Calcium Disorders Specialist

Introduction – Calcium Disorders Specialist in Montgomery County, Maryland

As a calcium disorders specialist in Montgomery County, I am committed to delivering specialized care to individuals facing calcium-related health challenges with a comprehensive and evidence-based approach.

Conveniently located in Rockville, my practice provides both virtual and in-person services, extending support to individuals in nearby areas such as Chevy Chase, Bethesda, North Bethesda, Potomac, North Potomac, Gaithersburg, Germantown, Frederick, Silver Spring, Northern Virginia, Western MD, and the Eastern Shore of Maryland for comprehensive care.

My goal is to enhance the health and quality of life of our community members by implementing personalized therapies to the management of calcium disorders.

The Importance of Calcium in the Human Body

Calcium, a double-charged ion, is the most prevalent mineral in the human body that performs a myriad of critical functions. Its essential roles include:

  • Glucose Metabolism: Calcium is key for glucose metabolism. In pancreatic beta cells, rising blood sugar levels trigger an influx of calcium ions, leading to the production and release of insulin. The released insulin interacts with muscle cells, facilitating calcium-dependent glucose uptake, which fuels their activity. Additionally, calcium in the liver assists in glycogen synthesis, storing excess glucose for future energy needs. This orchestrated interplay between calcium and insulin ensures the efficient utilization and storage of glucose throughout the body, maintaining healthy blood sugar levels.
  • Bone and Teeth: Around 99% of the body’s calcium resides within our bones and teeth, providing structure and strength. Calcium is the key ingredient of hydroxyapatite crystals, which make up the mineralized matrix of these structures.
  • Blood Pressure: Calcium plays a critical role in keeping our blood pressure in check by influencing the narrowing and widening of blood vessels. This helps maintain a healthy cardiovascular system.
  • Muscle Function: Calcium is essential for muscle contraction. When a nerve stimulates a muscle, it triggers the release of calcium ions from the muscle’s storage sites, initiating the contraction process. Following this action, calcium is efficiently pumped back into storage, allowing for muscle relaxation.
  • Blood Clotting: Calcium plays a vital role in the blood clotting process, known as coagulation. It is necessary for activating various clotting factors, such as Factors 2, 7, 9, and 10, which assist in stopping bleeding when an injury occurs.
  • Cell Signaling: Acting as messengers, calcium ions play a crucial role in cell signaling pathways. They facilitate the transmission of signals within and between cells, a function indispensable for numerous cellular processes like growth, division, and communication.
  • Nerve Function: Calcium actively participates in the transmission of nerve impulses. It plays a key role in facilitating the release of neurotransmitters, the tiny chemical messengers that enable nerve cells to communicate with each other and with muscles.
  • Enzyme Activity: Calcium serves as a cofactor for many enzymes, including Adenylyl cyclase, Phospholipase C, and Calcineurin. These enzymes assist proteins in their catalytic functions and play a crucial role in various biochemical reactions throughout the body.

Calcium-Rich Foods

Achieving good health involves maintaining a well-balanced diet that incorporates a variety of calcium-rich foods. Fortunately, many natural sources can provide ample amounts of calcium, including:

  • Leafy Green Vegetables: Broccoli, kale, collard greens, and bok choy are abundant in calcium. 
  • Nuts and Seeds: Almonds, chia seeds, and sesame seeds contain significant quantities of calcium. 
  • Fish: Canned sardines and salmon with bones offer good sources of calcium. 
  • Legumes: Beans and lentils provide some calcium. 
  • Fruits: Oranges and figs contain moderate amounts of calcium. 
  • Dairy Products: Milk, yogurt, and cheese are excellent sources of calcium. 
  • Fortified Foods: Including tofu, orange juice, and breakfast cereals, offer additional dietary calcium sources.

Calcium Regulation

Calcium homeostasis is a complex and dynamic process, involving several key organs and hormones working together via negative feedback loops to achieve and maintain a stable blood calcium level.

