Integrative Treatment Methods Reviewed for Hyperparathyroidism

Unlock the benefits of integrative treatment for hyperparathyroidism and take control of your health journey.

Abstract

This educational post offers a comprehensive exploration of hypercalcemia, with a primary focus on the diagnosis, management, and treatment of primary hyperparathyroidism (PHPT). Written from my clinical perspective as Dr. Alex Jimenez, I will guide you through an easy-to-understand journey, demystifying the complex physiological processes that underpin these conditions. We will begin by exploring the broad differential diagnosis of elevated calcium levels, extending beyond hyperparathyroidism to include conditions like malignancy, vitamin toxicities, and milk-alkali syndrome. The post will detail the systematic diagnostic workup, from initial lab rechecks to advanced imaging and specific hormonal assays, explaining the clinical reasoning behind each step. We will delve into the nuances of primary, secondary, and tertiary hyperparathyroidism, supported by the latest findings from leading researchers, including a 10-year randomized controlled trial examining quality-of-life outcomes and a comparative “Tale of Two Cities” cohort revealing striking regional differences in disease presentation.

Through three detailed case studies, I will unpack our clinical reasoning, lab interpretation, imaging, intraoperative monitoring, and longitudinal care—including medication-based management when surgery is deferred. A significant portion is dedicated to the clinical indications for surgical intervention—the only definitive cure for primary hyperparathyroidism—and the benefits patients can expect post-operatively. For those who are not surgical candidates or opt for non-surgical management, we will thoroughly review medical treatment protocols, including medication options like Cinacalcet (Sensipar) and crucial lifestyle modifications. Throughout this guide, I will integrate the concept of our multidisciplinary approach at Injury Medical Clinic, P.A. in El Paso, Texas. I will explain how my role as a Doctor of Chiropractic (DC) and Advanced Practice Registered Nurse (APRN) merges with the invaluable medical oversight of our Medical Director, Dr. Maria Guadalupe Cardenas, MD, an experienced internist. This collaborative model, combining chiropractic care, functional medicine, internal medicine, and rehabilitation, provides a holistic framework to manage not just the primary diagnosis but also the associated neuromusculoskeletal symptoms, ultimately enhancing patient outcomes and overall well-being. You will learn the physiological basis for symptoms, the rationale for each diagnostic and therapeutic step, and how we optimize outcomes through coordinated, patient-centered, and data-driven care.

Highlights

• Primary hyperparathyroidism fundamentals: pathophysiology, diagnostics, and risk stratification
• Surgery versus observation: what a decade of evidence tells us
• Regional phenotype differences in PHPT: United States vs. Beijing insights
• Three comprehensive case studies: operative cure, medical management, and functional outcomes
• Integrative chiropractic care: neuromusculoskeletal optimization, metabolic support, and rehabilitation
• Functional medicine lens: vitamin D, renal health, bone microarchitecture, and systemic inflammation
• Safety monitoring and long-term follow-up: labs, imaging, hydration, and medication stewardship
• How our multidisciplinary clinic ensures continuity, patient education, and shared decision-making

Our Integrated Approach: Dr. Maria Guadalupe Cardenas, MD, and Dr. Alex Jimenez, DC, APRN

At Injury Medical Clinic, P.A., also known as Mission Plaza Injury Medical Clinic, in El Paso, Texas, we have cultivated a unique and powerful healthcare environment built on the principles of integrative and multidisciplinary care. This model is the cornerstone of our practice and is personified by the collaborative partnership between myself, Dr. Alex Jimenez, and our esteemed Medical Director, Dr. Maria Guadalupe Cardenas, MD.

Dr. Cardenas is a highly respected physician, board-certified in Internal Medicine, with an impressive career spanning over 40 years. Her extensive experience provides an essential foundation of medical expertise and diagnostic acumen (NPI #1164426749, Texas MD License #J2933). As our Medical Director and Collaborative Physician, she provides critical medical oversight, ensuring that every patient receives care that is not only effective but also safe, comprehensive, and aligned with the highest standards of conventional medicine. This collaboration is particularly vital in a setting like ours, which frequently manages complex cases, including personal injuries and chronic conditions that often involve a web of systemic and musculoskeletal issues.

My own credentials as a Doctor of Chiropractic (DC), an Advanced Practice Registered Nurse (APRN) with a specialization as a Family Nurse Practitioner (FNP-BC), and certifications in Functional Medicine (CFMP, IFMCP), Applied Tensegrity Neurology (ATN), and Chiropractic Cranial Spinal Techniques (CCST), allow me to approach patient care from multiple perspectives. I can address the biomechanical and neurological aspects of health through chiropractic adjustments and rehabilitation. At the same time, my FNP role allows me to manage broader health concerns, order and interpret laboratory and imaging studies, and prescribe treatments within my scope.

Together, Dr. Cardenas and I form a synergistic team. This is not a siloed practice where different providers operate independently. Instead, it is a truly integrated system. For a patient presenting with symptoms suggestive of hyperparathyroidism, for instance, our process is seamless. I might identify the initial red flags through a patient history, physical examination, or functional medicine workup. Under the medical direction of Dr. Cardenas, we can order the necessary blood panels (CMP, PTH, Vitamin D) and imaging (DEXA scan, renal ultrasound). Dr. Cardenas’s internal medicine background is invaluable in interpreting these results, ruling out other medical causes of hypercalcemia, and co-managing the patient’s overall health, especially if they have comorbidities like hypertension or diabetes. Her four decades of experience ensure robust medical oversight for complex cases, medication stewardship, lab and imaging strategy, and interventional pathways (e.g., oncology consultations, infusion therapy coordination).

Simultaneously, my chiropractic and functional medicine expertise comes into play. A patient with hyperparathyroidism might present with “bones, stones, and groans”—bone pain, kidney stones, and abdominal discomfort. The bone pain and associated “proximal myopathy” (muscle weakness) are where chiropractic care becomes essential. I can perform a thorough neuromusculoskeletal evaluation to identify areas of spinal dysfunction, joint restriction, and muscular imbalance that contribute to the patient’s pain and functional limitations. Gentle, specific chiropractic adjustments can help restore proper joint mechanics, alleviate nerve irritation, and reduce pain. Our rehabilitation services can then be tailored to address the muscle weakness, improving strength, stability, and overall function. This dual-pronged approach ensures that we are not just managing the endocrine disorder at a biochemical level but are also actively treating the physical suffering it causes.

This collaborative model is the essence of modern integrative healthcare. It bridges the gap between different disciplines, allowing us to leverage the strengths of both conventional medicine and complementary therapies to provide a level of care that is far more comprehensive and patient-centered than either could achieve alone. Our philosophy is straightforward: use the best available evidence, communicate clearly, personalize care, and coordinate across disciplines so patients understand their options and feel confident in every step.

Unraveling Hypercalcemia: The First Clue

In my practice, the journey toward a diagnosis often begins with a single, unexpected finding on a routine lab report: an elevated serum calcium level. Hypercalcemia, the medical term for high calcium in the blood, is a significant clinical marker that demands a thoughtful and systematic investigation. While it can be alarming for patients, it’s my job to navigate this finding calmly and methodically. My first principle is always: don’t panic, verify.

