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Is embolization, rather than adrenalectomy, ever an option for

aldosterone-producing adenomas?

For example: http://www.ajronline.org/cgi/reprint/151/4/819.pdf

- msmith1928

45, female, 5'3 " , 120 lbs, 1cm left adrenal nodule, aldosterone 42.3, renin 0.5,

potassium <2.9 (when not taking supplements); 25mg spiro caused gynecomastia, no

HTN meds; other meds are 20MEQ K 2x/day, singulair 10mg, norethindrone .35mg,

and cyclobenzaprine 5mg as needed; low sodium, fructose- and grain-free diet

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Or, an even more relevant article:

http://radiology.rsna.org/content/227/2/401.full.pdf

>

> Is embolization, rather than adrenalectomy, ever an option for

aldosterone-producing adenomas?

>

> For example: http://www.ajronline.org/cgi/reprint/151/4/819.pdf

>

> - msmith1928

> 45, female, 5'3 " , 120 lbs, 1cm left adrenal nodule, aldosterone 42.3, renin

0.5, potassium <2.9 (when not taking supplements); 25mg spiro caused

gynecomastia, no HTN meds; other meds are 20MEQ K 2x/day, singulair 10mg,

norethindrone .35mg, and cyclobenzaprine 5mg as needed; low sodium, fructose-

and grain-free diet

>

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They have done this in Japan for aldosterone-producing adenomas. Can search for

the studies.

>

> Is embolization, rather than adrenalectomy, ever an option for

aldosterone-producing adenomas?

>

> For example: http://www.ajronline.org/cgi/reprint/151/4/819.pdf

>

> - msmith1928

> 45, female, 5'3 " , 120 lbs, 1cm left adrenal nodule, aldosterone 42.3, renin

0.5, potassium <2.9 (when not taking supplements); 25mg spiro caused

gynecomastia, no HTN meds; other meds are 20MEQ K 2x/day, singulair 10mg,

norethindrone .35mg, and cyclobenzaprine 5mg as needed; low sodium, fructose-

and grain-free diet

>

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Yes has been tried. Very painful from what I hear. But you could be our first here to have it and tell us about it.One problem is that you do not have the adrenal to see if it is likely on both sides.I have seen alcohol used for a renal tumor. CE Grim MDIs embolization, rather than adrenalectomy, ever an option for aldosterone-producing adenomas?For example: http://www.ajronline.org/cgi/reprint/151/4/819.pdf- msmith192845, female, 5'3", 120 lbs, 1cm left adrenal nodule, aldosterone 42.3, renin 0.5, potassium <2.9 (when not taking supplements); 25mg spiro caused gynecomastia, no HTN meds; other meds are 20MEQ K 2x/day, singulair 10mg, norethindrone .35mg, and cyclobenzaprine 5mg as needed; low sodium, fructose- and grain-free diet

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I'm seeing an interventional radiologist next week and will be discussing this

with her; I'm told she has experience with this as well as with AVS. From the

little bit I've read, they will still do AVS first and then the embolization

only if it's unilateral.

>

> > Is embolization, rather than adrenalectomy, ever an option for

> > aldosterone-producing adenomas?

> >

> > For example: http://www.ajronline.org/cgi/reprint/151/4/819.pdf

> >

> > - msmith1928

> > 45, female, 5'3 " , 120 lbs, 1cm left adrenal nodule, aldosterone

> > 42.3, renin 0.5, potassium <2.9 (when not taking supplements); 25mg

> > spiro caused gynecomastia, no HTN meds; other meds are 20MEQ K 2x/

> > day, singulair 10mg, norethindrone .35mg, and cyclobenzaprine 5mg as

> > needed; low sodium, fructose- and grain-free diet

> >

> >

> >

>

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Will do, Dr. Grim :) Already had the point about ACTH on my list of pre-AVS

questions, thanks to this group.

I don't think there is any solution that is " without risk " for this, but I'm

hoping to find the one that has the least risks, that still allows me to live a

normal life. (Aren't we all!)

> > >

> > > > Is embolization, rather than adrenalectomy, ever an option for

> > > > aldosterone-producing adenomas?