Primary Organs and Hormones:

  • Parathyroid Glands: Secrete parathyroid hormone (PTH) in response to low blood calcium levels. PTH has three key effects: stimulating the release of calcium from bones, enhancing calcium retention by the kidneys, and activating vitamin D25 from the liver into its active form, vitamin D1,25 (calcitriol), within the kidneys. Calcitriol, in turn, further increases calcium absorption in the intestines.
  • Thyroid Gland: Releases calcitonin, which opposes the actions of PTH by reducing calcium release from bones and promoting calcium loss in the kidneys.
  • Skin: Synthesizes vitamin D3 when exposed to sunlight. This initial form of D3 is then transported to the liver and kidneys for further conversion.
  • Liver: Converts vitamin D3 from the skin into its semi-active form, 25-hydroxyvitamin D (calcidiol).
  • Kidneys: play a crucial role in transforming the semi-active calcidiol, originating from the liver, into the active form of vitamin D, known as 1,25-dihydroxyvitamin D (calcitriol).
  • Gastrointestinal System: Absorbs dietary calcium, a process significantly influenced by the active form of vitamin D, calcitriol.
  • Bones: Act as a reservoir for calcium, releasing it into the bloodstream when needed, influenced by PTH.

Dynamic and Interconnected:

Calcium balance is maintained through a continuous, adaptive process. When blood calcium levels fall, the parathyroids release PTH, triggering a cascade of events to restore balance: bones release calcium into the bloodstream, kidneys retain more calcium, and the liver and kidneys activate vitamin D, leading to increased calcium absorption from the intestines.

Conversely, high blood calcium levels prompt the thyroid gland to release calcitonin, which counteracts the above PTH effects: bones take up calcium from the bloodstream, kidneys lose more calcium in the urine, and there is reduced activation of vitamin D, leading to a decrease in dietary calcium uptake by the intestines. This intricate network ensures that blood calcium levels remain within a narrow range, vital for optimal health and well-being.

Definition & Prevalence of Calcium Disorders

Definition: Calcium disorders are defined by deviations in blood calcium levels from the normal range (typically 8.5 to 10.5 mg/dL), leading to potential health consequences. These deviations are primarily classified into two conditions: hypocalcemia, indicating low blood calcium, and hypercalcemia, indicating high blood calcium.

Prevalence: Hypercalcemia affects 1-2% of the general population, with its prevalence increasing to 4.7% among hospital patients. Common culprits include primary hyperparathyroidism and cancer-related causes. The risk escalates with age, particularly after 65. In contrast, the prevalence of hypocalcemia in the general population remains unknown. However, within hospital settings, its incidence is notably high at 28%, reaching even higher rates of 70% to 80% in intensive care units. Various medical conditions and treatments, especially in older adults and infants, often trigger hypocalcemia.

Symptoms “Short-Term Manifestations”

Symptoms of calcium disorders, including both hypocalcemia (low calcium levels) and hypercalcemia (high calcium levels), are manifested by a range of effects on various organ systems.

  • Hypocalcemia: It is characterized by diverse symptoms impacting different aspects of health. Individuals with hypocalcemia may experience neuromuscular symptoms such as muscle cramps, spasms, and tingling, especially around the mouth and fingers. Additionally, cardiovascular issues like abnormal heart rhythms and low blood pressure can manifest, along with symptoms such as irritability, anxiety, fatigue, and difficulties swallowing. In severe cases, hypocalcemia can even lead to seizures.
  • Hypercalcemia: Conversely, it presents a distinct set of symptoms across various organ systems. Gastrointestinal symptoms encompass nausea, vomiting, and abdominal pain, while musculoskeletal effects may involve muscle weakness and joint pain. Renal complications can lead to excessive thirst, frequent urination, and the development of kidney stones. Neurological symptoms, including confusion and memory impairment, may also occur. Additional manifestations may include fatigue, bone pain, and, in rare instances, pancreatitis.

It’s noteworthy that both hypocalcemia and hypercalcemia may share certain symptoms, such as fatigue and bone pain. The severity and presence of these symptoms depend on factors such as the rate of calcium level changes, intensity of calcium deviation from the normal range, and the underlying causes of the disorders.

Complications “Long-Term Consequences”

Untreated calcium disorders, whether hyper- or hypocalcemia, can lead to various complications affecting multiple organ systems. The severity and specific consequences depend on the underlying cause and the magnitude of the calcium imbalance. Here are some potential sequelas:

