Thirty-four patients with Cushing's Syndrome: our clinical experience in the past 20 years/ Otuz dort Cushing's Sendromu olgusu: 20 yillik klinik deneyimlerimiz.
Abstract: Objective: Cushing's syndrome is a relatively rare disorder caused by chronic endogenous hypercortisolemia. We aimed to present patients with Cushing's syndrome who were diagnosed and followed at our endocrinology clinic.

Materials and Methods: 34 patients (26 female, 8 male) with Cushing's syndrome were enrolled in this retrospective study.

Results: Of 34 patients, 20 had Cushing's disease and 14 had Cushing's syndrome. Regarding the clinical signs of Cushing's syndrome, purple striae were present in 31 subjects (91.2%), hirsutismus in 21 (72.4 %), buffalo hump in 33 (97.1%), moon face in 33 (%97.1), plethora in 33 (%97.1), and menstrual irregularities in 21 (84%) subjects. Diabetes mellitus (DM), hypertension and osteoporosis were found to be 13/34 (39.4%), 23/34 (69.7%) and 18/34 (66.7%), respectively. Following the treatment, primary adrenal failure, secondary adrenal failure, central hypothyroidism, central hypogonadism and central diabetes insipidus were found to be 3 (8.8%), 3 8.8%), 4 (11.7%), 4 (11.7%) and 4 (11.7%), respectively.

Conclusions: As reported in the literature, Cushing's disease is the most common form of Cushing's syndrome and various complications such as adrenal failure, hypogonadism, diabetes insipidus can develop following the treatment.

Key words: Cushing's syndrome, Cushing's disease, hypercortisolemia

Amac: Cushing's sendromu nadir gorulen, kronik endojen hiperkortizoleminin yol actigi morbid bir hastaliktir. Biz klinigimizde tani konulan ve takip edilen 34 Cushing 's sendromlu hastayi sunmayi amacladik.

Gerec ve Yontemler: Bu retrospektif calismaya 34 (26 kadin, 8 erkek) Cushing 's sendromlu hasta dahil edildi.

Bulgular: Otuz dort hastanin 20'si Cushing's hastaligi, 14'u Cushing's sendromu tanisi aldi. Cushing's sendromunun klinik bulgularindan, mor strialar 31 (%91,2), hirsutismus 21 (%72,4 ), buffalo hump 33 (%97,1), aydede yuzu 33 (%97,1), pletore 33 (%97,1) ve adet duzensizligi 21 (%84) hastada goruldu. Diyabetes mellitus (DM), hipertansiyon ve osteoporoz sirasiyla 13/34 (%39,4), 23/34 (%69,7) ve 18/34 (%66,7) hastada bulundu. Tedavi sonrasinda takiplerde primer adrenal yetmezlik, sekonder adrenal yetmezlik, santral hipotroidizm, santral hipogonadizm ve santral diyabetes insipidus oranlari sirasiyla 3 (%8,8), 3 (%8,8), 4 (%11,7), 4 (%11,7) ve 4 (%11,7) olarak saptandi.

Sonuc: Literaturle uyumlu olarak, Cushing's hastaligi Cushing's sendromunun en cok gorulen seklidir ve tedavi sonrasi farkli komplikasyonlar, ornegin; adrenal yetmezlik, hipogonadizm, diyabetes insipidus gelisebilir.