> > > >

> > > > For example: http://www.ajronline.org/cgi/reprint/151/4/819.pdf

> > > >

> > > > - msmith1928

> > > > 45, female, 5'3 " , 120 lbs, 1cm left adrenal nodule, aldosterone

> > > > 42.3, renin 0.5, potassium <2.9 (when not taking supplements);

> > 25mg

> > > > spiro caused gynecomastia, no HTN meds; other meds are 20MEQ K 2x/

> > > > day, singulair 10mg, norethindrone .35mg, and cyclobenzaprine

> > 5mg as

> > > > needed; low sodium, fructose- and grain-free diet

> > > >

> > > >

> > > >

> > >

> >

> >

> >

>

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Small Functional Adrenal Cortical Adenoma: Treatment with CT-guided Percutaneous Acetic Acid Injection—Report of Three Cases1

Huei-Lung Liang, MD,

Huay-Ban Pan, MD,

Ying-Huei Lee, MD, PhD,

Jer-Shyung Huang, MD,

Tony D. L. Wu, MD,

Cheng-Tsung Chang, MD,

Hsin-Lee Liang, MD,

Tsung-Lung Yang, MD and

Chien-Fang Yang, MD

+ Author Affiliations

1From the Departments of Radiology (Huei-Lung L., H.B.P., J.S.H., T.L.Y., C.F.Y.), Surgery (Y.H.L., T.D.L.W.), and Medicine (C.T.C., Hsin-Lee L.), Kaohsiung Veterans General Hospital, 386 Ta-Chung 1st Rd, Kaohsiung, Taiwan 813, Republic of China, and National Yang-Ming University, Taipei, Taiwan. Received November 24, 1998; revision requested December 23; revision received January 25, 1999; accepted April 30. Address reprint requests to Huei-Lung L. (e-mail: hlliang@... .gov.tw).

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Abstract

Two patients with Conn syndrome and one patient with Cushing syndrome underwent computed tomography (CT)-guided tumor ablation with a total of 5–11 mL of 50% acetic acid injected into their adrenal nodule (1.3–3.3 cm in diameter). No major complications were encountered during or after the procedure. All patients were symptom free with normal laboratory test results for at least 1-year follow-up. CT images showed complete cystic change with tumor size regression. Our preliminary results suggest that percutaneous acetic acid injection is a safe and effective alternative for treatment of small functional adrenal cortical adenoma.

Percutaneous ethanol injection has become a widely accepted therapy for small hepatocellular carcinoma with an effect equal to or better than that with surgical resection (1–3). Ultrasonography-guided percutaneous ethanol injection has also been proposed as an alternative therapy to surgery in the management of parathyroid adenoma and autonomously functioning thyroid nodules (4,5). Ohnishi et al (6,7) reported that acetic acid had a stronger cytotoxic effect than did pure ethanol in both animal studies and treatment of hepatocellular carcinoma clinically. On the basis of the therapeutic effect of acetic acid, wider clinical application may be anticipated. The aim of this study was to evaluate the feasibility of one-time percutaneous acetic acid injection in the treatment of small functional adrenal cortical adenoma.

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Materials and Methods

Patients

From July 1997 through November 1997, three patients (two women, one man; mean age, 46 years; age range, 40–56 years) underwent computed tomography (CT)-guided percutaneous acetic acid injection for the treatment of their small functional adrenal cortical adenoma. The clinical diagnosis in two patients was Conn syndrome and in one patient was Cushing syndrome. The diagnosis of Cushing syndrome was confirmed by means of nonsuppression in the large-dose dexamethasone test. The clinical characteristics, blood pressure, and results of biochemical studies, including serum levels of potassium, aldosterone, renin activity, and morning cortisol, are listed in the Table.

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Baseline Characteristics and Biochemical Data before and after Percutaneous Acetic Acid Injection

In the two patients with Conn syndrome, CT images showed a nodule, 2.2 and 1.3 cm in anteroposterior diameter, respectively, in the right adrenal gland; in the patient with Cushing syndrome, a 3.3-cm-diameter nodule was depicted in the left adrenal gland (Fig 1). One of the patients with Conn syndrome also had Bechet syndrome for more than 20 years. He was not considered a good surgical candidate. The other two patients refused conventional surgical resection. The institutional research committee approved our study for patients in either of those two categories. With detailed explanation and full understanding of the advantages and risks of this therapy, written informed consent was obtained from each patient and family member(s). To avert hypokalemia, which might occur during or after the procedure owing to excessive release of aldosterone, a supplement of potassium chloride was given if the serum potassium level was less than 3 mmol/L before treatment.

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Figure 1.

A-C, CT scans before treatment in the three cases. A, Patient 1, Conn syndrome. CT scan depicts a 2.2 × 1.7-cm nodule (arrow) in the right adrenal gland. B, Patient 2, Conn syndrome. CT scan depicts a 1.3 × 1.3-cm nodule (arrow) in the right adrenal gland. C, Patient 3, Cushing syndrome. CT scan depicts a 3.3 × 3.0-cm nodule (arrow) in the left adrenal gland.

Procedure

The coagulation profile of each patient was checked, and they were instructed to fast for 6 hours. Meperidine hydrochloride (40 mg) was injected intramuscularly 30 minutes before treatment. Each patient was prone, and local anesthetic of 1% lidocaine was injected at the site of skin puncture. With CT guidance, a 10-cm-long guiding needle (19 gauge) was inserted into the posterior paraspinal muscle. Another thin (22-gauge) multiple-side-hole needle (Cliny, Yokohama, Japan) was advanced coaxially into the center of the lesion. To avoid a needle path through the posterior pleura, the CT gantry was angled for guidance in one patient. The needle was connected to a 1-mL tuberculin syringe, which was filled with 50% acetic acid via an extension tube.

