What you should know about otosclerosis

What Is Otosclerosis?

The term otosclerosis is derived from the Greek words for “hard” (scler-o) and “ear” (oto). It describes a condition of abnormal growth in the tiny bones of the middle ear which leads to a fixation of the stapes bone. The stapes bone must move freely for the ear to work properly and hear well.

Hearing is a complex process. In a normal ear sound vibrations are funneled by the outer ear into the ear canal where they hit the ear drum. These vibrations cause movement of the ear drum that transfers to the three small bones of the middle ear the malleus (hammer) incus (anvil) and stapes (stirrup). When the stapes bone moves it sets the inner ear fluids in motion which in turn start the process to stimulate the auditory (hearing) nerve. The hearing nerve then carries sound energy to the brain resulting in hearing of sound. When any part of this process is compromised hearing is impaired.

Who Gets Otosclerosis And Why?

It is estimated that ten percent of the adult Caucasian population is affected by otosclerosis. The condition is less common in people of Japanese and South American decent and is rare in African Americans. Overall Caucasian middle-aged women are most at risk.

The hallmark symptom of otosclerosis slowly progressing hearing loss can begin anytime between the ages of 15 and 45 but it usually starts in the early 20’s. The disease can develop in both women and men but is particularly troublesome for pregnant women who for unknown reasons often experience a rapid decrease in hearing ability.

Approximately 60 percent of otosclerosis cases are genetic in origin. On average a person who has one parent with otosclerosis has a 25 percent chance of developing the disorder. If both parents have otosclerosis the risk goes up to 50 percent.

Symptoms Of Otosclerosis

Gradual hearing loss is the most frequent symptom of otosclerosis. Often individuals with otosclerosis will first notice that they cannot hear low-pitched sounds or whispers. Other symptoms of the disorder can include dizziness balance problems or a sensation of ringing roaring buzzing or hissing in the ears or head known as tinnitus.

How Is Otosclerosis Diagnosed?

Because many of the symptoms typical of otosclerosis can also be caused by other medical conditions it is important to be examined by an otolaryngologist (ear nose and throat doctor) to eliminate other possible causes of the symptoms. After an ear exam the otolaryngologist may order a hearing test. Based on the results of this test and the exam findings the otolaryngologist will suggest treatment options.

Treatment For Otosclerosis

If the hearing loss is mild the otolaryngologist may suggest continued observation and a hearing aid to amplify the sound reaching the ear drum. Sodium fluoride has been found to slow the progression of the disease and may also be prescribed. In most cases of otosclerosis a surgical procedure called stapedectomy is the most effective method of restoring or improving hearing.

What Is A Stapedectomy?

A stapedectomy is an outpatient surgical procedure done under local or general anesthesia through the ear canal with an operating microscope. (No outer incisions are made.) It involves removing the immobilized stapes bone and replacing it with a prosthetic device. The prosthetic device allows the bones of the middle ear to resume movement which stimulates fluid in the inner ear and improves or restores hearing.

Modern-day stapedectomies have been performed since 1956 with a success rate of 90 percent. In rare cases (about one percent of surgeries) the procedure may worsen hearing.

Otosclerosis affects both ears in eight out of ten patients. For these patients ears are operated on one at a time; the worst hearing ear first.

What Should I Expect After A Stapedectomy?

Most patients return home the evening after surgery and are told to lie quietly on the un-operated ear. Oral antibiotics may be prescribed by the otolaryngologist. Some patients experience dizziness the first few days after surgery. Taste sensation may also be altered for several weeks or months following surgery but usually returns to normal.

Following surgery patients may be asked to refrain from nose blowing swimming or other activities that may get water in the operated ear. Normal activities (including air travel) are usually resumed two weeks after surgery.

Notify your otolaryngologist immediately if any of the following occurs:

  • Sudden hearing loss

  • Intense pain

  • Prolonged or intense dizziness

  • Any new symptom related to the operated ear

Since packing is placed in the ear at the time of surgery hearing improvement will not be noticed until it is removed about a week after surgery. The ear drum will heal quickly generally reaching the maximum level of improvement within two weeks.

Nose Bleed (Epistaxis) Regimen

  1. Nose bleeds occur after the mucus membrane (skin) of the nose is disrupted. Because the blood vessels of the nose are right beneath the surface bleeding occurs.
  2. Aspirin and ibuprofen (Motrin/Advil) should be avoided as they can cause bleeding.
  3. Dryness in the nose can cause bleeding. The best way to stop bleeding in the nose is to prevent the nose from getting dry. Saline spray should be used 3 puffs in each nostril 4 times a day. Bacitracin on a Q-tip should be gently place in the nose (wherever you can comfortably reach) three to four times a day. If you have a humidifier this should be used in the bedroom at night.
  4. If you have high blood pressure this can also promote bleeding from the nose. You should consult your internist regarding your blood pressure if this has not been checked or it is not completely under control Diabetes and arteriosclerosis can also predispose you to nose bleeds.
  5. If your nose is actively bleeding you should take Afrin (you can buy this without a prescription) and soak two pieces of cotton with this. Then place the cotton in each nostril and pinch the front of your nose for five minutes without letting up the pressure. Do not use Afrin on a daily basis use it only if there is actual bleeding. If after doing this your nose still bleeds you should go to the nearest emergency room so that your nose can be packed. If the emergency room doctor has difficulty they will then call our office.
  6. Packing will usually stay in the nose for 48 hours. Cauterization of the nose is sometimes necessary in addition to the packing. If your nose bleed is especially difficult to stop a posterior balloon packing may be placed you will have to remain in the hospital if this is used.