An isolated elevated calcium reading on a Comprehensive Metabolic Panel (CMP) is not, in itself, a diagnosis. Laboratory values can fluctuate, and errors can occur. Therefore, the very first step I take is simple and pragmatic: recheck the lab. I will have the patient return for a second blood draw, often ensuring they are well-hydrated, to confirm the finding. If this repeat test comes back within the normal range, we can generally be reassured. I would “move on” in the sense of not launching a full-scale workup at that moment, but I make a mental note and a chart note. If the elevation reappears on a subsequent routine lab check months later, the investigation will resume with more urgency. However, for a one-time, non-reproducible result, further immediate investigation is often unnecessary.

But what happens if the repeat test confirms the hypercalcemia? This is where the real detective work begins. The next logical step is to order a parathyroid hormone (PTH) level. This single test is the most critical fork in the road, as it immediately helps us differentiate between PTH-mediated and non-PTH-mediated causes of hypercalcemia. We are essentially asking the body’s primary calcium regulator, the parathyroid glands, “Are you the cause of this problem?”

Additionally, I may consider ordering an ionized calcium level. While total serum calcium is what we see on a CMP, about half of it is bound to proteins, primarily albumin. The ionized calcium is the biologically active form. In a patient who is critically ill or has a significant protein abnormality (low albumin), total calcium can be misleading. However, in a relatively healthy outpatient with a normal acid-base status, the total calcium is usually sufficient, and an ionized calcium test may not add significant value. But in ambiguous cases, it can provide crucial clarity.

The Differential Diagnosis of Hypercalcemia

When a patient presents with confirmed hypercalcemia, it is crucial to think broadly. While hyperparathyroidism is a common culprit, it is far from the only one. A thorough differential diagnosis is essential to avoid missing other serious conditions. The PTH level is our primary guide. If PTH is high or inappropriately normal in the face of high calcium, our suspicion for primary hyperparathyroidism skyrockets. If PTH is suppressed (low), we must look elsewhere.

Here are the key conditions to consider:

• Hypercalcemia of Malignancy: This is a major concern, especially in older or acutely ill patients. Certain cancers, such as lung cancer, breast cancer, and multiple myeloma, can produce a substance called parathyroid hormone-related peptide (PTHrP). This peptide mimics the action of PTH, leading to bone resorption and increased calcium levels, but the body’s own PTH production will be suppressed. Other cancers can cause hypercalcemia by directly invading and destroying bone (lytic bone metastases). Calcium levels in malignancy-related hypercalcemia are often very high, frequently exceeding 12 mg/dL, and patients are typically quite symptomatic.
• Vitamin D Toxicity: Vitamin D’s primary role is to increase the absorption of calcium from the gut. While it is difficult to reach toxic levels from sun exposure or food, excessive supplementation can lead to hypervitaminosis D. This causes the gut to absorb much calcium, overwhelming the body’s ability to regulate it, resulting in hypercalcemia. I always ask patients to bring in all their supplements—bottles in hand—because dosages and formulations can vary wildly.
• Vitamin A Toxicity: Though less common, excessive intake of Vitamin A can also lead to hypercalcemia, primarily by increasing bone resorption. This is usually seen with very high supplement doses.
• Milk-Alkali Syndrome: This condition is a classic example of “too much of a good thing.” It arises from the excessive absorption of calcium and absorbable alkali, most commonly from over-the-counter antacids like Tums (calcium carbonate). I had a memorable clinical experience with a patient who presented with persistent hypercalcemia. When I specifically and carefully questioned her about supplements, she initially denied taking any. But when I broadened the question to include over-the-counter medications, she revealed she was taking Tums for reflux. When I asked, “How many are you taking?” she casually replied, “Thirty a day.” This quantified number was the key. We had her stop the Tums, and her calcium levels normalized. This case underscores a vital clinical pearl: always ask specifically and quantitatively about all substances a patient is ingesting.
• Other Causes: Several other conditions can contribute to hypercalcemia, though they are less common:

• • Prolonged Immobilization: Being bedridden for a long time can lead to increased bone breakdown and a subsequent rise in serum calcium.
  • Hyperthyroidism: An overactive thyroid can accelerate bone turnover, sometimes leading to mild hypercalcemia.
  • Granulomatous Diseases: Conditions like sarcoidosis, tuberculosis (TB), and certain lymphomas can cause hypercalcemia. The granulomas in these diseases contain macrophages that can independently produce an active form of vitamin D (1,25-dihydroxyvitamin D), leading to increased intestinal calcium absorption.
  • Total Parenteral Nutrition (TPN): Patients receiving all their nutrition intravenously can sometimes develop hypercalcemia if the calcium content in their TPN formula is too high.
  • Adrenal Insufficiency: Also known as Addison’s disease, this condition can cause hypercalcemia through volume contraction and decreased renal calcium excretion.

Understanding this broad landscape is fundamental. Before focusing solely on the parathyroid glands, we must thoughtfully rule out these other possibilities, using the patient’s history, physical exam, and targeted laboratory tests as our guide.

The Parathyroid Glands: Masters of Calcium Homeostasis

To truly understand hyperparathyroidism, we must first appreciate the elegant and vital role of the parathyroid glands. Tucked behind the thyroid gland in the neck, most people have four of these tiny, rice-sized glands. Despite their small size, they are endocrine powerhouses, singularly responsible for producing parathyroid hormone (PTH).

PTH acts as the body’s primary calcium regulator. Its main job is to prevent hypocalcemia (low blood calcium). Calcium is not just for strong bones; it is absolutely critical for nerve transmission, muscle contraction, blood clotting, and cellular signaling. The body maintains blood calcium within a very narrow, tightly controlled range.

When blood calcium levels begin to dip, the parathyroid glands sense this change and ramp up their secretion of PTH. PTH then acts on three main targets to raise blood calcium levels:

1. The Bones: The skeletal system serves as the body’s vast calcium reservoir. PTH stimulates cells called osteoclasts to break down bone tissue, a process known as bone resorption. This releases calcium (and phosphate) from the bone matrix into the bloodstream.
2. The Kidneys: In the kidneys, PTH works in two ways. First, it increases the reabsorption of calcium in the renal tubules, preventing it from being lost in the urine. Second, and just as importantly, PTH stimulates the final and most crucial step in activating Vitamin D. It prompts the kidneys to convert the inactive form of Vitamin D (25-hydroxyvitamin D) into its potent, active form, 1,25-dihydroxyvitamin D (also known as calcitriol).
3. The Intestines (Indirectly): The active form of Vitamin D (calcitriol) then acts on the intestines, dramatically increasing the absorption of dietary calcium.

This entire system operates on a classic negative feedback loop. As PTH does its job and blood calcium levels rise back to normal, the parathyroid glands sense the increased calcium and decrease their secretion of PTH. This elegant, self-regulating mechanism ensures calcium homeostasis.

When the System Breaks: Primary, Secondary, and Tertiary Hyperparathyroidism

Hyperparathyroidism occurs when this finely tuned system goes awry. It is categorized into three distinct types: primary, secondary, and tertiary. Understanding the differences is crucial for accurate diagnosis and appropriate management.

Primary Hyperparathyroidism: The Autonomous Gland

Primary hyperparathyroidism (PHPT) is the focus of our discussion. In this condition, one or more of the parathyroid glands becomes overactive and produces an excessive amount of PTH, independent of the body’s calcium levels. The negative feedback loop is broken. The gland (or glands) essentially goes rogue, continuously pumping out PTH even when blood calcium is already high.

