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    "textoCompleto" => "<p class="elsevierStylePara"><span class="elsevierStyleBold">INTRODUCTION</span></p><p class="elsevierStylePara">Amyloidosis is a condition characterized by predominantly extracellular deposits of a protein material&#44; with a molecular beta tertiary structure that accounts for the insolubility and the resistance to proteolytic digestion&#46; The classification of the disorder is made according to the type of fibrillar protein&#46;</p><p class="elsevierStylePara">In secondary amyloidosis the deposits are typically constituted by a fibrillar protein AA with a non-immunoglobulin structure&#46; The origin of this protein &#40;SAA&#41; is a plasmatic precursor&#44; which is synthesized in the liver as an acute phase reactant in the presence of persistent inflammation or of tissue necrosis&#46; Several forms of SAA proteins have been identified&#46;<span class="elsevierStyleSup">1</span> Systemic amyloidosis AA can be a complication of many diseases or chronic disorders&#46; It is especially frequent in Mediterranean familiar fever&#44; rheumatoid arthritis&#44;<span class="elsevierStyleSup">2</span> juvenile idiopathic arthritis&#44;<span class="elsevierStyleSup">3</span> ankylosing spondylarthritis&#44;<span class="elsevierStyleSup">4-6</span> inflammatory bowel disease&#44; osteomyelitis and chronic respiratory infection with underlying bronchiectasis&#46; Other conditions can also be associated to amyloidosis AA&#44; like malignant neoplasm&#44; such as renal cancer or Hodgkin disease&#46;<span class="elsevierStyleSup">7&#44; 8</span> The association to benign proliferations has only sporadically been reported&#46;<span class="elsevierStyleSup">8 &#44;9</span></p><p class="elsevierStylePara">We present two cases to show the association between benign proliferations and the development of secondary amyloidosis &#40;AA&#41;&#46;</p><p class="elsevierStylePara"><span class="elsevierStyleBold">CASE REPORT &#40;1&#41;&#58; AMYLOIDOSIS ASSOCIATED TO HEPATIC ADENOMA AFTER TREATMENT WITH ORAL CONTRACEPTIVE</span></p><p class="elsevierStylePara">A 34 year-old patient with unremarkable family and personal history was on oral contraceptives from 1989 to 1996&#46; In 1999 she was pregnant and delivered a child without known complications&#46; In 2000 she took contraceptives once again&#46; She was again pregnant in 2001 and everything went out without complications&#46; After delivery&#44; she reinitiated again the treatment with contraceptives&#46; In 2002 hyperlipidemia was detected and she began simvastatine&#46; In May of 2003 she complained about progressive morning ankle and palpebral edema&#44; and she went to the Emergency Room&#46; The laboratory parameters were compatible with nephrotic syndrome&#44; together with a biochemical profile of cholestasis &#40;table I&#41;&#46;</p><p class="elsevierStylePara">The image investigations &#40;ultrasonography and abdominal CT scan&#41; showed a large lesion that appeared to be a hepatic adenoma in the right hepatic lobe &#40;fig&#46; 1a&#41;&#46; The kidneys were normal in size and structure&#46; A rectal biopsy was performed that revealed the existence of type AA amyloid deposits within the submucosal vessels &#40;immunohistochemistry technique&#41;&#46;</p><p class="elsevierStylePara">The diagnosis was nephrotic syndrome secondary to amyloidosis in a patient with probable hepatic adenoma&#46; The patient was referred to the Surgery Department for elective surgery&#46; In July of 2003 a partial right hepatectomy was performed &#40;fig&#46; 1b&#41;&#46; The diagnosis of hepatic adenoma was confirmed and type AA amyloid deposits were further observed within the kidney&#44; liver and tumor samples &#40;fig&#46; 1c&#44; d&#41;&#46;</p><p class="elsevierStylePara">The evolution after the surgery was torpid&#46; A high volume ascites appeared and the renal function deteriorated progressively&#46; A septic shock with E&#46; Coli of peritoneal origin complicated the clinical course and vasoactive drugs together with continuous renal replacement therapies were required&#46; Once the patient got over from the acute phase and after being