Identification Of Potential Markers For Cushing’s Disease

Posted on January 27, 2026 by MaryO

Endocr Pract. 2016 Jan 20. [Epub ahead of print]

Broder MS1, Chang E1, Cherepanov D1, Neary MP2, Ludlam WH2.

Author information

Abstract

OBJECTIVE:

Cushing’s disease (CD) causes a wide variety of nonspecific symptoms, which may result in delayed diagnosis. It may be possible to uncover unusual combinations of otherwise common symptoms using ICD-9-CM codes. Our aim was to identify and evaluate dyads of clinical symptoms or conditions associated with CD.

METHODS:

We conducted a matched case-control study using a commercial healthcare insurance claims database, designed to compare the relative risk (RR) of individual conditions and dyad combinations of conditions among patients with CD versus matched non-CD controls.

RESULTS:

With expert endocrinologist input, we isolated 10 key conditions (localized adiposity, hirsutism, facial plethora, polycystic ovary syndrome, abnormal weight gain, hypokalemia, deep venous thrombosis, muscle weakness, female balding, osteoporosis) with RR varying from 5.1 for osteoporosis to 27.8 for hirsutism. The RR of dyads of these conditions ranged from 4.1 for psychiatric disorders/serious infections to 128.0 for hirsutism/fatigue in patients with vs. without CD. Construction of uncommon dyads resulted in further increases in RR beyond single condition analyses, such as osteoporosis alone had RR of 5.3, which increased to 8.3 with serious infections and to 52.0 with obesity.

CONCLUSION:

This study demonstrated that RR of any one of 10 key conditions selected by expert opinion was ≥5 times greater in CD compared to non-CD, and nearly all dyads had RR≥5. An uncommon dyad of osteoporosis and obesity had an RR of 52.0. If clinicians consider the diagnosis of CD when the highest-risk conditions are seen, identification of this rare disease may improve.

KEYWORDS:

Cushing’s disease; delay in diagnosis; disease markers; insurance claims; relative risk

PMID:
26789346
[PubMed – as supplied by publisher]

From http://www.ncbi.nlm.nih.gov/pubmed/26789346

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COVID-19 May Be Severe in Cushing’s Patients

Posted on January 23, 2026 by MaryO

A young healthcare worker who contracted COVID-19 shortly after being diagnosed with Cushing’s disease was detailed in a case report from Japan.

While the woman was successfully treated for both conditions, Cushing’s may worsen a COVID-19 infection. Prompt treatment and multidisciplinary care is required for Cushing’s patients who get COVID-19, its researchers said.

The report, “Successful management of a patient with active Cushing’s disease complicated with coronavirus disease 2019 (COVID-19) pneumonia,” was published in Endocrine Journal.

Cushing’s disease is caused by a tumor on the pituitary gland, which results in abnormally high levels of the stress hormone cortisol (hypercortisolism). Since COVID-19 is still a fairly new disease, and Cushing’s is rare, there is scant data on how COVID-19 tends to affect Cushing’s patients.

In the report, researchers described the case of a 27-year-old Japanese female healthcare worker with active Cushing’s disease who contracted COVID-19.

The patient had a six-year-long history of amenorrhea (missed periods) and dyslipidemia (abnormal fat levels in the body). She had also experienced weight gain, a rounding face, and acne.

After transferring to a new workplace, the woman visited a new gynecologist, who checked her hormonal status. Abnormal findings prompted a visit to the endocrinology department.

Clinical examination revealed features indicative of Cushing’s syndrome, such as a round face with acne, central obesity, and buffalo hump. Laboratory testing confirmed hypercortisolism, and MRI revealed a tumor in the patient’s pituitary gland.

She was scheduled for surgery to remove the tumor, and treated with metyrapone, a medication that can decrease cortisol production in the body. Shortly thereafter, she had close contact with a patient she was helping to care for, who was infected with COVID-19 but not yet diagnosed.

A few days later, the woman experienced a fever, nausea, and headache. These persisted for a few days, and then she started having difficulty breathing. Imaging of her lungs revealed a fluid buildup (pneumonia), and a test for SARS-CoV-2 — the virus that causes COVID-19 — came back positive.