The most common cause, seen in 80-90% of cases, is a single, benign parathyroid adenoma—a non-cancerous tumor on one of the four glands. Less commonly, all four glands may become enlarged (four-gland hyperplasia), or, in about 15% of cases, multiple glands might be involved (multigland disease). Extremely rarely (in less than 1% of cases), the cause is a parathyroid carcinoma, a malignant tumor.

The result of this autonomous PTH secretion is chronic hypercalcemia. The body is constantly being told to release calcium from the bones, retain it in the kidneys, and absorb more from the gut, leading to the classic clinical picture of PHPT. Historically, before the advent of routine biochemical screening in the 1970s, PHPT was known as the disease of “bones, stones, abdominal groans, and psychic moans.” Patients were often symptomatic, presenting with bone pain and fractures, painful kidney stones, constipation and abdominal pain, and significant fatigue, depression, and cognitive fog. Today, thanks to the inclusion of calcium levels in routine blood work, the vast majority of cases (over 80%) are diagnosed in an asymptomatic or biochemically screened stage, long before these overt symptoms develop.

Secondary Hyperparathyroidism: A Compensatory Response

Secondary hyperparathyroidism is fundamentally different. In this case, the parathyroid glands are functioning correctly. They are not diseased; rather, they are responding appropriately to a different underlying problem that is causing or threatening to cause hypocalcemia. The high PTH level is a compensatory mechanism. The body is struggling to maintain normal calcium levels, so the parathyroid glands work overtime to correct the imbalance.

The most common causes of secondary hyperparathyroidism are:

• Chronic Kidney Disease (CKD): This is the leading cause. As kidney function declines, two things happen. First, the kidneys lose their ability to excrete phosphate, leading to hyperphosphatemia. PhosphaCalciums to calcium in the blood, effectively lowering the amount of frCalciumized calcium. Second, and critically, the damaged kidneys can no longer effectively convert Vitamin D into its active form (calcitriol). This lack of active Vitamin D severely impairs intestinal calcium absorption. Both of these factors lead to low blood calcium, which in turn triggers the parathyroid glands to produce massive amounts of PTH in a desperate attempt to normalize calcium levels.
• Vitamin D Deficiency: Even in people with healthy kidneys, severe Vitamin D deficiency can cause secondary hyperparathyroidism. Without enough Vitamin D, the gut cannot absorb sufficient calcium from the diet. The resulting low blood calcium stimulates the parathyroid glands to increase PTH secretion to maintain calcium levels, often by leaching it from the bones.
• Malabsorption Syndromes: Conditions like celiac disease or Crohn’s disease can impair the absorption of both calcium and Vitamin D from the intestines, leading to a state similar to Vitamin D deficiency and causing secondary hyperparathyroidism.

Tertiary Hyperparathyroidism: The Compensatory Gland Becomes Autonomous

Tertiary hyperparathyroidism is a late-stage complication that arises almost exclusively in patients with long-standing, severe secondary hyperparathyroidism, most often those with end-stage renal disease. After years or even decades of constant stimulation from chronic hypocalcemia, the parathyroid glands themselves transform. They become so enlarged and hyperplastic that they begin to function autonomously, much like in primary hyperparathyroidism.

At this point, even if the original problem is corrected (for example, through a successful kidney transplant), the parathyroid glands do not shut down. They continue to secrete enormous amounts of PTH, leading to severe hypercalcemia. In essence, a condition that started as a compensatory response has evolved into an autonomous, disease-producing state.

A Visual Guide to Diagnosis

To help visualize these distinctions, I often refer to a diagnostic algorithm, similar to one provided by major laboratories like Quest Diagnostics. It provides a clear pathway for interpreting lab results:

• High Calcium + High or Inappropriately Normal PTH: This is the classic signature of Primary Hyperparathyroidism. A “normal” PTH is inappropriate here; high calcium should be suppressing PTH to very low levels.
• Low or Normal Calcium + High PTH: This pattern points strongly toward Secondary Hyperparathyroidism. The body is trying to compensate for low calcium.
• High Calcium + Very High PTH (often in a patient with a history of CKD): This is characteristic of Tertiary Hyperparathyroidism. Both calcium and PTH are markedly elevated.

This framework is an invaluable tool for navigating the initial lab results and steering the diagnostic process in the right direction.

Investigating Elevated PTH: Medications and Rare Genetic Conditions

Once we’ve identified a patient with elevated calcium and an elevated PTH level, placing them squarely in the primary hyperparathyroidism category, the investigation isn’t quite over. Before finalizing the diagnosis and moving toward treatment discussions, we must consider two important confounding factors: medications and rare familial syndromes.

The Influence of Common Medications

Certain medications can directly interfere with calcium and PTH metabolism, mimicking the biochemical profile of primary hyperparathyroidism. It is essential to take a meticulous medication history to rule these out.

• Thiazide Diuretics: Medications like hydrochlorothiazide (HCTZ) are commonly prescribed for hypertension. Thiazides have a unique effect on the kidneys: they decrease urinary calcium excretion. By causing the body to retain more calcium, they can lead to mild hypercalcemia. This, in turn, can sometimes cause a mild, secondary elevation in PTH or unmask an underlying, mild case of primary hyperparathyroidism. If a patient on a thiazide presents with this lab pattern, a reasonable first step is to consult with their primary care provider or cardiologist about temporarily holding the diuretic (if medically safe) and rechecking the labs in a few weeks. If the calcium and PTH levels normalize, the medication was the likely culprit.
• Lithium: This medication, widely used to treat bipolar disorder, has a direct effect on the parathyroid glands themselves. Lithium decreases the sensitivity of the calcium-sensing receptors on the parathyroid cells. This means the glands require a higher level of blood calcium before they “shut off” PTH production. Essentially, it shifts the setpoint for calcium regulation upward, leading to both hypercalcemia and elevated PTH. Managing this situation requires careful collaboration with the patient’s mental health provider, as abruptly stopping lithium is often not an option.

Rare Familial (Genetic) Syndromes

While the vast majority of primary hyperparathyroidism cases are sporadic, involving a single adenoma in an older adult, it’s important to be aware of rare genetic forms, especially when certain red flags are present.

• Familial Hypocalciuric Hypercalcemia (FHH): This is a very rare, benign, autosomal dominant condition that can perfectly mimic the labs of primary hyperparathyroidism (high calcium, high PTH). It is caused by a genetic mutation in the calcium-sensing receptor, primarily in the kidneys and parathyroid glands. Because the kidneys’ calcium sensors are faulty, they reabsorb much calcium, leading to very low calcium in the urine (hypocalciuria). Faulty sensors in the parathyroid glands also contribute to the high PTH. The key to differentiating FHH from true primary hyperparathyroidism is a 24-hour urine calcium test.

• • In a patient with primary hyperparathyroidism, the high PTH and high blood calcium will overwhelm the kidneys, leading to high calcium in the urine (hypercalciuria), typically greater than 200 mg/24 hours.
  • In a patient with FHH, the urine calcium will be characteristically low, almost always less than 200 mg/24 hours.
  • A more specific calculation, the calcium-to-creatinine clearance ratio (CCCR), can be performed. A ratio of less than 0.01 is highly suggestive of FHH.

