Hyperparathyroidism Secondary
Disease Details
Family Health Simplified
- Description
- Hyperparathyroidism secondary is a condition where the parathyroid glands produce excessive amounts of parathyroid hormone in response to low calcium levels, often due to chronic kidney disease or vitamin D deficiency.
- Type
- Secondary hyperparathyroidism is not typically caused by genetic factors. Instead, it is usually a condition that results from other underlying issues such as chronic kidney disease or vitamin D deficiency, which lead to low calcium levels in the blood. The parathyroid glands overproduce parathyroid hormone in response to low calcium levels, not due to genetic transmission.
- Signs And Symptoms
-
Signs and symptoms of secondary hyperparathyroidism can include:
1. Bone pain and fragility
2. Muscle weakness and cramps
3. Joint pain
4. Fatigue
5. Depression or mood changes
6. Itching (pruritus)
7. Nausea
8. Loss of appetite
9. Increased urination
10. Kidney stones
Nan refers to "not a number" in computing and does not have a meaning in this medical context. - Prognosis
- The prognosis for secondary hyperparathyroidism varies depending on the underlying cause and the effectiveness of treatment. Generally, if the underlying condition—such as chronic kidney disease or vitamin D deficiency—is managed properly, the symptoms and complications related to secondary hyperparathyroidism can be controlled. Early detection and treatment are crucial to avoid long-term complications like cardiovascular disease and bone disorders. Regular follow-up care is important to monitor and adjust treatment as needed.
- Onset
- Secondary hyperparathyroidism typically has an insidious onset. It often develops as a consequence of chronic kidney disease (CKD) or conditions leading to prolonged hypocalcemia, vitamin D deficiency, or phosphate retention. The condition may progress gradually as the underlying cause affects the balance of calcium, phosphate, and parathyroid hormone (PTH) in the body.
- Prevalence
- The prevalence of secondary hyperparathyroidism can vary significantly depending on the underlying condition causing it, such as chronic kidney disease (CKD). In patients with advanced CKD (stages 3-5), the prevalence of secondary hyperparathyroidism can be as high as 40-100%.
- Epidemiology
- Hyperparathyroidism secondary (SHPT) is commonly associated with chronic kidney disease (CKD), which impairs the kidneys' ability to maintain phosphate homeostasis, vitamin D metabolism, and calcium balance. As CKD progresses, the prevalence of SHPT increases. It is particularly prevalent in patients with stage 3-5 CKD. SHPT can also be seen in conditions causing malabsorption of calcium and vitamin D, such as gastrointestinal surgeries or disorders. Demographically, SHPT affects both genders and all age groups, although it is more common in older adults due to the higher incidence of CKD in this population.
- Intractability
- Secondary hyperparathyroidism is typically not considered intractable. It often results from chronic kidney disease or vitamin D deficiency, and its management includes addressing the underlying cause, dietary modifications, and medications like phosphate binders, vitamin D analogs, and calcimimetics. In some cases, surgical intervention may be required if medical management is not effective.
- Disease Severity
- Secondary hyperparathyroidism is generally less severe than primary hyperparathyroidism, as it usually results from another underlying condition, such as chronic kidney disease or vitamin D deficiency. The severity can vary depending on the effectiveness of treatment for the underlying cause. Early diagnosis and management are crucial to prevent complications.
- Healthcare Professionals
- Disease Ontology ID - DOID:12466
- Pathophysiology
- Hyperparathyroidism secondary involves the overactivity of the parathyroid glands due to an external cause, often chronic kidney disease (CKD). In CKD, the kidneys' ability to filter phosphate decreases and their ability to produce active vitamin D (calcitriol) diminishes. This leads to hypocalcemia (low blood calcium levels) and hyperphosphatemia (high blood phosphate levels). The parathyroid glands respond to these imbalances by producing more parathyroid hormone (PTH) to increase calcium levels. Elevated PTH levels eventually cause bone resorption and contribute to complications such as renal osteodystrophy.
- Carrier Status
-
For secondary hyperparathyroidism:
Carrier Status: Not applicable. Secondary hyperparathyroidism is not a genetic disorder but rather a condition resulting from another underlying issue, such as chronic kidney disease or vitamin D deficiency. There are no carriers for this condition because it is not inherited. - Mechanism
-
Secondary hyperparathyroidism is a condition characterized by the overproduction of parathyroid hormone (PTH) due to a chronic stimulus, often related to chronic kidney disease (CKD) or vitamin D deficiency.
