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I didn't know where else to post this, so I apologize if this is in the wrong forum.


My university doesn't have access, and I need the full text of this article:


"Pitfall of the Accessory Spleen" by Sels J.P.J.E.; Wouters R.M.M.E.; Lamers R.; Wolffenbuttel B.H.R.

The Netherlands Journal of Medicine. Volume 56, Issue 4, April 2000, Pages 153-158


Here's the abstract:


"Two patients, one with insulinoma and one with Cushing's syndrome, are presented. Biochemical evaluation readily suggested the correct diagnosis. During radiologic imaging, the anatomic abnormality giving rise to these diseases, i.e. a pancreatic islet cell tumor, and an adrenal adenoma, at first were mistakenly interpreted as an accessory spleen on the basis of specific computed tomography and magnetic resonance imaging appearances. The insulinoma was identified as such during laparotomy, whereas additional jodo-cholesterol scintigraphy revealed the real nature of the lesion in the patient with Cushing's syndrome. Both patients were operated successfully."


I see so many links here of full-text articles, and I hoped someone had access to an organization that can save the pdf file and post it here. I found the citation in PubMed and Science Direct, but they both directed me to Elsevier.

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Hi, This is all i could find. Is this what you are after???

Page 2

154J.P.J.E. Sels et al. I Pseudo-accessory spleenCase historiesCase 1The first patient was a man, born in 1957. Hecomplained of episodes of changed behavior, con-sisting of aggressive mood, stubbornness and agita-tion without coma or epileptiform attacks. Theattacks were characterized additionally by generalmalaise, loss of concentration and retrograde am-nesia. There was no history of palpitations or profusesweating. These complaints were more frequent afterprolonged fasting and in the morning, and theyimproved after eating. His body weight had in-creased by 10 kg over a period of 2 years. Theexistence of an insulin-producing pancreatic tumorwas suspected, and he was admitted for evaluation.At admission, physical examination was unre-markable. Routine laboratory investigations werenormal. During a prolonged fasting, blood glucoselevels decreased to a value of 2.3 mmol/1 while thepatient experienced symptoms of sweating, agitationand mental confusion. At that time serum insulin(IRMA, Pharmacia, Uppsala, Sweden) was 20 mU/1and serum C-peptide (RIA, Mallinckrodt, Germany)740 pmol/1. These values are indeed evidence forinsulinoma. CT of the abdomen demonstrated anormal pancreas without any sign of enlargement ornodularity. An accessory spleen was found. Also,angiography and magnetic resonance imaging (MRI)did not reveal any abnormalities in the pancreas,whereas the presence of an accessory spleen wasconfirmed; on MRI, this lesion had the same tissuecharacteristics as the spleen (Fig. 1). It was decidedto perform an exploratory laparotomy with peropera-tive ultrasound examination. At laparotomy a tumorof 4.5 X 3 X 2 cm was found to be situated next tothe spleen at the exact location of the presumedaccessory spleen. The tumor was attached to the tailof the pancreas, and it was assumed that this lesionwas the insulinoma, especially since careful palpa-tion and ultrasound investigation of the pancreasrevealed no other abnormalities. Freeze-section ex-amination of a biopsy indicated that the tumorcontained endocrine tissue. The tumor was removed,and histologic examination confirmed that it was aninsulinoma. After the operation, the patient recoveredcompletely and all his hypoglycaemic complaintssubsided.Case 2The second patient was a woman, who was bornin 1939. She had been treated for non-insulin depen-dent diabetes mellitus since 1991 and hypertensionsince 1992. For these ailments she used oral bloodglucose lowering agents (a combination of metfor-min and glibenclamide); in 1994 insulin therapy wasinstituted because of worsening of metabolic control.Her hypertension was treated with the ACE inhibitorenalapril and the calcium-entry blocker felodipine. In1992 she suffered vertebral fractures, which wereconsidered to be caused by postmenopausal os-teoporosis, treated with a combination of oestradioland norethisterone (Kliogest).Despite dietary measures her body weight was stillincreasing and diabetes control remained unsatisfac-tory. During one of the visits to the outpatient clinicher physician noted that she had a more congestivered face and that gradually truncal obesity and a thin,easy bruising skin had developed. Cushing'ssyndrome was suspected. Laboratory screening re-vealed that fasting serum Cortisol was 1125 nmol/1after 1 mg dexamethasone overnight (normal value< 100 nmol/1). A random plasma ACTH determi-nation was below 10 pg/ml (normal value 20-110pg/ml). Since this biochemical profile is characteris-tic for Cushing's syndrome due to an adrenal abnor-mality (adenoma, carcinoma), CT of the abdomenwas performed. This indicated normal adrenal glandsand an additional mass above the left kidney wasinterpreted as an accessory spleen. MRI showed amass situated in the left suprarenal region with tissuecharacteristics identical to the spleen (Fig. 2). Sub-sequently, an I13'-cholesterol scan was performed,and revealed enhanced activity in this region. It wasdecided that the 'accessory spleen' in fact was anadrenal adenoma, and the lesion was removed bylaparoscopy. Histologic examination confirmed thatit was an adrenal adenoma. The patient recoveredcompletely and all symptoms of Cushing's syndromesubsided. Antihypertensive medication could bestopped, and her diabetes is now satisfactorily treatedwith dietary measures only.The Netherlands Journal of Medicine 2000;56:153-158