Acetic acid was injected slowly into the three adrenal nodules for a total of 5, 5, and 11 mL (Fig 2). The injected volume was determined on the basis of two factors. (a) The potency of 50% acetic acid is presumed to be three times that of absolute alcohol (7). (B) The formula for the injected volume in the treatment of a malignancy is V = 4/3 Ï€(R + 0.5)3, where V is volume and R is radius of the tumor. Less volume may be used in the treatment of a benign nodule because there seems to be no requirement for a 0.5-cm safe margin. We injected at least 3–5 mL acetic acid into lesions because the small dose was well tolerated and small foci of the lesion were protected from agent diffusion as a result of needle tip insertion that might not be exactly at the center of the lesion.

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Figure 2.

A-C, Images depict CT-guided percutaneous acetic acid injection in adrenal tumors with the patient prone. A thin needle was inserted coaxially into the nodule. Because there is no end hole in this thin needle, the needle tip was inserted to the anterior surface of the lesion. The lesion in A appears smaller than the lesion in Figure 1, A because the needle tip was slightly off center in the lesion.

During the whole procedure, the electrocardiogram, blood pressure, and peripheral blood oxygen saturation level were carefully monitored. Vital signs were also closely observed for another 4 hours after the patients were sent back to their ward. To evaluate the efficacy of treatment, follow-up biochemical studies were performed every 2–4 months, and follow-up CT was performed every 6 months in each patient.

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Results

The whole procedure lasted 30–50 minutes. All the patients tolerated the procedure well. Transient elevation in blood pressure (≥20–30 mm Hg) was noted during and shortly after the procedure, and it was easily controlled with oral nifedipine. Mild to moderate flank tenderness was experienced during and after the percutaneous acetic acid injection, and two of the patients needed one injection of meperidine hydrochloride (40 mg) for pain relief. The tenderness may be related to reflux of a small amount of acetic acid along the needle track, tumor necrosis, or both.

The two patients with Conn syndrome were discharged in stable condition 2 days after the procedure. The patient with Cushing syndrome developed symptoms of adrenal insufficiency 24 hours after percutaneous acetic acid injection that were similar to those seen after surgical resection. A supplemental double dose of cortisone acetate (50 mg daily) was prescribed for her for 4 days. She was discharged on the 4th day after percutaneous acetic acid injection with a supplemental physiologic dose (25 mg daily) of cortisol.

All the patients were symptom free at 1½-year follow-up and as of May 1999. Follow-up CT images obtained at 6 and 12 months showed complete cystic change with regression of tumor size (Fig 3). No renal parenchymal damage was noted on the follow-up CT images or in the laboratory study results (Table).

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Figure 3.

A-C, Follow-up CT images show cystic change in each nodule (arrow) 12 months after percutaneous acetic acid injection. Mild fibrotic change in the perirenal fat space (arrowhead in B and C) is a result of reflux of acetic acid during injection.

Previous SectionNext Section

Discussion

Primary hyperaldosteronism accounts for less than 1% of disease in the hypertensive population. Unilateral benign adrenal tumor is the most common cause of low renin aldosteronism, which occurs in 80%–90% of patients. The remaining cases are caused by bilateral adrenal hyperplasia (8). Adrenocortical carcinoma that produces aldosterone is a rare disorder, occurring in 1%–2% of patients with aldosteronism. The tumors are almost always larger than 4 cm in diameter and are often very large (9). Cushing syndrome is caused by autonomic excessive secretion of cortisol by an adrenal adenoma or carcinoma. Carcinoma tumors that weigh less than 100 g (<5.5-cm diameter) are rare (8). The treatment of choice for patients with endocrine-producing adenoma is unilateral total adrenalectomy (10). Recently developed laparoscopic techniques have gained wide acceptance because of their ease and feasibility, with limited surgical problems. The disadvantages include a longer surgery time (135–269 minutes) and the risk of vascular or internal organ injuries (11–13).

Rossi et al (14) report a case of aldosterone-producing adenoma successfully treated with percutaneous local injection of pure ethanol. They injected 4 mL of pure ethanol into a 2-cm-diameter adrenal adenoma. The injected volume was far less than the standard volume (14 mL) used in the treatment of hepatocellular carcinoma, as calculated by means of the formula V = 4/3 π(R + 0.5)3. With a benign functional adenoma, even partial ablation of the tumor may have noticeable clinical benefits.

