Is Your Difficult-to-Control Type 2 Diabetes Due to Underlying Hypercortisolism: Are Doctors Missing the Diagnosis?

Primary care physicians are often the gatekeepers and initial caretakers of most patients. They need to be aware of the risks when hypercortisolism goes undiagnosed.

What is Diabetes?

Diabetes is defined by hyperglycemia. Characteristics include insulin resistance in tissues and dysfunction of the pancreatic beta cell in insulin secretion. Essentially, the body becomes resistant to insulin or fails to produce enough of it. There are 2 kinds: Type 1 and Type 2. Type 1 is an autoimmune disorder that destroys beta cells, resulting in an absolute deficiency of insulin. Type 2 diabetes (T2D) is a hormonal disorder characterized by pancreatic beta-cell dysfunction and insulin resistance. 

38.4 million people in the U.S. have T2D and 90% of diabetes cases are T2. ¹,²,³

Causes of T2D are multiple and often multifactorial. Researchers are still unsure of what, exactly, causes insulin production dysfunction and insulin resistance.⁴

Risk factors include:⁴,⁵

• Age

• Obesity

• Lack of physical activity

• Racial, ethnic, genetic predisposition

• Pregnancy

• Certain medications (ie, steroids)

• Visceral fat distribution

Around 25% of T2D patients have an HbA1c of greater than 8%, which is considered uncontrolled. 

Hemoglobin A1c (HbA1c) is a blood test used to assess average blood glucose levels over the last 2 to 3 months, indicating blood sugar control during that period. This test helps diagnose type 2 diabetes and monitors blood glucose regulation in individuals with diabetes. A glycemic index below 7.5% is the goal.⁵

Consequences of Uncontrolled T2D:¹,⁶,⁷

Uncontrolled T2D causes a significant number of complications, morbidity, and mortality:

• Retinopathy: retinal nerve damage leads to blindness

• Neuropathy and neuropathology: nerve damage

• Atherosclerosis and cardiovascular disease lead to heart attack, vascular complications, and amputations

• Cerebrovascular disease leads to stroke, memory and psychiatric issues, and cognitive decline

• Nephropathy: Kidney damage leads to chronic kidney disease and kidney failure

• Impaired wound healing leads to infection

• Cancer, including liver, colorectal, pancreatic, endometrial, breast, and bladder cancer

What is considered "difficult to control" T2D?

• Sustained hyperglycemia: Blood sugar levels ≥ 130 mg/dL before meals for over a year⁸

• HbA1c > 7%⁸

• Physical symptoms: increased thirst and urination, blurred vision, fatigue⁸

• Complications like chronic kidney disease, nephropathy, neuropathy, heart disease, and difficult-to-control high blood pressure (HTN)⁹

• Glycemic index not reached despite being on multiple antihyperglycemic medications⁹

38.9-76.9% of people with T2D are considered uncontrolled⁸

The presence of long-term difficulty in controlling blood sugar despite optimal therapies may mean that hypercortisolism is present.

What is Hypercortisolism (CS)?

CS occurs when the body produces excessive cortisol, often without the classic symptoms of overt hypercortisolism. This results in a systemic hormonal disorder caused by prolonged exposure to high circulating levels of the hormone (also known as glucocorticoid) cortisol. It leads to hyperglycemia and a variety of other symptoms throughout the body.^7,11

Hypercorticism is caused by endogenous sources (within the body), such as tumors of the adrenal gland(s) or pituitary, or from exogenous sources (outside the body), like chronic steroid use.^7,11 

In this paper, we will discuss “mild” ACTH-independent Endogenous Hypercortisolism, which will be referred to as Cushing’s Syndrome (CS). 

Confusingly, it is referred to by several different names in scientific literature:⁷

• Subclinical CS

• Adrenal autonomous CS

• Less severe CS

• Mild CS/Mild Autonomous CS (MACS)

• Hidden CS

• Cushing's Syndrome

What is Cortisol?

Known as the "stress hormone", it is present in most body tissues and affects nearly every organ system. The activation of the HPA axis, or hypothalamic-pituitary axis, produces it. Production begins in the brain, with the hypothalamus being stimulated to release CRH (corticotropin-releasing hormone). This stimulates the pituitary (also in the brain) to release ACTH (adrenocorticotropic hormone). ACTH stimulates the adrenal glands, found on top of both kidneys, to produce cortisol¹².