Noise Induced Hearing Loss

What is noise-induced hearing loss?

Every day we experience sound in our environment such as the sounds from television and radio household appliances and traffic. Normally these sounds are at safe levels that don’t damage our hearing. However when we’re exposed to harmful noise—sounds that are too loud or loud sounds that last a long time—sensitive structures in our inner ear can be damaged causing noise-induced hearing loss (NIHL).

What causes NIHL?

NIHL can be caused by a one-time exposure to an intense “impulse” sound such as an explosion or by continuous exposure to loud sounds over an extended period of time such as noise generated in a woodworking shop.

Sound is measured in units called decibels. Sounds of less than 75 decibels even after long exposure are unlikely to cause hearing loss. However long or repeated exposure to sounds at or above 85 decibels can cause hearing loss. The louder the sound the shorter the amount of time it takes for NIHL to happen.

Here are the average decibel ratings of some familiar things:

  • The humming of a refrigerator45 decibels

  • Normal conversation60 decibels

  • Noise from heavy city traffic85 decibels

  • Motorcyles95 decibels

  • An MP3 player at maximum volume105 decibels

  • Sirens120 decibels

  • Firecrackers and firearms150 decibels

Although being aware of decibel levels is important to help us protect our hearing how far away we are from the source and how long we are exposed to the sound are equally important. A good rule of thumb is to avoid noises that are too loud too close or last too long.

Who is affected by NIHL?

People of all ages including children teens young adults and older people can develop NIHL. Approximately 15 percent of Americans between the ages of 20 and 69—or 26 million Americans—have hearing loss that may have been caused by exposure to loud sounds or noise at work or in leisure activities. Recreational activities that can put someone at risk for NIHL include target shooting and hunting snowmobile riding listening to MP3 players at high volume through earbuds or headphones playing in a band and attending loud concerts. Harmful noises at home may come from lawnmowers leaf blowers and shop or woodworking tools.

How can noise damage our hearing? 

To understand how loud noises can damage our hearing we have to understand how we hear. Hearing depends on a series of events that change sound waves in the air into electrical signals. Our auditory nerve then carries these signals to the brain through a complex series of steps.

  1. Sound waves enter the outer ear and travel through a narrow passageway called the ear canal which leads to the eardrum.

  2. The eardrum vibrates from the incoming sound waves and sends these vibrations to three tiny bones in the middle ear. These bones are called the malleus incus and stapes.

  3. The bones in the middle ear couple the sound vibrations from the air to fluid vibrations in the cochlea of the inner ear which is shaped like a snail and filled with fluid.  An elastic partition runs from the beginning to the end of the cochlea splitting it into an upper and lower part. This partition is called the basilar membrane because it serves as the base or ground floor on which key hearing structures sit.

  4. Once the vibrations cause the fluid inside the cochlea to ripple a traveling wave forms along the basilar membrane. Hair cells—sensory cells sitting on top of the basilar membrane—ride the wave.

  5. As the hair cells move up and down microscopic hair-like projections (known as stereocilia) that perch on top of the hair cells bump against an overlying structure and bend. Bending causes pore-like channels which are at the tips of the stereocilia to open up. When that happens chemicals rush into the cell creating an electrical signal.

  6. The auditory nerve carries this electrical signal to the brain which translates it into a “sound” that we recognize and understand.

Most NIHL is caused by the damage and eventual death of these hair cells. Unlike bird and amphibian hair cells human hair cells don’t grow back. They are gone for good.

What are the effects and symptoms of NIHL?

When we’re exposed to loud noise over a long period of time we gradually start to lose our hearing. Over time the sounds we hear may become distorted or muffled and it may be difficult to understand other people when they talk. If you have NIHL you might not even be aware of it but it can be detected with a hearing test.

NIHL can also be caused by extremely loud bursts of sound such as gunshots or explosions which can rupture the eardrum or damage the bones in the middle ear. This kind of NIHL could result in immediate hearing loss that may be permanent.

Loud noise exposure can also cause tinnitus—a ringing buzzing or roaring in the ears or head. Tinnitus may subside over time but can sometimes be permanent continuing constantly or occasionally throughout a person’s life.  Hearing loss and tinnitus can occur in one or both ears.

Sometimes exposure to impulse and continuous loud noise causes a temporary hearing loss which disappears 16 to 48 hours later. Recent research suggests however that although the loss of hearing seems to disappear there may be residual long-term damage to your hearing.

Can NIHL be prevented?

NIHL is the only type of hearing loss that is completely preventable. If you understand the hazards of noise and how to practice good hearing health you can protect your hearing for life. Here’s how:

  • Know which noises can cause damage (those at or above 85 decibels).