A week after symptoms developed, the patient required supplemental oxygen. Her condition worsened 10 days later, and laboratory tests were indicative of increased inflammation.

To control the patient’s Cushing’s disease, she was treated with increasing doses of metyrapone and similar medications to decrease cortisol production; she was also administered cortisol — this “block and replace” approach aims to maintain cortisol levels within the normal range.

The patient experienced metyrapone side effects that included stomach upset, nausea, dizziness, swelling, increased acne, and hypokalemia (low potassium levels).

She was given antiviral therapies (e.g., favipiravir) to help manage the COVID-19. Additional medications to prevent opportunistic fungal infections were also administered.

From the next day onward, her symptoms eased, and the woman was eventually discharged from the hospital. A month after being discharged, she tested negative for SARS-CoV-2.

Surgery for the pituitary tumor was then again possible. Appropriate safeguards were put in place to protect the medical team caring for her from infection, during and after the surgery.

The patient didn’t have any noteworthy complications from the surgery, and her cortisol levels soon dropped to within normal limits. She was considered to be in remission.

Although broad conclusions cannot be reliably drawn from a single case, the researchers suggested that the patient’s underlying Cushing’s disease may have made her more susceptible to severe pneumonia due to COVID-19.

“Since hypercortisolism due to active Cushing’s disease may enhance the severity of COVID-19 infection, it is necessary to provide appropriate, multidisciplinary and prompt treatment,” the researchers wrote.

From https://cushingsdiseasenews.com/2021/01/15/covid-19-may-be-severe-cushings-patients-case-report-suggests/?cn-reloaded=1

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Insulin Resistance Unveiled: Cushing’s Disease in a Patient with Type 1 Diabetes Mellitus and Worsening Glycemic Control

Posted on January 22, 2026 by MaryO

Highlights

  • Coexistence of hypercortisolism secondary to ACTH-producing pituitary adenoma and type 1 diabetes mellitus.
  • Presentation of Cushing’s disease in individuals with type 1 diabetes mellitus.
  • Automated insulin delivery utilization in type 1 diabetes with comorbid refractory hypercortisolism.

ABSTRACT

Background/Objective

Type 1 diabetes mellitus is an autoimmune disease often characterized by endogenous insulin deficiency and often sensitivity to endogenous insulin administration. Cushing’s disease, though rare, should be considered as a cause of insulin resistance and increased insulin requirements in individuals with type 1 diabetes mellitus.

Case Presentation

A 21-year-old female with type 1 diabetes mellitus presented with steadily increasing insulin requirements via her hybrid closed-loop insulin pump. She subsequently developed hypertension, weight gain, violaceous striae, and cystic acne. Laboratory evaluation revealed unsuppressed cortisol of 16.6 μg/dL after a 1-mg dexamethasone suppression test, with a simultaneous adrenocorticotropin hormone level of 73.3 pg/mL. Pituitary MRI showed a 1.9 cm sellar mass with local invasion. She underwent transsphenoidal hypophysectomy. Postoperative cortisol was 8.9 μg/dL after intraoperative dexamethasone exposure. Residual hypercortisolism was confirmed, necessitating gamma knife radiation and pharmacologic treatment with a steroidogenesis inhibitor.

Discussion

We present a case of Cushing’s disease due to a corticotropin-secreting pituitary macroadenoma in a young woman with type 1 diabetes. Her initial presentation included rising insulin requirements, followed by overt hypercortisolism. Despite surgery, persistent hypercortisolism required further intervention with gamma knife radiation and osilodrostat. She experienced reductions in both weight and insulin needs, with normalization of cortisol levels on maintenance osilodrostat.

Conclusion

Cushing’s syndrome should be considered in the differential diagnosis of patients with type 1 diabetes and increasing insulin requirements. This case underscores the importance of regular review of automated insulin delivery data and consideration of endocrine causes of insulin resistance and increased insulin requirements in those with type 1 diabetes.