**Mechanism:**
1. **Chronic Kidney Disease (CKD):** In CKD, the kidneys lose the ability to efficiently excrete phosphate and convert inactive vitamin D to its active form (calcitriol). The decreased levels of calcitriol lead to reduced calcium absorption from the intestine.
2. **Phosphate Retention:** CKD causes phosphate retention, which results in hyperphosphatemia. Increased phosphate levels bind to calcium, precipitating calcium-phosphate, and lowering serum calcium levels.
3. **Hypocalcemia:** The low serum calcium levels stimulate the parathyroid glands to secrete more PTH in an attempt to restore calcium homeostasis.
4. **Vitamin D Deficiency:** Inadequate vitamin D levels, whether due to reduced dietary intake, lack of sunlight, or impaired conversion (as seen in CKD), result in decreased calcium absorption from the gut and contribute to hypocalcemia.
**Molecular Mechanisms:**
1. **Calcium-Sensing Receptor (CaSR):** Located on the surface of parathyroid cells, the CaSR detects low serum calcium levels and stimulates PTH secretion. With persistent hypocalcemia, there’s an upregulation of PTH synthesis.
2. **Vitamin D Receptor (VDR):** The active form of vitamin D (calcitriol) binds to the VDR in parathyroid cells, typically exerting a negative feedback to inhibit PTH secretion. In CKD, reduced calcitriol levels lead to a loss of this inhibitory feedback, promoting PTH release.
3. **FGF23 (Fibroblast Growth Factor 23):** FGF23 is released from bone osteocytes in response to high phosphate levels. It reduces the synthesis of calcitriol in the kidneys, exacerbating hypocalcemia and indirectly increasing PTH levels.
4. **Phosphatonin Mechanisms:** These are hormonal pathways that regulate phosphate homeostasis. In CKD, dysregulation of these pathways (e.g., increased FGF23) can lead to decreased calcitriol production and increased PTH secretion.
Overall, secondary hyperparathyroidism is a complex interplay of impaired kidney function, disrupted mineral metabolism, and altered hormonal controls, leading to chronic overstimulation of the parathyroid glands. - Treatment
-
Treatment for secondary hyperparathyroidism primarily focuses on addressing the underlying cause and may include:
1. **Management of underlying conditions**: Correcting the deficiencies such as vitamin D deficiency or addressing chronic kidney disease.
2. **Medications**:
- **Vitamin D supplements**: Used to treat vitamin D deficiency.
- **Phosphate binders**: Help to reduce phosphate levels in patients with chronic kidney disease.
- **Calcimimetics**: Help to control parathyroid hormone levels, such as cinacalcet.
3. **Dietary modifications**: Reducing phosphate intake in diet, especially in patients with kidney disease.
4. **Dialysis**: For patients with advanced kidney failure, regular dialysis can help manage phosphate levels.
5. **Surgery**: In cases where medical management is ineffective, parathyroidectomy (surgical removal of the parathyroid glands) may be considered.
It's crucial to consult with a healthcare provider for a personalized treatment plan. - Compassionate Use Treatment
-
Secondary hyperparathyroidism, commonly associated with chronic kidney disease, involves elevated parathyroid hormone levels due to external factors like vitamin D deficiency or imbalanced calcium and phosphate levels. Compassionate use treatments, off-label, or experimental therapies for secondary hyperparathyroidism may include:
1. **Nutritional Vitamin D (Cholecalciferol or Ergocalciferol)**: Sometimes used off-label to manage vitamin D deficiency, which can contribute to secondary hyperparathyroidism.
2. **Calcimimetics (e.g., Cinacalcet)**: Approved for secondary hyperparathyroidism in patients with chronic kidney disease on dialysis, but can be considered off-label in predialysis stages.
3. **Active Vitamin D Analogues (e.g., Calcitriol, Paricalcitol)**: Often used to regulate calcium and phosphate metabolism and control parathyroid hormone levels.
4. **Phosphate Binders (e.g., Sevelamer, Lanthanum carbonate)**: These are standard but might be considered off-label for managing secondary hyperparathyroidism by controlling serum phosphate levels.
5. **Bisphosphonates**: Though primarily used for osteoporosis, they may be explored experimentally to mitigate skeletal complications.