• This distinction is critically important because patients with FHH do not benefit from parathyroid surgery. Removing their parathyroid glands will not cure their hypercalcemia, which is a lifelong, generally asymptomatic condition. Misdiagnosing FHH as primary hyperparathyroidism could lead to an unnecessary and ineffective operation.

• Multiple Endocrine Neoplasia (MEN) Syndromes: If I encounter a patient with primary hyperparathyroidism who is unusually young, typically under the age of 30, a red flag should be raised for a possible underlying MEN syndrome. These are rare genetic disorders that cause tumors in multiple endocrine glands.

• • MEN Type 1: This syndrome is characterized by the “3 P’s”: Parathyroid tumors (hyperparathyroidism is the most common and usually the first manifestation), Pituitary tumors, and Pancreatic neuroendocrine tumors.
  • MEN Type 2A: This syndrome involves Parathyroid hyperplasia, Pheochromocytoma (a tumor of the adrenal glands), and Medullary thyroid carcinoma.

• A young patient with PHPT, especially if they have a family history of endocrine issues or multi-gland involvement, requires a referral for genetic counseling and testing to rule out these syndromes.

Normocalcemic Primary Hyperparathyroidism: The Subtle Variant

In recent years, a more subtle variant of the disease has been recognized: Normocalcemic Primary Hyperparathyroidism (NPHPT). As the name suggests, these are patients who have a persistently elevated PTH level but consistently normal total and ionized calcium levels. This diagnosis can be challenging and requires careful exclusion of all causes of secondary hyperparathyroidism.

To make a diagnosis of NPHPT, the following criteria must be met:

1. Normal Calcium: Both the albumin-adjusted calcium and Calcium-corrected calcium must be consistently within the normal range.
2. Elevated PTH: The parathyroid hormone level must be elevated on at least two separate occasions over a three- to six-month period.
3. Exclusion of Secondary Causes: This is the most critical step. We must meticulously rule out all potential reasons for a compensatory rise in PTH. This includes:

• • Vitamin D Deficiency: The 25-hydroxyvitamin D level must be sufficient (generally defined as greater than 30 ng/mL).
  • Renal Insufficiency: The estimated Glomerular Filtration Rate (eGFR) must be greater than 60 mL/min/1.73 m².
  • Medications: The patient must not be taking lithium or thiazide diuretics.
  • Malabsorption Issues: There should be no clinical evidence of conditions like celiac disease that would impair calcium absorption.
  • Other Bone Diseases: Conditions such as Paget’s disease, which can affect bone metabolism, must be ruled out.

NPHPT is considered an early form of primary hyperparathyroidism. A significant percentage of these patients will eventually develop hypercalcemia over time. The management and monitoring of these patients are similar to those with asymptomatic hypercalcemia, with a focus on regular surveillance of their calcium levels and bone density.

“Cracking the Low Thyroid Code: A Comprehensive Assessment Guide”- Video

The Diagnostic Workup: Putting the Pieces Together

Once we have a strong suspicion of primary hyperparathyroidism (either classic or normocalcemic), a structured workup is necessary to confirm the diagnosis, assess the severity of the disease’s impact on the body, and determine the best course of action. This workup involves a specific set of laboratory tests and imaging studies.

Essential Laboratory Tests

• Comprehensive Metabolic Panel (CMP): This is our starting point. It provides the serum calcium, which needs to be confirmed. It also provides the albumin level, which is necessary to calculate the corrected calcium, and, crucially, the creatinine level and eGFR, allowing us to assess renal function.
• Parathyroid Hormone (PTH): The cornerstone of the diagnosis. As discussed, an elevated or inappropriately normal PTH in the setting of hypercalcemia is the key finding.
• 25-Hydroxyvitamin D: This test is non-negotiable. Vitamin D deficiency is rampant and is the most common cause of secondary hyperparathyroidism. We must rule it out and replete vitamin D levels if they are low before finalizing a diagnosis of primary hyperparathyroidism.
• Serum Phosphorus: In primary hyperparathyroidism, PTH causes the kidneys to waste phosphate, so the serum phosphorus level is often low or in the low-normal range. This can be a supportive finding.
• 24-Hour Urine Calcium: This test is vital for two reasons. First, as mentioned, it is essential to rule out Familial Hypocalciuric Hypercalcemia (FHH). Second, a very high level of urinary calcium is an independent indicator of disease severity and is one of the criteria for recommending surgery. It reflects a high risk of kidney stone formation.

Essential Imaging Studies

Imaging in primary hyperparathyroidism serves two purposes: assessing end-organ damage and, for surgical candidates, localizing the diseased gland(s) before an operation.

• DEXA (Dual-Energy X-ray Absorptiometry) Scan: This is a bone mineral density scan. It is essential for assessing one of the primary targets of PTH: the skeleton. Chronic PTH excess preferentially removes calcium from cortical bone, which is the dense outer layer of bone. Therefore, the DEXA scan must include not only the standard sites (lumbar spine and hip) but also the distal one-third of the radius in the forearm, as this site is rich in cortical bone and is often the first and most severely affected area. A finding of osteoporosis (a T-score of -2.5 or lower at any site) is a major indication for surgery. Optional additions to the DEXA scan, if available, include a Vertebral Fracture Assessment (VFA), which can detect silent compression fractures in the spine, and a Trabecular Bone Score (TBS), which gives an indirect measure of bone quality.
• Renal Ultrasound: This imaging study is used to look for evidence of kidney damage. Its primary purpose is to detect nephrolithiasis (kidney stones), even if the patient has never had symptoms. It can also identify nephrocalcinosis, a more diffuse deposition of calcium salts within the functional tissue (parenchyma) of the kidney, which indicates more advanced damage.
• Localization Studies (for Surgical Planning): These studies are not for diagnosis. The diagnosis of primary hyperparathyroidism is a biochemical one, made with blood and urine tests. Localization studies are used only after the diagnosis is confirmed and a decision for surgery is being considered. Their purpose is to help the surgeon plan the operation. The two main studies are:

• • Neck Ultrasound: Performed by a skilled sonographer, this can often identify an enlarged parathyroid adenoma in the neck.
  • Sestamibi Scan (Parathyroid Scintigraphy): This is a nuclear medicine scan. A small amount of a radioactive tracer (technetium-99m sestamibi) is injected. This tracer is preferentially taken up by overactive parathyroid tissue (and thyroid tissue). Images are taken to see if a “hot spot” corresponding to a parathyroid adenoma lights up. Combining this with a SPECT/CT scan (single-photon emission computed tomography) can provide a precise 3D location of the adenoma.

The success of parathyroid surgery does not depend on these scans being positive. An experienced parathyroid surgeon can find the diseased gland(s) over 95% of the time even with negative preoperative scans. However, a positive scan that clearly identifies a single adenoma allows the surgeon to perform a minimally invasive parathyroidectomy, a much quicker procedure with a smaller incision.

The Role of Chiropractic Care in Managing Hyperparathyroidism Symptoms

While the underlying endocrine disorder of hyperparathyroidism requires medical or surgical management, the physical symptoms it produces fall squarely within the scope of integrative chiropractic care. The classic “bones and groans” are not just abstract concepts; they represent real pain and dysfunction that can severely impact a patient’s quality of life. This is where my role as a chiropractor becomes particularly valuable within our integrated team at Injury Medical Clinic.