  • Wear earplugs or other protective devices when involved in a loud activity (activity-specific earplugs and earmuffs are available at hardware and sporting goods stores).

  • Be alert to hazardous noises in the environment.

  • Protect the ears of children who are too young to protect their own.

  • Make family friends and colleagues aware of the hazards of noise.

  • Have your hearing tested if you think you might have hearing loss.  

What research is being done about NIHL?

The National Institute on Deafness and Other Communication Disorders (NIDCD) supports research on the causes diagnosis treatment and prevention of hearing loss. NIDCD-supported researchers have helped to identify some of the many genes important for hair cell development and function and are using this knowledge to explore new treatments for hearing loss.

NIDCD-supported researchers also are investigating potential ways to prevent NIHL after noise exposure. Noise exposure triggers the formation of destructive molecules called free radicals which can cause hair cell death. Researchers are now testing the ability of nutrients such as vitamins and minerals to prevent the damage caused by free radicals and to determine if there is a window of opportunity in which it is possible to rescue hearing from noise trauma or prevent the damage. Researchers are also looking at the protective properties of supporting cells in the inner ear which appear to be capable of lessening the damage to sensory hair cells upon exposure to noise.

Nasal Vestibulitis

Nasal vestibulitis is caused by infection with the bacteria staphylococcus (the same organism that causes strep throat) in the area just inside the nostrils otherwise known as the nasal vestibule.

Typical symptoms are swelling redness tenderness pimples around nasal hairs or crusting.

In most cases simple application of Bacitracin ointment and hot washcloths or a course of antibiotics are sufficient to treat the infection. Occasionally though infections can cause boils spread beneath the skin (cellulitis) and rarely spread through facial veins to the brain in a potentially fatal condition called cavernous sinus thrombosis. For this reason infections that persist should be examined by a physician.

Laboratory, Radiology and Hospital Charges

Radiology and Hospital Charges Due to the requirements of some insurance companies or the nature of certain laboratory studies your lab tests may be sent from our office to a reference laboratory. Reference laboratories are independent of our practice and will bill separately for their services. For all laboratory radiology and hospital charges it is the patient's responsibility to determine if these providers are covered by your individual plan. Most will bill your insurance directly. If you have questions about bills and cannot resolve them with insurance company or other provider directly please talk to a member of our billing staff.

Instructions for Nasal Surgery

Before Surgery:

  1. No Aspirin or Vitamin E two weeks before surgery. Do not eat or drink after midnight prior to surgery.
  2. No make-up and arrange for a ride home after surgery. Under no circumstances will you be allowed to drive back by yourself.

After Surgery:

  1. Bed rest with head elevated for two days following surgery. Sleep with head elevated on two pillows for five days following surgery. No heavy lifting or bending for two weeks.
  2. Cold compresses over eyes for the first 48 hours following surgery to reduce swelling. Take pain medicine and/or antibiotics as prescribed.
  3. Bathing may be resumed three days postoperatively but if there is splint or cast it must not get wet.
  4. The day after surgery a soft normal diet may be resumed.
  5. It is extremely important that the inside of your nose is moist and humidified after nasal surgery to prevent crusting and recurrent symptoms. If you have a humidifier it should be used. Saline nasal spray (Ocean/Ayr) should be used three times a day to continually keep the inside of your nose moist. After sinus surgery: a steam inhaler should be purchased at a local pharmacy and used three times daily. Alternatively the nose can be washed out with a water-pik set at the low setting with 8 oz. of water with one tablespoon of salt and a tablespoon of baking soda. Alternatively the nose can be irrigated out as directed on the accompanying sheet. It is normal for the mouth to be dry after surgery. You may rinse with mouthwash or salt water as needed.
  6. Replace the nasal dressing (over the lip) as necessary. Blood tinged drainage is to be expected the first 48 hours. Should there be a significant amount of bright red blood remain calm and call our office or the emergency room immediately. If the phone is answered by the answering service the doctor will be notified immediately. Should there be any problem or difficulty with contacting the doctor report to the emergency room. The emergency room physician will have to see you in this situation and contact the covering surgeon as necessary.
  7. Do not try breathing through your nose when it is packed as it may displace the packing into your throat.
  8. Sneeze and blow your nose gently.
  9. If packing remains in your nose after surgery make an appointment to see Dr. Gordon the following day in the office for packing removal. Take your pain medication after you arrive at the office to ease the discomfort of the packing removal. Otherwise make an appointment for 1-2 weeks following surgery.
  10. After packing removal the nostrils may be cleaned periodically with Q-tips soaked in hydrogen peroxide and then coated lightly with Vaseline or Antibiotic ointment.
  11. Do not tamper with the cast on your nose (if you have one). It will be removed 6-8 days after your surgery. The morning it is to be removed take a warm shower and get the cast wet. This will make removing the cast easier.
  12. Do not judge the result too soon. Swelling persists for six weeks and the healing process goes on for six months. Avoid contact sports for at least three months if your surgery was rhinoplasty or nasal fracture surgery.