Anahtar kelimeler: Cushig's sendromu, Cushing's hastaligi, hiperkortizolemi
Article Type: Report
Subject: Cushing syndrome (Risk factors)
Cushing syndrome (Diagnosis)
Cushing syndrome (Research)
Authors: Evran, Mehtap
Sert, Murat
Tetiker, Tamer
Pub Date: 12/01/2009
Publication: Name: Turkish Journal of Endocrinology and Metabolism Publisher: Galenos Yayincilik Audience: Academic Format: Magazine/Journal Subject: Health Copyright: COPYRIGHT 2009 Galenos Yayincilik ISSN: 1301-2193
Issue: Date: Dec, 2009
Topic: Event Code: 310 Science & research
Geographic: Geographic Scope: Turkey Geographic Code: 7TURK Turkey
Accession Number: 219520154
Full Text: Introduction

In Cushing's syndrome the most frequent signs are gaining excess weight and central obesity. Also, hypertension, plethorea, hirsutismus, glucose intolerance, DM, menstrual irregularities, osteoporosis and hepatosteatosis are the other frequent findings (1,2). 85% of endogenous Cushing's syndrome is ACTH-dependent. Of these, 68% is pituitary adenoma, whereas 15% is ectopic ACTH syndrome. Adrenal causes account for approximately 15% of Cushing's syndrome (3,4,5). Low-dose dexamethasone suppression test (DST), 24-h urinary free cortisol (UFC) levels, highdose DST, corticotropin-releasing hormone (CRH) test and imaging modalities are among the current diagnostic approaches (4). In treatment, unilateral adrenalectomy is method of choice in adrenal adenomas, while transsphenoidal hypophyseal surgery is such in hypophyseal microadenomas.

In this study, we report our clinical experience in 34 patients with Cushing's syndrome.

Materials and Methods

Population and Study Design

34 patients diagnosed and treated as Cushing's syndrome, as general term, at our university endocrinology clinic between 1989 and 2008 years, were included in this retrospective study. Iatrogenic Cushing's cases were excluded from the study. Data consisting of age, sex, height, weight, body-mass index (BMI), systolic and diastolic blood pressure (BP) and pulse rate were recorded. The typical clinical findings were determined.Osteoporosis, DM and gonadal dysfunction were assessed from a metabolic point of view. Screening for osteoporosis was performed with bone mineral density (BMD) measurement by DEXA at lumbar spine (L1-L4) and femural neck.

Laboratory Examination

Plasma basal cortisol and ACTH levels, low-dose (1 mg) and highdose (8 or 16 mg) of dexamethasone suppression tests and 24-h UFC levels were measured. 24-hour UFC levels which were >2-fold above the normal levels were considered as consistent with Cushing's syndrome. Following 1-mg DST, cortisol level below 3 [micro]g/dl was accepted to be a positive response. For 8-mg or 16-mg DST, 50% or more decrease in the basal cortisol level was accepted to be a positive response for Cushing's disease. Radyological screening with CT or MRI were obtained focusing on the suspected site (pituitary or abdominal). The treatment modalities and the outcomes were also studied. Plasma cortisol levels were measured by ELISA or RIA methods, serum ACTH levels--by HPLC. Normal limits of ACTH and cortisol levels are 10-50 pg/ml and 3-25 [micro]g/dl at the central laboratory of our hospital. Remission was assessed at one and six months with performed basal cortisol level and 1mg DST.

Statistics

Data obtained from patients were analysed by using SPSS 10.0 program. The results were presented as mean [+ or -] SEM. The frequencies of all parameters were calculated. The differences between pre- and post-treatment measures were assessed by using paired-samples t-test and p< 0.05 was accepted as significant in 95% confidence interval.

Results

Clinical Findings

Mean age, BMI, systolic and diastolic blood P, cortisol and ACTH levels of the patients are shown in Table 1, and clinical and metabolic findings of patients with Cushing's syndrome are shown in Table 2. MRI/BT showed microadenoma in most of the patients with Cushing's disease (CD) (n=15, 75%), (See Table 3). Visual field defects were detected in 2 patients (10%). Inferior petrosal sinus sampling (IPSS) was performed only in one patient and confirmed the diagnosis of CD. Adrenal CT/MRI revealed adrenal hyperplasia in 5 (36%) and adrenal adenoma in 9 (64%) patients with diagnosed Cushing's syndrome (CS) (See Table 4).

