Understanding the Condition

Mechanisms of Disease

(Mechanism of disease is a term that is used to describe the way a disease occurs. It explains the chain of events that go wrong within cells and how the problem causes symptoms and consequences. It is important for researchers to know the mechanism of disease so that they can design treatments to fix what is going wrong.)

Insulin is a hormone made by the pancreas that regulates blood glucose levels through a very controlled process. Normally, when we eat or drink, our blood glucose levels go up, signaling the pancreas to release insulin. Insulin helps move glucose from the blood into the body’s cells, where it’s used for energy. The shift of glucose into the cells and out of the blood, lowers blood glucose levels. Once blood glucose returns to normal levels, the pancreas slows down insulin production. Between meals, when blood glucose levels drop, the body relies on stored energy sources to maintain balance.

In HI, the finely tuned system described above does not work as expected. The pancreas releases too much insulin, even when blood glucose levels are within a normal range or already low. The signals that tell the pancreas that more insulin is not needed are misread or ignored. The result is that high amounts of insulin are released into the blood regardless of blood glucose levels. This makes long times of fasting (not eating), like overnight or between meals, particularly dangerous for people with HI, as blood glucose can go down quickly without warning, causing severe hypoglycemia.

One of the most serious consequences of hypoglycemia is the risk of neurological complications. The brain uses glucose for energy, but it can switch to ketones (another fuel source that your body makes to help provide energy) when glucose levels are low. However, insulin also plays a role in making ketones: when insulin levels are high, the body slows down ketone production. For individuals with HI, this creates a double problem—both glucose and ketone levels are too low, depriving the brain of the energy it needs to function and develop properly. When the brain is deprived of the fuels it needs, someone may develop learning disabilities, seizure disorders, blindness, or even death.

Causes of Hyperinsulinism

HI can have different causes. Knowing the cause of an individual’s HI may be helpful in predicting whether the condition is temporary (sometimes referred to as transient) or lifelong (sometimes referred to as persistent). Some types of HI are known to be caused by genetic changes, and others are non-genetic (also known as acquired). However, in some people, the cause of HI may not be clear.

Studies estimate that about half of people with HI have an identified genetic cause. Genetic forms of HI are typically caused by variants in specific genes that regulate insulin release from the pancreas. These variants may cause high insulin release even when blood glucose is low, leading to dangerous hypoglycemia. In some cases, an exact genetic cause may not be found. This could suggest that additional genes may be involved that have not been identified yet. Ongoing research continues to discover new genetic changes that may contribute to HI. Finding these currently unknown genetic causes of HI will improve diagnosis and treatment options in the future.

Non-genetic causes of HI may result from complications during pregnancy or birth. These may include diabetes in the mother (gestational diabetes), perinatal stress, birth asphyxia (oxygen deprivation), intrauterine growth restriction, exposure to drugs in the womb, or high rates of maternal glucose infusions during delivery. While some of these factors are often associated with transient HI that may resolve over time, they still pose a significant risk of neurological disorders in the baby if not treated properly.

Regardless of whether HI is transient or life-long, or genetic or acquired, rapid diagnosis and treatment are critical to preventing neurodevelopmental disorders. However, understanding the cause of someone’s HI can help guide individual treatment strategies.

Types of HI

Over the years, as the understanding of HI has gotten better, the words used to describe the condition have changed. In the past and in older literature, HI was referred to by several names including nesidioblastosis, islet cell dysregulation syndrome, idiopathic hypoglycemia of infancy, and persistent hyperinsulinemic hypoglycemia of infancy. Despite our knowledge of HI improving, there are still many ways that doctors might describe HI, such as according to genetics, pathology (in the case of HI, pathology can refer to a doctor looking at the pancreas tissue to determine HI type), or how someone responds to medications. On this page, we will be describing HI types according to genetics and tissue pathology.

Identifying the specific type of HI that someone has is important because it can guide treatment decisions and long-term management. To figure out what type of HI someone has, doctors can use genetic testing, advanced imaging techniques, and confirmation through pathology/biopsy testing during surgery (if applicable).

Focal hyperinsulinism: Focal HI is characterized by a lesion in a localized area of the pancreas, but the surrounding pancreatic tissue is normal. Focal HI can sometimes be linked to specific genetic variants that cause only some cells to have abnormal insulin regulation. More information about this scenario can be found on the genetics page.