Instructions For Collection Of Second Voided Urin

You will be collecting a “spot urine” specimen specifically the second urine you void in the morning. Here are the specific instructions:

  1. The first urine you void in the morning (i.e. when you first get out of bed) should be discarded.
  2. Collect the sample the next time you urinate. You do not need to collect the entire specimen: 2-3 ounces(about 1/3 cup)is adequate. Store it in a clean dry bottle made of clear plastic or glass(a soft drink or snapple bottle is fine) until you bring it to the lab.
  3. Keep the specimen in the refrigerator if more than several hours will elapse prior to submitting it.
  4. If you take supplements such as Glucosamine chondroitin or “shark cartilage” please STOP taking these at least 3 DAYS before you collect your urine for this test.

Instructions For Collecting A 24hr Urine Specimen

  1. This specimen can be collected up to one week before submission to the laboratory. -Be sure to CONTINUE ALL YOUR CALCIUM SUPPLEMENTS vitamins and dietary calcium to ensure that this collection properly reflects your calcium intake(unless your physician has given you speciifc instructions to do otherwise).
  2. On the morning of the collection day rise at your usual time and discard the first urine(this urine is from the night before). Start the collection from this point on.
  3. Collect all the urine you make through the day and night. End the collection with the first morning urine of the following day when you wake up.
  4. Store the urine in a clean plastic bottle of at least 2 liters or a half-gallon in volume. A mineral water bottle is satisfactory. DO NOT USE AN EMPTY MILK CONTAINER. -Most labs prefer that you use their bottle for collection(therefore you may want to visit a QUEST LAB center to pick up a specimen bottle to ensure lab results( call 1-800-631-1390 to locate a center near you; for LABCORP call: 1-888-522-2677). Request two bottles if you drink 8 or more cups of fluid a day). 
  5. Please label the container with your name and the doctor's name. When complete refrigerate the specimen until you bring it into the lab particularly if more than one day will elapse. the specimen will keep for approximately one week.


Hypercalcemia is a relatively common clinical problem. It typically manifests as a mild chronic calcium level elevation although hypercalcemic emergencies do exist. Calcium homeostasis is tightly regulated and hypercalcemia can affect almost every organ system in the body.


Usually hypercalcemia is reported as elevation of total plasma calcium levels rather than ionized calcium levels. Approximately 50% of total calcium is protein bound and the total calcium level will vary with protein-binding capacity. This phenomenon may rarely result in pseudohypercalcemia—for example in patients with hyperalbuminemia secondary to dehydration and in some patients with multiple myeloma. More commonly lowering of total calcium levels is observed in patients with low levels of binding proteins (hypoalbuminemia). This physiology requires that the total plasma calcium level be corrected for the albumin level. Normal calcium levels may range from 8.5 to 10.5 mg/day assuming an albumin level of 4.5 g/dL. The calcium concentration [Ca] usually changes by 0.8 mg/dL for every 1.0-g/dL change in plasma albumin concentration. Thus this formula estimates the actual total plasma calcium level:

Corrected [Ca] = Total [Ca] + (0.8 × [4.5 − albumin level])

Acidosis decreases the amount of calcium bound to albumin whereas alkalosis increases the bound fraction of calcium. A small amount of calcium (about 6%) is complexed to anions such as citrate and sulfate. The remainder is ionized calcium that is biologically active.

The most common causes of hypercalcemia affecting 90% of all patients are primary hyperparathyroidism (HPT) and malignancy. Other causes are summarized in Box 1.

Box 1: Causes of Hypercalcemia
Primary hyperparathyroidism
  • Sporadic
  • Familial
Hypercalcemia of malignancy
  • Osteolytic hypercalcemia
  • Humoral hypercalcemia of malignancy
  • Ectopic production of calcitriol (by lymphoma)
Hypercalcemia of granulomatous disease
Chronic renal failure with aplastic bone disease
Tertiary hyperparathyroidism
Acute renal failure
Familial hypercalcemic hypocalciuria
Lithium-associated hypercalcemia
Vitamin D intoxication
Other causes
  • Increased calcium intake
  • Pheochromocytoma
  • Congenital lactase deficiency
  • Hyperthyroidism
  • Vitamin A intoxication
  • Thiazides
  • Milk-alkali syndrome
  • Immobilization
  • Theophylline

Signs and symptoms

Symptoms of hypercalcemia ( Table 1) are nonspecific and are related to the severity and rate of change of the serum calcium level. Symptoms are more severe with acute changes than with chronic calcium level elevation. Patients with a chronic calcium level as high as 12 to 14 mg/dL may tolerate those levels well whereas sudden development of hypercalcemia in this range or higher may lead to dramatic changes in a patient’s mental status. Symptoms of underlying diseases causing hypercalcemia may dominate the clinical picture.