A patient with chronic hyperparathyroidism often experiences:

• Bone Pain (Ostealgia): This can be a deep, aching pain, often felt in the bones of the legs, arms, and back. It results from the constant osteoclastic activity stimulated by excess PTH.
• Proximal Myopathy: This is a characteristic weakness in the large muscles closer to the center of the body—the shoulders, hips, and thighs. Patients may complain of difficulty getting up from a chair, climbing stairs, or lifting their arms above their head.
• Joint Pain and Stiffness: The metabolic changes and inflammation associated with the condition can lead to generalized arthralgias.
• Increased Fracture Risk: The loss of bone density, especially in the spine, can lead to vertebral compression fractures, causing acute back pain and postural changes.

My approach to a patient with these symptoms is multifaceted. After a thorough history and a focused neuromusculoskeletal examination, I develop a care plan tailored to their specific presentation:

1. Spinal and Extremity Adjustments: The goal of chiropractic adjustments is to restore normal motion and function to joints that have become restricted or misaligned (subluxated). In a patient with bone and joint pain, gentle, specific adjustments can help alleviate mechanical stress on the joints, reduce nerve irritation, and decrease pain signaling. For a patient with osteoporosis, I would modify my technique, using low-force methods (like Activator or drop-table techniques) to ensure safety while still achieving the desired therapeutic effect. Restoring proper spinal alignment can also improve overall neurological function, which may help modulate the body’s pain perception.
2. Soft Tissue and Myofascial Release: The muscle weakness (myopathy) and pain can lead to the development of tight, painful knots of muscle tissue known as trigger points. Techniques like myofascial release, trigger point therapy, and instrument-assisted soft tissue mobilization (like Graston Technique) can be used to break up these adhesions, improve blood flow to the muscles, and reduce pain and stiffness.
3. Targeted Rehabilitation and Exercise Prescription: This is a critical component. To combat the proximal myopathy, we design a specific, progressive strengthening program. This program focuses on the weak muscles of the pelvic and shoulder girdles. We start with gentle, controlled exercises and gradually increase the resistance and complexity as the patient’s strength improves. This not only helps restore function but also places mechanical stress on the bones, which is a powerful stimulus for osteoblastic (bone-building) activity and helps counteract the effects of PTH.
4. Postural Correction and Biomechanical Education: Chronic pain and weakness often lead to poor posture and faulty movement patterns, which can perpetuate the pain cycle. I educate patients on proper body mechanics for daily activities and prescribe exercises to strengthen core postural muscles, helping to offload stress on the spine and reduce the risk of further injury or vertebral fracture.
5. Functional Medicine Support: From my functional medicine perspective, I can also provide guidance on an anti-inflammatory diet and lifestyle modifications that support bone health and reduce systemic inflammation, complementing the medical management overseen by Dr. Cardenas.

By integrating these chiropractic and rehabilitative strategies, we are not just waiting for surgery or medication to solve the problem. We are actively managing the patient’s symptoms, improving their function, reducing their pain, and empowering them to take an active role in their recovery. This holistic approach ensures that the patient’s whole-body health is addressed, leading to better outcomes and a higher quality of life throughout their treatment journey.

Understanding Primary Hyperparathyroidism: Physiology, Symptoms, and Why It Can Be So Subtle

Primary hyperparathyroidism (PHPT) is a disorder of excessive parathyroid hormone (PTH) secretion, most often due to a benign parathyroid adenoma, less commonly from parathyroid hyperplasia or carcinoma. Elevated PTH results in increased serum calcium primarily through:

• Increased osteoclastic bone resorption (calcium and phosphate from bone)
• Enhanced renal tubular calcium reabsorption
• Increased renal conversion of 25-hydroxyvitamin D to 1,25-dihydroxyvitamin D, boosting intestinal calcium absorption

Many patients are discovered incidentally on routine labs. Hypercalcemia may be mild and chronic; the body adjusts, masking classic symptoms. Yet subtle issues—fatigue, muscle aches, mood changes, concentration difficulties—often improve after definitive management. The disconnect between labs and symptoms can make decision-making difficult for patients, which is why clear education, careful surveillance, and precise criteria for surgery matter.

Physiological Touchpoints

• Bone: Chronic PTH excess stimulates osteoclast-mediated resorption, degrading trabecular connectivity, reducing bone mineral density at cortical sites (e.g., distal one-third radius) and sometimes trabecular sites. Microarchitectural changes predispose to fractures even with near-normal DXA in early disease.
• Kidney: Hypercalciuria increases nephrolithiasis risk; PTH also influences phosphate handling. Hydration and urinary calcium tracking are critical in risk assessment.
• Neuromuscular: Hypercalcemia can disrupt neuromuscular excitability, producing weakness, fatigue, proximal myopathy, and cramps. After biochemical cure, many patients report improved vitality.
• Neurocognitive: Patients describe brain fog, mood changes, or sleep disturbance. Randomized data show mixed quality-of-life outcomes, but clinically, selective symptom improvement is common.
• Cardiovascular: PHPT may associate with hypertension, arrhythmias, vascular stiffness, and left ventricular hypertrophy, though mechanisms and causality remain debated. Correcting hypercalcemia can beneficially affect hemodynamics in select patients.

Surgery vs. Observation in Asymptomatic PHPT: What a Decade-Long Trial Tells Us

Deciding on surgery when you “feel fine” is challenging. That’s why I often share the evidence from a significant prospective randomized controlled trial that followed patients for 10 years. This study compared parathyroidectomy to simple observation in patients with asymptomatic PHPT, measuring quality of life using standardized tools (SF-36 and CPRS) at baseline and then at 2, 5, and 10 years. Patients who had surgery achieved a biochemical cure, while those in the observation group maintained elevated calcium and PTH levels. The results were revealing:

• On the SF-36 survey, which has eight different scales, only one scale—vitality—showed an improvement after surgery.
• The CPRS, another symptom score, improved similarly in both the surgical and observation groups.
• Most importantly, at the 10-year mark, having a parathyroidectomy did not necessarily lead to a better overall quality of life compared to observation, and importantly, observation did not worsen it.

Why This Matters in Practice

This evidence is incredibly useful when counseling patients. It tells us:

• For asymptomatic patients who do not meet the strict criteria for surgery, watchful waiting is a very reasonable and evidence-backed approach.
• For patients who do meet the guidelines for surgery, the procedure still offers the clear and durable benefit of a biochemical cure, as it is the only definitive treatment.
• Individual experiences vary greatly. While average quality-of-life scores may not change dramatically, some of my patients experience immediate and meaningful improvements in their energy levels and pain after surgery. This individual variability is a key part of our shared decision-making process.

“Tale of Two Cities” in PHPT: Phenotypes Across Regions and Why They Differ

The way primary hyperparathyroidism presents can be dramatically different depending on where you are in the world. A fascinating comparative analysis of 100 patients from the United States and 100 patients from Beijing highlighted this disparity.

• United States Cohort:

• • Presentation: Typically discovered through asymptomatic hypercalcemia on routine blood tests.
  • Timing: Often diagnosed within a decade after menopause. Calcium: Mean calcium was only mildly elevated at approximately 10.4 mg/dL, with modest PTH elevations around 118 pg/mL.
  • Vitamin D: Average levels were around 21 ng/mL.
  • Complications: Severe bone disease (osteitis fibrosa cystica) was rare, and the rate of kidney stones had dropped to about 15–20%. DEXA scans, not overt fractures, mainly detected bone issues.