for several days in the intensive care unit&#44; the evolution was favorable&#44; except for renal function that was not recovered&#44; and the patient was scheduled for periodic hemodialysis program&#46; Ten months after&#44; the patient received a kidney transplant&#44; and the evolution to date was good &#40;serum creatinine&#58; 120 &#956;mol&#47;L&#44; plasma albumin&#58; 35 g&#47;L&#44; proteinuria&#58; 0&#46;5 g&#47;day&#41;&#46;</p><p class="elsevierStylePara"><span class="elsevierStyleBold">DISCUSSION OF CASE REPORT 1</span></p><p class="elsevierStylePara">The association between hepatic adenoma and chronic use of contraceptives was first described in 1973&#46;<span class="elsevierStyleSup">10</span> Since then it has been increasingly reported&#44; probably because of the increasing use of contraceptives&#46; The incidence among women who have never taken contraceptives is approximately 1 per million population &#40;pmp&#41;&#44; whereas among women who are chronically treated with this drug is 30-40 pmp&#46; Young age&#44; high content in estrogens&#44; and doses and duration of the treatment have been reported as possible risk factors&#46;<span class="elsevierStyleSup">11&#44; 12</span> The hepatic adenomas that appear in relation to contraceptives are frequently multiple&#44; of a greater size and with higher tendency to bleeding than primary adenomas&#46;<span class="elsevierStyleSup">13-16</span> In some cases withdrawal of the treatment was accompanied with a regression of the adenomas&#44; which recurred in case of pregnancy or if the treatment was reintroduced&#44; that is to say during hyper-estrogenic states&#46;<span class="elsevierStyleSup">17-20</span> The pathophysiologic mechanism underlying the development of hepatic adenomas while on estrogenic therapy is not clear&#44; although the most plausible hypothesis is hepatocytes transformation and proliferation through steroid receptors present on these cells&#46;<span class="elsevierStyleSup">21</span> The risk for malignization is not universally accepted&#44; although some authors have found that it is probably not exceptional&#46;<span class="elsevierStyleSup">22</span> The management of the adenomas remains controversial&#46; Asymptomatic patients who chronically take contraceptives and have small hepatic lesions &#40;&#60; 5 cm&#41; should discontinue the treatment and are to be observed&#44; as complete regression of the lesions after drug withdrawal has been documented&#46;<span class="elsevierStyleSup">23-25 </span>Other authors propose surgical resection&#44; independently of tumor size&#44; because of the risk for tumor growth&#44; malignization or rupture&#46;<span class="elsevierStyleSup">26</span> Surgical resection is the first choice therapy in asymptomatic patients with adenomas larger than 5 cm&#46;</p><p class="elsevierStylePara">We found very few reports in the literature on the association between hepatic adenomas and development of secondary systemic amyloidosis &#40;AA&#41;&#46; It was described that the appearance of secondary amyloidosis &#40;AA&#41; is due to hyperproduction of TNF-&#945; by tumoral cells&#44; which can stimulate the production of amyloid substance&#46;<span class="elsevierStyleSup">27</span> Some cases of deposits regression after the surgical removal of the tumor have been reported&#46;<span class="elsevierStyleSup">28</span> For this reason&#44; surgical resection was indicated in this case despite the risk of intervention in a patient with systemic amyloidosis&#46; Tumor removal was not accompanied by improvement in renal insufficiency&#44; probably because of postoperative hemodynamic complications&#46; To date&#44; 30 months after the intervention&#44; the patient has received a kidney transplant and maintains an excellent renal function&#46;</p><p class="elsevierStylePara"><span class="elsevierStyleBold">CASE REPORT &#40;2&#41;&#58; CASTLEMAN&#191;S DISEASE AND SECONDARY AMYLOIDOSIS</span></p><p class="elsevierStylePara">A20 year-old female&#44; with unremarkable personal and pathological history was admitted to our Department because of asthenia and ankle edema for one month&#46; The remaining physical examination was