The International Guidelines for the Diagnosis and Management of HI recommend the use of advanced pancreatic imaging to locate the focal lesion if someone is suspected of having focal HI. The current standard for imaging is the 6-fluoro-(18F)-L-3,4-dihydroxyphenylalanine positron emission tomography (18F-DOPA PET) scan, which may be done in combination with CT or MRI. This technique is highly sensitive and specific when interpreted by an experienced radiologist, but its availability is limited to a few specialized HI centers worldwide. These centers include those who have been designated as Centers of Excellence. At some centers, a new kind of imaging, called &sup68;Ga-NODAGA-Exendin-4 PET/CT, is being tested as an alternative to 18F-DOPA PET. Some studies suggest this new technique may have better image quality, which may help with more accurate determination of HI type. More studies are being done using this technique in larger groups of people with HI to better compare which is better to diagnose HI.

Surgery to remove the focal lesion will typically cure someone of their HI. This is because the surgeon removes only the damaged cells and leaves the normal pancreatic tissue alone. Outcomes for focal HI are generally excellent, and most individuals no longer have problems regulating blood glucose levels. Because there is less tissue removed in a focal HI lesionectomy compared to a diffuse HI pancreatectomy, there is less of a chance of developing diabetes following focal surgery. However, many people with focal disease can still face complications related to prolonged hypoglycemia that may have happened prior to surgery.

Diffuse hyperinsulinism: Diffuse HI occurs when beta-cells throughout the entire pancreas are causing too much insulin to be released into the blood. The most common known causes of diffuse HI are associated with genetic changes in KATP channel genes, such as ABCC8 or KCNJ11, which are important for releasing insulin into the blood to keep blood glucose levels in a healthy range. (See the Genetics section below for more information on these variants.) Diffuse HI is not limited to K_ATP HI and includes all types that are not focal (i.e. atypical HI, mosaic HI, syndromic HI, HI caused by non-K_ATP channel genes, etc.). Some of these diffuse HI types are discussed in more detail below.

When diffuse HI is suspected from genetic testing results, the most common approach to treat the condition is medical management to control blood glucose. Diffuse HI can be mild or severe and for some people with HI, medication may not work well enough to manage hypoglycemia, and surgery may be necessary. For those with diffuse HI that do not respond to medicine, a 90-98% pancreatectomy may be needed to reduce insulin release.

Typically, the goal of a pancreatectomy to treat diffuse HI is to decrease the severity of HI and allow for more effective medical treatment by removing beta-cells within the pancreas. This procedure is often not curative for diffuse HI. About 50% of people who have a pancreatectomy for diffuse HI still take medication for hypoglycemia after surgery. In some cases, doctors may perform more than one pancreatectomy. In the long-term, people that have a pancreatectomy tend to have a high risk of developing insulin-dependent diabetes. One study found that 91% of people who had a pancreatectomy to treat HI in childhood required insulin therapy by 14 years old. In addition to diabetes, some people report experiencing pancreatic insufficiency which may require enzymes to be taken with meals to help with digestion. More information is provided about surgical options and outcomes may be found in the Surgery section below.

Atypical hyperinsulinism: Atypical HI is characterized by unique histological (biological tissue structure) patterns that may have features of both focal and diffuse disease. For example, some regions of the pancreas may have characteristics of diffuse HI, while others appear more similar to focal HI.

Atypical HI is sometimes associated with genetic variants in genes such as ABCC8, GCK, and HK1. Certain forms of syndromic HI (hyperinsulinism occurring alongside other disorders) can present with atypical HI.

Diagnosing atypical HI is often done through a combination of advanced imaging technology, genetic testing, and detailed analysis of pancreatic tissue obtained during surgery. Treatment strategies can differ for people with atypical HI depending on the severity of the condition. Medical management is often the first step in treating atypical HI, but surgical intervention may be necessary if hypoglycemia cannot be controlled.

Transient hyperinsulinism: Transient HI is typically considered an acquired (non-genetic) form of hyperinsulinism that occurs in some newborns. While this condition is considered temporary, these babies are still at risk of neurological disorders from prolonged hypoglycemia during this early period. It is important to know that transient hyperinsulinism is most often a retrospective diagnosis, meaning someone is often determined to have this form once the hyperinsulinism has resolved and they are not experiencing hypoglycemia any longer.