KEY WORDS

Type 1 Diabetes Mellitus
T1DM
Cushing’s disease
Insulin resistance
Insulin pump
Total Daily Dose
TDD

Introduction

Cushing’s syndrome occurs as the result of prolonged elevation in plasma cortisol which can lead to adverse effects including insulin resistance, hyperglycemia, hypertension, weight gain, immunosuppression, and neurocognitive changes. Cushing’s syndrome can occur due to exogenous exposure to corticosteroids or endogenous cortisol hypersecretion. The most common etiology of endogenous hypercortisolism is Cushing’s disease secondary to a corticotrophin-secreting pituitary tumor. In 90% of cases of Cushing’s disease, patients present with pituitary microadenomas, with only 10% of patients presenting with pituitary tumors >1 cm1.
Type 1 diabetes mellitus is an autoimmune condition characterized by T-cell mediated destruction of pancreatic beta cells with ultimate inability to produce insulin and subsequent insulin dependence2. Over the last decade, there has been significant advancement in diabetes management strategies and insulin delivery with creation of hybrid closed-loop insulin pump technology used in conjunction with continuous glucose monitoring systems to provide automated insulin delivery. Within the field of endocrinology, this has required a shift in both the interpretation of glycemic data, insulin utilization data, as well as a pivot to approaching titration of insulin pump settings. Assessment of total daily basal and total daily dose (TDD) in automated mode is of utmost importance when utilizing automated insulin delivery as the amount of insulin utilized can vary significantly in comparison to fixed quantities seen with use of manual mode in an insulin pump2,3.
Type 1 diabetes mellitus is typically characterized by relative insulin sensitivity, particularly early in the disease course. Patients can develop insulin resistance over time, particularly in the setting of comorbid obesity. However, we present a case of a young woman with type 1 diabetes mellitus presenting with steadily increasing insulin requirements followed by development of overt Cushing’s secondary to corticotropin-secreting pituitary macroadenoma. She was utilizing a hybrid-closed loop insulin pump technology with insulin pump download indicating diminished glycemic control despite a steady increase in total daily insulin requirements. This is only the third reported case of Cushing’s disease in a person living with type 1 diabetes mellitus4,5.

Case Presentation

A 21-year-old female with a history of type 1 diabetes diagnosed at age 11 in the context of admission for diabetic ketoacidosis initially presented to adult endocrinology for routine outpatient diabetes management. Type 1 Diabetes Mellitus was managed with automated hybrid-closed loop insulin pump technology (Tandem T-slim X:2 with Dexcom G6 continuous glucose monitoring system). Her hemoglobin A1c was 6.2% with a review of her continuous glucose monitoring system indicating time in range of 73% with 21% of blood glucose levels >180 mg/dL. At that time, she reported concerns regarding high insulin requirements despite an active lifestyle as she was running out of insulin for use in pump early. She was noted to have significant prandial insulin requirements with insulin to carbohydrate ratio of 1 unit for every 3.0-4.5 carbohydrates, raising concern for insulin resistance. Over the next 16 months, she had weight gain of 15.8 kg with elevation in blood pressure and worsening hyperglycemia. Review of her insulin pump downloads indicated a steady increase in her total daily insulin requirements of close to 30%, coupled with reduced time in range and increase in HbA1c.
On repeat physical examination, the development of cystic acne, trace pitting pedal edema, and purple violaceous striae on the abdomen, hips, and thighs were observed. She was also noted to have a new elevation of blood pressure to 162/101 mm Hg. She declined exposure to exogenous corticosteroids (including oral, topical or intra-articular formulations). Based on clinical examination and changes in insulin requirements, the decision was made to evaluate for hypercortisolism. Laboratory evaluation at that time revealed unsuppressed 08:00 AM cortisol level of 16.6 ug/dL after 1 mg of dexamethasone the evening prior. Dexamethasone level was confirmed to be more than adequate at 418 ng/dL (reference range for 8:00 AM level following 1 mg dexamethasone previous evening: 140-295 ng/dL). A simultaneous ACTH level was elevated at 73.3 pg/mL (reference range: 7.2-63.3 pg/mL). She was also noted to have midnight salivary cortisol levels of 0.646, 0.290, and 0.350 ug/dL on three consecutive evenings (reference range <0.010-0.090 ug/dL).
She then underwent MRI pituitary with and without gadolinium enhancement which revealed 1.8 x 1.9 cm enhancing sellar mass with invasion of the right cavernous sinus, extension around the right internal carotid artery, as well as posteriorly down the dorsal aspect of the clivus (Figures 1 and 2). As both hypercortisolism as well as type 1 diabetes mellitus have been implicated as etiologies for lower bone density with subsequent increased risk of osteoporosis later in life, bone densometry was also obtained for this patient. She was found to have low bone mineral density for her age with Z-score of the lumbar spine of -3.2, Z-score of the femoral neck of -2.3, and Z-score of the total hip of -2.8.