Table 1: Clinical Manifestations of Hypercalcemia
Symptoms and Signs Associated Conditions
Depression Organic brain syndromes
Cognitive dysfunction
Polyuria Nephrolithiasis
Polydipsia Nephrogenic diabetes insipidus
Nocturia Cardiovascular calcifications
Constipation Peptic ulcer disease
Anorexia Acute pancreatitis
Abdominal pain
Muscle weakness Osteopenia osteoporosis
Aches pains Gout pseudogout
Fractures Chondrocalcinosis
Osteitis fibrosa cystica
Brown tumors
Hypercalcemic crisis

A normal extracellular calcium concentration is necessary for normal neuromuscular function and neurologic dysfunction is the major feature of hypercalcemic states. Changes vary from slight difficulties in concentrating to depression confusion and coma. Some of these symptoms may resolve or improve after correction of the hypercalcemia. 1 Muscle weakness is another clinical manifestation.

Chronic hypercalcemia may result in the formation of renal calculi. Hypercalciuria is the main factor in stone formation but increased calcitriol production in HPT also plays a role. Nephrogenic diabetes insipidus resulting in polydipsia and polyuria is seen in about 20% of patients. Mechanisms include downregulation of water channels (aquaporin 2) and tubulointerstitial injury caused by calcium deposition. Renal tubular acidosis and renal insufficiency are rare. Chronic hypercalcemic nephropathy may continue to worsen after correction of hypercalcemia.

Hypertension is seen with increased frequency in patients with hypercalcemia and may be caused by renal insufficiency calcium-mediated vasoconstriction or both. Hypertension may or may not resolve after correction of hypercalcemia. Cardiac effects include short QT intervals which may increase sensitivity to digitalis and deposition of calcium in heart valves myocardium or coronary arteries.

Constipation anorexia nausea and vomiting are often prominent symptoms whereas acute pancreatitis (via activation of trypsinogen in pancreatic parenchyma) and peptic ulcer disease (via stimulation of gastrin secretion) are unusual. Fatigue musculoskeletal weakness and pain are the only symptoms known to correlate with increasing levels of serum calcium.

Primary hyperparathyroidism

Sporadic Primary Hyperparathyroidism

Primary HPT occurs at all ages but is most common in the sixth decade of life. It is three times more common in women than in men. When HPT affects children it is likely to be a component of familial endocrinopathies such as the multiple endocrine neoplasia (MEN) syndromes type I and II or familial HPT. The incidence of HPT is approximately 4 per 100 000 per year. 2

The underlying pathophysiology of HPT is caused by excessive secretion of parathyroid hormone (PTH) which leads to increased bone resorption by osteoclasts increased intestinal calcium absorption and increased renal tubular calcium reabsorption. The consequent hypercalcemia is also often accompanied by low-normal or decreased serum phosphate levels because PTH inhibits proximal tubular phosphate reabsorption.

Most cases of HPT (80%) are discovered accidentally by automated blood sample analyzers that were initially introduced into clinical practice in the 1970s. These cases have minimal or no symptoms and calcium levels are only mildly elevated (lower than 12 mg/dL). Patients with HPT can present with any of the clinical manifestations summarized in Table 1 and this diagnosis needs to be considered especially in any patient presenting with kidney stones bone disease or hypercalcemic crisis.

Renal calculi are seen in 15% to 20% of patients with HPT and conversely about 5% of patients with renal calculi have HPT. Some of these patients may have calcium levels in the upper range of normal. Most calculi are composed of calcium oxalate and the main factor in pathogenesis is hypercalciuria. Although PTH stimulates calcium reabsorption in the distal tubule the kidney is overwhelmed by the increase in the amount of filtered calcium resulting from increased serum calcium levels. Patients with increased vitamin D levels are more likely to have hypercalcemia and nephrolithiasis.

Classic bone disease of HPT manifests with brown tumors osteitis fibrosa cystica and subperiosteal resorption on the radial aspect of middle phalanges. These findings are present only in severe and long-standing disease and today are seen rarely usually when disease is caused by parathyroid carcinoma and in secondary or tertiary HPT is associated with chronic renal insufficiency. 3 Low bone mineral density is found in some patients with HPT but it is unclear whether this occurs more often than in the normal population. Some studies have shown decreased bone mineral density in untreated cases 3 but others have not. 4 However most studies have shown an increased risk for vertebral fractures in patients with HPT. Hip fractures were studied in a cohort of 1800 patients in Uppsala Sweden and revealed no extra risk for women but an increased risk in men. 5

Hypercalcemic crisis is a rare manifestation and is characterized by calcium levels usually above 15 mg/dL and severe symptoms of hypercalcemia particularly central nervous system (CNS) dysfunction. Abdominal pain pancreatitis peptic ulcer disease nausea and vomiting are also seen more commonly in these patients. The mechanism whereby a crisis develops is not clear but dehydration intercurrent illness and possibly infarction of parathyroid adenoma in some patients all play roles.

Several studies have found excessive mortality in patients with HPT with most of the excess caused by cardiovascular disease. The largest study included 4461 patients and measured an increased mortality risk of 1.71 for men and 1.85 for women. 6


The diagnosis of HPT requires an elevated serum calcium level with simultaneous demonstration of elevated PTH levels (in 80% to 90% of patients) or within normal limits (in 10% to 20% of patients). Note that patients with hypercalcemia should have their PTH level suppressed and that the “normal” level is inappropriately high in these patients. The PTH elevated should be determined by an assay that measures the intact PTH molecule. The phosphorus level may be low but is usually just in the low-normal range. Urinary calcium excretion is measured by a 24-hour urine collection that should also specify total volume and urine creatinine levels; hypercalciuria should be considered if the urinary calcium level is higher than 400 mg/day. In addition low calcium excretion (lower than 150 mg/day) may signify familial hypercalcemic hypocalciuria which is not surgically treatable.