What does it do?

Since cortisol is ubiquitous in the body, it has a wide range of functions and effects:^12,13

• Regulates immune function and anti-inflammatory mechanisms

• Maintains normal BP and vascular tone

• Controls the "fight or flight" response

• Helps regulate metabolism and blood sugar

• Helps regulate cognition and mood

• Regulates menstruation and fetal development

• Helps control the sleep-wake cycle

What Happens When There Is Too Much Cortisol?

CS affects almost every system in the body. Favero, et al. Pathophysiology of Mild Hypercortisolism: From Bench to Bedside. Int J Mol Sci. 2022; 23(2), 673: https://doi.org/10.3390/ijms23020673

Physical Symptoms of hypercortisolism:^14,15

• Atherosclerotic heart disease, left ventricular hypertrophy

• Hypercoagulability leads to clots = heart attacks/strokes/amputations

• HTN, high cholesterol

• Weight gain, especially around the mid-section and torso; unusual dispersion of fat: around the collar between the shoulder blades, known as a buffalo hump. An increase in visceral fat, located around the organs, is particularly dangerous.

• Skin changes: striae/purple stretch marks, easy bruising, acne; rounded, pale face known as moon face

• Decreased immune function = delayed healing, infections, sepsis

• Hirsutism (unwanted, dark, coarse hair in women, usually on face, neck, and back)

• Delayed puberty or increased weight with slowing growth in youths

• Muscle weakness and fatigue

• High blood sugar, difficult to control T2D

• Osteoporosis = increased bone fragility and fractures

• Increased thirst and urination

• H20 and electrolyte imbalances, like hypokalemia.

Cognitive Symptoms: (14,15)

• Chronically increased levels of cortisol cause irreversible functional and structural changes to the brain in regions responsible for emotional and cognitive functions.

• Mood swings and disturbances: anxiety (66%), depression (50-81%), bipolar (30%), and psychosis.

• Fatigue, insomnia, obstructive sleep apnea

• Impaired cognitive function: memory, language, visual and spatial information, along with verbal learning and language.

Due to its wide range of clinical manifestations, recognizing and diagnosing CS can be challenging unless obvious symptoms are present. Patients with endogenous CS don't have severe enough cortisol elevation for these to be recognized until the disease has progressed. Patients often present with nonspecific symptoms in common with the general public: 

• Weight gain/obesity

• Diabetes

• High blood pressure and cholesterol

• Osteoporosis

• Reproductive and psychiatric disorders.

"Hidden CS" may have no outward symptoms and is only detectable 5-30% of the time in patients with adrenal incidentalomas (adrenal abnormalities found on imaging, during a workup for something else).^17,18

Up to 2% of people over 60 may have CS, and that number is even higher in people with unexplained, difficult-to-control T2D and/or HTN and/or osteoporosis. ¹⁶

Despite milder symptoms, CS is associated with an increased risk of other chronic diseases, including progressive type 2 diabetes and hypertension (HTN). CS is associated with an increased risk of cardiovascular and cerebrovascular events, sepsis, and thromboembolism. Over time, cumulative adverse outcomes, including increased morbidity and mortality, will ensue.⁹ 

These patients have been found to have:

• 10% increase in cardiovascular events⁹

• 4.5x increased risk of heart attack¹⁴

• 19.1% decrease in overall survival from cardiovascular events⁹

• 3.5- 5x increase in mortality compared with the general population¹⁴

How Does CS Affect T2D

The association between T2D and long-term complications may be linked to HPA axis dysfunction, which is a cause of CS. In turn, CS causes T2D and makes it difficult to control.

CS leads to T2D in 1/3 of affected patients by causing:

Insulin resistance: High cortisol levels impair the body's sensitivity to insulin, resulting in elevated blood sugar levels, skeletal muscle insulin resistance, and impaired glucose metabolism.

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Visceral fat: Cortisol promotes the accumulation of visceral fat (hidden fat surrounding the organs), leading to further insulin resistance, obesity, hypertension, increased cholesterol, and other metabolic disturbances.

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Gluconeogenesis: (production of glucose) Increased glucose production by the liver raises blood sugar.

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Beta cell dysfunction: Decreased function of the pancreatic beta cells, which create insulin. Decreased insulin = increased blood sugar.