Ohnishi et al (6) report the capacity to necrotize a hepatocyte with 50% acetic acid is more than three times that with absolute alcohol. They treated small hepatocellular carcinomas (≤3-cm diameter) with small-volume, multiple injections. They stated that percutaneous acetic acid injection was superior to percutaneous ethanol injection in terms of both survival and local recurrence rates (7).

In our study, we selected patients with lesions less than 3.5 cm in diameter because smaller lesions (a) are rarely malignant and (B) can be treated completely with one-time percutaneous acetic acid injection. In rare instances in a small malignant adrenal lesion, alcohol injection with incomplete ablation or surgical resection by means of laparoscopic removal may result in tumor recurrence or dissemination.

Imaging-guided adrenal intervention is considered a safe procedure. The posterior approach involves the risk of pneumothorax from transgression of the posterior costophrenic sulcus (15,16). Hussain (17) reported a method for adrenal biopsy to reduce the risk of pneumothorax by using an angled CT gantry and angled insertion of a biopsy needle with the patient prone. In our study, we used a posterior approach, combined if necessary with an angled CT gantry, to avoid major visceral organ transgression. No pneumothorax or hemorrhage was encountered in any of our patients, but transient elevation of blood pressure was noted during and shortly after the procedure. The temporary hypertension did not cause a crisis and could be easily controlled with oral nifedipine. This reaction is most likely related to a transient release of aldosterone and cortisol into the blood circulation that is induced by cytolysis of a functioning adenoma, stress stimulation, or both.

In our limited experience, CT-guided percutaneous acetic acid injection has been a safe, effective, and minimally invasive therapy for the treatment of small functional adrenal cortical adenoma. It can be a good alternative treatment in patients with high surgical risk. However, the application of this technique to replace surgical adrenalectomy in all patients with small functional adenoma requires further investigations in larger numbers of patients.

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Previous SectionNext Section

Footnotes

Author contributions: Guarantor of integrity of entire study, Huei-Lung L.; study concepts and design, Huei-Lung L.; definition of intellectual content, Huei-Lung L.; literature research, Huei-Lung L., H.B.P., T.L.Y., Hsin-Lee L.; clinical studies, Huei-Lung L., Y.H.L., T.D.L.W., C.T.C.; data acquisition and analysis, Huei-Lung L., J.S.H.; manuscript preparation, Huei-Lung L.; manuscript editing, Huei-Lung L., C.F.Y.; manuscript review, Huei-Lung L., H.B.P., Y.H.L. Index terms: Acetic acid; Adrenal gland, neoplasms, 86.31; Interventional procedures, 86.1266

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References

↵

Shina S, Tagawa K, Niwa Y, et al. Percutaneous ethanol injection therapy for hepatocellular carcinoma: results in 146 patients. AJR 1993; 160:1023-1028.

Livraghi T, Giorgio A, Marin G, et al. Hepatocellular carcinoma and cirrhosis in 746 patients: long-term results of percutaneous ethanol injection. Radiology 1995; 197:101-108.

↵

Castells A, Bruix J, Bru C, et al. Treatment of small hepatocellular carcinoma in cirrhotic patients: a cohort study comparing surgical resection and percutaneous ethanol injection. Hepatology 1993; 18:1121-1126.

↵

Solbiati L, Giangrande A, De Pra L, Bellotti E, Cantu PP, Ravetto C. Percutaneous ethanol injection of parathyroid tumors under US guidance: treatment for secondary hyperparathyroidism. Radiology 1985; 155:607-610.

↵

Livraghi T, Paracchi A, Ferrari C, Reschini E, Macchi RM, Bonifacino A. Treatment of autonomous thyroid nodules by percutaneous ethanol injection: 4 years experience. Radiology 1994; 190:529-534.

↵

Ohnishi K, Ohyama N, Ito S, Fujiwara K. Small hepatocellular carcinoma: treatment with US-guided intratumoral injection of acetic acid. Radiology 1994; 193:747-752.

↵

Ohnishi K, Yoshioka HF, Ito S, Fujiwara K. Prospective randomized controlled trial comparing percutaneous acetic acid injection and percutaneous ethanol injection for small hepatocellular carcinoma. Hepatology 1998; 27:67-72.

↵

JD, DW. Textbook of endocrinology 8th ed. Philadelphia, Pa: Saunders, 1992; 557-563.

↵

Mazzaferri EL, Samaan NA. Endocrine tumors Boston, Mass: Blackwell, 1993; 409-411.

↵

Young WF, Jr, Hogan MJ, Klee GG, Grant CS, van Heerden JA. Primary aldosteronism: diagnosis and treatment. Mayo Clin Proc 1990; 65:96-110.

↵

Ganger M, Lacroix A, Prinza RA, et al. Early experience with laparascopic approach for adrenalectomy. Surgery 1993; 114:1120-1125.