• Beijing Cohort:

• • Presentation: Patients were much younger (average age 37) and highly symptomatic.Calcium: Mean calcium was significantly higher (~12 mg/dL), and PTH levels were astronomical, often over 20 times the upper limit of normal.
  • Vitamin D: Levels were profoundly low, averaging just 8.8 ng/mL.
  • Complications: Severe bone disease was evident in about 60% of patients, osteoporosis was nearly universal, and pathological fractures were common (~35%). Kidney stones were also more frequent (~42%).

Why the Disparity?

These striking differences are largely driven by public health and nutritional factors. In the U.S., routine lab screening catches the disease in its early, milder stages. In other regions, where screening is less common and vitamin D deficiency is more severe, the disease is often discovered only after it has caused significant damage. This “Tale of Two Cities” powerfully illustrates how nutritional status, sunlight exposure, and healthcare system practices shape the clinical face of PHPT.

Treatment of Primary Hyperparathyroidism: The Surgical Solution

For confirmed primary hyperparathyroidism, there is only one definitive cure: surgery. The procedure, called a parathyroidectomy, involves the surgical removal of the overactive parathyroid gland or glands. Medical management can control symptoms and slow disease progression, but only surgery can permanently resolve the underlying problem.

Indications for Surgery: When I Recommend a Surgical Consult

The decision to proceed with surgery is based on a set of internationally recognized criteria developed through consensus workshops. These guidelines help identify patients who are most likely to benefit from surgery and are at the highest risk of complications if left untreated. A patient should be offered a surgical consultation if they meet any one of the following criteria:

1. Age: Patient age less than 50 years. Younger patients have a longer lifetime ahead of them to suffer the consequences of chronic hypercalcemia, making surgery a more compelling option.
2. Serum Calcium Level: A serum calcium level that is more than 1.0 mg/dL above the upper limit of the laboratory’s normal range. This indicates a significant degree of hypercalcemia and a higher burden of disease. I make it a point to educate my patients on how to interpret this. I show them their lab report, point out their value, and compare it to the normal range listed on that specific lab’s report. This empowers them to understand their own results, even if they have tests done elsewhere in the future.
3. Renal Involvement: Evidence of kidney damage, which can manifest in two ways:

• • A creatinine clearance or eGFR of less than 60 mL/min/1.73 m², indicating significantly reduced kidney function.
  • A history of kidney stones (nephrolithiasis) or the presence of stones or nephrocalcinosis on a renal ultrasound.

• Skeletal Involvement: Evidence of significant bone loss:

• • A diagnosis of osteoporosis, defined as a T-score of -2.5 or lower at the lumbar spine, total hip, femoral neck, or distal one-third radius.
  • A history of a fragility fracture (a fracture from a low-impact fall), particularly a vertebral compression fracture.

• Urinary Calcium Excretion: A 24-hour urine calcium level greater than 400 mg/day. (Note: some guidelines use different cutoffs, such as >250 mg for women and >350 mg for men). This high level indicates a significant risk for future kidney stone formation.

It’s important to note that even if a patient does not meet any of these formal criteria, a surgical consult can still be offered. If a patient with asymptomatic, mild PHPT is anxious about the condition or wishes to be cured rather than undergo lifelong monitoring, they have the right to explore the surgical option.

The Importance of an Experienced Surgeon

If I could emphasize one point about parathyroid surgery, it would be this: the single most important factor for a successful outcome is the surgeon’s experience. Parathyroid surgery is a delicate, nuanced operation. The glands are tiny, can be located in unusual places (ectopic locations), and can be difficult to distinguish from surrounding fat and thyroid tissue.

A general surgeon who performs this operation only a few times a year may not have the same level of expertise as a dedicated endocrine surgeon or a high-volume parathyroid surgeon who performs hundreds of these cases annually. I learned this lesson early in my career. I was referring patients who I felt were clear surgical candidates to a particular general surgeon. Time and again, he would send them back with a note saying he didn’t think surgery was necessary. After a discussion, he admitted that it simply wasn’t an operation he enjoyed or felt particularly comfortable with. From that point on, I established relationships with surgeons who specialized in this procedure and had a passion for it. These are the meticulous surgeons who are comfortable exploring the neck to find all four glands if necessary, and who have the highest cure rates.

The Surgical Procedure and Its Benefits

Today, if preoperative imaging has successfully pinpointed a single adenoma, most patients can undergo a minimally invasive parathyroidectomy. This involves a small incision (about 1-2 cm) through which the surgeon can directly access and remove the identified adenoma. Often, the surgeon will use an intraoperative PTH assay. This involves measuring the patient’s PTH level just before the operation, and then again 10-15 minutes after the suspected adenoma is removed. A drop of more than 50% from the baseline level confirms that the correct, hypersecreting gland was removed and that no other overactive glands are present. This allows the surgeon to conclude the operation quickly.

If localization studies are negative or suggest multi-gland disease, the surgeon will perform a more traditional four-gland neck exploration, which involves a larger incision and a systematic identification of all four parathyroid glands to determine which ones are abnormal and need to be removed.

The benefits of a successful parathyroidectomy are profound and well-documented:

• Biochemical Cure: Surgery achieves a cure—meaning normalization of calcium and PTH levels—in approximately 98% of patients when performed by an experienced surgeon. It is a very safe and highly effective procedure.
• Improvement in Bone Density: This is the most consistent and dramatic benefit. Following surgery, bone density begins to improve, often significantly, within the first year. This leads to a substantial reduction in future fracture risk.
• Decreased Kidney Stone Risk: By normalizing blood and urine calcium levels, surgery dramatically reduces the risk of forming new kidney stones.
• Stabilization of Renal Function: While surgery cannot reverse existing kidney damage, it can halt the progressive decline in renal function caused by chronic hypercalcemia.
• Improvement in Neurocognitive Symptoms: Many patients report a significant improvement in symptoms like fatigue, “brain fog,” depression, and anxiety after surgery, often describing it as “a cloud lifting.”

Risks are low but important to discuss, including a ~1% risk of permanent hoarseness from recurrent laryngeal nerve injury, a ~5% risk of temporary hoarseness, a ~1 in 300 risk of postoperative bleeding, and a ~4-5% chance of persistent or recurrent disease. In patients with severe skeletal disease, a phenomenon called “hungry bone syndrome” can occur post-op, requiring extensive calcium and vitamin D support.

Medical Management: The Non-Surgical Pathway

What about patients who do not meet the criteria for surgery, are too frail to undergo an operation, or refuse surgery? For these individuals, we have a well-defined pathway for medical management and surveillance. The goals of this approach are twofold: to keep the serum calcium level in a safe range to prevent symptoms of severe hypercalcemia, and to preserve bone density to minimize fracture risk.

Regular Monitoring and Surveillance

Patients managed non-surgically require lifelong follow-up. In my practice, I typically see these patients at least twice a year. The monitoring protocol includes:

• Annual Laboratory Tests: At a minimum, I check a serum calcium and serum creatinine (for eGFR) every year to track for any significant changes.
• Vitamin D Management: I monitor the 25-hydroxyvitamin D level and supplement as needed to maintain a level of at least 20 ng/mL, and preferably above 30 ng/mL. Adequate vitamin D levels can help modestly suppress PTH and are crucial for bone health.
• Bone Density Scans (DEXA): A DEXA scan should be performed every one to two years to monitor for any progressive bone loss that might push the patient toward meeting a surgical indication.