normal&#46; The laboratory findings were compatible with pure nephrotic syndrome &#40;table I&#41;&#46; Immunological and serological examinations yielded no abnormalities&#46; An ultrasound-guided kidney biopsy was performed that showed extended deposits of type AA proteinic amyloid material &#40;immunohistochemistry technique&#41; &#40;fig&#46; 2&#41;&#46; With the diagnosis of secondary renal amyloidosis &#40;AA&#41; the etiological study was undertaken&#46; The bone biopsy aspirate was normal&#46; The abdominal CT disclosed a retroperitoneal mass 6 x 5 x 6 cm adjacent to the inferior vena cava together with several retroperitoneal lymphadenopathies&#46; The mass was excised by laparoscopy&#46; The pathological examination revealed a lymphadenopathic structure with nodular proliferation of dendritic cells and hyaline appearance&#44; typical of Castleman&#180;s disease &#40;CD&#41;&#44; as well as deposits of type AA amyloid material&#46; Nephrotic syndrome remained despite the surgical removal of the lymphadenopathic mass&#46; Colchicine was initiated together with symptomatic medical treatment with no response&#44; and the clinical picture evolved to chronic end-stage renal failure&#44; which 9 months after required replacement treatment&#46; Six years later&#44; the patient received a kidney transplant from a cadaver donor and the course has been good to date &#40;serum creatinine&#58; 110 &#956;mol&#47;L&#44; plasma albumin&#58; 37 g&#47;L&#44; proteinuria&#58; 0&#46;2 g&#47;day&#41;&#46;</p><p class="elsevierStylePara"><span class="elsevierStyleBold">DISCUSSION OF CASE 2</span></p><p class="elsevierStylePara">Giant lymph node hyperplasia or Castleman&#191;s disease &#40;CD&#41; is a heterogeneous clinicopathological entity included in the group of atypical lymphoproliferative diseases&#46; Castleman et al&#46; described the disease for the first time in 1956 as a big lymphadenopathic mass&#44; localized in the mediastinum and with a benign behavior&#46; Other studies have demonstrated that the disease can also localize outside the mediastinum&#46;<span class="elsevierStyleSup">29</span> The classical pathological patterns of CD are vascular hyaline in 80&#37;-90&#37; of the cases&#44; and the plasma cell type&#44; in 10&#37;-20&#37;&#46; The vascular hyaline variant originates from capillary proliferation inside the germinal center of the lymph follicles&#46; It has a hyaline appearance&#44; with only one&#44; frequently mediastinal localization&#44; and a benign course after its removal&#46; The less frequent plasma cell variant is characterized by follicular hyperplasia with plasma cells&#44; often multicentric&#44; and can present as a clinical picture resembling a systemic inflammatory syndrome&#46; The prognosis is worse than that of vascular hyaline type&#44; and progression to lymphoma is not an exception&#46; The multicentric form is frequently associated to HIV infection&#44; as well as infection or co-infection by HHV 8&#46;<span class="elsevierStyleSup">30</span> Antiviral therapy can be useful to achieve disease regression&#46;<span class="elsevierStyleSup">31</span> Some mixed forms have also been described&#46; <br></br></p><p class="elsevierStylePara">Few cases of Castleman&#191;s disease associated to amyloidosis have been reported in the literature&#46; Only 9 out of 17 cases presented with nephrotic syndrome secondary to renal amyloidosis&#46;<span class="elsevierStyleSup">32</span> Other renal conditions have also been described in CD&#58; minimal changes nephropathy&#44; membranous and membranoproliferative nephropathy&#46;<span class="elsevierStyleSup">33</span> The pathogenesis of the amyloidosis AA associated to CD is not clear&#46; Some authors have pointed out cytokine IL-6&#44; present in great amounts inside the germinal centers of the lymph nodes&#44; as a possible factor responsible for the release of acute phase reactants that promote the formation of amyloid deposits &#40;PCR&#44; SAA&#41;&#46;<span class="elsevierStyleSup">34&#44; 35</span> Some authors have shown that lymphoid mass resection leads to CD healing&#44; and consequently to amyloid deposits regression with disappearance of the associated nephrotic