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Figure 1. MRI pituitary coronal image revealing sellar mass with invasion of the right cavernous sinus, extension around the right internal carotid artery.

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Figure 2. MRI pituitary sagittal image revealing 1.8 x 1.9 cm sellar mass.

She was evaluated by neurosurgery and underwent endoscopic trans-sphenoidal resection of pituitary macroadenoma. Pathology revealed immunoreactivity for neuroendocrine marker INSM1 (Insulinoma-associated protein 1) and adrenocorticotropic hormone. The lesion was negative for immunoreactivity for prolactin, growth hormone, thyroid-stimulating hormone, follicle-stimulating hormone, and beta-luteinizing hormone.
The cortisol level was 8.9 ug/dL on post-operative day 1. It is notable that she had received 10 mg of intravenous Dexamethasone intraoperatively, raising concern for residual tumor. On post-operative day 3, cortisol level was 4.1 mcg/dL with ACTH level of 94.5 pg/mL. Repeat random cortisol level was 16.3 mcg/dL with simultaneous ACTH level of 63.3 pg/mL. Upon being discharged home, a repeat 24-hour urinary free cortisol was obtained in the outpatient setting and found to be elevated at 464 ug/24 hours (reference range: 6-42 ug/24 hours), consistent with refractory hypercortisolism (Table 1, Figure 4). She was then initiated on osilodrostat, a steroidogenesis inhibitor approved by the FDA in 2020 for use in refractory Cushing’s disease after pituitary surgery. Osilodrostat works via inhibition of 11β-hydroxylase and aldosterone synthase to inhibit the production of cortisol and aldosterone6,7. She underwent ongoing up titration to a maintenance dose of osilodrostat 7 mg twice daily with additional insulin pump titrations over a 2-year duration. Urinary free cortisol was monitored as this is the gold standard for monitoring refractory Cushing’s and the preferred modality for monitoring cortisol levels in individuals on osilodrostat. Final repeat 24-hour urine free cortisol level normalized to 35 ug/24 hours and TDD of insulin via automatic insulin delivery system was lower than time of diagnosis of pituitary Cushing’s at 96 units per day despite having had a roughly 27 kg weight gain (Table 1, Figure 4).

Table 1. Weight trends as well as TDD of insulin listed along with glycemic parameters from automated insulin dosing system Tandem T-slim X:2 with automated mode utilizing Decom G6 CGM. 24-hour urine cortisol collection data included to highlight degree of hypercortisolism. Treatments denoted by asterisk in table include

Date Weight (kg) Total daily insulin dose (units/day) HbA1c (%) Time in range (%) Urine cortisol (mcg/24 hours); RR 6-42 mcg/24 hours
03/2021 72.7 99.25 6.2 73
06/2021 74.5 109.56 6.6 73
12/2021 80.0 117.17 6.9 62
05/2022 88.5 126.84 6.9 57
11/2022∗ – – – –
12/2022 93.8 124.15 7.0 61 464
01/2023∗∗ – – – –
02/2023 35
06/2023∗∗∗ – – – –
06/2023 100.4 122.76 7.0 54
07/2023 137
12/2023 100.9 130.34 6.8 48 48
08/2024 106 125 6.9 58 76
02/2025 100 96 5.8 76 42
∗
Transsphenoidal resection.
∗∗
Osilodrostat initiated.
∗∗∗
Gamma knife radiosurgery.

