Hypoparathyroidism Causes, Symptoms, Diagnosis, Treatment, and More

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What is hypoparathyroidism?

What causes hypoparathyroidism?

What are symptoms of hypoparathyroidism?

Symptoms are different for each person. These are the most common ones:

  • Uncontrollable, painful spasms of your face, hands, arms, and feet
  • A burning or prickling feeling (pins and needles) in your hands and feet, and around your mouth

These symptoms may look like other health problems. Always see your healthcare provider for a diagnosis.

How is hypoparathyroidism diagnosed?

How is hypoparathyroidism treated?

Your health care provider will figure out the best treatment for you based on:

  • How old you are
  • Your overall health and past health
  • How sick you are
  • How well you can handle specific medicines, procedures, or therapies
  • How long the condition is expected to last
  • Your opinion or preference

An IV (intravenous) infusion of calcium may be able to ease your symptoms right away. You may also need to take calcium and vitamin D pills every day.

When should I call my healthcare provider?

Key points about hypoparathyroidism

  • Hypoparathyroidism happens when 1 or more of your parathyroid glands are not active enough. They don’t make enough parathyroid hormone. This lowers the level of calcium in your blood.
  • The most common cause is injury to or removal of all 4 parathyroid glands. That can accidentally happen during surgery to remove the thyroid.
  • Symptoms may include painful spasms of your face, hands, arms, and feet. They may also include a burning or prickling feeling in your hands and feet, and around your mouth.
  • Blood tests can spot low levels of calcium and parathyroid hormones.
  • An IV (intravenous) infusion of calcium may be able to ease your symptoms right away. You may also need to take calcium and vitamin D pills every day.

Next steps

Tips to help you get the most from a visit to your healthcare provider:

  • Know the reason for your visit and what you want to happen.
  • Before your visit, write down questions you want answered.
  • Bring someone with you to help you ask questions and remember what your provider tells you.
  • At the visit, write down the name of a new diagnosis, and any new medicines, treatments, or tests. Also write down any new instructions your provider gives you.
  • Know why a new medicine or treatment is prescribed, and how it will help you. Also know what the side effects are.
  • Ask if your condition can be treated in other ways.
  • Know why a test or procedure is recommended and what the results could mean.
  • Know what to expect if you do not take the medicine or have the test or procedure.
  • If you have a follow-up appointment, write down the date, time, and purpose for that visit.
  • Know how you can contact your provider if you have questions.

What Is Hypoparathyroidism?

Your Guide To

What Is Hypoparathyroidism?

What Is Hypoparathyroidism?

What Is Hypoparathyroidism?

  • What Is Hypoparathyroidism?
  • Causes
  • Symptoms
  • Getting a Diagnosis
  • Questions to Ask Your Doctor
  • Treatment
  • Taking Care of Yourself
  • What to Expect
  • Getting Support

What Is Hypoparathyroidism?

Your neck has fourВ pea-sized glands called the parathyroid glands. Hyperparathyroidism happens when they don’t make enough parathyroid hormone (PTH), are surgically removed, are damagedВ or when your body is resistant to that hormone. PTH controls the blood level of important vitamins and minerals such as vitamin D and calcium.

You may also have hypoparathyroidism because you have another condition that affects how much PTH is in your body, such as a low magnesium level.

Your body uses calcium to keep your nerves, muscles, and heart working. Low levels of calcium can result in symptoms ranging from mild to severe muscle spasms, tingling, heart problems, and seizures. The good news is you can treat the condition.

Treatment mostly means making sure your body has enough calcium and vitamin D, which you can do by eating a balanced diet, taking supplements, and keeping an eye on blood levels. If you stick with your treatment plan and see your doctor regularly, you can lead a full, active life with hypoparathyroidism.