6. **Investigational Drugs**: Experimental treatments in clinical trials may include new calcimimetics or other agents targeting the parathyroid gland or calcium/phosphate metabolism.
Patients considering these options should be closely monitored by healthcare professionals to balance benefits and risks. - Lifestyle Recommendations
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For secondary hyperparathyroidism, lifestyle recommendations may include:
1. **Dietary Modifications**:
- **Increase Calcium Intake**: Consume calcium-rich foods like dairy products, leafy green vegetables, and fortified cereals.
- **Limit Phosphorus**: Reduce intake of foods high in phosphorus, such as red meats, dairy products, processed foods, and sodas, especially if you have kidney disease.
- **Vitamin D**: Ensure adequate vitamin D through either sun exposure, diet (e.g., fatty fish, fortified foods), or supplements as advised by your healthcare provider.
2. **Hydration**: Drink plenty of water to support kidney function and reduce the risk of kidney stones.
3. **Medication Adherence**: Follow your doctor's recommendations regarding medications that manage phosphate levels and vitamin D analogs.
4. **Regular Exercise**: Engage in weight-bearing and muscle-strengthening exercises to support bone health.
5. **Regular Medical Follow-up**: Attend all medical appointments for blood tests to monitor calcium, phosphorus, and parathyroid hormone (PTH) levels. Adjustments to treatment may be needed based on these results.
Consult with a healthcare professional before making significant changes to diet or lifestyle. - Medication
-
Secondary hyperparathyroidism, often associated with chronic kidney disease, can be managed with medications that address the underlying causes of the condition. These medications may include:
1. **Phosphate Binders**: These help reduce phosphate levels in the blood, which can contribute to parathyroid hormone (PTH) overproduction. Examples include:
- Calcium acetate
- Sevelamer hydrochloride or carbonate
- Lanthanum carbonate
2. **Vitamin D Analogues**: These help reduce PTH secretion by increasing the levels of active vitamin D. Examples include:
- Calcitriol
- Paricalcitol
- Doxercalciferol
3. **Calcimimetics**: These mimic calcium and can help decrease PTH secretion by increasing the sensitivity of the calcium-sensing receptors on the parathyroid gland. An example is:
- Cinacalcet
These medications should be used under the guidance of a healthcare provider, who can tailor treatment to the specific needs and health condition of the individual. - Repurposable Drugs
-
There are currently no widely recognized and specific repurposible drugs identified for secondary hyperparathyroidism. The management primarily includes the use of phosphate binders, active vitamin D analogs, and calcimimetics. These include:
1. **Phosphate Binders**:
- Sevelamer
- Lanthanum carbonate
2. **Vitamin D Analogs**:
- Calcitriol
- Paricalcitol
- Doxercalciferol
3. **Calcimimetics**:
- Cinacalcet
These therapies help manage the biochemical abnormalities associated with secondary hyperparathyroidism, often seen in chronic kidney disease. - Metabolites
-
In secondary hyperparathyroidism, key metabolites affected include:
1. **Calcium**: Often decreased due to chronic kidney disease, leading to increased parathyroid hormone (PTH) secretion.
2. **Phosphate**: Typically elevated in secondary hyperparathyroidism because failing kidneys cannot excrete phosphate effectively.
3. **Vitamin D**: Often decreased, as kidneys are less able to convert it to its active form (calcitriol), resulting in lower calcium absorption from the gut, which further stimulates PTH release.
4. **PTH**: Elevated as a compensatory response to low calcium levels and ineffective vitamin D metabolism.
These imbalances contribute to the pathophysiology of secondary hyperparathyroidism, primarily seen in patients with chronic kidney disease. - Nutraceuticals
- For managing secondary hyperparathyroidism, nutraceuticals like vitamin D and its analogs (e.g., calcitriol) and calcium supplements can be beneficial. Vitamin D improves calcium absorption, which can help regulate parathyroid hormone (PTH) levels. Calcium supplements help maintain appropriate serum calcium levels, thereby reducing PTH secretion. Always consult a healthcare provider before starting any supplements.
- Peptides
- For secondary hyperparathyroidism, the peptide of interest is parathyroid hormone (PTH). Elevated levels of PTH are a hallmark of this condition as the parathyroid glands respond to chronic hypocalcemia, often due to chronic kidney disease or vitamin D deficiency. Monitoring PTH, calcium, and phosphorus levels is crucial in managing secondary hyperparathyroidism.