Lifestyle and Dietary Education

Patient education is a cornerstone of medical management. I provide patients with a few key, actionable guidelines:

• Hydration: This is paramount. Dehydration concentrates the blood and can cause a sharp increase in serum calcium levels. I counsel patients to drink plenty of fluids, primarily water, throughout the day to stay well-hydrated. This is a simple, powerful tool for calcium control and stone prevention.
• Encourage Physical Activity: Weight-bearing exercise is one of the best non-pharmacological ways to maintain bone density. Regular activity is strongly encouraged.
• Calcium Intake: This is a frequent source of confusion for patients. It seems counterintuitive, but they should not strictly avoid calcium. Drastically restricting calcium intake can actually stimulate the parathyroid glands even further, worsening the problem. The goal is to maintain a normal, moderate dietary calcium intake, aiming for a total of around 1000-1200 mg per day from food sources. They must avoid concentrated calcium supplements and calcium-fortified antacids like Tums.

Pharmacological Treatment

For patients who opt for medical management but have persistently high or symptomatic calcium levels, we can use medication. This requires vigilant monitoring under the medical direction of Dr. Cardenas.

• Calcimimetics (Cinacalcet/Sensipar): This is the primary medication used to treat hypercalcemia in primary hyperparathyroidism. Cinacalcet is not a cure; it is a treatment. It works by blocking calcium. It binds to the calcium-sensing receptors on the parathyroid glands and tricks them into thinking that calcium levels are higher than they actually are. This causes the glands to reduce PTH secretion, which in turn decreases serum calcium. The starting dose is typically 30 mg twice a day, titrated upwards based on the patient’s calcium response. It is effective at lowering serum calcium but does not appear to have a significant positive effect on bone mineral density.
• Bisphosphonates: If a patient with PHPT also has osteoporosis, they should be treated for the osteoporosis. Medications like alendronate (Fosamax) or zoledronic acid (Reclast) are anti-resorptive agents. They work by inhibiting the osteoclasts, the very cells that PTH stimulates to break down bone. By putting the brakes on bone resorption, bisphosphonates can effectively increase bone mineral density and reduce fracture risk. They can also cause a modest decrease in serum calcium levels. Zoledronic acid, given as an infusion, is particularly useful for acute severe hypercalcemia or for long-term bone protection but requires careful renal monitoring.
• Denosumab: This is an alternative for patients with low GFR. It also requires vigilance for hypocalcemia, particularly in those with vitamin D deficiency.
• Hormone Replacement Therapy (HRT): For postmenopausal women with mild PHPT, estrogen replacement therapy can be a consideration. Estrogen has a protective effect on bone and can help increase bone density and slightly lower serum calcium.

The decision to use these medications is made in collaboration with the patient, weighing the potential benefits against the side effects and costs, and always in the context of our integrated care model with Dr. Cardenas’s medical oversight. Our goal is to create a personalized, sustainable plan that keeps the patient safe, functional, and living well with their condition.

How We Practice Together: MD Medical Direction and Integrative Chiropractic Care

At Injury Medical Clinic PA, our structure is designed for synergy. Dr. Maria Guadalupe Cardenas, as Medical Director, provides the essential internal medicine oversight for diagnostics, medication and infusion therapy management, surgical coordination, and ensuring renal and hepatic safety. I integrate chiropractic care, functional medicine, rehabilitation programming, and education to support the patient’s musculoskeletal efficiency, improve mobility, and assist with symptom relief, whether they are under observation or recovering from surgery.

How Integrative Chiropractic Care Fits into PHPT

• Neuromusculoskeletal Optimization: We use gentle, evidence-informed spinal and extremity mobilization to address compensatory postures and muscle guarding that are often exacerbated by chronic pain or fatigue. Myofascial techniques relieve soft tissue tension that frequently coexists with mineral imbalance-related muscle symptoms.
• Exercise-Based Rehabilitation: We design programs with progressive resistance and balance training tailored to bone health and fall prevention, especially for patients with osteopenia or osteoporosis. Low-impact conditioning helps maintain cardiovascular health and, via hydration and movement, reduces stone risk.
• Functional Medicine Alignment: We assess vitamin D status, dietary calcium adequacy, and hydration behaviors. We also incorporate stress-modulating strategies that can indirectly support autonomic tone and sleep quality.
• Postoperative Support: We guide a gradual return to activity, closely monitoring for hypocalcemic symptoms and coordinating with the medical team on supplementation. We also employ pain management strategies that minimize the burden on the kidneys.

As I’ve shared on my professional platforms like dralexjimenez.com and my LinkedIn profile, patients frequently report marked improvements in subjective energy, sleep, and diffuse musculoskeletal pain following adequate disease control, especially after a surgical cure. Even when quality-of-life surveys show modest average changes, individual patients often experience meaningful gains that accelerate their rehabilitation goals.

Case Study 1: Asymptomatic Male With Elevated PTH, Surgery, and Symptom Insight

A 68-year-old male with a complex cardiac history was referred to me for abnormal calcium. His calcium was 10.8 mg/dL, PTH was elevated (158-190 pg/mL), and his vitamin D was low at 16.3 ng/mL. Though his DEXA scan was normal, his 24-hour urine calcium was high, meeting a criterion for surgery. After localization scans identified a suspicious nodule, he underwent surgery. Intraoperative PTH monitoring confirmed a successful excision of a left superior adenoma, with PTH levels dropping from a baseline of 533 to 42 within 15 minutes.

The outcome was striking. He reported an immediate postoperative improvement in energy and resumed activities like golf that had been limited for years. Interestingly, his PTH remained slightly elevated post-op, despite normal calcium, which can reflect ongoing vitamin D insufficiency or the body’s process of bone remineralization. This case highlights that even “asymptomatic” patients may have subtle limitations they’ve adapted to, and it underscores the need for close postoperative follow-up, including vitamin D repletion and ongoing monitoring. Our integrative support focused on a graded return to activity and thoracic mobility exercises to support his cardiopulmonary health.

Case Study 2: Elderly Female With Severe Hypercalcemia Managed Medically

An 85-year-old female with dementia presented to the emergency room with weakness and confusion, found to have a critically high calcium of 15.8 mg/dL. After an extensive hospital workup ruled out malignancy, the diagnosis was primary hyperparathyroidism. Given her overall frailty, her family declined surgery, opting for medical management under our care.

Her course was challenging, with fluctuating calcium levels that required multiple medication adjustments. We initiated cinacalcet and titrated it up to the maximum dose of 90 mg twice daily. Despite this, she had breakthrough hypercalcemia spikes requiring hospital readmission for IV fluids and infusions of zoledronic acid, which were coordinated through oncology. A key clinical pearl from this case was that her outward appearance was not a reliable indicator of her biochemical severity; vigilant lab monitoring was essential. Our integrative care focused on gentle mobility drills to prevent deconditioning and extensive family education on hydration and recognizing delirium. Her calcium rose. This case is a powerful example of how our team, with Dr. Cardenas’s internal medicine expertise, manages complex, high-risk patients who are not surgical candidates.

Case Study 3: Middle-Aged Male, Foot Pain, and Postoperative Functional Gains

A 57-year-old male pilot came to our clinic with calcium (11.5 mg/dL) and PTH (107-111 pg/mL). His workup revealed a non-obstructing kidney stone, meeting a surgical indication. He also suffered from chronic bilateral foot pain for years. He underwent a successful parathyroidectomy, and by his follow-up visit in August, his labs had normalized.