Causes

Several things can trigger hypoparathyroidism. They include:

  • Injury or removal of the glands during surgery
  • Autoimmune diseases
  • Radiation therapy to your neck or head
  • Low levels of magnesium
  • Genetic disorders

Symptoms

Some of the symptoms of low blood calcium are:

  • Muscle cramps or spasms in your legs, feet, lower back, or face
  • Tingling in your fingers, toes, or lips
  • Anxiety and depression
  • Heart failure
  • An irregular heartbeat
  • Low blood pressure
  • Seizures
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Low calcium in the long term can lead to:

  • Cataracts
  • Dental problems
  • Movement disorders like tremors
  • Hair loss and brittle nails

Getting a Diagnosis

Your doctor will test your blood and your urine for calcium, PTH, phosphorus, and magnesium.

Questions to Ask Your Doctor

  • What caused my hypoparathyroidism?
  • Do I need any more tests?
  • How often will I need to see a doctor?
  • What kind of treatments can help? Which do you recommend?
  • How can I keep my calcium levels normal?
  • What kind of lifestyle changes do I need to make?
  • Will it ever go away?
  • Will my children get hypoparathyroidism?

If your child has the disease, ask her doctor how you can make sure she gets the nutrients she needs to grow.

Continued

Treatment

Calcium and vitamin D supplements can keep hypoparathyroidism in check. A healthy diet helps, too. Your doctor may tell you to:

  • Limit foods with phosphates, like soda and other fizzy drinks. These can pull calcium from your bones.
  • Eat foods high in calcium such as low-fat dairy products, dark green vegetables like collard greens and kale, and foods with added calcium like some cereals and orange juices.

A dietitian can help you plan meals to keep you or your child healthy. Your child’s doctor will check her regularly to see that her growth is on track.

If normal calcium levels in your body are hard to maintain, you may need to get an injection of PTH. Once your calcium levels are normal again, you can go back to your regular treatment.

Taking Care of Yourself

You can take steps to make living with hypoparathyroidism easier.

  • Take calcium supplements with food. They’re more easily absorbed that way.
  • Drink plenty of water every day. That makes it easier for your body to digest vitamins and minerals.
  • See your dentist regularly. Too little calcium can hurt your teeth.

What to Expect

As long as you get enough calcium and vitamin D and have your blood checked regularly, you should be able to keep your hypoparathyroidism under control. If you don’t take your daily supplement and watch your diet, the condition can be dangerous.

Getting Support

For more information, visit the web site of the Hypoparathyroidism Association.

Sources

Hormone Health Network: «Hypoparathyroidism.»

Hypopara UK: «Hypoparathyroidism.»

Hypoparathyroidism Association: «A Quick Guide to Understanding Hypoparathyroidism.»

National Osteoporosis Foundation: «A Guide to Calcium-Rich Foods.»

NIH Office of Rare Disease Research: «Hypoparathyroidism.»

Parathyroid Diseases: Hyperparathyroidism and Hypoparathyroidism

Table of Contents

Image: “Intermediate magnification micrograph of the parathyroid gland” by Nephron. License: CC BY 3.0

Function of the Parathyroid Hormone

Image: The role of parathyroid hormone in maintaining blood calcium Homeostasis. By OpenStax College, License: CC BY 3.0

The parathyroid hormone is synthesized by the parathyroid gland as a polypeptide consisting of 84 amino acids, with a relatively short half-life of approx. 5 min. Its effects on kidneys and bones are mediated via stimulation of the adenylyl cyclase.

In the kidneys, the parathyroid hormone increases the secretion of phosphate and the resorption of calcium. The decreased phosphate levels stimulate the renal 1-α-hydroxylase to increase the synthesis of the biologically active form of vitamin D (calcitriol). Calcitriol, in turn, stimulates enteral calcium resorption.

The effect on the bone is mediated via activation of the osteoclasts, which is indirectly caused by activation of the osteoblasts expressing the PTH receptor. This activation releases more calcium from the bones, which does not lead to a negative calcium balance in the bone if PTH concentration is physiologically elevated.

The secretion of the parathyroid hormone thus leads to increased calcium levels, and higher concentrations are released at lower levels of calcium ( Hyperparathyroidism

Pathologically elevated PTH levels are summarized under the term hyperparathyroidism. Depending on the pathogenesis, primary, secondary, and tertiary forms of hyperparathyroidism are distinguished.