Transient HI may be associated with complications during pregnancy, birth, or the early neonatal period. Perinatal stress-induced hyperinsulinism (PSHI) is known to be associated with babies who are small for gestational age, born prematurely, or delivered to mothers with diabetes. PSHI usually presents within the first 24 hours of life and often resolves within two weeks. However, in rare cases, a more severe form of PSHI persists beyond the neonatal period and may require more intensive management.

Typically, the goal of treating transient HI involves keeping blood glucose levels in the normal range. Some clinicians may recommend frequent feedings (i.e. every 3-4 hours) to minimize hypoglycemia. In more severe cases, glucose infusion or medications may be needed to maintain safe blood glucose levels. As the condition begins to resolve, the infant’s glucose levels will often improve, and a doctor may suggest a decrease in treatment dose and/or frequency until the baby maintains stable blood glucose levels without intervention.

Persistent HI: If someone is diagnosed with persistent HI, this typically means their condition may not go away on its own. These individuals may require long-term treatment to avoid hypoglycemia, or in some cases surgery may be presented as an option to manage hypoglycemia. Sometimes what may seem like transient HI may turn out to be persistent HI.

Genetics

Click here for a more in-depth discussion of HI genetics.

Genetic testing can play an important role in diagnosing and understanding HI. Sometimes, a treatment team may personalize treatment based off genetic testing results. The most common genetic causes of HI include variants in the K_ATP channel genes ABCC8 and KCNJ11. Genetic testing may not necessarily be performed for cases of transient HI.

It is important to remember that a negative genetic test result may not necessarily rule out a genetic cause of the condition. About 50-60% of individuals who undergo genetic testing receive a clear genetic HI diagnosis, but many people can receive negative genetic testing results because current testing cannot identify all possible genetic causes of HI. A negative genetic testing result does not mean that the person does not have HI. As researchers learn more about HI, they may be able to identify new genetic causes of this condition.

Access to genetic testing remains a challenge for some families, particularly in underserved regions of the world. The Open Hyperinsulinism Genes Project aims to expand access to genetic testing worldwide, supporting individuals and families affected by HI.

The following subsections will very briefly describe some known genetic forms of HI. This does not include all genetic causes for HI. As HI research continues to grow, scientists are finding new genes that may contribute to the development of HI, such as PMM2 and HK1. While the more common genetic causes of HI are discussed below, descriptions of some less common genetic causes of HI can be found here.

K_ATP Hyperinsulinism: The K_ATP channel plays a major role in releasing insulin into the blood. Normally, this channel receives signals to allow insulin to be released when blood glucose levels are high. However, when this channel is defective or not present, which can be the case with certain ABCC8 and KCNJ11 gene variants, the channel no longer works properly. As a result, insulin is released into the blood continuously, including when blood glucose is not high, causing persistent hypoglycemia.

Variants in genes affecting the K_ATP channel account for up to 70% of known genetic HI cases. Knowing the exact genetic variant and the way it was inherited can be helpful because sometimes genetics can reveal whether someone has focal or diffuse HI and potentially clue clinicians into the best method of treatment.

GDH-HI (HI/HA): Glutamate dehydrogenase (GDH) HI, also known as hyperinsulinism/hyperammonemia syndrome (HI/HA), is caused by variants in the GLUD1 gene, which codes for the enzyme glutamate dehydrogenase. This enzyme is important for releasing insulin into the blood in response to amino acids such as leucine. Individuals with GDH-HI may experience leucine-sensitive hypoglycemia, where eating protein-rich foods can trigger severe hypoglycemia. GDH-HI can present later than other forms of HI, such as when a child transitions from breast milk to infant formula.

GCK-HI: Glucokinase (Gck) is an enzyme that has the important role as the glucose sensor on beta-cells. This means that Gck acts like a mediator, telling the cells to make more insulin when glucose levels cross a particular threshold. In someone with a variants in the GCK gene that causes HI, the threshold for insulin release is lowered. This means more insulin is released when blood glucose levels are at or below a healthy level, causing hypoglycemia. Individuals with GCK-HI may develop ketotic hypoglycemia (low blood glucose but high ketone levels) with prolonged fasting. Ketotic hypoglycemia is different than other forms of HI, where ketone production is low.