A careful family history is paramount for the recognition of familial forms of primary HPT. In these cases urinary screening for catecholamine overproduction is important before surgical treatment.

Localization of abnormal parathyroid glands preoperatively by means of ultrasound Tc 99m-sestamibi scintigraphy or magnetic resonance imaging (MRI) may offer a possibility for a less invasive surgical approach. The accuracy of these radiologic modalities is variable. They are not required for the diagnosis of HPT but serve mainly as guides for surgical strategy and the selection of these tests should be left to the surgeon.

Indications for Treatment.

Removal of the abnormal and hyperfunctioning parathyroid tissue results in a long-term cure of HPT in 96% of patients and significant improvement in associated symptoms. The following criteria were proposed as indications for parathyroidectomy based on a National Institutes of Health–sponsored panel and endocrine specialty societies: 7

  1. Serum Ca level more than 1 mg/dL above the upper limit of normal
  2. Marked hypercalciuria higher than 400 mg/day
  3. Creatinine clearance reduced more than 30% compared with age-matched controls
  4. Reduction in bone mineral density of the femoral neck lumbar spine or distal radius of more than 2.5 standard deviations below peak bone mass (T score lower than -2.5)
  5. Age younger than 50 years
  6. Patients for whom medical surveillance is not desirable or possible
  7. Presence of any complications (e.g. nephrolithiasis overt bone disease)
  8. An episode of hypercalcemic crisis

However because no effective medical therapy for HPT exists all patients with HPT who are otherwise healthy for surgery should be referred for surgical treatment.

Surgical Treatment.

Parathyroid surgery remains the single most effective treatment option in HPT and requires removal of all abnormal parathyroid tissue. Traditionally in the vast majority of U.S. practices this has meant bilateral exploration of the neck to identify all (typically four) parathyroids assess which ones are abnormal and remove only the abnormal glands. The setting of multiglandular hyperplasia requires subtotal parathyroidectomy or total parathyroidectomy with reimplantation of parathyroid tissue into the sternocleidomastoid or forearm muscles. The parathyroids may then also be cryopreserved as a safeguard against future hypocalcemia in which case the patient may undergo autotransplantation of autogenous stored parathyroid tissue. In experienced hands this approach has an exceptional rate of successful long-term cure of HPT (more than 96%) and a low rate of surgical complications (hypocalcemia less than 1% recurrent laryngeal nerve injury 2% to 5% neck hematoma or infection less than 1%). 8

In recent years parathyroid procedures have been developed using smaller incisions under sedation and local anesthesia and with the opportunity for outpatient surgery. Minimally invasive parathyroid surgery has become more frequently requested by patients and primary care physicians alike even though it does not represent a uniform set of techniques. Depending on regional practices minimally invasive parathyroid surgery can include laparoscopic radio-guided or most frequently only unilateral neck surgery. The success of these approaches in curing HPT and minimizing complications is relatively unknown because clinical follow-up periods are still short. Minimally invasive parathyroid surgery is appropriate only for patients who have a single clearly defined parathyroid abnormality on ultrasound sestamibi scan or both and when parathyroid hormone levels can be monitored intraoperatively. Bilateral neck exploration is mandatory in all other cases and for patients with familial or genetic syndromes.

Medical Treatment.

Patients who are not treated surgically should be managed to ensure good hydration and to avoid thiazide diuretics. Ambulation should be encouraged. Calcium intake should be average because excessive intake may aggravate hypercalcemia especially in patients with high calcitriol levels whereas low calcium intake may stimulate PTH secretion. Bisphosphonates may be used to lower the serum calcium level in patients with symptomatic hypercalcemia (see later “Treatment of Hypocalcemia”) although they are usually not effective.

Familial Forms of Hyperparathyroidism

Up to 10% of cases of primary HPT are hereditary forms. Recognition is important because management of many patients and their families may be affected.

The most common familial form is multiple endocrine neoplasia syndrome type I (MEN-I). In this disorder primary HPT is almost invariably present (in more than 95% of patients) by the age of 65 years but may be diagnosed in children and even in infants. Indications for surgical intervention are generally the same as for sporadic cases. Pancreatic tumors are present in 30% to 80% of patients. These are usually islet cell tumors secreting gastrin and causing Zollinger-Ellison syndrome in about two thirds of cases. The second most common pancreatic tumor is insulinoma. Tumors secreting various substances have been described.

Pituitary adenomas affect 15% to 50% of patients and are mostly prolactinomas although tumors causing acromegaly and Cushing’s disease also occur. Adrenocortical hyperplasia is seen in about one third of patients.

MEN-I is caused by autosomal dominant mutation of the menin gene on chromosome 11. Genetic testing is cumbersome and screening of family members should be done by determining serum calcium levels. Some patients develop MEN-1–associated lesions as late as age 35 years.