Primary Hyperparathyroidism

Definition of primary hyperparathyroidism

Primary hyperparathyroidism directly affects the parathyroid glands, resulting in elevated PTH levels.

Etiology of primary hyperparathyroidism

The most frequent cause of primary hyperparathyroidism include adenomas of the parathyroid gland (approx. 85%). In most cases, a solitary adenoma is involved. Multiple adenomas are significantly rare. Approx. 15% of all cases of primary hyperparathyroidism are caused by hyperplasia of the parathyroid glands.

Malignant diseases of the epithelial cells very rarely contribute to primary hyperparathyroidism (less than 1%). Multiple endocrine neoplasia (MEN) is another rare cause.

Image: Parathyroid adenoma. B y THWZ, License: CC BY 3.0

Pathophysiology of primary hyperparathyroidism

Due to the effect of PTH on the target structures including kidneys and bones (see above), elevated PTH levels increase the calcium levels as well as decrease the serum phosphate levels.

Clinical signs of primary hyperparathyroidism

More than 50% of patients with primary hyperparathyroidism are asymptomatic or only exhibit non-specific symptoms.

Clinical manifestations of primary hyperparathyroidism are typically restricted to kidneys, bones, and the gastrointestinal tract. Therefore, the classic triad of symptoms is also summarized as ‘stones, bones, and abdominal groans’.

Nephrolithiasis is the most common renal manifestation of primary hyperparathyroidism, resulting in the formation of calcium phosphate or calcium oxalate stones. Occasionally, it results in nephrocalcinosis with a highly unfavorable prognosis.

Image: Brown tumors of the hands in a patient with hyperparathyroidism. By Frank Gaillard, License: CC BY 3.0

The increased osteoclast activity and the resulting increased calcium release leads to osteopenia and subperiosteal resorption lacunae as well as osteolysis of hands and feet. In part, this pathophysiology may lead to bleeding into the resorption cysts, which are then referred to as ‘brown tumors’ (osteitis fibrosa cystica, osteodystrophy cystica generalisata, or von Recklinghausen’s disease).

A range of non-specific gastrointestinal symptoms may include obstipation, meteorism, nausea, loss of appetite, and weight loss. Other more uncommon manifestations include ulcera ventriculi and duodeni as well as pancreatitis.

Aside from the three primary manifestations of primary hyperparathyroidism, increased calcium levels may lead to neuromuscular as well as psychiatric symptoms. The neuromuscular symptoms include general muscle weakness, rapid muscle fatigue as well as changes in ECG readings, i.e., shortened QT time.

Depression is the most common psychiatric manifestation.

Diagnosis of primary hyperparathyroidism

Laboratory diagnosis should be specifically highlighted. According to the definition, hyperparathyroidism is accompanied by elevated PTH values. In addition, elevated serum calcium levels (> 2.6 mmoL/L) are found.

However, kidney function, as well as serum protein content (especially albumin), influence the serum calcium levels.

In a few cases, primary hyperparathyroidism may occur despite normal serum calcium levels, for instance, in patients diagnosed with concomitant deficiency of vitamin D (especially in the winter months) and albumin as well as kidney insufficiency.

Other laboratory parameters, which may point toward primary hyperparathyroidism, are lower serum phosphate concentrations as well as an increase in alkaline phosphatase. The secretion of hydroxyproline and phosphate in urine may be increased as well.

The increased secretion of hydroxyproline is attributed to increased bone turnover comparable to increased serum alkaline phosphatase, whereas the phosphate content in urine is increased due to the phosphaturic effect of PTH.

Imaging modalities such as sonography, CT, MRT as well as 99mTc-MIBI (metoxyisobutylisonitrile scintigraphy) may be used to detect localized changes.

Image: Parathyroid adenoma in sonography. Well-defined, rounded to the ovoid formation (arrow ) next to the thyroid lobes (blue border). By Hellerhoff, License: CC BY 3.0

Differential diagnoses (DD) of primary hyperparathyroidism

The differential diagnoses associated with primary hyperparathyroidism include diseases involving increased serum calcium levels.