HI with a family history of MODY: Maturity-onset diabetes of the young (MODY) is a condition that is separate from both Type 1 and Type 2 diabetes, where a single genetic variant causes diabetes that is often diagnosed at a young age. In families with a history of MODY, it is often recommended to consider genetic testing for mutations in the HNF1A and HNF4A genes. Variants found in HNF1A and HNF4A genes may lead to transient hyperinsulinism soon after birth. For some people, hyperinsulinism may resolve over time, but in others, it may be long-lasting. Variants in these genes may increase the risk of developing early-onset diabetes, typically in adolescence or early adulthood.

Syndromic HI: Syndromic HI means HI is caused by another genetic condition. In addition to HI and the pancreas, other organ systems are often affected. Identifying syndromic HI can be important because it may influence treatment strategies for both HI and other health needs. Some of the most common syndromes associated with HI include (but are not limited to) Beckwith-Wiedemann Syndrome, Polycystic Kidney Disease, Rubeinstein-Taybi Syndrome, and Kabuki Syndrome.

Diagnosis

There are several tests that may be used to indicate that someone may have HI. HI is typically diagnosed when tests show an increased in insulin action and/or amount during times of hypoglycemia. This means that when someone is experiencing hypoglycemia, a blood sample may be taken to measure the amount of insulin and other important molecules (such as glucose, beta-hydroxybutyrate/BOHB, and free fatty acids). From this sample, which is sometimes called a critical sample, doctors can see how the body responds to being in a condition of low blood glucose. A typical indicator of HI is high insulin levels during hypoglycemia because in people that don’t have HI, insulin is often low when blood glucose is low. The threshold for what is considered high or low for each molecule of interest is described in the International Guidelines for the Diagnosis and Management of HI.

Newborn babies may have lower blood glucose levels during the first 72 hours of life. This is known as “transitional hypoglycemia.” If tests to diagnose HI are done before 72 hours of age, these tests are typically repeated after 72 hours of age to confirm the diagnosis of HI if the child still has hypoglycemia and high insulin levels.

Treatment

Typically, the most important goal in treating HI is to maintain blood glucose levels between 70-100 mg/dL (3.9-5.6 mmol/L). The lower limit of 70 mg/dL (3.9 mmol/L) was established as a safety threshold to avoid hypoglycemia-induced neurodevelopmental disorders. Some countries have a lower threshold for treating hypoglycemia in someone with HI of 63 mg/dL (3.5 mmol/L). Therefore, the acceptable range for an individual may vary depending on your national guidelines.

During mild hypoglycemic episodes, a fast-acting carbohydrate-containing drink or snack may be helpful (e.g. fruit juice or candies). In times of severe hypoglycemia, a glucagon injection or nasal spray may be used to raise blood glucose levels or i.v. glucose may be suggested by your clinician. We suggest talking with your doctor about plans for responding to hypoglycemia.

Medical therapy is typically the first line of treatment for managing HI. Specific medications are discussed in the next section. In addition to medication, glucose monitoring can play a role in HI management. The frequency of glucose checks are typically individualized based on the severity of HI and may include testing before meals and at bedtime, with additional checks as suggested by your care team.

Continuous glucose infusion can become necessary for some people with HI. If needed, glucose may be delivered through a nasogastric (NG) tube or a gastrostomy tube. In some cases, tube feeding may impact feeding by mouth, but feeding therapy can help support the development of these skills. It may be helpful to have back-up plans in place in case of accidental disconnection of feeding tubes, especially overnight. Some techniques that have been reported to help at night time include a continuous glucose monitor (CGM) that can alarm at low glucose readings or a nocturnal enuresis alarm pad to detect fluid leaks.

Medications

Some of the currently available medications are described below. There are new HI therapies that are being tested in clinical research trials that are not listed here.

Diazoxide: Diazoxide is the first-line medication for controlling hypoglycemia in children with HI, and it is the only FDA-approved medication for children with HI. Diazoxide interacts with KATP channels to slow insulin release. Diazoxide is typically taken 2-3 times per day, depending on physician recommendations. It is manufactured in both a pill or liquid form; however, within many countries only one form or another is available.

In many cases, a five-day trial may be used to determine whether someone responds to diazoxide. Typically, diazoxide responsiveness can be determined by a fasting test and ketone analysis. However, not everyone responds to diazoxide and other medications may be recommended. People with HI who are diazoxide-unresponsive often have genetic variants in ABCC8 and KCNJ11. This is true for up to 90% of people with HI who are diazoxide-unresponsive, although other genetic forms of HI can also fall into this category.