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Figure 3. MRI pituitary coronal image revealing right eccentric heterogenous enhancing sellar mass which is decreased in size. Redemonstrated residual tissue around the right carotid artery.

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Figure 4. Graphical representation of weight (kg), total daily dose of insulin (units per day), and 24-hour urine cortisol measurements (mcg/24 hours).

Due to ongoing hypercortisolism, repeat MRI pituitary with and without gadolinium enhancement was obtained and revealed residual disease in the right sella with right cavernous sinus involvement and extending posteriorly along the dorsal aspect of the clivus (Figure 3). She had subsequent consultation with neurosurgery at which time the decision made to proceed with single-fraction gamma knife stereotactic radiosurgery. She received additional treatment of gamma knife radiosurgery with dose of 18 Gy to target residual pituitary disease.

Discussion

We present, to our knowledge, the third reported case of Cushing’s disease due to a corticotropin-secreting pituitary adenoma in an individual with type 1 diabetes. Prolonged hypercortisolism, as seen in this case, is associated with obesity, hypertension, decreased bone density, insulin resistance, and decreased glucose control. Hypercortisolism is most commonly caused by chronic exogenous corticosteroid exposure however, endogenous hypercortisolemia should be considered as a potential etiology of worsening glycemia and insulin resistance in individuals with diabetes mellitus.
The coexistence of Cushing’s disease secondary to a corticotropin-secreting pituitary macroadenoma in an individualwith type 1 diabetes mellitus is exceedingly rare. Furthermore, only 10% of pituitary Cushing’s cases present with macroadenomas at the time of diagnosis. Several studies indicate that smaller lesions at the time of diagnosis and earlier diagnosis of Cushing’s disease are associated with reduced risk of disease recurrence6,7,8. In this case, a young female presented with a macroadenoma at the time of diagnosis and had residual post-operative hypercortisolism requiring gamma knife radiation and pharmacologic intervention with osilodrostat, a steroidogenesis inhibitor approved by the FDA in 2020 for use in refractory Cushing’s disease after pituitary surgery. Osilodrostat works via inhibition of 11β-hydroxylase and aldosterone synthase to inhibit the production of cortisol and aldosterone9,10. Of the two other reported cases of comorbid type 1 diabetes and Cushing’s disease, one individual presented with a macroadenoma at the time of diagnosis. This case occurred in a pediatric male with type 1 diabetes mellitus who was ultimately admitted to the hospital with worsening headaches in the setting of pituitary apoplexy. Prior to hospitalization, this individual showed numerous clinical stigmata of hypercortisolism.
Other contributors to increased insulin resistance, such as obesity, infection, stress, and concurrent glucocorticoids, should also be considered in the differential diagnosis when evaluating etiologies for unexplained changes in glycemic control. However, this case emphasizes the importance of considering the possibility of comorbid Cushing’s disease in persons with type 1 diabetes mellitus. This is imperative to mitigate the consequences of prolonged hypercortisolism and to potentially aid in earlier diagnosis. In this case, declining glucose control and increasing insulin requirements were noted prior to other overt clinical findings of hypercortisolism. Thus, this case also underscores the importance of steadfast evaluation of insulin dose requirements for individuals using continuous insulin infusion devices (particularly hybrid closed-loop automated insulin delivery [AID] systems). With growing emphasis on the review and utilization of the one-page ambulatory glucose profile, it is important to also review insulin pump settings and insulin delivery for those utilizing these systems as automated insulin delivery profile for total daily dose can change and should be reviewed at each visit.

Conclusion

In closing, this case emphasizes the importance of considering secondary endocrine disorders in those living with diabetes mellitus who experience sudden or unexplained changes in glycemic control and insulin requirements. Although rare, coexistence of type 1 diabetes and Cushing’s disease can occur. Prompt recognition and treatment of the underlying Cushing’s disease can lead to significant improvements in insulin sensitivity and glycemic outcomes. This report reinforces the need for multidisciplinary management of vigilant monitoring in patients with coexisting endocrine pathologies, particularly when advanced diabetes technologies are in use. Ultimately, it highlights the critical role of clinical suspicion and timely intervention in optimizing outcomes for complex endocrine cases.

