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Hypervitaminosis D

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Description: Hypervitaminosis D is a condition caused by excessive intake of vitamin D, leading to elevated calcium levels in the blood and potential damage to bones, kidneys, and other organs.
Type: Hypervitaminosis D is not a genetic condition; rather, it is a toxicity condition resulting from excessive intake of vitamin D. It does not involve genetic transmission.
Signs And Symptoms: An excess of vitamin D causes abnormally high blood concentrations of calcium, which can cause overcalcification of the bones, soft tissues, heart and kidneys. In addition, hypertension can result. Symptoms of vitamin D toxicity may include the following:

Dehydration
Vomiting
Diarrhea
Decreased appetite
Irritability
Constipation
Fatigue
Muscle weakness
Metastatic calcification of the soft tissues
InsomniaSymptoms of vitamin D toxicity appear several months after excessive doses of vitamin D are administered. In almost every case, a low-calcium diet combined with corticosteroid drugs will allow for a full recovery within a month. It is possible that some of the symptoms of vitamin D toxicity are actually due to vitamin K depletion. One animal experiment has demonstrated that co-consumption with vitamin K reduced adverse effects, but this has not been tested in humans. However the interconnected relationships between vitamin A, vitamin D, and vitamin K, outlined in a 2007 paper published in the journal Medical Hypotheses, describes potential feedback loops between these three vitamins that could be elucidated by future research.
A mutation of the CYP24A1 gene can lead to a reduction in the degradation of vitamin D and to hypercalcemia (see Vitamin D: Excess).
Prognosis: Prognosis:
The prognosis for hypervitaminosis D varies depending on the severity and duration of excessive vitamin D intake. Mild cases often resolve with the cessation of vitamin D supplements and dietary adjustments. However, severe cases can lead to lasting complications such as kidney damage and cardiovascular issues. Early detection and timely treatment significantly improve outcomes.

Nan:
The "nan" acronym is unclear in this context. If you mean "nan" in a statistical software sense (Not a Number), it is not applicable. If you meant a different term, please provide more context.
Onset: The onset of hypervitaminosis D, or vitamin D toxicity, can vary depending on the amount and duration of excessive intake. Symptoms may take weeks or months to appear after prolonged ingestion of high doses of vitamin D supplements. The nan value, or serum concentration of 25-hydroxyvitamin D, often exceeding 150 ng/mL (375 nmol/L) indicates hypervitaminosis D.
Prevalence: The prevalence of hypervitaminosis D, or vitamin D toxicity, is relatively rare. This condition typically results from excessive intake of vitamin D supplements rather than from dietary sources or sun exposure.
Epidemiology: Hypervitaminosis D is relatively rare and usually occurs due to excessive intake of vitamin D, often from supplements rather than diet or sun exposure. It can affect individuals at any age but is more common in those taking high-dose vitamin D supplements without medical supervision. The exact prevalence is not well-documented but is considered low, particularly in countries where vitamin D supplementation is regulated.
Intractability: Hypervitaminosis D, caused by excessive intake of vitamin D, is generally not considered intractable. It can usually be managed by discontinuing vitamin D supplementation and addressing any complications arising from elevated calcium levels, such as dehydration and kidney damage. Treatment may include hydration, diuretics, and medications to manage hypercalcemia. With appropriate medical intervention, most individuals recover fully.
Disease Severity: Hypervitaminosis D, which results from excessive intake of vitamin D, can vary in severity. Mild cases may include symptoms such as nausea, vomiting, and weakness. More severe cases can lead to serious health issues like hypercalcemia, which manifests as frequent urination, kidney stones, and even kidney failure. It can also cause calcification of the bones and soft tissues.
Healthcare Professionals: Disease Ontology ID - DOID:9971
Pathophysiology: **Pathophysiology of Hypervitaminosis D:**

Hypervitaminosis D refers to the toxic condition resulting from excessive intake of vitamin D. This condition leads to elevated levels of calcium in the blood (hypercalcemia) because vitamin D plays a crucial role in the regulation of calcium and phosphate metabolism.

1. **Increased Absorption of Calcium:** Excessive vitamin D increases intestinal absorption of calcium.
2. **Bone Resorption:** Elevated vitamin D levels enhance osteoclast activity, leading to increased bone resorption and release of calcium into the bloodstream.
3. **Renal Effects:** High calcium levels lead to impaired function of the kidneys, causing reduced renal function and potential kidney damage, including nephrocalcinosis and renal failure.
4. **Tissue Calcification:** Sustained hypercalcemia can lead to ectopic calcification, particularly in soft tissues including the kidneys, heart, and blood vessels.

These pathological changes can result in a variety of clinical symptoms such as nausea, vomiting, weakness, frequent urination, kidney stones, and in severe cases, may cause cardiac arrhythmias and neuropsychiatric disturbances.
Carrier Status: Hypervitaminosis D is related to excessive intake of vitamin D and is not a genetic condition; therefore, concepts such as "carrier status" do not apply to this condition.
Mechanism: Hypervitaminosis D refers to a condition caused by excessive intake of vitamin D, leading to toxic levels in the body.

**Mechanism:**
- Excessive intake of vitamin D leads to increased absorption of calcium from the gut.
- High levels of circulating vitamin D metabolites (especially 1,25-dihydroxyvitamin D) enhance calcium reabsorption in the kidneys and mobilize calcium from bones, raising blood calcium levels (hypercalcemia).