Diazoxide has side effects that can be severe for some people taking the medicine. One of the most common side effects that may be experienced includes rapid hair growth all over the body. Another common side effect is fluid retention. Your doctor may recommend taking a diuretic with diazoxide, particularly at high doses (>10 mg/kg/day). Diazoxide is also known to cause coarsening of facial features. Less frequently reported side effects include neutropenia, thrombocytopenia, hyperuricemia, and pulmonary hypertension. Most side effects typically resolve after discontinuing diazoxide. It is important to discuss any side effects that you notice or experience during appointments with your clinician.

There are different ways clinicians may monitor you or your child while taking diazoxide. Clinicians may request blood tests every 6 months to assess complete blood count and differential and serum uric acid levels. Similarly, you may be asked to have an echocardiogram performed on your child before starting diazoxide and again one week after starting treatment to monitor for signs of pulmonary hypertension.

Octreotide: Octreotide, a somatostatin analog (a medicine that acts like a normal hormone in the body), is another medication used to treat HI. It may be prescribed to individuals with HI who are diazoxide-unresponsive, or who may stop taking diazoxide due to side effects. Somatostatin is a hormone known to slow the release of other hormones, including insulin. By decreasing the amount of insulin released from the pancreas, octreotide helps stabilize blood glucose levels.

Depending on the region you live in, octreotide may be available in both short-acting and long-acting forms. The short-acting form is typically given by subcutaneous (under the skin) injection 2-4 times daily or through a continuous infusion pump. Long-acting octreotide is delivered as a single dose given monthly, which may be more convenient for some families.

One of the most common side effects of octreotide is tachyphylaxis (meaning the effect becomes weaker over time). A less common side effect is necrotizing enterocolitis (a serious condition affecting the intestines of premature or very young babies). Children taking octreotide may be regularly monitored by undergoing blood tests to check growth factor, gall bladder, liver enzyme, and thyroid function panels.

Lanreotide: Lanreotide is another somatostatin analog that can be used to treat HI. Similar to octreotide, lanreotide works by acting like the hormone somatostatin to slow down insulin release from the pancreas. Lanreotide is typically given as a once-monthly injection into the muscle. Regular monitoring may include blood tests for liver enzyme and growth factor levels, as well as gall bladder and thyroid function.

Surgery

The International Guidelines for Diagnosis and Management of Hyperinsulinism recommend surgery when someone is suspected of having focal HI and their focal lesion can be seen by imaging and removed. Surgery typically has a high success rate (>95% cure rate) when the lesion is located in a part of the pancreas where very little normal tissue needs to be removed. In rare cases, a focal lesion may be in an area of the pancreas that makes surgery more difficult, like the pancreatic head. This surgery can sometimes be more complicated because other important parts of the body, like the small intestine, make it riskier.

Surgery for diffuse HI is usually more complex. This surgery is typically not curative but a subtotal or near-total pancreatectomy (95-98% removal) may help with the management of hypoglycemia. After pancreatectomy for diffuse HI, studies show 50-60% of individuals continue to require medication for hypoglycemia. For some, an additional surgery to remove more of the pancreas may be needed.

Studies show that up to 25% of people who have a pancreatectomy to treat diffuse HI develop diabetes right after surgery, and 91% require insulin by 14 years old. If a child has surgery that removes more than 50% of the pancreas, you or your child may be monitored for pancreatic insufficiency. This means that the remaining pancreas tissue does not make enough enzymes to break down food during digestion. Typically, enzymes will be prescribed to take with meals if pancreatic insufficiency develops.

A team of medical experts may form to prepare your child for surgery and maintain proper care after. This team may include endocrinologists, radiologists, pathologists, and surgeons. Your team may suggest imaging strategies such as 18F-DOPA PET scans before surgery, especially if focal HI is suspected. In some cases, your medical team may consult or contact one of the CHI Centers of Excellence (COE) for advice. Sometimes, a transfer of care may be suggested if a local hospital is not equipped to perform a pancreatectomy and provide proper post-surgical care.

