Imaging Technique Measures Tumor Stiffness to Aid Surgical Planning

Posted on January 28, 2026 by MaryO

screenshot-2017-01-27-11-04-44

 

Important steps in planning tumor surgery include identifying borders between tumor and healthy tissue and assessing the tumor stiffness, e.g. hard and calcified or soft and pliant. For decades, tumors near the surface of the body have been evaluated for stiffness by simple palpation—the physician pressing on the tissue. Because tumors within the skull cannot be palpated, researchers used Magnetic Resonance Elastography (MRE) to assess pituitary tumor stiffness by measuring waves transmitted through the skull into pituitary macroadenomas (PMAs). MRE reliably identified tumors that were soft enough for removal with a minimally-invasive suction technique versus harder tumors requiring more invasive surgery.

“The group developed brain MRE several years ago and is now successfully applying it to clinical diagnosis and treatment,” explained Guoying Liu, Ph.D., Director of the NIBIB Program in Magnetic Resonance Imaging. “This development of a new imaging technique followed by its practical application in surgical planning for better patient outcomes is an outstanding example of one of the main objectives of NIBIB-funded research.”

MRE is a special magnetic resonance imaging technique that captures snapshots of shear waves that move through the tissue and create elastograms—images that show tissue stiffness. John Huston III, M.D., Professor of Radiology at the Mayo Clinic in Rochester, MN, and senior author of the study, explains how MRE works. “MRE is similar to a drop of water hitting a still pond to create the ripples that move out in all directions. We generate tiny, harmless ripples, or shear waves, that travel through the brain of the patient. Our instruments measure how the ripples change as they move through the brain and those changes give us an extremely accurate measure–and a color-coded picture–of the stiffness of the tissue.”

MRE data enables non-invasive surgical planning

Ninety percent of PMAs are soft—nearly the consistency of toothpaste. Therefore, without MRE, surgeons would routinely plan for a procedure called transphenoidal resection that employs very thin instruments that are threaded through the nasal cavity to the pituitary gland at the base of the skull, where suction is used to remove the tumor. However, in about 10% of the cases, the surgeon will encounter a hard tumor. At that point an attempt is made to break-up the tumor—essentially chipping away at it with sharp instruments. If that is not successful, the surgeon must perform a fully-invasive craniotomy that involves removing a piece of the skull bone in order to fully expose the tumor.

The more extensive procedure means added risk and discomfort for patients, and up to a week-long recovery in the hospital compared to the transphenoidal approach that allows patients to leave the hospital in a day or two. Using MRE, hard PMAs can be identified and the more extensive craniotomy can be planned before starting the surgery, which makes the more invasive procedure less taxing for both the surgeon and patient. Similarly, MRE showing a soft PMA gives surgeons confidence that the nasal entry and removal by suction will be successful-eliminating the likelihood that the surgeon may need to perform a second fully-invasive craniotomy.

In the study of PMA reported in the January 2016 issue of the journal Pituitary, the group performed pre-surgical MRE evaluation of the PMAs of 10 patients.The MRE measurements were compared to tumor classifications made by inspection of the tumor during surgery. The surgeons categorized six tumors as soft and four tumors as medium. No tumors were deemed to be hard. The comparison of the MRE results and reports of stiffness by the surgeons when the tumor was removed and inspected were in close agreement, which was confirmed by statistical analysis.

Future plans

Although brain MRE is not yet widely available, Huston explained that the surgeons at the Mayo Clinic are now routinely using MRE to plan the best procedure for the removal of PMAs as well as several other types of brain tumor. And, even though this study of the 10 PMA patients is a very small set, Huston believes that as Mayo surgeons continue to use MRE in planning, the technique will likely begin to be adopted by other surgical centers.

Huston explained that an important aspect of some of the other brain tumor types, which the surgeons are finding extremely useful, is the ability of MRE to identify tumor adhesion to the brain. Adhesion refers to whether the brain tumor and healthy brain tissue are connected by an extensive network of blood vessels and connective tissue. This is in comparison with a tumor that is in the brain but is isolated from healthy tissue.

When MRE is used to analyze this aspect of the tumor, it clearly identifies those that are non-adhered, showing a border around the tumor through which there are no vascular connections. Conversely, MRE of adhered tumors show no border between the tumor and healthy brain, indicating extensive vascular and soft tissue connections between brain and tumor. Mutual blood vessels make removal of adherent tumors much more difficult, with a much higher chance of damage to healthy tissue and potential loss of function for the patient.

Huston and his colleagues are continuing to apply MRE, often called “palpating by imaging” to diagnosis of other brain disorders. In addition to characterizing focal brain disorders such as tumors, the group is testing the potential for MRE to provide diagnostic information about diffuse brain disease, and are currently using MRE brain stiffness patterns to identify different types of neural disorders including dementia.

This research was funded by the National Institutes of Health through the National Institute of Biomedical Imaging and Bioengineering grant EB001981.

Magnetic resonance elastography detects tumoral consistency in pituitary macroadenomas. Hughes JD, Fattahi N, Van Gompel J, Arani A, Ehman R, Huston J 3rd. Pituitary. 2016 Jun;19(3):286-92

From http://www.rdmag.com/news/2017/01/imaging-technique-measures-tumor-stiffness-aid-surgical-planning

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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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Cushing’s Syndrome Subtype Affects Postoperative Time to Adrenal Recovery

Posted on January 25, 2026 by MaryO

Berr CM. J Clin Endocrinol Metab. 2014;doi:10.1210/jc.2014-3632.