Go H, Takeda M, Imai T, Komeyama T, Nishiyama T, Morishita H. Laparoscopic adrenalectomy for Cushing's syndrome: comparison with primary aldosteronism. Surgery 1995; 117:11-17.

↵

Chee C, Ravinthiran T, Cheng C. Laparoscopic adrenalectomy: experience with transabdominal and retroperitoneal approaches. Urology 1998; 51:29-32.

↵

Rossi R, Savastano S, Tommaselli AP, et al. Percutaneous computed tomography-guided ethanol injection in aldosterone-producing adrenocortical adenoma. Eur J Endocrinol 1995; 132:302-305.

↵

Welch TJ, Sheedy PF, II, s DH, CM, Swensen SJ. Percutaneous adrenal biopsy: review of a 10-year experience. Radiology 1994; 193:341-344.

↵

Regge D, Balma E, Lasciarrea P, a C, Serrallonga M, Gandini G. Interventional radiology of the adrenal glands. Minerva Endocrinol 1995; 20:15-26.

↵

Hussain S. Gantry angulation in CT-guided percutaneous adrenal biopsy. AJR 1996; 166:537-539.

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November 1999 Radiology, 213, 612-615.

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> > > >> > > > > Is embolization, rather than adrenalectomy, ever an option for> > > > > aldosterone-producing adenomas?> > > > >> > > > > For example: http://www.ajronline.org/cgi/reprint/151/4/819.pdf> > > > >> > > > > - msmith1928> > > > > 45, female, 5'3", 120 lbs, 1cm left adrenal nodule, aldosterone> > > > > 42.3, renin 0.5, potassium <2.9 (when not taking supplements); > > > 25mg> > > > > spiro caused gynecomastia, no HTN meds; other meds are 20MEQ K 2x/> > > > > day, singulair 10mg, norethindrone .35mg, and cyclobenzaprine > > > 5mg as> > > > > needed; low sodium, fructose- and grain-free diet> > > > >> > > > >> > > > >> > > >> > >> > >> > >> >>

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The Journal of Clinical Endocrinology & Metabolism, doi:10.1210/jc.2003-030530

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CT ScansThe Journal of Clinical Endocrinology & Metabolism Vol. 88, No. 12 5814-5817Copyright © 2003 by The Endocrine Society

Computed Tomography-Guided Percutaneous Acetic Acid Injection Therapy for Functioning Adrenocortical Adenoma Shigeru Minowada, Tetsuya Fujimura, Naoki Takahashi, Hiroichi Kishi, Kanehiro Hasuo and Manabu Minami

Departments of Urology (S.M., T.F., H.K.) and Radiology (N.T., K.H.), International Medical Center of Japan, Tokyo 162-8655, Japan; and Department of Radiology (M.M.), Faculty of Medicine, The University of Tokyo, Tokyo 113-8655, Japan

Address all correspondence and requests for reprints to: Shigeru Minowada, Department of Urology, International Medical Center of Japan, 1-21-1, Toyama, Shinjuku-ku Tokyo, 162-8655, Japan. E-mail: sminowad@...

..

Abstract

TopAbstractIntroductionPatients and MethodsResultsDiscussionReferences We reported the outcomes of computed tomography (CT)-guided percutaneous acetic acid injection therapy for functioning adrenocortical adenomas. With the patient in a prone position, the puncture needle was inserted vertically downward into the adenoma with frequent CT scanning. After confirmation by pilot injection with contrast medium, a small aliquot of 40–50% acetic acid was injected and repeated. Between 1997 and 2002, 18 sessions of CT-guided injection therapy, including one session of ethanol injection, were performed on 10 patients (five patients with primary aldosteronism and five patients with Cushing's or subclinical Cushing's syndrome) without any complications except transient upper abdominal pain during the acetic acid injection. The follow-up period ranged from 5–69 months. The treatment resulted in almost an extirpation of the adrenocortical hyperfunction in seven patients after one or two sessions. CT-guided percutaneous acetic acid injection might be a simple, cost-effective, and far less invasive treatment for small functioning adrenocortical adenomas.

Introduction

TopAbstractIntroductionPatients and MethodsResultsDiscussionReferences PERCUTANEOUS ETHANOL INJECTION (PEI) has been commonly used as a simple and effective treatment for hepatocellular carcinomas measuring 3 cm or less in diameter (1, 2). In addition, PEI has also been employed for the treatment of endocrine tumors of the thyroid and parathyroid (3, 4). On the other hand, the use of a high concentration of acetic acid instead of ethanol has achieved safer and stronger cytotoxic effects in both animal studies and the clinical treatment of hepatocellular carcinomas (5, 6). Acetic acid induces swelling of the fibers and promotes dissociation of collagen in the tumor tissue owing to its low pH.