Discharge

Before being discharged from the hospital, a fasting study (sometimes called a cure fast) may be performed to assess the ability to maintain normal blood glucose levels. Sometimes these tests may be done to determine whether people suspected to have transient HI no longer need treatment. In other cases, this kind of test can be performed to establish appropriate medical management, safe feeding schedules, sleeping routines, and glucose monitoring protocols to be followed at home.

Typically during a fasting test a child’s blood glucose levels and ketone levels will be monitored over time without food. Once their blood glucose or ketones hit a pre-determined low level, a blood sample will be drawn and sent to the lab, and the child will be given glucagon (a medication that raises blood glucose). The child will continue to be monitored for changes in blood glucose levels.

To help the transition to live with HI at home, some families may find it helpful to create a plan with their care team for blood glucose monitoring, what to do during hypoglycemia episodes, how to handle illnesses, etc. These plans may change throughout the lifetime, but may provide guidance in caring for yourself or your child.

On-Going Management

Blood glucose monitoring: The main goal of treating HI is to keep blood glucose levels within the range of 70-100 mg/dL (3.9 mmol/L). For some people with HI, they may show symptoms when they experience dysglycemia (blood glucose outside of the normal range). However, some people may experience hypoglycemia unawareness (when someone does not recognize they are having symptoms of low blood glucose). To monitor blood glucose, some families use point-of-care glucometer devices for regular testing. For others, continuous glucose monitors (CGMs) may be helpful, though these devices have not been approved by a regulatory body (a regulatory body is a government agency or other organization that is responsible for making and enforcing laws) for use in HI and may have reduced accuracy in the low glucose ranges. More information about CGM use in HI, written by members of the CHI CRN, can be found here.

Post-surgical monitoring: After pancreatectomy for diffuse HI, screening for diabetes is typically performed every 6-12 months. Screening may include testing hemoglobin A1c and monitoring for hyperglycemia symptoms such as increased thirst and frequent urination. If diabetes develops, life-long insulin therapy will often be required.

Post-surgery follow-up exams typically check for enzyme deficiencies that can lead to malabsorption. If pancreatic insufficiency develops following surgery, enzyme replacement medication may be suggested to help with digestion.

Neurodevelopmental follow-up: Neurodevelopmental delays and neurological disorders have been reported in individuals with HI, including those with transient HI. Neurological conditions can vary in severity and may include epilepsy, microcephaly, infantile spasms, motor and speech delay, and difficulties with attention, memory, visual, and sensorimotor functions.

Regular neurodevelopmental testing, especially in early childhood, may be helpful for early identification of potential learning disabilities in children with HI. In some cases, people with HI can benefit from neurodevelopmental pediatricians, physiotherapists, occupational therapists, or speech and language therapists depending on their needs. While the most severe long-term complications of HI are neurological conditions, many people with HI report having no neurological problems. Other times, children who have developmental delays in the early years may catch up with their peers. It is important to remember that those who do have ongoing neurodevelopmental issues can lead full, happy, and meaningful lives.

Feeding and nutritional support: Feeding problems can be common in children with HI, and the root cause of these difficulties is not well understood. Some of the most commonly reported feeding issues associated with HI include difficulties with sucking, swallowing, and food aversion. Vomiting and discomfort while feeding are also known to occur in some cases. Intervention by a feeding specialist may be helpful if issues arise. For some families, feeding issues may get better over time as the child grows.

Outcomes

Early recognition of hypoglycemia and effective continuous management of HI are key to preventing complications associated with hypoglycemia. However, even in the centers most experienced in treating HI, there are still children who have long-term complications. Prognosis for HI is often influenced by the severity of the condition, time to diagnosis, and the effectiveness of treatment. Families with HI may face challenges including frequent medical appointments, strict dietary monitoring and frequent feeding needs, and the emotional toll of living with a rare condition. However, with the right support, access to medication and glucose monitoring tools, and a dedicated care team, many individuals with HI can achieve milestones, go to school, and live independently.

To help support individuals and families with HI, CHI hosts a private Facebook Forum where parents can ask questions and provide support to each other from around the world. Some families have shared short interviews on their HI journey on our website, which we call HI-Stories. We encourage all HI families (individuals and caregivers) to share their experiences with HI and contribute to HI research through the HI Global Registry. To stay connected with CHI, we invite you to join our mailing list where you will get information about all our upcoming events!

Several resources were used to prepare this resource, including several articles published in medical journals. To view the references to these materials, click here.