Abdominal ultrasound was performed in 26 patients and the findings were as follows: completely normal in 8 (30.8%) subjects, hepatosteatosis in 8 patients, hepatosteatosis with hepatomegaly in 5 patients, adrenal hyperplasia in 2, nephrolithiasis in 2, and hepatomegaly alone in 1 patient.

Metabolic Abnormalities

The mean basal serum cortisol level of all patients was 71.49[+ or -]27.7 [micro]g/dl (range: 9-744 [micro]g/dl). Among the patients considered to have CS, serum ACTH levels were found to be 11.1[+ or -]6 pg/ml. In patients with CS, the mean 24-h UFC level was 195.6[+ or -]35 [micro]g/24 h (n=5, range: 35.4-685 [micro]g/24h).

In patients with CD, the mean ACTH level was 197[+ or -]57 (range 43.6-886 pg/ml) and the mean 24-h UFC level was 483[+ or -]163 [micro]g/24h (n=6, range: 37-1015 [micro]g/24h).

1-mg DST was applied to 30 patients and the mean cortisol level was 32.02[+ or -]8.6 (range: 3.4-275 [micro]g/dl). Out of 20 patients with CD, 12 (60%) showed suppression (>50% vs. basal level) during the 8 mg DST. 16-mg DST was performed in 8 patients who had no supression with 8-mg dexamethasone, and 6 of them showed suppression.

The mean white blood cell (WBC) and eosinophil counts were 9417[+ or -]389 and 169[+ or -]14.5, respectively. There was no significant difference between pre- and post-treatment WBC and eosinophil levels (p=0.22, p=0.28, respectively).

The diagnosis was confirmed with IPSS in the patient considered to have CD, but with normal pituitary imaging (presented in Table 3 as number 15). Metabolic investigations of 34 patients with Cushing's syndrome showed DM in 13 (39.4%) patients. Of 27 patients who had BMD measurements, 17 (63%) had osteoporosis at left femoral neck and 18 (66.7%) at anteroposterior lumbar vertebrae (mean T-score was -2.7[+ or -]0.4 and -2.9[+ or -]0.2, respectively).

Managements of the Patients

The management and the outcomes of the patients are shown briefly in Table 3 and 4. Surgery was performed focusing on the targets which were disclosed by CT or MRI scans. Among surgical methods performed in the study: Transsphenoidal pituitary surgery was in 11 (55%), and transcranial pituitary surgery was in 6 (30%) subjects. Macroadenoma was detected in 3 patients who underwent transcranial pituitary surgery. The patients with CD were assessed by neurosurgery department to make the decission about transcranial pituitary surgery. For patients with CS, unilateral adrenalectomy and bilateral adrenalectomy were performed in 6 (42.8%) and 4 (28.5%), respectively. Data on medical treatments of 28 patients were obtained. 53.6% of them did not take any medication. 7 (25%) and 6 (21.4%) patients were administered aminoglutethimide and ketoconazole, respectively. As mentioned above, surgical treatment was performed along with medical treatment in some patients.

The efficacy of all treatment modalities was assessed based on the data from 26 patiens (the patients were assesed at one and 6 months after surgery): cure rate was 76%, on the other hand, failure of treatment was seen in the remaining 16%. The complications related to the treatment of 26 patients included secondary adrenal insufficiency in 3 patients (8.8%), primary adrenal insufficiency 3 in patients (8.8%) and central hypothyroidism in 4 patients (11.7%). Central hypogonadism and central diabetes insipidus were seen in 4 (11.7%) and 4 patients (11.7%), respectively. Transient diabetes insipidus, neurological complications and recurrence were not observed.

Discussion

Cushing's syndrome is usually seen between the third and fifth decades of life, and causes morbidity and mortality associated with chronic hypercortisolemia. Women are affected more than men (5,6). In this study, the mean age of the patients was 31.8[+ or -]2.2 years, and the frequency of female patients (26/34) was consistent with the reported studies (7).