The most common cause of hypercalcemia is hypercalcemia caused by tumors. However, they may lead to hypercalcemia due to osteolysis caused by bone metastases and ectopic PTH secretion, i.e., in cases of bronchial carcinoma.

Other causes include increased vitamin D levels, i.e., due to intoxication or sarcoidosis.

Treatment of primary hyperparathyroidism

Basically, 2 treatment options are available: surgical and conservative.

Surgery is indicated in case of symptomatic primary hyperparathyroidism as well as certain constellations associated with asymptomatic primary hyperparathyroidism, for instance, impaired kidney function (increased creatinine levels), reduced bone density, serum calcium levels greater than 0.25 mmol/L above normal levels as well as age above 50 years.

During surgery, the solitary adenoma is removed; however, in the case of hyperplasia of the epithelial cells, a total parathyroidectomy with simultaneous transplantation of the remains of the parathyroid tissue into the forearm is performed. The transplantation of the remaining tissue into the brachialis muscle (m. brachioradialis) facilitates easy surgical access, as needed.

The short half-life of PTH ensures a successful surgical outcome, with levels decreased by approx. 50% compared with the initial stage. In the days following surgery, the calcium levels, in particular, must be closely monitored for signs of hypocalcemia, for instance, Chvostek’s and Trousseau’s signs.

If surgery is contraindicated, conservative therapy is initiated using symptomatic measures such as sufficient fluid intake or osteoporosis prophylaxis with bisphosphonates in postmenopausal women.

Complications with primary hyperparathyroidism

The hypercalcemic crisis is a complication of primary hyperparathyroidism. However, it is relatively rare with less than 5% incidence. Symptoms of the hypercalcemic crisis include polyuria and polydipsia, vomiting, nausea as well as the loss of consciousness, somnolence, and even coma.

Secondary Hyperparathyroidism

Definition of secondary hyperparathyroidism

The increased PTH levels in secondary hyperparathyroidism are not caused by the parathyroid glands.

Etiology of secondary hyperparathyroidism

Renal secondary hyperparathyroidism can be grossly distinguished from hyperparathyroidism with normal kidney function.

Pathophysiology of secondary hyperparathyroidism

The pathophysiology of renal secondary hyperparathyroidism is based on diminished calcitriol synthesis due to renal insufficiency. The low calcitriol levels, in turn, have a stimulating effect on PTH secretion. However, in cases of renal insufficiency, calcium resorption and phosphate secretion are inhibited. Both factors also induce PTH release.

Non-renal causes include decreased enteral calcium resorption as well as increased incidence of hepatic diseases such as liver cirrhosis, which also impairs vitamin D synthesis. The lack of UV light also impairs vitamin D synthesis.

Clinical signs of secondary hyperparathyroidism

Treatment is targeted at the underlying diseases contributing to secondary hyperparathyroidism.

Diagnosis of secondary hyperparathyroidism

In contrast to primary hyperparathyroidism, the serum calcium levels are lower and the serum phosphate levels are usually normal in secondary hyperparathyroidism. In cases of impaired kidney function, the serum phosphate levels are partially elevated as the phosphate secretion is impaired. Subsequently, the PTH levels are also elevated.

Treatment of secondary hyperparathyroidism

Treatment is tailored and individualized depending on the underlying disease, supported by calcitriol or calcium substitution.

Tertiary Hyperparathyroidism

Tertiary hyperparathyroidism develops from secondary hyperthyroidism. Thus, secondary hyperparathyroidism can lead to hyperplasia of the epithelial cells and subsequent decrease in PTH secretion.

Therapy entails the surgical removal of hyperplastic epithelial cells.

Hypoparathyroidism

Definition of hypoparathyroidism

In the case of hypoparathyroidism, the PTH levels are reduced due to the poor function of the parathyroid glands.

Etiology of hypoparathyroidism

The cause of hypoparathyroidism is most commonly iatrogenic following neck surgery. Thyroidectomy can cause hypoparathyroidism, which is why calcium levels should always be closely monitored following such surgeries.