January 16, 2015

In patients undergoing curative surgical tumor resection for Cushing’s syndrome, the time to recovery of adrenal function is contingent upon the underlying etiology of the disease, according to recent findings.

In the retrospective study, researchers reviewed case records of 230 patients with Cushing’s syndrome. All patients were seen at a tertiary care center in Munich between 1983 and 2014, whose cases were documented in the German Cushing’s Registry. Patients were divided into three subgroups of Cushing’s syndrome: Cushing’s disease, adrenal Cushing’s syndrome and ectopic Cushing’s syndrome.

After applying various exclusion criteria, the researchers identified 91 patients of the three subgroups who were undergoing curative surgery at the hospital. The patients were followed for a median of 6 years. The researchers defined adrenal insufficiency as the need for hydrocortisone replacement therapy, and collected this information from patient records and laboratory results.

The duration of adrenal insufficiency was calculated as the interval between successful surgery and the completion of hydrocortisone replacement therapy. Cushing’s syndrome recurrence was defined as biochemical and clinical signs of hypercortisolism.

The researchers found a significant difference between Cushing’s syndrome subtypes in the likelihood of regaining adrenal function within 5 years of follow-up: The probability was 82% in ectopic Cushing’s syndrome, 58% in Cushing’s disease and 38% in adrenal Cushing’s syndrome (P=.001). Among the 52 participants who recovered adrenal function, the median type to recovery also differed between subtypes and was 0.6 years in ectopic Cushing’s syndrome, 1.4 years in Cushing’s disease and 2.5 years in adrenal Cushing’s syndrome (P=.002).

An association also was found between younger age and adrenal recovery in the Cushing’s disease participants (P=.012).

This association was independent of sex, BMI, symptom duration, basal adrenocorticotropic hormone and cortisol levels. No association was seen between adrenal recovery and length of hypercortisolism or postoperative glucocorticoid replacement dosage.

“It is the main finding of this series that the median duration of tertiary adrenal insufficiency was dependent on the etiology of [Cushing’s syndrome]: It was shortest in the ectopic [Cushing’s syndrome], intermediate in [Cushing’s disease] and longest in adrenal [Cushing’s syndrome] caused by unilateral cortisol producing adenoma,” the researchers wrote. “The significant difference to [Cushing’s disease] is an unexpected finding since by biochemical means cortisol excess is generally less severe in adrenal [Cushing’s syndrome]. If confirmed by others, our data have clinical impact for the follow-up of patients after curative surgery: Patients should be informed that adrenocortical function may remain impaired in benign conditions such as cortisol-producing adenoma.”

Disclosure: The study was funded in part by the Else Kröner-Fresenius Stiftung.

The original article is here: Healio

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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.

Uncited reference

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References

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Cushing’s Syndrome Etiology Affects Adrenal Function Recovery

Posted on January 21, 2026 by MaryO
Abstract
Context:
Successful tumor resection in endogenous Cushing’s syndrome (CS) results in tertiary adrenal insufficiency requiring hydrocortisone replacement therapy.
Objective:

The aim was to analyze the postsurgical duration of adrenal insufficiency of patients with Cushing’s disease (CD), adrenal CS and ectopic CS.

Design:

We performed a retrospective analysis based on the case records of 230 CS patients in our tertiary referral center treated from 1983 to 2014. The mean follow-up time was 8 years.

Patients:
We included 91 patients of the three subtypes of CS undergoing curative intended surgery and documented follow-up after excluding cases with persistent disease, pituitary radiation, concurrent adrenostatic or somatostatin analogue treatment, and malignant adrenal disease.
Results:

The probability of recovering adrenal function within a 5 years follow-up differed significantly between subtypes (p=0.001). It was 82 % in ectopic CS, 58 % in Cushing’s disease and 38 % in adrenal CS. In the total cohort with restored adrenal function (n=52) the median time to recovery differed between subtypes: 0.6 (IQR 0.03–1.1) years in ectopic CS, 1.4 (IQR 0.9–3.4) years in CD, and 2.5 (IQR 1.6–5.4) years in adrenal CS (p=0.002). In CD the Cox proportional-hazards model showed that the probability of recovery was associated with younger age (hazard ratio 0.896, 95% CI 0.822–0.976, p=0.012), independently of sex, BMI, duration of symptoms, and basal ACTH and cortisol levels. There was no correlation with length and extend of hypercortisolism or postoperative glucocorticoid replacement doses.

Conclusions:

Time to recovery of adrenal function is dependent on the underlying etiology of CS.

Affiliations
  • 1Medizinische Klinik und Poliklinik IV, Ludwig-Maximilians-Universität München, Germany;
  • 2Institut für Klinische Radiologie, Klinikum der Ludwig-Maximilians-Universität München, Germany;
  • 3Chirurgische Klinik und Poliklinik – Innenstadt, Klinikum der Ludwig-Maximilians-Universität München, Germany;
  • 4Klinik für Neurochirurgie, Klinikum Grosshadern, Ludwig-Maximilians-Universität München, Germany;
  • 5IMSE, Klinikum rechts der Isar der TU München, München, Germany

From http://press.endocrine.org/doi/abs/10.1210/jc.2014-3632

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