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Lipolysis (breakdown of fats) is activated, causing free fatty acids to be released, which can lead to high cholesterol and arterial plaques.

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What is the Prevalence of CS in Difficult to Control T2D?

There has been a paucity of research done on this debilitating duo, but recently, studies have been looking into the prevalence and treatment of people with T2D and CS. Current research suggests the prevalence is as follows:

• Approximately 2.9% (575,000-2.5 million people) with resistant T2D in the U.S. may have T2D as a result of underlying CS.⁹

• The recent and ongoing CATALYST study found up to 24% of patients with difficult-to-control T2D have underlying CS. 

• That number increased to 40% in patients who also had difficult-to-control HTN (BP > 135mmHg despite being on ≥ 3 BP meds).⁸

• Up to 50% of people with adrenal incidentaloma will have CS^15,18

Untreated CS is associated with a marked increase in major health complications, including early death and decreased quality of life. Endogenous CS is often missed, leading to an unnecessary progression of disease and comorbidities. 

Leading causes of death:

• Cardiovascular events

• Cerebrovascular events

• Thromboembolism

• Sepsis

• Opportunistic infections. 

Early detection and treatment are critical for decreasing adverse outcomes.^15,18

Who Should be Screened for CS?

Patients displaying these presentations should be considered for CS screening:^15,18

• Resistant or suddenly worsening T2D, metabolic syndrome and/or HTN

• Worsening cardiovascular symptoms or events despite optimal therapy

• Proximal myopathy (muscle weakness of the limbs)

• Distinctive pigmented striae and easy bruising

• Unexplained, progressive weight gain

• Sudden or suddenly worsening osteoporosis/bone fragility

• Young patients with unusual symptoms for their age, especially early onset T2D, HTN, and/or osteoporosis.

• Adrenal incidentaloma

  
  

Why Aren't More At-Risk Patients Being Screened?

Knowledge Gaps: Until recently, the prevalence of underlying CS was unknown and poorly understood. Primary care physicians are the first individuals to see the patient and are responsible for referring them for further evaluation if CS is a possibility. However, since CS was relatively unthought of until now, physicians may have unknowingly become stymied when traditional attempts failed to control their patients' diabetes. They may suffer from "clinical inertia," a phenomenon that occurs when, despite guidelines, patients are not transitioned to the next tier of treatment when current therapies are ineffective.^25,26

PCP Perspectives: Doctors want to achieve targets. When T2D is uncontrolled, they may become frustrated and blame the patient. They may feel a sense of failure, on their part, that will turn to resignation and further clinical inertia. Also, some PCPs may only refer patients to a specialist as a "last resort", perhaps not realizing the gravity of waiting to enlist help. Delayed diagnosis could cause progression of symptoms with permanent pain and suffering.^25,26

Therapeutic Limitations: There is no widely accepted protocol for screening and treating patients with CS. Once CS is suspected, multiple tests are needed that are expensive and time-consuming. The MD and the patient may not want to accept this, even though it is the most prudent course of action.^27,28

Living with CS: The Patient Journey

CS is a life-altering, devastating illness, often leading to joblessness, isolation, depression, and loneliness.

• Once patients are screened, multiple tests are required and, even then, they may not be entirely reliable. 

• The therapeutic regimen is grueling, requiring a multidisciplinary team that should collaborate regularly, which may prove difficult. 

• Complications may require multiple hospitalizations and surgeries. 

• Different combinations of medications to try, each with side effects. 

• Racial/ethnic disparities, sociodemographics, lack of access to health care, and high cost make it difficult for patients to navigate issues like time and transportation while attempting to honor occupational commitments. 

It can be challenging for both the patient and the primary care physician to maintain long-term participation.

The symptoms of CS are life-altering, involving numerous comorbidities that affect self-esteem, body image, personal relationships, and overall quality of life. They affect the patient both physically and cognitively, and many become chronic or lifelong conditions.^15,31

Physical symptoms: Can significantly alter the patient's appearance (e.g., weight gain, moon face, buffalo hump, striae, acne, hirsutism), creating a negative body image and self-perception.

Psychiatric and cognitive symptoms: Mental illness, insomnia, and cognitive decline create more issues with relationships and job life.

