, because someone—a patient, a clinician, a compounding pharmacy, a food manufacturer—treated vitamin D as if it were incapable of harm. It is not. Respect the molecule. Test. Dose thoughtfully. Monitor. And never assume that more is better.

References

1. Marcinowska-Suchowierska E, Kupisz-Urbańska M, Łukaszkiewicz J, Płudowski P, Jones G. Vitamin D Toxicity—A Clinical Perspective. Front Endocrinol. 2018;9:550. DOI: 10.3389/fendo.2018.00550.

2. Nguyen T, Joe D, Shah AD. Forget the phosphorus: A case of hypervitaminosis D-induced symptomatic hypercalcemia. Clin Nephrol Case Stud. 2021;9:1–3. DOI: 10.5414/CNCS110414.

3. Jha V, Rouniyar R, Rao SD, Dua A, Bhadada SK. An Outbreak of Vitamin D Toxicity in a Family: Report of 3 Cases From Unregulated Fortification. JCEM Case Reports. 2025;3(12):luaf230. DOI: 10.1210/jcemcr/luaf230.

4. Gordon L, Zipursky R, Cheung CC, Sasidharan Pillai S. Vitamin D Intoxication in an Adolescent due to Over-Supplementation: A Case Report and Review of Literature. AACE Endocrinol Diabetes. 2026;13(1):93–97. Online October 15, 2025. DOI: 10.1016/j.aed.2025.10.008.

5. Marins TA et al. Vitamin D intoxication: case report. Einstein (São Paulo). 2014;12(2):242–244. DOI: 10.1590/S1679-45082014RC2860.

6. Kasiri H, Farzaneh AH, Khosravi N. A 3-Year-Old Child With Incidental High-Dose Vitamin D Intoxication: A Case Report and Literature Review. Case Rep Endocrinol. 2025;2025:6614996. DOI: 10.1155/crie/6614996.

7. Zittermann A, Trummer C, Theiler-Schwetz V, Pilz S. Long-term supplementation with 3200 to 4000 IU of vitamin D daily and adverse events: a systematic review and meta-analysis of randomized controlled trials. Eur J Nutr. 2023;62(4):1833–1844. DOI: 10.1007/s00394-023-03124-w.

8. Krinsky D, Mazori A. A Case of Severe Hypercalcemia Secondary to Supplement-Associated Vitamin D Toxicity. Endocr Pract. 2026;32(4 Suppl):S153 (abstract). DOI: 10.1016/j.eprac.2026.01.365.

Additional References

9. Anık A, Çatlı G, Abacı A, Dizdarer C, Böber E. Acute vitamin D intoxication possibly due to faulty production of a multivitamin preparation. J Clin Res Pediatr Endocrinol. 2013;5(2):136–139. DOI: 10.4274/Jcrpe.896.

10. Bansal RK et al. Iatrogenic hypervitaminosis D as an unusual cause of persistent vomiting: a case report. J Med Case Rep. 2014;8:74. DOI: 10.1186/1752-1947-8-74.

11. Bahadori AR, Rahimi M, Mostafazadeh B, Erfan Talab Evini P, Shadnia S. A Rare Case Report of Acute Vitamin D Toxicity due to Suicide Attempt. J Emerg Med Case Rep. 2025;16(3):126–128. DOI: 10.33706/jemcr.1656965.

12. Szawłoga T, Sobieszczańska-Droździel A. Vitamin D toxicity with acute kidney injury in siblings: a case report and literature review. Pediatria Polska – Polish J Paediatrics. 2025;100(4):387–393. DOI: 10.5114/polp.2025.156651.

13. Van den Ouweland J, Fleuren H, Drabbe M, Vollaard H. Pharmacokinetics and safety issues of an accidental overdose of 2,000,000 IU of vitamin D3 in two nursing home patients: a case report. BMC Pharmacol Toxicol. 2014;15:57. DOI: 10.1186/2050-6511-15-57. (Note: neither patient developed clinical toxicity; relevant as evidence that acute single-dose kinetics differ from chronic overexposure.)