Regarding the etio-pathogenesis, of 34 patients, 20 had CD (58.8%) and 14 had CS (41.2%). CD was found to be more frequent among our patients (3,4). In a study by Erem C et al. from Turkey, CD was reported in 39 patients (71%), adrenal adenoma in 13 patients (23.6%) and adrenal carsinoma in 3 patients (5.5%) (8). Among the morbidities due to Cushing's syndrome, impaired glucose tolerance, DM and fasting hyperglycemia have been reported to be 35%, from 15 to 20%, and from 10 to 15% respectively (1,2). In the present study, DM was found in 13 patients (39.4%), which was a higher rate than that in the reported studies. We can speculate that this high rate of DM is due to delay in the diagnosis of CS. In addition, obesity (n=23, 82%) and the relatively advanced age of the patients might also be involved. There was a positive correlation between the age of our patients and DM (p=0.004). The rate of nephrolithiasis associated with Cushing's syndrome was found to be lower than that of the reported studies (7.7% vs 15%, respectively) (7,9). Hypertension rate and skin findings were observed to be similar to the reported studies (2,10). The rate of osteoporosis was relatively higher in our study than in the reported studies (59% and 66.7 %, respectively) (6). However, this difference could be related to many factors including ethnicity, gender, age, nutrition.

Currently, in the differential diagnosis of CD and CS, HDDST (8/16 mg) has not routinely been recommended in the clinical practice due to its low sensitivity and specifity (65-100%) (11,12). Among the patients with CD in whom HDDST was performed, of 20 subjectssuppression (>50% vs. basal serum cortisol) was observed in 18 (90%). Only 6 of the patients with CS showed supression during HDDST (HDDST was not performed in all patients with CS).

Plasma ACTH measurement is also an important step in the differential diagnosis of Cushing's syndrome (2). In CS of adrenal origin, plasma ACTH level is expected to be below <5pg/ml. When ACTH level is found to be >20 pg/ml, ACTH-dependent CS should be considered (5,13). In our 20 patients with CD, serum ACTH level was 197[+ or -]57 pg/ml, which was consistent with other studies (7,8). Recently, midnight plasma cortisol measurements have been performed for establishing the diagnosis of Cushing's syndrome. We had only 4 patients with midnight cortisol measurements and their results were found to be higher than those in Cushing's syndrome. Regarding the sensitivity and specifity, these measurements were reported to be comparable to the 24-h urine cortisol measurement and low-dose DST (5,14). Likewise, salivary cortisol measurement is also a sensitive method used in the diagnosis of Cushing's syndrome (15,16). But, we had no patient whose salivary cortisol level was measured. In the subjects who have findings of Cushing's syndrome, if 24-h urine cortisol level is 2-fold higher than the normal range, Cushing's syndrome is confirmed (17). Out of 34 patients, 11 had results of 24-h urine cortisol measurements, as variable, which were similar to that in the study by Bos Kuil MJ, et al (18).

IPSS was performed in 1 patient who had normal pituitary MRI scan, central to peripheral venous ACTH ratio was found to be >2/1. In a study on ACTH-dependent CS, Wiggam et al. confirmed the diagnosis of CS in 82% of total of 53 patients by using IPSS (19). As general, following the pituitary surgery, complication rate is nearly 5%, and the mortality is low, and transient diabetes insipidus can be seen in 10% of patients. Haemorrhagia, rhinorrhea, vision loss and persistent diabetes insipidus are rare (2,20). In the present study, the high complication rates (in 10 patients, 29.4%; with more than one complication in some patients) may be due to delay in diagnosis and admittance for surgery, and due to absence of experienced pituitary surgeons.

One of the two patients, who developed Nelson syndrome following the bilateral surrenalectomy, underwent transsphenoidal adenomectomy, and the other was treated with conventional radyotherapy (5000 Rad). In a study including 53 patients, by Assie et al., Nelson syndrome was reported in half of the patients who had bilateral surrenalectomy (21).