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References

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Topical Ocular Glucocorticoid Leads to Cushing’s Syndrome in 9-Year-Old

Posted on January 21, 2026 by MaryO

In a case report published online January 19 in Pediatrics, iatrogenic Cushing’s syndrome (CS) is described in a 9-year-old girl who received topical ocular glucocorticoid (GC) treatment for bilateral iridocyclitis.

Daisuke Fukuhara, MD, PhD, from the Kyorin University School of Medicine in Mitaka, Japan, and colleagues present the case of a 9-year-old girl suffering from idiopathic uveitis. She arrived at the ophthalmology department with a complaint of painful eyes, and was diagnosed with bilateral iridocyclitis and started on betamethasone sodium phosphate eye drop treatment.

The authors note that the patient was referred to the pediatric department with stunted growth, truncal obesity, purple skin striae, buffalo hump, and moon face six months after initiation of topical ocular GC treatment. She was diagnosed with iatrogenic CS as her serum cortisol and plasma adrenocorticotropic hormone levels were undetectable. The clinical symptoms of CS were improved after the doses of topical ocular GC were reduced. On genetic analysis, the patient was found to have a single heterozygous nucleotide substitution in the 3′ untranslated region of the NR3C1 gene.

“However, additional investigations are required to determine if our findings can be extrapolated to other patients,” the authors write. “In conclusion, clinicians should be aware that even extremely low doses of topical ocular steroid therapy can cause iatrogenic CS.”

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From http://www.empr.com/news/iatrogenic-cushings-syndrome-topical-ocular-glucocorticoid-iridocyclitis/article/632840/

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Cushing’s Disease: When Symptoms Are Mistaken for Menopause

Posted on January 11, 2026 by MaryO

After 8 years of menopause-like symptoms, a 62 year old patient discovered she actually had Cushing’s disease. Read about her long journey to get a diagnosis and her success in finding her dream-come-true neurosurgeon.

A Mysterious Decline in Health

When Elisabeth N., 62, started developing symptoms that included obesity, osteoporosis, insomnia, kidney stones and hair loss, she attributed it to what most women her age would: menopause. Back in 2000 she never would have thought those seemingly normal symptoms for a woman her age would lead her to Santa Monica to be treated eight years later by Daniel Kelly, MD., neurosurgeon and director of the Pacific Pituitary Disorders Center at Pacific Neuroscience Institute and Saint John’s Health Center. In fact, it wasn’t till February of 2008 that she learned it could all be caused by something completely different.

A Sister’s Observation Leads to a Breakthrough

“I wouldn’t have known about Cushing’s disease if it weren’t for my youngest sister; I’m 25 years older and so fortunate she has her medical degree,” explained Elisabeth, a kitchen and bath designer in Mesa, Arizona. “We hadn’t seen one another for five years when we visited in February of 2008. My appearance had drastically changed by then. She told me, ‘Don’t be scared, Bethie, but I think you should be tested for Cushing’s.’”

Learning About Cushing’s Disease

cushing's disease symptoms infographic

Elisabeth started researching Cushing’s disease right away and was relieved to learn that a cure was possible. Cushing’s is a hormonal disorder caused by high levels of the hormone cortisol. Symptoms include upper-body obesity, fragile skin that bruises easily, weakened bones, severe fatigue, weak muscles, high blood pressure, high blood glucose, increased thirst and urination, depression and a fatty hump between the shoulders. Women can also experience irregular menstrual periods and excess hair growth on their bodies. It can be caused by taking glucocorticoids such as prednisone or if there is a problem with a person’s pituitary gland or hypothalamus.