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J.P.J.E. Sels et al. I Pseudo-accessory spleen155(a)GYROSCftN ftCS-ITRANSESATsenteNSA 2TRTE15FLIP135FOW375THK 18/' 1.2SLICE IE1/ 12ANT30.0RIGHTC 13CAUD?22.3:.eneftZM MAASTRICHT81-0CT-93SCftM 18L U 1899L 954GYROSCftN ACS-11(b)Fig. 1. (a) Tl-weigted turbofield-echo images showed a 2 X 3 cm circumscribed markedly hyperintensive lesion in the region of the hilus ofthe spleen (arrow), and isointense relative to the spleen. On gadolinium enhanced Tl-weighted images (:) the signal intensity is similar tothe spleen.The Netherlands Journal of Medicine 2000;56:153-158


Page 4

15 fiJ. f. J.E. Sels el al. ! Pseudo-accessory spleen(a)(b)Fig. 2. MR imaging reveals a mass. 3 cm in size, in the region of the left adrenal gland with a low signal intensity on Tl weighted images(a) and an intermediate signal intensity on T2-weighted turbospin-ccho images (:). The mass has sharp borders and is isuintense to thespleen on both sequences.The Netherlands Journal of Medicine 2000:56:153-158


Page 5

J.P.J.E. Sels et al. I Pseudo-accessory spleen157DiscussionWe describe Lwo patients in whom Lhc clinical andbiochemical abnormalities were clear and undoubted,and pointed to the existence of an insulin-producingislet cell tumor, and a corti sol-producing adrenaladenoma, respectively. Yet, the results of the radiolo-gic examinations initially caused us to doubt theresults of our biochemical evaluation. In both in-stances, CT of the abdomen revealed abnormal tissuein the splenic region, which was considered to betypical for an accessory spleen. In our two patients,CT as well as MRI indicated thai the abnormal tissuewas isointense relative to the spleen, both in nativesections and alier contrast injection (iodide-contain-ing contrast or gadolinium).Imaging techniques are primarily based on thedemonstration of anatomic abnormalities. In addi-tion, they may employ specific differences in densitylo classify the nature of a mass. For instance, thespecific density of an adrenal mass may be indicativeof the existence of a pheochromoeyioma. It isreported frequently in the literature that a 'tumor',found in the left upper abdominal region, initiallycaused alarm, but eventually proved to be an acces-sory spleen [3?7]. The term accessory spleen refersto a congenital location of normal splenic tissuewhich is separate from the main body of the spleen|4]. This anatomical variant may be found in up lo10% of the population. In 80% of the cases it islocated in the splenic hilus [8? 10J and in 16% in thepancreatic tail [5,7,11-14]. Freeman et al. havesuggested that a round or ovoid mass near the splenichilus, with the same attenuation of that of normalspleen both before and after i.v. administration ofcontras! material, is pathognomonic [3J. In theirclassic series of 3 ?1 patients with accessory spleen,Halpcrl and Gyorkey [8] reported six patients inwhom the splenic tissue was situated in the tail of thepancreas. None of them had an islet-ecll tumor,although in one subject islet cells were found insidethe capsule of the accessory spleen. This was notwhat was found in our first patient: the lesionremoved at operation