Medical treatment with ketoconazole or aminoglutethimide was administered in a short period (a few months) in certain patients, but their results and data were not enough to be discussed here. When we reviewed all our treatment modalities, we assessed the cure rate as 76% (26 patients), which was relativelly good. In conclusion, in this retrospecitive study consisting of 34 patients with Cushing's syndrome, we found that the general findings of Cushing's syndrome were similar to those reported in the literature, with a little variation in the rate of frequency. However, the rates of Cushing's syndrome and DM were higher than in the literature, and the complication rates following the surgery were found to be also high.

Recevied: 03.01.2010 Accepted: 30.01.2010

References

(1.) Raff H and Findling JW. A physiologic approach to the diagnosis of Cushing syndrome. Ann Intern Med 2003; 138: 980-991.

(2.) Arnaldi G, Angeli A, Atkinson AB, et al. Diagnosis and complications of Cushing's syndrome: A consensus statement. J Clin Endocrinol Metab 2003; 88: 5595-5602.

(3.) Biller BMK. Pathogenezis of Pituitary Cushing's syndrome. Endoc. And Meth. Clin of. North Am 1994; 23: 547-554.

(4.) Stewart PM. The adrenal cortex. Williams Textbook of Endogrinology 10.edition (Ed: Larsen PR, Kronenberg HM, Melmed S, Polonsky KS). Philadelphia, Saunders, 2003, 491-541.

(5.) John Newell-Price. Cushing's syndrome. Medicine 2005; 33: 11-13.

(6.) Melmed S, Jameson JL. Disorders of the Anterior Pituitary and Hypothalamus. Harrison' s Principles of Internal Medicine 16.edition (Ed: Kasper DL, Fauci AS, Longo DL, Braunwald E, Hauser SL, Jameson JL) . Mc Graw Hill, 2005, 2076-2097.

(7.) Newell-Price J, Grossman AB. The differential diagnosis of Cushing's syndrome. Ann Endocrinol (Paris) 2001; 62: 173-179.

(8.) Erem C, Algun E, Ozbey N, et al. Clinical laboratory findings and results of therapy in 55 patients with Cushing's syndrome. J Endocrinol Invest 2003; 26: 65-72.

(9.) Faggiano A, Pivonello R, Melis D, et al. Nephrolithiasis in Cushing's disease: prevalance, etiopathogenesis, and modification after disease cure. J Clin Endocrinol Metab 2003; 88: 2076-80.

(10.) Dluhy RG, Lawrence JE, Williams GH. Endocrine Hypertension. Williams Textbook of Endogrinology 10. edition (Ed: Larsen PR, Kronenberg HM, Melmed S, Polonsky KS). Philadelphia, Saunders, 2003, 552-579.

(11.) Lindsay JR, Nieman LK. Differantial diagnosis and imaging in Cushing's syndrome. Endocrinol Metab Clin N Am 2005; 34: 403-421. Evran et al.

(12.) Aron DC, Findling JW, and Tyrrell JB. Glucocorticoids and adrenal androgens. Basic and Clinical Endocrinology 8.edition (Ed: Greenspan FS and Gardner DG.). New York, Lange/McGraw Hill, 2007, 346-395.

(13.) Hermus AR, Pieters GF, Pesman GJ, et al. The corticotropin-releasing-hormone test versus the high-dose dexamethasone test in the differantial diagnosis of Cushing's syndrome. Lancet 1986; 2: 540-544.

(14.) Gorges R, Knappe G, Gerl H, et al. Diagnosis of Cushing's syndrome: reevaluation of midnight plasma cortisol vs urinary free cortisol and lowdose dexamethasone suppression test in a large patient group. Journal of Endocrinological Investigation 1999; 22: 241-249.