A Long and Uncertain Testing Journey

Elisabeth immediately set up a doctor’s appointment to get her cortisol and adrenocorticotropic hormone (ACTH – the pituitary hormone that stimulates the adrenal glands to make cortisol) levels tested. Over the next nine months Elisabeth went through several blood, urine, saliva and plasma tests for her cortisol and ACTH production and had an MRI. The tests showed elevated cortisol and ACTH levels but the initial impression was that her levels were not high enough to indicate Cushing’s disease and her pituitary MRI showed no apparent tumor. Elisabeth met with both a pituitary neurosurgeon and an endocrinologist, but both determined her condition not to be Cushing’s.

“My cortisol was not high enough; I wasn’t obese enough; I wasn’t disabled enough; I wasn’t depressed enough,” Elisabeth said.

Finding the Missing Clue

She felt frustrated by the diagnosis and continued to research possibilities online. It was during this research that she stumbled upon an article comparing MRI Tesla strengths. It recommended getting a Tesla 3.0 with contrast to pick up small abnormalities. Elisabeth scheduled a new MRI at the beginning of November. This time the scan detected a 6 mm tumor on the right side of her pituitary gland. Additional hormonal testing also confirmed that she did indeed have high ACTH and cortisol levels consistent with Cushing’s, “I was thrilled to finally have proof I had Cushing’s, but terrified because I knew I’d have to have brain surgery to remove it,” Elisabeth said. “I knew I wanted transsphenoidal surgery – the safest, most successful procedure with the least complications if done by an experienced surgeon.”

Understanding the Endonasal Transsphenoidal Approach

endonasal procedure illustration

Endonasal transsphenoidal tumor removal, aka endoscopic endonasal approach, such as what Elisabeth needed, is a surgery that uses the nostril as the entry point with visualization from the operating microscope and endoscope. The approach passes through the back of the nasal cavity and into the sphenoid sinus to the skull base without facial incisions, brain retraction or post-operative nasal packing.

“This type of surgery is ideal for removing over 99% of pituitary adenomas, like what Elisabeth had and is considered first-line therapy for patients with Cushing’s disease,” Dr. Kelly explained. “Untreated or incompletely treated, Cushing’s disease is a very serious condition leading to uncontrolled hypertension, diabetes, weight gain and increased mortality.”

Choosing the Right Surgeon

With all the months she had to prepare for a diagnosis, Elisabeth knew exactly what needed to be done.

“I’d known I wanted Dr. Kelly to perform surgery but never imagined it could happen,” Elisabeth said. “I found him online. He’s ranked as one of the world’s top neurosurgeons specializing in this type of surgery. While watching his YouTube videos, I was awed by his kindness, patience, sense of humor, approachability, professionalism and complete lack of arrogance in spite of his fame. I’m still pinching myself that I had the fortune and honor to become one of his patients.”

A Life-Changing Call

Dr. Daniel Kelly and Dr. Chester Griffiths perform surgery

Figuring she didn’t have anything to lose, Elisabeth called Dr. Kelly’s office and asked if he was accepting new patients (he was) and how long was his waiting list (she could see him next week). Elisabeth was astounded. She immediately mailed Dr. Kelly all the test results, films and reports she could gather.

“Two days later, Dr. Kelly personally called and left a message, indicating it appeared there was indeed an ACTH secreting adenoma on my pituitary gland and to call him back,” Elisabeth said. “I was blown away. I’d have expected to win the lottery first.”

Successful Surgery and a New Beginning

Dr. Kelly arranged to perform Elisabeth’s surgery two weeks later on November 26 – the day before Thanksgiving. Her cortisol levels fell dramatically within 24 hours of surgery. She has remained in remission since then. Years after surgery, she continues to feel like a new person and regularly stays in contact with Dr. Kelly and his office staff.

About Dr. Daniel Kelly

Dr. Daniel Kelly, a board-certified neurosurgeon, is the director and one of the founders of the Pacific Neuroscience Institute, director of the Pacific Brain Tumor Center and Pacific Pituitary Disorders Center, and is Professor of Neurosurgery at Saint John’s Cancer Institute at Providence Saint John’s Health Center. Considered to be one of the top neurosurgeons in the US, he is a multiple recipient of the Patients’ Choice Award and Southern California Super Doctors distinction.

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