was completely made up ofendocrine tissue.It is not infrequent that preoperative location ofan insulinoma poses problems. Pavone et al. [15]described thai with the use of MRI it was possible tolocale more insulinomas than with CT or ultrasound.In contrast, Hammond et al. [lj considered MRI notto be superior to other imaging techniques. At leastin 25% of cases, exact localisation is made duringthe surgical procedure by palpation and intra-opera-tive ultrasound. It can be argued that prior scinti-graphy with tcchnctiutu-99tn sulfur colloid or Tc-99heal damaged red blood cells |13] could have beenhelpful in our palienls: such an investigation couldprobably indicate that the tissue which was noted,was not functioning splenic tissue. Indeed, in thesecond patient radionuclide imaging indeed washelpful: we used a specific method to demonstratefunctional adrenal tissue, i.e. scintigraphy with jodo-cholesterol. This investigation clearly indicated thatthe tissue which was considered to be an accessoryspleen, did not consist of functioning splenic tissue,hut in fact was adrenal tissue. Thus, the correctdiagnosis of a cortisol-producing adenoma could bemade preoperati vel y, which made it possible toremove the tumor by laparoscopy.We would like lo emphasize that our two casehistories demonstrate that the interpretation of imag-ing techniques has always to be correlated to thefunctional hormonal status of the patient with anendocrine disorder. Once the diagnosis has beenfirmly established on the basis of the endocrinologi-cal work-up, the physician should pursue a thoroughradiologic examination, while being aware of itspossible pitfalls.References|1[ Hammond FJ, Jackson JA. Bloom SR. Localisation ofpancreatic endocrine tumours. Clin Endocrin 1994;40:3 14.|2| Norton JA. S hawker TH, Doppman JL et al. Localisation ofsurgical treatment ot occult insulinomas. Ann Surg1990:212:615-20.PJ Freeman JL, Jal'ri SZH. Roberts JL, Me/wa DG, ShirkhodaA. CT of congenital and acquired abnormalities of thespleen. Radiographics 1993;13:597-610.[4] Seo T. Ito T, Watanabe Y, Umeda T. Torsion of an accessoryspleen presenting as an acute abdomen with an inflammatorymass. PediaLr Radiol 1994;24:532-4.[51 Hayward 1, Mindcb.un RE, Brooke Jeffrey R. Intra pancreaticaccessory spken mimicking pancreatic mass on CT. .1Compul Assist Tomngr 1992:16:984-5.L6| Stiris MG. Accessory spleen versus left adrenal tumor:computed tomography and abdominal angiographic evalua-tion. J Compul Assis Tomogr 1980:4:543-4.The Netherlands Journal of Medicine 20U0;56:153-158




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That was my pleasure Mustangsally,


I found the artical very interesting..........Below i will add my post opp diagnosis on adrenal gland for extra information on adrenal mass.



I had a partial adrenalectomy 18 months ago (Left adrenal gland). The mass measured 4.6cmx3.3 x3. The principal diagnosis- Adrenal cortical Adenoma - cortisole secreting.


I only found out months later that they left a slither of my adrenal. Wether it is a good thing or not, i don't know.



Best wishes


Edited by Anka
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