**Molecular Mechanisms:**
- Vitamin D is metabolized in the liver to 25-hydroxyvitamin D and then in the kidney to the active form, 1,25-dihydroxyvitamin D (calcitriol).
- Calcitriol binds to the vitamin D receptor (VDR) in target tissues (intestine, bone, kidney) forming a complex that acts as a transcription factor, regulating gene expression.
- Overactivation of VDR leads to increased expression of calcium-binding proteins and transporters such as TRPV6 and calbindin in the intestinal epithelium, boosting calcium uptake.
- In bone, elevated calcitriol enhances osteoclast activity, increasing bone resorption and calcium release into the bloodstream.
- In the kidney, enhanced VDR activity increases calcium reabsorption, decreasing urinary calcium excretion.

This cascade ultimately results in hypercalcemia, which can cause various symptoms and complications, including renal stones, bone loss, and tissue calcification.
Treatment: Treatment for hypervitaminosis D involves stopping vitamin D intake and restricting dietary calcium. Intravenous fluids and medications such as corticosteroids or bisphosphonates may be administered to manage hypercalcemia. Monitoring and supportive care are essential to address any organ damage or complications.
Compassionate Use Treatment: Hypervitaminosis D, or vitamin D toxicity, occurs when there is an excessive accumulation of vitamin D in the body, often leading to hypercalcemia and associated complications. Treatment primarily focuses on stopping vitamin D intake and managing hypercalcemia.

1. **Compassionate Use Treatment**:
- **Glucocorticoids**: These may be used to reduce calcium levels in cases of severe hypercalcemia. Glucocorticoids help to decrease intestinal calcium absorption.
- **Bisphosphonates**: Medications like pamidronate or zoledronic acid can be administered to inhibit bone resorption, thereby lowering serum calcium levels.
- **Calcitonin**: This hormone can be used to reduce calcium levels acutely. It works by inhibiting osteoclastic bone resorption.

2. **Off-label or Experimental Treatments**:
- **Denosumab**: While primarily used for osteoporosis and certain cancers, denosumab may be used off-label for managing hypercalcemia by inhibiting osteoclast formation and function.
- **Cinacalcet**: This medication, typically used for secondary hyperparathyroidism, may be considered to manage hypercalcemia by increasing the sensitivity of calcium-sensing receptors on the parathyroid glands, thus reducing PTH secretion.

Management of severe hypervitaminosis D often requires individualized care, including enhanced hydration, dietary modifications, and careful monitoring of calcium levels. Always consult with a healthcare professional for appropriate diagnosis and treatment options.
Lifestyle Recommendations: Lifestyle recommendations for hypervitaminosis D (vitamin D toxicity) include:

1. **Cease Excess Vitamin D Intake**: Stop taking vitamin D supplements and avoid foods fortified with high levels of vitamin D.
2. **Hydration**: Increase fluid intake to help flush out excess calcium through the kidneys.
3. **Low-Calcium Diet**: Reduce dietary calcium to manage hypercalcemia; avoid dairy products and calcium-rich foods.
4. **Medical Monitoring**: Regularly monitor blood calcium and vitamin D levels under the guidance of a healthcare provider.
5. **Avoid Prolonged Sun Exposure**: Although rare from UV exposure, managing sun exposure can help prevent additional vitamin D synthesis.
6. **Medication Management**: Follow any prescribed treatments or medications to reduce calcium levels, such as corticosteroids or bisphosphonates, as directed by a healthcare professional.

Consulting with a healthcare provider for tailored advice and monitoring is crucial.
Medication: For hypervitaminosis D (an excess of vitamin D in the body), immediate steps typically involve discontinuing vitamin D supplementation and reducing dietary calcium intake to lower calcium levels in the blood. Some medication options that may be considered include:

1. **Corticosteroids**: To reduce inflammation and lower calcium levels.
2. **Bisphosphonates**: To slow down the release of calcium from bones.
3. **Intravenous fluids**: To promote renal excretion of calcium.
4. **Calcitonin**: To decrease blood calcium levels.

It is essential to manage hypervitaminosis D under medical supervision to avoid complications such as hypercalcemia, which can affect various organs.
Repurposable Drugs: There are currently no well-established repurposable drugs specifically for hypervitaminosis D. Treatment primarily involves discontinuing vitamin D supplements and reducing dietary calcium intake. In severe cases, medical interventions like hydration, corticosteroids, or bisphosphonates may be used to manage symptoms and reduce calcium levels in the blood.
Metabolites: Hypervitaminosis D, an excessive intake of vitamin D, leads to high levels of its metabolites, primarily 25-hydroxyvitamin D (25(OH)D) and 1,25-dihydroxyvitamin D (1,25(OH)2D). Elevated levels of these metabolites can result in hypercalcemia and hypercalciuria, causing symptoms such as nausea, vomiting, weakness, and in severe cases, kidney damage and bone loss. Monitoring and managing vitamin D intake is crucial to prevent toxicity.
Nutraceuticals: Nutraceuticals related to hypervitaminosis D typically involve the excessive intake of vitamin D supplements. The condition results from consuming vitamin D in amounts significantly higher than the recommended dietary allowance. It is important to monitor and regulate the intake of vitamin D supplements to prevent toxicity. If hypervitaminosis D occurs, discontinuing the vitamin D supplement and avoiding further intake is crucial. Management may involve hydration, corticosteroids, and bisphosphonates to manage symptoms and reduce elevated calcium levels. Always consult with a healthcare provider before beginning any supplementation, especially at high doses.
Peptides: Hypervitaminosis D, also known as vitamin D toxicity, is a condition resulting from excessive intake of vitamin D. It is not directly associated with peptide levels. Instead, this condition leads to hypercalcemia, which causes symptoms such as nausea, vomiting, weakness, and serious complications like kidney damage. Management focuses on discontinuing vitamin D intake, reducing dietary calcium, and in severe cases, administering medications such as bisphosphonates or corticosteroids. Use of nanotechnology or nanoparticles is not standard in the treatment of hypervitaminosis D.