MEN-II is characterized by the development of medullary thyroid carcinoma which occurs in almost all patients. Hyperparathyroidism occurs in about one half of affected individuals; most are asymptomatic. Pheochromocytoma or adrenal medullary hyperplasia is an associated feature. The mutated gene is the RET protooncogene. Genetic testing of family members is desirable because it clearly identifies individuals at risk and timely thyroidectomy is lifesaving.

Other familial syndromes are rare and include the HPT–jaw tumor syndrome and familial isolated primary HPT.

Other types and causes of hypercalcemia

Tertiary Hyperparathyroidism

In cases of prolonged states of secondary HPT as seen in patients with end-stage renal disease vitamin D deficiency and states of vitamin D resistance the parathyroid glands undergo hypertrophy and eventually develop autonomous PTH secretion which in turn leads to hypercalcemia and resembles primary HPT. This condition is called tertiary HPT. The cure requires surgical intervention to reduce the amount of parathyroid tissue.

Familial Hypocalciuric Hypercalcemia

Familial hypocalciuric hypercalcemia (FHH) is a rare familial condition caused by an inactivating disorder of calcium-sensing receptors that is expressed in many tissues but has a major function in regulating calcium metabolism through effects on parathyroid tissue and on handling of renal calcium. The disorder is autosomal dominant with high penetrance. Several mutations are described but all decrease the sensitivity of receptors to calcium requiring higher calcium levels to suppress PTH secretion. Heterozygous patients present with hypercalcemia hypocalciuria and mild hypermagnesemia. Fractional excretion of calcium is lower than 1% despite hypercalcemia. The PTH level is normal or slightly elevated (up to twice the normal in our clinical experience).

The clinical significance of this disease lies mostly in mistaken diagnosis of HPT and referral for parathyroidectomy. A commonly performed subtotal parathyroidectomy cannot correct hypercalcemia and these patients sometimes undergo multiple surgeries.

Genetic testing is not routinely available and usually is unnecessary. Patients are free of symptoms a family history will uncover more family members with hypercalcemia and urinary calcium excretion is low (about 75% of patients excrete less than 100 mg/day). Such a low calcium excretion in the face of hypercalcemia indicates increased renal tubular calcium absorption and low calcium clearance. The ratio of calcium (Ca) clearance to creatinine (Cr) clearance may be used for the diagnosis of FHH using the following formula:

where Cau = urinary Ca concentration Crs = serum Cr concentration Cru = urinary Cr concentration and Cas = serum Ca concentration. A ratio of 0.01 or less is typically seen in individuals with FHH.

Hypercalcemia of Malignancy

Humoral Hypercalcemia of Malignancy

Humoral hypercalcemia of malignancy (HHM) is a clinical syndrome in which elevated calcium levels are caused by effects of the humoral factor synthesized by the tumoral process. Usually this term is applied to patients with excessive tumoral production of PTH-related peptide (PTHrP). However rare cases characterized by excessive production of PTH and calcitriol have also been described. Patients with HHM constitute about 80% of all patients with hypercalcemia associated with malignancy.

PTHrP and PTH share the same receptor but there are some differences in clinical presentation. HHM patients have a markedly larger degree of renal calcium excretion—PTH potently stimulates tubular calcium resorption and hypercalciuria is less pronounced. HHM is usually associated with low serum calcitriol levels—PTH stimulates calcitriol production and its level is usually elevated. Also PTH stimulates bone resorption and formation whereas PTHrP stimulates only bone resorption with very low osteoblastic activity and therefore usually normal alkaline phosphatase levels.

These patients have suppressed levels of immunoreactive PTH whereas the immunoreactive PTHrP level is elevated. In addition patients with HHM are usually dehydrated in part because of hypercalcemia and in part because of poor oral intake.

Patients with HHM usually have clinically obvious malignant disease and have a poor prognosis. The only exceptions to this rule are patients with small well-differentiated endocrine tumors (e.g. pheochromocytomas or islet cell tumors). However these tumors constitute a minority of cases and HHM is most commonly seen with squamous cell carcinomas (e.g. lung esophagus cervix head and neck) and renal bladder and ovarian cancers. The therapy of HHM is aimed at reducing the tumor burden reducing osteoclastic resorption of the bone and increasing calcium excretion through the urine.

Most hypercalcemia cases associated with Hodgkin’s disease and about one third of those seen in non-Hodgkin’s lymphoma are caused by increased production of calcitriol by the malignant cells. Hypercalcemia usually responds well to treatment with corticosteroids.

Hypercalcemia of Malignancy Associated with Localized Bone Destruction

Multiple myeloma affects the skeleton extensively in almost all patients. In addition common malignant tumors (e.g. breast prostate and lung) frequently metastasize to the bone. Most bone metastases are destructive to the bone tissue (osteolytic).