(15.) Castro M, Elias PC, Quidute AR, et al. Out-patient screening for Cushing's syndrome: the sensitivity of the combination of circadian rhythm and overnight dexamethasone suppression salivary cortisol tests. Journal of Clinical Endocrinology & Metabolism 1999; 84: 878-882.

(16.) Raff H. Salivary cortisol: a useful measurement in the diagnosis of Cushing's syndrome and the evaluation of the hypothalamic-pituitaryadrenal axis. Endocrinologist 2000; 10: 9-17.

(17.) Williams GH, Dluhy RG. Disorders of the Adrenal Cortex Harrison' s Principles of Internal Medicine 16.edition (Ed: Kasper DL, Fauci AS, Longo DL, Braunwald E, Hauser SL, Jameson JL). Mc Graw Hill, 2005, 2127-2148.

(18.) de Bos Kuil MJ, Endert E, Fliers E, et al. Establishment of reference values for endocrine tests. I: Cushing's syndrome. Netherlands Journal of Medicine 1998; 53: 153-163.

(19.) Wiggam MA, Heaney AP, McIlrath EM, et al. Bilateral Inferior Petrosal Sinus Sampling in the Differential Diagnosis of Adrenocorticotropin-Dependent Cushing's Syndrome: A Comparison with Other Diagnostic Tests. The Journal of Clinical Endocrinology & Metabolism 2000; 85: 1525-1532.

(20.) Sepple PL, Laws ERJ. Complications in a contemporary series of patients who underwent transsphenoidal surgery for Cushing's disease. J Neurosurg 1999; 91: 175-179.

(21.) Assie G, Bahurel H, Coste J, et al. Corticotroph Tumor Progression after Adrenalectomy in Cushing's Disease: A Reappraisal of Nelson's Syndrome. The Journal of Clinical Endocrinology & Metabolism 2007; 92: 172-179. Evran et al.

Address for Correspondence: Mehtap Evran, MD, Cukurova University Faculty of Medicine, Department of Endocrinology, Balcali, 01330, Adana, Turkey Phone: +90 322 33868 79/232 05 20 Gsm: +90 532 781 86 34 E-mail: mehtapevran@mail.com Mehtap Evran, Murat Sert, Tamer Tetiker

Cukurova University Faculty of Medicine, Department of Endocrinology, Adana, Turkey
Table 1. The certain characteristics of the patients with Cushing's
disease and Cushing' syndrome

                               Cushing          Cushing
                            disease (n=20)   syndrome (n=14)

Mean Age(years)             30[+ or -]2.2      31.8[+ or -]1.2

Mean BMI(kg/[m.sup.2])    33.4[+ or -]2.1    31.13[+ or -]1.06

Mean SBP(mmHg)             145[+ or -]7.2    148.3[+ or -]6.02

Mean DBP(mmHg)              95[+ or -]3.8        96[+ or -]3.2

Mean serum basal           97.5[+ or -]25        26.8[+ or -]9
cortisol levels
([micro]g/dl)

Mean serum ACTH             197[+ or -]57        11.1[+ or -]6
levels ([micro]g/ml)

Urine free cortisol        483[+ or -]163      195.6[+ or -]35
levels ([micro]g/24 h)

1 mg DST (cortisol          31[+ or -]8.2      16.4[+ or -]3.4
levels)

8/16 mg DST              14.4[+ or -]0.78        15[+ or -]8.5
(cortisol levels)

Table 2. Clinical and metabolic findings of patients with CS

                              Patients (n)   Frequency (n/(%)

Obesity                           28               23/82
Plethorea                         34             33/97.1
Hypertension                      33             23/69.7
Hirsutismus                       29             21/72.4
Menstruel irregularities          25               21/84
Strias                            34             31/91.2
Moon face                         34             33/97.1
Buffalo Hump                      34             33/97.1
Acne                              34             21/61.8
Osteoporosis (AP vertebrae)       27             18/66.7
Diabetes Melllitus                33             13/39.4
Hepatosteatosis                   26              8/30.8
Nepfrolitiasis                    26               2/7.7