syndrome&#46;<span class="elsevierStyleSup">36&#44; 37</span> However&#44; others have showed that the amyloid deposits persist after surgery&#46;<span class="elsevierStyleSup">38&#44; 39</span></p><p class="elsevierStylePara">In the present case it is possible that the amount of amyloid material in the kidneys was too big to disappear&#44; even after the elimination of the causative stimulus&#46;</p><p class="elsevierStylePara"><span class="elsevierStyleBold">CONSIDERATIONS</span></p><p class="elsevierStylePara">It is well known that the presence of type AAamyloid in a tissue sample obliges to discard a possible underlying chronic inflammatory disease as the cause of the deposit&#46; The two reported cases illustrate that benign proliferations are also to be taken into account together with other more frequent conditions as the possible cause of secondary amyloidosis&#46; It is important to note that early recognition of these entities can lead to healing of secondary amyloid disease&#44; and therefore to avoidance of the multiorgan parenchymal injury that can be a feature of the disease&#46; In the two cases&#44; the amyloid insult to the kidney&#44; which presented as nephrotic syndrome&#44; did not regress despite the elimination of the causative stimulus&#46; The first patient presented severe complications after the surgical procedure with hemodynamic collapse&#44; which probably prevented the potential renal function recovery&#46; The second patient had such extensive deposits of amyloid material in all renal compartments&#44; mainly within the glomeruli and the vessels&#44; that their elimination was impossible despite the disappearance of the primary stimulus&#46; However&#44; the favorable clinical renal and extrarenal evolution for both patients two years receiving a kidney transplant point out that systemic amyloid disease is resolved&#46;</p><p class="elsevierStylePara">Amyloidosis AA is a systemic disease and cardiac injury has a special relevance regarding the vital prognosis as well as the possible indication for kidney transplantation&#46; In the formerly commented cases&#44; ultrasonic myocardial assessment revealed no functional abnormalities&#44; both at diagnosis and before the transplantation&#44; and it was assumed that there was no cardiac affectation&#46; It can be concluded that once the causative stimulus for the amyloid disease disappears&#44; renal transplantation is indicated with excellent clinical outcome&#46;<br></br></p>"
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        "resumen" => "La amiloidosis se caracteriza por el dep&#243;sito de prote&#237;nas de caracter&#237;sticas ultraestructurales fibrilares&#44; con plegamiento &#946; en capas e insolubles&#44; que se depositan mayoritariamente a nivel de los espacios extracelulares de &#243;rganos y tejidos&#46; Se clasifica t&#237;picamente seg&#250;n la naturaleza bioqu&#237;mica de la prote&#237;na fibrilar&#44; y seg&#250;n su distribuci&#243;n en el organismo podr&#225; ser sist&#233;mica o localizada&#46; La amiloidosis sist&#233;mica m&#225;s frecuente en la pr&#225;ctica cl&#237;nica es la denominada AL &#40;idiop&#225;tica primaria o asociada a mieloma m&#250;ltiple&#41; cuyas fibrillas est&#225;n formadas por cadenas ligeras&#46; En cambio&#44; la amiloidosis AA &#40;secundaria&#44; reactiva o adquirida&#41; es aquella que se desarrolla t&#237;picamente como complicaci&#243;n de una enfermedad inflamatoria cr&#243;nica&#44; destacando entre las m&#225;s habituales&#59; enfermedades de origen reumatol&#243;gico &#40;artritis reumatoide&#44; espondilitis anquilopoy&#233;tica&#44; artritis psori&#225;sica&#41;&#44; la fiebre mediterr&#225;nea familiar&#44; la enfermedad inflamatoria intestinal&#44; as&#237; como infecciones cronificadas &#40;tuberculosis&#44; osteomielitis&#41;&#46; No obstante&#44; otras causas responsables de su desarrollo y en muchas ocasiones infravaloradas&#44; son las tumoraciones benignas&#46; Algunas de estas entidades&#44; tambi&#233;n tendr&#225;n capacidad de actuar como est&#237;mulo responsable de la formaci&#243;n de estas prote&#237;nas&#44; que finalmente se depositar&#225;n en diferentes tejidos del organismo&#46; Es importante resaltar&#44; que el diagn&#243;stico precoz as&#237; como el tratamiento eficaz de la enfermedad subyacente ha permitido disminuir su incidencia&#44; as&#237; como en algunos casos incluso revertirla&#46; Aqu&#237;&#44; presentamos dos casos cl&#237;nicos paradigm&#225;ticos de tumoraciones benignas&#44; adenoma hep&#225;tico y Enfermedad de Castlemann&#44; que desarrollaron posteriormente amiloidosis AA con afectaci&#243;n renal principalmente en forma de s&#237;ndrome Nefr&#243;tico&#46;"