Bone involvement in multiple myeloma may be in the form of discrete lesions or can affect the axial skeleton diffusely. Bone involvement is responsible for pathologic fractures bone pain (about 80% patients first present with bone pain) and hypercalcemia (seen in 20% to 40% of patients in the course of disease). Myelomas cause bone destruction by cytokine secretion that activates osteoclasts. The exact nature of the responsible cytokines is unknown. In vitro lymphotoxin produced by myeloma cells accounts for the major portion of bone resorption activity. Interleukin-1 interleukin-6 and PTHrP may also be involved in the process in some patients. The fact that most patients with multiple myeloma demonstrate extensive bone destruction whereas far fewer develop hypercalcemia may be explained by impaired glomerular filtration—a result of nephropathy caused by Bence-Jones protein uric acid nephropathy amyloidosis or infection—and the inability to excrete calcium efficiently in those who do develop hypercalcemia.

How to Use Alkalol

Nasal rinsing with Alkalol provides relief from congestion caused by allergies cold flu and sinus symptoms. Alkalol’s unique blend of invigorating extracts and essential oils loosens and washes away mucus helping to reduce nasal congestion and sinus pressure.

How does nasal irrigation work?

Alkalol’s blend of natural ingredients helps clean mucus from your nasal passages. During nasal irrigation Alkalol flows through your sinuses clearing irritants such as dust and pollen. It also helps improve overall nasal hygiene by preventing mucus from gathering in your sinuses where it can become the breeding ground for bacteria. Alkalol helps you breathe easier.


Some people use Alkalol when they feel a cold coming on. Others use it daily as a preventative measure. Alkalol is formulated for use as often as needed and we believe it remains your choice as to how often you use it.


Alkalol is intended for use at variable strengths depending on personal preference and thickness of mucus. We recommend starting with a “mild” dose and adjusting accordingly. Alkalol is recommended for use with the Alkalol Nasal Wash Cup. But please feel free to use it with another nasal pot or irrigation device. Just remember that each delivery system is different and you may want to adjust the amount of Alkalol to compensate. Please consult the following directions or download the instructions by clicking here.

If this is your first time using a nasal wash it may take some practice to become comfortable with it but the benefits far outweigh the challenges.

Let’s begin

STEP 1: Thoroughly rinse and dry your Alkalol Nasal Wash Cup removing any dust that may have settled in or on it.
STEP 2: Add Alkalol to the Alkalol Nasal Wash Cup following the guide below:

Mild: Add one teaspoon of Alkalol to the Alkalol Nasal Wash Cup filling it approximately 20% and the balance with saline or warm distilled or sterilized water

Medium: Add two teaspoons of Alkalol to the Alkalol Nasal Wash Cup filling it approximately 40% and the balance with saline or warm distilled or sterilized water

Strong: Add three teaspoons of Alkalol to the Alkalol Nasal Wash Cup filling it approximately 60% and the balance with saline or warm distilled or sterilized water

Very Strong: Add four teaspoons of Alkalol to the Alkalol Nasal Wash Cup filling it approximately 80% and the balance with saline or warm distilled or sterilized water


STEP 3:Holding one finger over the larger opening place the spout end of the Alkalol Nasal Wash Cup into one nostril.

STEP 4:While facing forward release your finger.

The Alkalol Nasal Wash Cup allows Alkalol to flow naturally and gently into one nostril across the nasal cavity and out the other nostril. Do not inhale gravity will allow the solution to flow properly. You may tilt your head slightly to one side if you like.

The Alkalol Nasal Wash Cup is specifically designed to properly regulate the flow to be comfortable and effective. Inhaling can interrupt the flow and may cause unnecessary discomfort. This part may take some practice but after the first few attempts you’ll be on your way.

 Blow through your nose without closing off either nostril. This is recommended because if one nostril is closed forceful blowing could injure your inner ear. Always blow gently.

STEP 6:Repeat steps 2-5 in the opposite nostril.

STEP 7:Rinse your Alkalol Nasal Wash Cup thoroughly with distilled sterile or boiled and cooled water. Dry with a paper towel or let it air dry between uses.


Should you experience any irritation or burning sensations there are some likely culprits:

  1. Solution is too weak: Rinsing your nasal passages with plain water will result in a burning sensation. Make sure there is enough Alkalol in your mix.
  2. Solution is too strong: Make sure Alkalol is thoroughly mixed by shaking well or try a milder solution.
  3. Water temperature: If the water temperature is either too hot or too cold you may experience discomfort. Aim for a lukewarm temperature. Remember to test the water first with your finger.
  4. Boldly refreshing: Upon initial use you may experience an invigorating sensation lasting a few seconds. This sensation is part of the process that allows Alkalol to work.

Neti pots & other nasal irrigation devices

Many people use Alkalol in neti pots and other rinse devices. Some tips to remember:

  • An Alkalol Nasal Wash Cup holds 1 fluid ounce. Many neti pots hold 8 fl oz. Simply follow the directions above adjusting the amount accordingly.
  • When using a neti pot or other large-volume irrigation device we recommend mixing Alkalol with a salt water solution instead of plain water to ensure the best experience. Too much plain water in the mix can cause a burning sensation.
  • Wash and dry your hands before using your nasal rinse device and make sure you clean and dry your nasal rinse device before and after use.

WARNING: Keep out of reach of children. For children under 3 years of age consult a physician. Avoid swallowing. Do not use if safety seal on bottle is broken or missing.