  • Endocrine Disruption: Calcium disorders can affect the function of the parathyroid glands, thyroid C cells, glucose metabolism, and vascular resistance in the context of blood pressure control, among other anomalies. In brief, calcium imbalance can have a cascade effect on multiple physiological functions.
  • Osteoporosis: In primary hyperparathyroidism-induced hypercalcemia, excess calcium may leach from the bones, weakening them and elevating the risk of fractures. Conversely, hypocalcemia resulting from decreased dietary intake or urinary loss can reduce bone density, increasing the risk of developing osteoporosis.
  • Kidney Stones & Function: Both hypercalcemia and hypocalcemia can negatively impact the kidneys. Hypercalcemia may contribute to the formation of kidney stones, while hypocalcemia can lead to impaired kidney function.
  • Seizures: Hypocalcemia can cause neurological symptoms, including muscle cramps, tingling sensations, and seizures. In severe, untreated cases, hypocalcemia may lead to life-threatening complications such as tetany and respiratory failure.
  • Arrhythmias: Hypercalcemia can impact the heart, potentially leading to arrhythmias and other cardiac issues. For example, hypocalcemia may prolong the QT interval on an electrocardiogram, increasing the risk of irregular heart rhythms.
  • Depression: Both hypercalcemia and hypocalcemia can affect cognitive function and mood. Symptoms may include confusion, irritability, and, in severe cases, psychosis.
  • Abdominal Pain: Hypercalcemia can lead to constipation, nausea, and abdominal pain. Hypocalcemia may contribute to increased muscle tone in the digestive tract, causing symptoms like abdominal cramping.
  • Infections: Prolonged imbalances in calcium levels can weaken the immune system, compromising the function of T-cells, B-cells, and cytokines and potentially increasing susceptibility to infections.

Causes of Calcium Disorders

Calcium disorders are classified based on which direction calcium levels deviate from the normal range in the bloodstream. The two main types of calcium disorders are hypercalcemia and hypocalcemia.

Hypercalcemia Causes

1. Primary Hyperparathyroidism (PHPT)

Primary hyperparathyroidism, characterized by overactive parathyroid glands, results in the over-secretion of parathyroid hormone (PTH). This excess PTH disrupts calcium metabolism, leading to increased calcium release from bones, enhanced absorption in the intestines, and augmented retention by the kidneys. Ultimately, these changes contribute to elevated blood calcium levels, potentially causing complications such as kidney stones, osteoporosis, and neurological symptoms.

2. Familial Hypocalciuric Hypercalcemia (FHH)

Familial hypocalciuric hypercalcemia, a rare genetic disorder, results in elevated blood calcium levels due to mutations in the calcium-sensing receptor (CaSR) gene, which renders CaSR less sensitive to blood calcium levels. Unlike other hypercalcemic conditions, FHH is characterized by low urinary calcium excretion. Symptoms are typically mild or absent, rendering this condition generally benign.

3. Hypervitaminosis D

Excessive vitamin D intake, a fat-soluble nutrient, can lead to hypervitaminosis D. This condition occurs when an individual significantly surpasses the recommended daily limits. Hypervitaminosis D is characterized by serum vitamin D25 (25-hydroxyvitamin D or calcidiol) levels exceeding 100 ng/ml, resulting in increased calcium absorption in the intestines and elevated blood calcium concentrations. Symptoms of hypercalcemia may include nausea, vomiting, weakness, and, in rare cases, kidney damage and cardiovascular problems.

4. Thiazide Diuretics

Thiazide diuretics, a class of medications commonly used to manage hypertension, can cause hypercalcemia via its dual action in the kidneys. This primarily occurs in the distal convoluted tubules, where thiazides promote both enhancing calcium retention and reducing calcium loss in the urine, resulting in elevated serum calcium levels. Thiazide-induced hypercalcemia may pose significant consequences for individuals with predisposing conditions like primary hyperparathyroidism. This underscores the importance of vigilant monitoring of calcium levels during thiazide therapy.

5. Lithium 

Although rare, long-term lithium therapy for mood disorders can lead to hypercalcemia. This is primarily attributed to lithium’s role as a calcium antagonist, disrupting the parathyroid glands and triggering excess production of parathyroid hormone (PTH). Elevated PTH levels prompt bones to release more calcium into the bloodstream and signal the kidneys to reabsorb additional calcium, further contributing to hypercalcemia. Therefore, it is crucial to regularly monitor blood calcium levels for early detection and management of hypercalcemia. This proactive approach helps prevent complications such as kidney damage, constipation, nausea, and even heart issues.