What was remarkable was his report of a notable improvement in his chronic foot pain, a phenomenon sometimes described by patients as immediate relief upon waking from surgery. While the exact mechanism is unclear, it is thought that Calcium and PTH may reduce micro-inflammation and improve neuromuscular efficiency. This biochemical cure created a window of opportunity for our integrative care. We were able to leverage this pain relief to restore his gait mechanics and load tolerance through targeted foot mobilization, strengthening exercises, and a progressive return to weight-bearing activity, enhancing his functional recovery.

Shared Decision-Making: Helping Patients Choose Between Surgery and Observation

A crucial part of my role is helping patients navigate the choice between surgery and observation. I discuss the evidence showing that observation doesn’t typically worsen quality of life over a decade in truly asymptomatic patients. I also explain the high cure rates and clear benefits of surgery for those who meet the criteria. We use decision aids, like visual checklists of the surgical indications, and focus on the patient’s individual goals. Is their primary concern preventing fractures, or is it regaining the energy to play with their grandchildren? By aligning the evidence with the patient’s lived experience and goals, we can arrive at a decision that feels right for them.

Practical Takeaways You Can Use Today

• An elevated calcium level on routine labs is a call to action. It warrants further testing with a PTH level and a 25-hydroxyvitamin D assessment.
• Surgery is the only definitive cure for primary hyperparathyroidism, but observation is a reasonable, evidence-based strategy when surgical criteria are not met, and symptoms are minimal.
• When surgery is deferred, medications like cinacalcet and bisphosphonates can stabilize calcium and protect bones, but they require vigilant monitoring by a knowledgeable medical team.
• Hydration is a simple, powerful, and non-negotiable tool for managing calcium levels and reducing kidney stone risk.
• Integrative chiropractic care and rehabilitation can meaningfully improve a patient’s functional recovery and quality of life by addressing the musculoskeletal consequences of the disease, especially after surgery.
• Long-term follow-up with labs, imaging, and functional reassessment is the key to keeping patients with PHPT safe and thriving for years to come.

References

1. Anderson, J. L., et al. (2012). Cardiovascular implications of primary hyperparathyroidism. Journal of Clinical Endocrinology & Metabolism.
2. Bilezikian, J. P. (2018). Global differences in primary hyperparathyroidism presentation and management. Journal of Clinical Endocrinology & Metabolism.
3. Bilezikian, J. P., Brandi, M. L., Eastell, R., Silverberg, S. J., Udelsman, R., Marcocci, C., & Potts, Jr., J. T. (2014). Guidelines for the management of asymptomatic primary hyperparathyroidism: summary statement from the Fourth International Workshop. The Journal of Clinical Endocrinology & Metabolism, 99(10), 3561–3569.
4. Curhan, G. C. (2018). Nutritional strategies in kidney stone prevention. The New England Journal of Medicine.
5. Eastell, R., Brandi, M. L., Costa, A. G., D’Amour, P., Shoback, D. M., & Thakker, R. V. (2014). Diagnosis of asymptomatic primary hyperparathyroidism: proceedings of the Fourth International Workshop. The Journal of Clinical Endocrinology & Metabolism, 99(10), 3570–3579.
6. Felsenfeld, A. J., & Levine, B. S. (2015). Evaluation of hypercalcemia: diagnostic approach. The New England Journal of Medicine.
7. Irvin, G. L., et al. (1999). Intraoperative parathyroid hormone monitoring for surgical guidance. The New England Journal of Medicine.
8. Jamal, S. A., et al. (2017). Denosumab use in renal impairment: safety and monitoring. Kidney International.
9. Johnson, N. A., et al. (2017). Imaging in parathyroid disease: ultrasound, sestamibi, and advanced modalities. Radiology.
10. Marcocci, C., Bollerslev, J., D’Amour, P., & Shoback, D. (2008). Medical management of primary hyperparathyroidism: a consensus statement from the 3rd International Workshop on the Management of Asymptomatic Primary Hyperparathyroidism. The Journal of Clinical Endocrinology & Metabolism, 94(2), 333–342.
11. Miniaci-Coxhead, S., et al. (2016). Musculoskeletal manifestations of endocrine disorders: focus on PHPT. Rheumatology.
12. Pallan, S., Rahman, M. O., & Khan, A. A. (2012). Diagnosis and management of primary hyperparathyroidism. BMJ, 344, e1013.
13. Parmar, M. S. (2017). Trends in nephrolithiasis among patients with primary hyperparathyroidism. Kidney International.
14. Peacock, M., Bilezikian, J. P., Bolognese, M. A., Borofsky, M., Scumpia, S., & Sterling, L. R. (2005). Cinacalcet HCl reduces hypercalcemia in primary hyperparathyroidism. The Journal of Clinical Endocrinology & Metabolism, 90(1), 135–141.
15. Rolighed, L., et al. (2014). Vitamin D status influences severity of primary hyperparathyroidism. Endocrine Connections.
16. Roman, S. A., et al. (2011). Quality of life after parathyroidectomy: SF-36 changes and clinical correlates. JAMA Surgery.
17. Rubin, M. R., et al. (2008). Bone mineral density and microarchitecture after parathyroidectomy. The New England Journal of Medicine.
18. Silverberg, S. J., & Bilezikian, J. P. (2017). Primary hyperparathyroidism: clinical manifestations, diagnosis, and evaluation. The New England Journal of Medicine.
19. Silverberg, S. J., Clarke, B. L., Peacock, M., Bandeira, F., Boutroy, S., Cusano, N. E., … & Bilezikian, J. P. (2014). The diagnosis of normocalcemic primary hyperparathyroidism: proceedings of the Fourth International Workshop. The Journal of Clinical Endocrinology & Metabolism, 99(10), 3654-3660.
20. Sosa, J. A., et al. (2013). Postoperative care and complications in parathyroid surgery. JAMA Surgery.
21. Udelsman, R., Åkerström, G., Biagini, C., Duh, Q. Y., Miccoli, P., & Sforza, N. (2014). The surgical management of asymptomatic primary hyperparathyroidism: proceedings of the Fourth International Workshop. The Journal of Clinical Endocrinology & Metabolism, 99(10), 3595–3606.
22. Walker, M. D., & Silverberg, S. J. (2018). Primary hyperparathyroidism. Nature Reviews Endocrinology, 14(2), 115–125.

About Our Team and Contact

• Dr. Maria Guadalupe Cardenas, MD

• • Board Certified in Internal Medicine
  • NPI #1164426749
  • Texas MD License #J2933
  • Medical Director and Collaborative Physician, Injury Medical Clinic PA (Mission Plaza Injury Medical Clinic), El Paso, Texas

• Dr. Alex Jimenez, DC, APRN, FNP-BC, CFMP, IFMCP, ATN, CCST

• • Integrative chiropractic physician and nurse practitioner
  • Focus: neuromusculoskeletal care, functional medicine, rehabilitation, and personal injury care
  • Clinical observations and educational content: dralexjimenez.com and LinkedIn (Dr. Alex Jimenez)

If you have questions about PHPT evaluation, whether surgery is appropriate, or how integrative chiropractic care supports recovery, our team is here to help.

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