Patty, living with Hypoparathyrodism

What is Hypoparathyroidism?

Hypoparathyroidism is a rare endocrine disorder in which the parathyroid glands produce insufficient amounts of parathyroid hormone (PTH), a key hormone responsible for regulating calcium in the body.1

Hypoparathyroidism Impact

~80,000

~80,000 people in the United States are estimated to be living with hypoparathyroidism1

~75%

of cases result from damage to the parathyroid glands during neck surgery2

Up to 40%

of patients with chronic hypoparathyroidism develop kidney complications, which may include nephrocalcinosis or kidney stones3

About Hypoparathyroidism

Parathyroid hormone plays a central role in maintaining the body's calcium balance. It signals the bones to release calcium into the blood, tells the kidneys to retain calcium and excrete phosphorus, and activates vitamin D to help the intestines absorb calcium from food.4 In hypoparathyroidism, the parathyroid glands are either damaged, absent, or dysfunctional, resulting in insufficient PTH production.1 Without adequate PTH, blood calcium levels fall and phosphorus levels rise, a persistent imbalance that can affect the muscles, nerves, kidneys, brain, and heart.4 The current approach of supplementing with calcium and active vitamin D attempts to compensate for this deficit, but many patients continue to live with abnormal blood and urine calcium levels, highlighting the need for new approaches that can achieve normal calcium homeostasis.1,3,4

Patty, living with Hypoparathyroidism

Clinical Features of Hypoparathyroidism

People living with hypoparathyroidism commonly experience muscle cramping, spasms, and tingling or numbness in the fingers, toes, and around the mouth, symptoms driven by chronically low calcium levels. In more severe cases, patients may develop seizures, cardiac arrhythmias, and laryngospasm. Over time, the chronic calcium and phosphorus imbalance can lead to calcium deposits in the kidneys (nephrocalcinosis), kidney stones, cataracts, and calcifications in the brain (basal ganglia calcifications).2,4 Many patients also report persistent fatigue, cognitive difficulty often described as "brain fog," and anxiety, symptoms that are frequently underrecognized but deeply affect day-to-day functioning. 1,2,4Despite treatment with calcium and active vitamin D, many patients continue to live with abnormal blood and urine calcium levels, meaning these symptoms and complications often persist.1,3,4

Community’s Unmet Need

The current standard of care for hypoparathyroidism, oral calcium supplements and active vitamin D, does not achieve normal calcium homeostasis for many patients. Large and frequent doses are often required throughout the day, and even with diligent adherence, many continue to experience abnormal blood calcium levels. Long-term use of high-dose calcium and active vitamin D also carries its own risks, including progressive kidney damage, kidney stones, and soft tissue calcification, meaning the treatment itself can contribute to the very complications it seeks to prevent.1,3,4 Elevated urine calcium remains a particular concern, as current supplementation approaches add exogenous calcium without addressing the excess calcium that passes through the kidneys.2–4

Diagnosis of hypoparathyroidism can also be significantly delayed, particularly in nonsurgical cases where there is no obvious precipitating event. Symptoms such as fatigue, muscle cramping, and cognitive difficulty overlap with many other conditions, leading to years of misdiagnosis or incomplete diagnosis.1,4 For patients and caregivers, this delay means prolonged uncertainty and a condition that is often not managed until complications have already developed.3,4

References