With respect to therapy for the adrenal gland, only a small number of patients with adrenocortical solid tumors have been successfully treated by percutaneous injection treatment (7, 8). In a previous paper published in 2000 we reported the preliminary results of three cases treated with computed tomography (CT)-guided acetic acid injection therapy (9). Here we present 10 cases with adrenal functioning adenoma, including five cases with primary aldosteronism and five with Cushing's syndrome, who underwent CT-guided percutaneous acetic acid injection (PAI) therapy between 1997 and 2002.

Patients and Methods

TopAbstractIntroductionPatients and MethodsResultsDiscussionReferences Patients The PAI treatment was performed on 10 patients aged a mean of 50 yr (range 32–67 yr) who presented with hormonally functioning adrenocortical adenomas. Five hypertensive patients showed the following biochemical data: hypopotassemia, high serum aldosterone levels, and low plasma renin concentration (Table 1). CT scans revealed tumors of the adrenal gland with tumor diameters ranging from 10–20 mm. [131I]Adosterol scintigrams showed unilaterally increased uptake at the tumor sites. Hypertension and hypopotassemia were normalized before the treatment sessions by the administration of spironolactone, 50–100 mg a day. The five patients with Cushing's syndrome or subclinical Cushing's syndrome were confirmed by findings of increased serum cortisol on circadian changes, suppressed ACTH, and clinical features (Table 2). The cortisol levels remained above 3.0 µg/dl after overnight suppression with 1 mg dexamethasone. [131I]Adosterol scintigrams showed unilateral uptake, and CT scans showed adrenal tumors ranging from 16–38 mm in diameter. A dosage of hydrocortisone, 10 mg a day, was administrated for 2–4 wk after the injections.

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TABLE 1. Patient characteristics, PAI treatment, and clinical outcome in primary aldosteronism

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TABLE 2. Patient characteristics, PAI treatment, and clinical outcome in Cushing's syndrome Methods The patient was placed prone on the bed of a CT scanner. The scout scan confirmed the location of tumor, the appropriate puncture point on the skin vertically above the tumor, and the distance from the puncture point to the tumor (Fig. 1A). We used the same type of needle used for treatment of hepatocellular carcinoma, a 21-gauge PEI puncture needle with three pores 4 mm from the tip (Hakko Shoji Co., Tokyo, Japan). The needle was inserted along the puncture line toward the adenoma with frequent CT scanning. The monitoring was repeated four to six times until we delivered the needle tip precisely inside the tumor (Fig. 1B). After confirmation by pilot injection of 1% lidocaine hydrochloride mixed with approximately 10% contrast medium, an aliquot of 0.5 ml of 40–50% acetic acid with 10% contrast medium was injected and repeated with repetitive CT imaging (Fig. 1C). When the injection fluid leaked outside the tumor, the treatment session was stopped. The patient was monitored carefully during and after the treatment procedures. All patients were followed by regular hormonal examinations and CT scans. If the first PAI treatment did not achieve success, subsequent PAI sessions were planned at intervals of 4–8 months.

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FIG. 1. CT scan images during the PAI with the patient in a prone position. A, The appropriate skin point was selected. B, The needle was inserted and placed precisely within the tumor after repetitive CT monitoring. C, Acetic acid solution containing contrast medium was injected. This study was approved by the local ethical committee and conducted in accordance with the Helsinki Declaration. Informed written consent was obtained from the patients.

Results

TopAbstractIntroductionPatients and MethodsResultsDiscussionReferences Eighteen sessions of CT-guided injection therapy (17 PAIs and one PEI) were performed on five patients with primary aldosteronism and five patients with Cushing's syndrome without any serious complications except transient upper abdominal pain between 1997 and 2002. The duration of the puncture procedure varied from 45–120 min. Hospitalization had been 6–8 d in primary aldosteronism and 10–14 d in Cushing's syndrome, respectively. The follow-up period ranged from 5–69 months. Follow-up CT scans revealed regression of the tumor size in all cases (Tables 1 and 2).

One or two PAI sessions brought about a good outcome in four of the five patients with primary aldosteronism at a mean follow-up period of 42.4 months (Table 1). Plasma aldosterone levels fell to within normal range, and blood pressures returned to normotensive. In case 1 the CT image at 69 months showed a cystic degenerative tumor with marked regression of tumor size in contrast to before treatment (Fig. 2). The levels of plasma aldosterone have been kept normal over 5 yr. The remaining patient, case 2, with plasma aldosterone of 234 pg/ml, required a prescription of spironolactone, 25 mg a day, after three PAI sessions.