6. Glucocorticoids

The prolonged use of high-dose glucocorticoids, including prednisone, hydrocortisone, and dexamethasone, can disturb calcium homeostasis, resulting in hypercalcemia. This disturbance primarily stems from elevated bone resorption, driven by heightened osteoclast activation. Consequently, bone resorption leads to skeletal demineralization and the release of calcium into the bloodstream. Although this form of hypercalcemia is uncommon, it emphasizes the need for careful monitoring of calcium levels in patients undergoing extended, high-dose glucocorticoid therapy.

7. Sarcoidosis and Tuberculosis

Both sarcoidosis and tuberculosis share a common pathway that can lead to hypercalcemia. This shared mechanism involves immune system activation, resulting in the formation of granulomas. Within these granulomas, macrophages excessively produce 1,25-dihydroxyvitamin D, the active form of vitamin D. This overproduction enhances calcium absorption in the intestines, causing a rise in blood calcium concentration. The parallel pathways in sarcoidosis and tuberculosis highlight the pivotal role of granulomas and vitamin D activation in the development of hypercalcemia.

8. Immobilization

Prolonged bed rest or insufficient physical activity can trigger the release of calcium from bones into the bloodstream, potentially leading to hypercalcemia and an increased risk of developing osteopenia or osteoporosis. This form of hypercalcemia is particularly prevalent in individuals with limited mobility, such as those recovering from surgery or experiencing extended bed rest due to neurological conditions like Guillain-Barre syndrome and myasthenia gravis. The occurrence of hypercalcemia due to immobility underscores the intricate interplay between physical activity and calcium homeostasis in the body.

9. Malignancies

Hypercalcemia from malignancies can be classified into PTHrp-dependent and non-PTHrp-dependent types. In the PTHrp-dependent category, tumors generate parathyroid hormone-related protein (PTHrp), acting as a mimic of parathyroid hormone (PTH). PTHrp, like PTH, enhances calcium absorption in the intestines and calcium retention in the kidneys, contributing to elevated calcium levels. Squamous cell carcinomas and renal cell carcinomas are typical examples in this group. On the other hand, non-PTHrp-dependent hypercalcemia occurs when tumors directly release excess calcium from the bones, as observed in multiple myeloma and bone metastases from breast and prostate cancers. In the end, both malignancy categories disturb calcium homeostasis, compromising physiological functions.

Hypocalcemia Causes

1. Hypoparathyroidism

Hypoparathyroidism is marked by inadequate secretion of parathyroid hormone (PTH), causing low blood calcium concentrations. PTH plays a vital role in calcium regulation by facilitating calcium release from bones, promoting absorption in the intestines, and preventing excessive calcium loss in the kidneys. In hypoparathyroidism, these functions are compromised, resulting in hypocalcemia and associated symptoms like muscle cramps, tingling, and seizures. In the absence of direct PTH supplementation, the standard treatment involves boosting calcium and vitamin D intake to address the PTH deficiency.

2. Thyroid Surgery

Thyroid surgery may result in hypocalcemia, a rare complication stemming from the manipulation of nearby parathyroid glands. This manipulation disrupts the secretion of parathyroid hormone, potentially causing hypoparathyroidism and, consequently, hypocalcemia, as explained in the previous section.

3. Vitamin D Deficiency

Insufficient vitamin D often leads to hypocalcemia. When vitamin D levels are low, the intestines cannot absorb enough dietary calcium, resulting in reduced serum calcium concentrations. Calcium deficiency, in turn, adversely affects bone health, muscle function, and nerve signaling. Therefore, addressing vitamin D insufficiency is crucial to restoring calcium balance and preventing complications associated with hypocalcemia.

4. Magnesium Deficiency

The role of magnesium in parathyroid gland function is important, as insufficient magnesium hinders the release of parathyroid hormone (PTH). PTH typically triggers calcium release from bones and improves calcium absorption by the intestines. Insufficient PTH subsequently leads to hypocalcemia, causing symptoms like muscle cramps and neurological issues. Therefore, addressing magnesium levels is essential for restoring optimal calcium regulation.

5. Kidney Disorders

Kidney disorders, including chronic kidney disease, can cause hypocalcemia by disrupting the activation of vitamin D. Diminished kidney function impairs the conversion of vitamin D into its active form, thus restricting the dietary calcium entry in the intestines. Additionally, high phosphorus levels in kidney disorders can bind with calcium, further reducing its availability in the bloodstream. These combined factors contribute to hypocalcemia and its associated clinical consequences.