Fatigue and muscle weakness: Can Impair activities of daily living, restricting social interaction, leading to joblessness, and necessitating a reliance on others for daily chores, personal hygiene, and financial needs.^15,31,32 

What Treatments Are Available?

Currently, surgery serves as the primary line of defense against CS.  Aimed at removing the tumor causing the CS, it is often located on the adrenal gland(s) but can appear in other parts of the body. However, research indicates that surgery may not provide a definitive cure or therapy for CS, and not all patients will be eligible for this surgical intervention.

Up to 75% of patients diagnosed with CS were not candidates or refused surgery. 

 Pharmacotherapy can offer an acceptable approach for people who can not or will not have surgery. In addition, just treating the comorbidities, as some therapeutic regimens suggest, is not effective enough. If the underlying cause of CS is not addressed, adverse events will persist and become more numerous.⁹

Drugs that are available or being studied have several targets, but which is best? Diagram: free full text(16)

As of now, there is only one drug approved to treat T2D with CS, but there are several other promising new drugs that may be approved soon:

1. Mifepristone (Korlym)²⁰: Competitive glucocorticoid receptor (GR) antagonist. 

   • Blocks cortisol at the receptor, stopping it from causing its effects.

   • Of the medications currently available, Mifeprisone (Korlym) is the only FDA-approved agent to treat hyperglycemia due to endogenous Cushing Syndrome in adults with T2D or impaired glucose tolerance who have failed or are not candidates for surgery.

   • However, due to its antiprogestational effects (blocks progesterone as well), which causes abortion, it has a box warning and is contraindicated in pregnant women.

   • May also cause hypokalemia and abnormal menstrual bleeding.

   • Blocks the effects of cortisol but does not affect cortisol levels in the body.

     
     

2. Relacorilant²¹: Selective GR modulator/cortisol antagonist.

   • Works similarly to Korlym, blocking the effects of cortisol at the receptor site. 

   • Unlike Korlym, it does not block progesterone, reducing the risk of side effects .

   • The FDA recently accepted an NDA (new drug application), meaning the drug is one step closer to approval.

     
     

3. Isturisa (Osilodrostat)²²: Cortisol synthesis inhibitor

   • Blocks the activity of an enzyme (11-beta-hydroxylase) involved in the production of cortisol.

   • Reduces cortisol production and cortisol levels in the body, thereby relieving the symptoms of the disease.

   • May cause heart palpitations, hypokalemia, hypocortisolemia

   • The FDA recently granted expanded approval to treat patients with Cushing’s syndrome who are not surgical candidates.

     
     

4. Clofutriben^23,24: HSD-1 inhibitor 

   • Blocks cortisol intracellularly.

   • A new, novel approach to treat CS intracellularly, stopping it before it converts to its active form.

   • Currently, an FDA-approved orphan drug for endogenous CS.

   • May soon be approved for autonomous CS. 

Conclusions:

Endogenous CS may be considered a milder form of CS, and it is easily overlooked. Symptoms can be nonspecific and overlap with those of the general population. Patients may not report symptoms that develop gradually, and primary care physicians (PCPs) may not recognize them for what they are. 

PCPs serve as the gatekeepers to patients, playing a crucial role in initial recognition, diagnosis, and referral. They are also often responsible for long-term follow-up, medication management, and interdisciplinary care for these patients. Until recently, the medical community has been unaware of the high prevalence of CS in difficult to control T2D. PCPs may have "given up" on patients they believe are noncompliant. The sole symptom of CS may be progressive, difficult-to-control T2D, despite optimal antihyperglycemic treatments. Physicians should be strongly encouraged to test patients presenting in this manner. 

Patients with CS often require a multidisciplinary team of physicians to address all the comorbidities associated with the disease. Care can be time-consuming, costly, and confusing for many individuals, particularly when dealing with the cognitive manifestations of the disease. Sociodemographic factors and limited access to healthcare further complicate this issue. 

When CS is overlooked, it leads to unnecessary disease progression and comorbidities, resulting in chronic and often permanent debilitating complications for the patient. This can result in isolation, unemployment, and a decreased quality of life. Currently, there is a lack of widely accepted pharmacological therapies proven to be safe and effective, that work quickly, can be used long term, and have minimal side effects. Ongoing research aims to develop better pharmacological treatments for CS. Once approved, PCPs should receive education on the uses and side effects of these medications. 

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