Table 3. Caracteristics of the 20 patients with Cushing's disease

Subject    Typical      Low-dose     High-dose      Pituitary
          Cushingoi    (1mg) dex-     (8/16mg         MRI/CT
          Features *    sup test    dex-sup test

   1        yes            NS             S            8 mm
   2        yes            NS             S            4 mm
   3        yes            NS             S            6 mm
   4        yes            NS             S            8 mm
   5        yes            NS             S            3 mm
   6        yes            NS            NS            4 mm
   7        yes            NS             S            8 mm
   8        yes            NS            --            4 mm
   9        yes            NS            --           16 mm
  10        yes            NS            --           20 mm
  11        yes            NS            --        hyperplasia
  12        yes            NS            NS            8 mm
  13        yes            NS            NS            4 mm
  14        yes            NS             S            5 mm
  15        yes            NS             S            normal
  16        yes            NS             S            3-4 mm
  17        yes            NS             S            normal
  18        yes            NS             S            9 mm
  19        yes            NS            --            10mm
  20        yes            NS             S            7 mm

Subject     Type of           Cure
            Surgery

   1          TS               yes
   2          TS               yes
   3          TS               yes
   4          TS               yes
   5          TS               yes
   6          TS               yes
   7          TS               yes
   8          TC               yes
   9          TC               yes
  10          TC               yes
  11          TS               yes
  12      ketaconasole          ?
  13          TS               yes
  14          TC               yes
  15          TC               yes
  16      ketaconasole/TS      yes
  17      aminoglutetimid   following
  18      following         following
  19          TC               yes
  20          TS               yes

(*)Truncal obesity, buffalo hump, plethorea, violesance stria (>1cm
widht), easy bruisability...

S: supression; NS: no supression; TS: Transsphenoidal pit

Table 4. Caracteristics of the 14 patients with Cushing's syndrome

Subject     Typical        Low-dose       High-dose
           Cushingoid       (1mg)         (8/16mg)
          Features (*)   dex-sup test   dex-sup test

 1           yes             NS              NS
 2           yes             NS               S
 3           yes             NS              --
 4           yes             NS              --
 5           yes             NS               S
 6           yes             NS              NS
 7           yes             NS              NS
 8           yes             NS               S
 9           yes             NS               S
10           yes             NS              --
11           yes             NS              --
12           yes             NS              --
13           yes             NS               S
14           yes             NS               S

Subject   Abdominal MRI/CT              Surgery        Cure

 1        Adrenal adenoma (5x3cm)    R.adrenalectomy    yes
 2        B. adrenal hyperplasia     ketaconasole       yes
 3        Adrenal adenoma (2.5cm)    R.adrenalectomy    yes
 4        Adrenal adenoma            B.adrenalectomy    yes
 5        Normal                     ?                   ?
 6        Adrenal adenoma (4.5cm)    R.adrenalectomy    yes
 7        Adrenal adenoma            B.adrenalectomy   Nelson
 8        B.Adrenal hyperplasia      B.adrenalectomy    yes
 9        B.adrenal hyperplasia      B.adrenalectomy   Nelson
10        Adrenal hyperplasia        Following
11        Adrenal adenoma (2cm)      L.adrenalectomy    yes
12        Adrenal adenoma            L.adrenalectomy    yes
13        Adrenal adenoma (3.5x2cm   Following
14        Adrenal adenoma (4x3cm)    R.adrenalectomy    Yes

(*)Truncal obesity, buffalo hump, plethorea, violesance stria
(>1cm widht), easy bruisability...

S: supression; NS: no supression; R: Right; L: Left; B: Bilateral
Gale Copyright: Copyright 2009 Gale, Cengage Learning. All rights reserved.