6. Gastrointestinal Malabsorption

Gastrointestinal conditions, such as celiac disease, inflammatory bowel disease, or surgical alterations, may hinder both general absorption processes and, more specifically, calcium absorption. Reduced uptake of calcium by the intestines can lead to hypocalcemia, impacting both bone health and neuromuscular function. It is crucial to monitor and address the root cause of malabsorption to effectively prevent and manage complications, including hypocalcemia.

7. Medications

Various medications can lead to hypocalcemia via distinct mechanisms of action. Below is a list of some commonly used medications that may contribute to low calcium levels.

  • Phenytoin and Phenobarbital: These anticonvulsants can cause hypocalcemia by increasing vitamin D catabolism. This process lowers vitamin D levels, impacting calcium absorption in the intestines and ultimately leading to decreased calcium levels in the bloodstream.
  • Cinacalcet. Utilized in the treatment of hyperparathyroidism, lowers blood calcium levels within the normal range by increasing the sensitivity of calcium-sensing receptors (CaSR), thereby reducing parathyroid hormone secretion. However, higher doses may exacerbate calcium reduction, potentially leading to hypocalcemia.
  • Bisphosphonates: Osteoporosis medications such as alendronate and zoledronic acid may contribute to hypocalcemia, particularly with high doses or prolonged use. Bisphosphonates hinder bone resorption, thus preventing the release of calcium from bones into the bloodstream
  • Denosumab: Used in treating osteoporosis and certain cancers, reduces bone resorption similarly to bisphosphonates. The limitation on calcium release from the bones may potentially result in hypocalcemia.
  • Furosemide: A loop diuretic, promotes calcium loss in the urine, thereby contributing to hypocalcemia.
  • Gentamicin: In rare circumstances, this aminoglycoside antibiotic can cause renal tubular injury, potentially leading to hypocalcemia.

Evaluation

To comprehensively assess calcium disorders, a multi-step approach is crucial. Initially, a thorough medical history is conducted, delving into the patient’s family history, details about medications and supplements, and especially symptoms related to calcium imbalance. This background information is essential for pinpointing the root cause of calcium disorders.

The subsequent stages of this assessment involve critical laboratory tests, examining serum levels of calcium, vitamin D, calcitriol (activated vitamin D), parathyroid hormone, magnesium, phosphorus, and urinary calcium. These comprehensive measurements offer detailed insights into the disease process, shedding light on the intricacies of the patient’s calcium metabolism.

Additionally, imaging studies, such as bone X-rays and Dual-Energy X-ray Absorptiometry (DEXA) scans, can be utilized to assess bone health and identify potential abnormalities. This thorough, stepwise approach ensures a detailed examination, facilitating a precise diagnosis that leads to meaningful, tailored therapies for patients with calcium disorders.

Therapy and Management

Effective management of calcium disorders hinges on addressing the underlying causes to ensure positive outcomes in both the short-term and long-term. For instance, in primary hyperparathyroidism, the most prevalent reason for hypercalcemia, surgical removal of overactive parathyroid glands serves as the key intervention. This procedure aims to normalize parathyroid hormone (PTH) levels and restore calcium balance. In cases where hypercalcemia is associated with malignancies, a comprehensive approach involves managing the underlying cancer via surgical procedures, chemotherapy, or radiation therapy, ultimately achieving normalization of calcium levels.

Similarly, managing hypocalcemia requires specific therapies tailored to the root cause. In instances of hypoparathyroidism, where parathyroid hormone deficiency is at the core of the disease process, the main treatment is supplementation with calcium and vitamin D. Until direct PTH replacement becomes available, maintaining a consistent intake of oral calcium and vitamin D is vital. This helps compensate for the absence of PTH, ensuring that normal serum calcium levels are attained. For hypocalcemia resulting from severe vitamin D deficiency, a multifaceted approach includes high-dose vitamin D supplements, dietary modifications, and increased exposure to sunlight to correct the deficiency and enhance calcium absorption.

In essence, the management of calcium disorders revolves around addressing the root cause. The overarching goal is to restore and maintain optimal calcium balance. This is accomplished via ongoing supervision to ensure the effectiveness of personalized interventions.

Summary

As a specialist in calcium disorders in Rockville, my dedication focuses on providing specialized care to individuals grappling with these conditions. Employing a comprehensive approach supported by medical evidence and clinical expertise, my objective is to improve the overall well-being of my patients through tailored therapeutic interventions. My ultimate aim is to optimize the health and quality of life for community members confronting calcium disorders.

Dr. Tashko