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        "resumen" => "Amyolidosis is a systemic disorder characterized by the extracelllular tissue deposition of insoluble&#44; toxic aggregates in bundles of &#946;- sheet fibrillar proteins&#46; These deposits are typically identified on the bases of their apple-green birrefringence under a polarized light microscope after staining with Congo red&#44; and by the presence of rigid&#44; nonbranching fibrils 8 to 10 nm in diameter on electron microscopy&#46; The type of amyloid fibril unit can be further defined by immunohistology or by immunoelectron microscopy&#46; It has been described at least 25 different human protein precursors of amyloid fibrils&#44; which will describe its corresponding amyloid disease&#46; The most common types of amyloidosis are AL &#40;primary&#41; and AA &#40;secondary&#41; types&#59; the former&#44; is the most frequent and is due to deposition of proteins derived from immunoglobulin light chain fragments&#44; occurring alone or in association with multiple myeloma&#46; The later &#40;AA&#41;&#44; is caused by deposition of fibrils composed of fragments of the acute phase reactant serum amyloid A &#40;SAA&#41; and complicates chronic diseases with ongoing or recurring inflammation&#44; namely&#59; rheumatoid arthritis &#40;RA&#41;&#44; juvenile chronic polyarthritis&#44; ankylosing spondylitis&#44; familial periodic fever syndromes &#40;Familial Mediterranean Fever&#41;&#44; chronic infections and furthermore&#44; some neoplasms &#40;mainly renal cell carcinoma and Hodking&#191;s disease&#41;&#46; Despite its less frequent association&#44; some benign neoplasms can subsequently complicate to AA amyloidosis&#44; therefore&#44; an early diagnose and successful treatment may lead indeed&#44; to regression of the amyloid disease&#46; Herein&#44; we present two cases of AA amyloidosis&#44; both of them caused by 2 different benign neoplasms&#58; 1&#46; A 34 year-old woman&#44; after chronic oral contraceptive use&#44; developed an hepatic adenoma &#40;fig&#46; 1&#41; which finally lead to AA amyloidosis with primary kidney presentation &#40;pure nephrotic syndrome&#41; &#40;table 1&#41;&#46; Post-surgical complications yield to acute renal failure from which unfortunately could not be recovered&#46; After being on hemodialysis therapy during 10 months she received a first renal allograft without any complication&#46; 2&#46; A 20 yearold woman&#44; was diagnosed of AA amyloidosis after a renal biopsy &#40;fig&#46; 2&#41; because of nephrotic syndrome &#40;table 1&#41;&#46; Further investigation lead to the finding of a hialyne-vascular type Castleman&#191;s disease located in the retroperotoneum &#40;fig&#46; 2&#41;&#46; Despite surgical resection and medical treatment &#40;colchicine&#41; she developed progressive renal failure requiring initialization of hemodialysis therapy&#46; After 6 years being on hemodialysis&#44; she received a first renal allograft which is currently functioning after one year of follow- up&#46; Although other chronic inflamatory diseases complicate more frequently to AA amyloidosis&#44; benign tumors have to be taken into account as a potential ethiological cause for secondary amyloidosis&#46;"
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Systemic AA amyloidosis induced by benign neoplasms
Amiloidosis secundaria (AA) asociada a tumoraciones benignas
Oriol Bestard Matamorosa, R.. Poveda Monjea, M.. Ibernon Vilaróa, M.. Carrera Plansa, J. M.. Grinyó Boiraa
a Hospital de Bellvitge, Hospitalet de Llobregat, Barcelona, España,