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FIG. 2. Follow-up CT images showed cystic change with marked regression of tumor size and changes of plasma aldosterone in case 1 in the primary aldosteronism group. A, Before treatment. B, CT image with oil contrast medium 12 months after PAI. C, CT image 69 months after PAI. D, The basal levels of plasma aldosterone have been kept normal over 5 yr. The clinical outcomes of the five patients with Cushing's syndrome or subclinical Cushing's syndrome are presented in Table 2. Case 1 could not undergo surgery using general anesthesia due to chronic heart failure and severe diabetes mellitus. The serum cortisol levels were normalized a few months after the two PAIs, but cortisol levels and blood pressure had soon risen. The hyperproduction of cortisol was almost extirpated by one or two sessions in cases 3, 4, and 5. The cortisol levels after overnight suppression with 1 mg dexamethasone were reduced to <2.0 µg/dl. Follow-up CT images in case 3 obtained at 5 and 11 months showed cystic degenerative change with tumor regression (Fig. 3). The basal cortisol levels slightly increased for a few days after PAI and then reduced into the normal range.

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FIG. 3. Follow-up CT scans showed cystic change with tumor regression and changes of serum cortisol in case 3 in the Cushing's syndrome group. A, Before treatment. B, CT image 5 months after PAI. C, CT image 11 months after PAI. D, Slight elevation of basal cortisol levels was temporarily observed after PAI, and then cortisol levels were reduced into normal range. All the patients experienced transient upper abdominal pain associated with elevation in blood pressure during the acetic acid injection. Most of the patients needed one iv injection of 15 mg pentazocine for pain relief. One patient, case 4 with Cushing's syndrome, experienced severe pain in the upper abdomen and marked hypertension at the initial injection of a small amount of acetic acid, prompting us to discontinue the PAI session immediately. In the second PAI procedure, the use of epidural local anesthesia eliminated all pain and other complaints in this case.

Discussion

TopAbstractIntroductionPatients and MethodsResultsDiscussionReferences Laparoscopic adrenalectomy has been widely employed for various adrenal lesions as a less invasive therapy in recent years (10, 11, 12). However, some complications involving major vascular injuries have been known to occur, mostly at the beginning of the learning curve (11, 12). In our study, 18 percutaneous injection procedures were performed in 10 cases with adrenocortical adenoma without any adverse complications. Excellent clinical outcomes were obtained in seven of those patients after one or two injections. The most important practical point of acetic acid injection is to minimize the injection volume per shot. An excess of injection volume in a single session to achieve complete tumor ablation should be avoided, because the PAI treatment can be repeated at appropriate intervals. Because we became used to achieving PAI, we believe that a small aldosteronoma can be treated with single session with one night of hospitalization. Compared with laparoscopic adrenalectomy, CT-guided PAI or PEI is a simpler, more cost-effective, and far less invasive treatment for small, hyperfunctioning adrenocortical tumors.

CT-guided adrenal intervention at the posterior approach is considered a safe procedure. In most cases, the procedure can be performed very easily and reliably to insert the puncture needle into the adrenal tumor vertically. On the other hand, the puncture involves the risk of pneumothorax when the lower edge of the lung extends downward over the adrenal gland. In these cases we should employ the angled CT gantry method (13). However, the angled gantry procedure to avoid pneumothorax could not achieve tumor ablation in cases 1 and 2 of the Cushing's syndrome group.

A disadvantage of the injection therapy is the lack of histological confirmation of the lesions. However, we have so far experienced a large number of adrenocortical lesions, including primary aldosteronism, Cushing's syndrome, and incidentally discovered adrenal tumors (14, 15, 16, 17). Owing to the various advanced diagnostic examinations such as endocrinological survey, CT scan, magnetic resonance imaging, and scintigraphy, accurate pretreatment diagnosis is now feasible in almost all cases. Tumor malignancy should be considered when the following findings are encountered: larger than 4 cm in diameter, faster velocity of tumor growth, irregular tumor shape, and heterogeneity of tumor contents (14, 15, 16, 17).

We propose that PAI may be a good alternative for the treatment of functioning adrenocortical adenomas, especially in high-risk patients for surgical treatment. Furthermore, with the recent amazing advances in medical technologies such as radiofrequency ablation and robotic surgeries (18, 19, 20), the development of a novel interventional treatment can be anticipated in the near future.

Footnotes Abbreviations: CT, Computed tomography; PAI, percutaneous acetic acid injection; PEI, percutaneous ethanol injection.

Received for publication March 26, 2003 . Accepted for publication August 24, 2003 .