Idiopathic hypoparathyroidism or aplasia of the parathyroid glands is rare, i.e., in cases of DiGeorge syndrome.

Pathophysiology of hypoparathyroidism

PTH deficiency results in low levels of serum calcium as well as elevated phosphate levels.

Clinical signs of hypoparathyroidism

Calcium deficiency and the resulting increase in neuromuscular excitability may manifest as a series of neuromuscular symptoms including hypocalcemic tetany, which is characterized by muscle cramps, muscle spasms in hands (claw) or paresthesia. For instance, abdominal pains may be triggered by contractions of the visceral musculature in the gastrointestinal tract.

Other clinical signs for hypocalcemia are Chvostek’s and Trousseau’s signs. In the case of positive Chvostek’s sign, tapping on the facial nerve (m. facialis) in the area of the cheek results in the twitching of the oral musculature.

Image: Trousseau sign . By Huckfinne, License: Public Domain

In case of positive Trousseau’s sign, however, a couple of minutes after the application of blood pressure cuff and inflation to a pressure greater than the systolic pressure, muscle spasms of the hand are induced, the so-called claw. Here, the thumb is withdrawn into the palm.

Prolongation of the QT interval (electrocardiogram) is another neuromuscular sign of hypoparathyroidism.

Aside from neuromuscular signs and symptoms, psychiatric changes such as depression, psychotic disorder or dementia may occur as well. These symptoms are attributed to calcification of the basal ganglia (Fahr’s syndrome), which occurs in approx. 50% of patients diagnosed with hypoparathyroidism.

Image: Fahr’s disease in computer tomography . By Hellerhoff, License: CC BY 3.0

Other organic changes are, for instance, disturbances in hair and nail growth as well as tetanic cataracts, which lead to paradoxical intraocular lens calcification, probably resulting from fluctuating hyperphosphatemia with simultaneous low calcium levels.

The calcifications in cases of Fahr’s syndrome are also paradox calcifications.

Hypoparathyroidism can also trigger osteosclerosis and osteoporosis, suggesting that the overall bone-related findings are not conducive to a diagnosis of hypoparathyroidism.

Diagnosis of hypoparathyroidism

A diagnosis of hypoparathyroidism is based on the measurement of calcium and phosphate levels in serum as well as in urine. In addition to low serum PTH, the serum levels of calcium are low and the serum phosphate levels are elevated whereas the levels of both calcium and phosphate in urine are low.

Differential diagnoses (DD) of hypoparathyroidism

The differential diagnoses of hypoparathyroidism include diseases with comparable laboratory parameters, i.e., low calcium levels and/or elevated serum phosphate levels as well as diseases with similar clinical symptoms.

Possible causes of low calcium levels with physiological PTH levels are, for instance, malabsorption syndrome, acute pancreatitis (see above) as well as kidney insufficiency.

However, low levels of calcium, as well as serum PTH, are detected in pseudohypoparathyroidism, which is very rare. Pseudohypoparathyroidism can be divided into several subtypes (type 1a, 1b, 1c, and type 2) and often occurs in familial clusters. Clinical signs typically include short bones in the hand and feet in pseudohypoparathyroidism type 1a.

The symptoms of pseudohypoparathyroidism are attributed to abnormal PTH receptor or subsequent signaling cascade.

Differential diagnosis of hypoparathyroidism includes decreased levels of ionized calcium in cases of alkalosis, which can also lead to clinical manifestations of tetany despite normal serum calcium levels. Alkalosis represents the most common cause of tetany, and respiratory alkalosis involves acid-base imbalance caused by alveolar hyperventilation.

Treatment of hypoparathyroidism

Treatment of long-term hypoparathyroidism involves substituting vitamin D and calcium, and monitoring of serum calcium levels on a regular basis in order to prevent hypercalcemia and nephrocalcinosis. Additional phosphate binders may be indicated if the serum phosphate levels do not decline adequately during therapy.

Tetany is an indication for intravenous injection of 10% calcium glucose. Patients undergoing digitalis treatment may not absorb intravenous calcium due to the synergistic effect between calcium and digitalis, which must be ruled out before administration.

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