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    "textoCompleto" => "<p class="elsevierStylePara"><span class="elsevierStyleBold">INTRODUCTION</span></p><p class="elsevierStylePara">Amyloidosis is a condition characterized by predominantly extracellular deposits of a protein material&#44; with a molecular beta tertiary structure that accounts for the insolubility and the resistance to proteolytic digestion&#46; The classification of the disorder is made according to the type of fibrillar protein&#46;</p><p class="elsevierStylePara">In secondary amyloidosis the deposits are typically constituted by a fibrillar protein AA with a non-immunoglobulin structure&#46; The origin of this protein &#40;SAA&#41; is a plasmatic precursor&#44; which is synthesized in the liver as an acute phase reactant in the presence of persistent inflammation or of tissue necrosis&#46; Several forms of SAA proteins have been identified&#46;<span class="elsevierStyleSup">1</span> Systemic amyloidosis AA can be a complication of many diseases or chronic disorders&#46; It is especially frequent in Mediterranean familiar fever&#44; rheumatoid arthritis&#44;<span class="elsevierStyleSup">2</span> juvenile idiopathic arthritis&#44;<span class="elsevierStyleSup">3</span> ankylosing spondylarthritis&#44;<span class="elsevierStyleSup">4-6</span> inflammatory bowel disease&#44; osteomyelitis and chronic respiratory infection with underlying bronchiectasis&#46; Other conditions can also be associated to amyloidosis AA&#44; like malignant neoplasm&#44; such as renal cancer or Hodgkin disease&#46;<span class="elsevierStyleSup">7&#44; 8</span> The association to benign proliferations has only sporadically been reported&#46;<span class="elsevierStyleSup">8 &#44;9</span></p><p class="elsevierStylePara">We present two cases to show the association between benign proliferations and the development of secondary amyloidosis &#40;AA&#41;&#46;</p><p class="elsevierStylePara"><span class="elsevierStyleBold">CASE REPORT &#40;1&#41;&#58; AMYLOIDOSIS ASSOCIATED TO HEPATIC ADENOMA AFTER TREATMENT WITH ORAL CONTRACEPTIVE</span></p><p class="elsevierStylePara">A 34 year-old patient with unremarkable family and personal history was on oral contraceptives from 1989 to 1996&#46; In 1999 she was pregnant and delivered a child without known complications&#46; In 2000 she took contraceptives once again&#46; She was again pregnant in 2001 and everything went out without complications&#46; After delivery&#44; she reinitiated again the treatment with contraceptives&#46; In 2002 hyperlipidemia was detected and she began simvastatine&#46; In May of 2003 she complained about progressive morning ankle and palpebral edema&#44; and she went to the Emergency Room&#46; The laboratory parameters were compatible with nephrotic syndrome&#44; together with a biochemical profile of cholestasis &#40;table I&#41;&#46;</p><p class="elsevierStylePara">The image investigations &#40;ultrasonography and abdominal CT scan&#41; showed a large lesion that appeared to be a hepatic adenoma in the right hepatic lobe &#40;fig&#46; 1a&#41;&#46; The kidneys were normal in size and structure&#46; A rectal biopsy was performed that revealed the existence of type AA amyloid deposits within the submucosal vessels &#40;immunohistochemistry technique&#41;&#46;</p><p class="elsevierStylePara">The diagnosis was nephrotic syndrome secondary to amyloidosis in a patient with probable hepatic adenoma&#46; The patient was referred to the Surgery Department for elective surgery&#46; In July of 2003 a partial right hepatectomy was performed &#40;fig&#46; 1b&#41;&#46; The diagnosis of hepatic adenoma was confirmed and type AA amyloid deposits were further observed within the kidney&#44; liver and tumor samples &#40;fig&#46; 1c&#44; d&#41;&#46;</p><p class="elsevierStylePara">The evolution after the surgery was torpid&#46; A high volume ascites appeared and the renal function deteriorated progressively&#46; A septic shock with E&#46; Coli of peritoneal origin complicated the clinical course and vasoactive drugs together with continuous renal replacement therapies were required&#46; Once the patient got over from the acute phase and after being for several days in the intensive care unit&#44; the evolution was favorable&#44; except for renal