References

TopAbstractIntroductionPatients and MethodsResultsDiscussionReferences

Ebara M, Ohto M, Sugihara N, Okuda K, Kondo F, Kondo K 1990 Percutaneous ethanol injection for the treatment of small hepatocellular carcinoma: study of 95 patients. J Gastroenterol Hepatol 5:616–626[Medline] Livraghi T, Giorgio A, Marin G, Salmi A, Siode I, Bolondi L, Pompili M 1995 Hepatocellular carcinoma and cirrhosis in 746 patients: long-term results of percutaneous ethanol injection. Radiology 197:101–108[Abstract/Free Full Text] Bennedbk FN, Karstrup S, Hegedüs L 1997 Percutaneous ethanol injection therapy in the treatment of thyroid and parathyroid diseases. Eur J Endocrinol 136:240–250[Abstract/Free Full Text] Zingrillo M, Collura D, Ghiggi MR, Nirchio VN, Trischitta V 1998 Treatment of large cold benign thyroid nodules not eligible for surgery with percutaneous ethanol injection. J Clin Endocrinol Metab 83:3905–3907[Abstract/Free Full Text] Ohnishi K, Yoshioka H, Ito S, Fujiwara K 1998 Prospective randomized controlled trial comparing percutaneous acetic acid injection and percutaneous ethanol injection for small hepatocellular carcinoma. Hepatology 27:67–72[CrossRef][Medline] Lau WY, Leung TWT, Yu SCH, Ho SKW 2002 Percutaneous local ablative therapy for hepatocellular carcinoma. A review and look into the future. Ann Surg 237:171–179 Rossi R, Savastano S, Tommaselli AP, Valentino R, Iaccarino V, Tauchmanova L, Gigante M, Luciano A, Lombardi G 1995 Percutaneous computed tomography-guided ethanol injection in aldosterone-producing adrenocortical adenoma. Eur J Endocrinol 132:302–305[Abstract/Free Full Text] Liang H-L, Pan H-B, Lee Y-H, Huang J-S, Wu TDL, Chang C-T, Liang H-L, Yang T-L, Yang C-F 1999 Small functional adrenal cortical adenoma: treatment with CT-guided percutaneous acetic acid injection: report of three cases. Radiology 213:612–615[Abstract/Free Full Text] Minowada S, Enomoto Y, Korenaga T, Kamijo T, Homma Y, Kitamura T 2000 CT-guided acetic acid injection therapy for aldosterone-producing adrenocortical adenoma: a preliminary report of three cases. Endocr J 47:185–189[Medline] Higashihara E, Tanaka Y, Horie S, Aruga S, Nutahara K, Minowada S, Aso Y 1993 Laparoscopic adrenalectomy: the initial 3 cases. J Urol 149:973–976[Medline] Gagner M 1996 Laparoscopic adrenalectomy. Surg Clin N Am 76:523–537 Meria P, Kempf BF, Hermieu JF, Plouin PF, Duclos JM 2003 Laparoscopic management of primary hyperaldosteronism: clinical experience with 212 cases. J Urol 169:32–35[CrossRef][Medline] Hussian S 1996 Gantry angulation in CT-guided percutaneous adrenal biopsy. Am J Roentgenol 166:537–539[Abstract/Free Full Text] Barzon L, Scaroni C, Sonino N, Fallo F, Gregianin M, Macri C, Boscaro M 1998 Incidentally discovered adrenal tumors: endocrine and scintigraphic correlates. J Clin Endocrinol Metab 83:55–62[Abstract/Free Full Text] Mantero F, Terzolo M, Arnaldi G, Osella G, Masini M, Ali A, Giovagnetti M, Opocher G, Angeli A 2000 A survey on adrenal incidentaloma in Italy. J Clin Endocrinol Metab 85:637–644[Abstract/Free Full Text] Bulow B, Ahren B 2002 Adrenal incidentaloma: experience of a standardized diagnostic programme in the Swedish prospective study. J Intern Med 252:239–246[CrossRef][Medline] Ng L, Libertuno JM 2003 Adrenocortical carcinoma: diagnosis, evaluation and treatment. J Urol 169:5–11[CrossRef][Medline] Wood BJ, Abraham J, Hvizda JL, HR, Fojo T 2003 Radiofrequency ablation of adrenal tumors and adrenocortical carcinoma metastases. Cancer 97:554–560[CrossRef][Medline] Desai MM, Gill IS, Kaouk JH, Matin SF, Sung GT, Bravo EL 2002 Robotic-assisted laparoscopic adrenalectomy. Urology 60:1104–1107[CrossRef][Medline] Bentas W, wolfram M, Brautigam R, Binder J 2002 Laparoscopic transperitoneal adrenalectomy using a remote-controlled robotic surgical system. J Endourol 16:373–376[CrossRef][Medline]

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> > >> > > Is embolization, rather than adrenalectomy, ever an option for aldosterone-producing adenomas?> > > > > > For example: http://www.ajronline.org/cgi/reprint/151/4/819.pdf> > > > > > - msmith1928> > > 45, female, 5'3", 120 lbs, 1cm left adrenal nodule, aldosterone 42.3, renin 0.5, potassium <2.9 (when not taking supplements); 25mg spiro caused gynecomastia, no HTN meds; other meds are 20MEQ K 2x/day, singulair 10mg, norethindrone .35mg, and cyclobenzaprine 5mg as needed; low sodium, fructose- and grain-free diet> > >> >>

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