function that was not recovered&#44; and the patient was scheduled for periodic hemodialysis program&#46; Ten months after&#44; the patient received a kidney transplant&#44; and the evolution to date was good &#40;serum creatinine&#58; 120 &#956;mol&#47;L&#44; plasma albumin&#58; 35 g&#47;L&#44; proteinuria&#58; 0&#46;5 g&#47;day&#41;&#46;</p><p class="elsevierStylePara"><span class="elsevierStyleBold">DISCUSSION OF CASE REPORT 1</span></p><p class="elsevierStylePara">The association between hepatic adenoma and chronic use of contraceptives was first described in 1973&#46;<span class="elsevierStyleSup">10</span> Since then it has been increasingly reported&#44; probably because of the increasing use of contraceptives&#46; The incidence among women who have never taken contraceptives is approximately 1 per million population &#40;pmp&#41;&#44; whereas among women who are chronically treated with this drug is 30-40 pmp&#46; Young age&#44; high content in estrogens&#44; and doses and duration of the treatment have been reported as possible risk factors&#46;<span class="elsevierStyleSup">11&#44; 12</span> The hepatic adenomas that appear in relation to contraceptives are frequently multiple&#44; of a greater size and with higher tendency to bleeding than primary adenomas&#46;<span class="elsevierStyleSup">13-16</span> In some cases withdrawal of the treatment was accompanied with a regression of the adenomas&#44; which recurred in case of pregnancy or if the treatment was reintroduced&#44; that is to say during hyper-estrogenic states&#46;<span class="elsevierStyleSup">17-20</span> The pathophysiologic mechanism underlying the development of hepatic adenomas while on estrogenic therapy is not clear&#44; although the most plausible hypothesis is hepatocytes transformation and proliferation through steroid receptors present on these cells&#46;<span class="elsevierStyleSup">21</span> The risk for malignization is not universally accepted&#44; although some authors have found that it is probably not exceptional&#46;<span class="elsevierStyleSup">22</span> The management of the adenomas remains controversial&#46; Asymptomatic patients who chronically take contraceptives and have small hepatic lesions &#40;&#60; 5 cm&#41; should discontinue the treatment and are to be observed&#44; as complete regression of the lesions after drug withdrawal has been documented&#46;<span class="elsevierStyleSup">23-25 </span>Other authors propose surgical resection&#44; independently of tumor size&#44; because of the risk for tumor growth&#44; malignization or rupture&#46;<span class="elsevierStyleSup">26</span> Surgical resection is the first choice therapy in asymptomatic patients with adenomas larger than 5 cm&#46;</p><p class="elsevierStylePara">We found very few reports in the literature on the association between hepatic adenomas and development of secondary systemic amyloidosis &#40;AA&#41;&#46; It was described that the appearance of secondary amyloidosis &#40;AA&#41; is due to hyperproduction of TNF-&#945; by tumoral cells&#44; which can stimulate the production of amyloid substance&#46;<span class="elsevierStyleSup">27</span> Some cases of deposits regression after the surgical removal of the tumor have been reported&#46;<span class="elsevierStyleSup">28</span> For this reason&#44; surgical resection was indicated in this case despite the risk of intervention in a patient with systemic amyloidosis&#46; Tumor removal was not accompanied by improvement in renal insufficiency&#44; probably because of postoperative hemodynamic complications&#46; To date&#44; 30 months after the intervention&#44; the patient has received a kidney transplant and maintains an excellent renal function&#46;</p><p class="elsevierStylePara"><span class="elsevierStyleBold">CASE REPORT &#40;2&#41;&#58; CASTLEMAN&#191;S DISEASE AND SECONDARY AMYLOIDOSIS</span></p><p class="elsevierStylePara">A20 year-old female&#44; with unremarkable personal and pathological history was admitted to our Department because of asthenia and ankle edema for one month&#46; The remaining physical examination was normal&#46; The laboratory findings were compatible with pure nephrotic syndrome &#40;table I&#41;&#46; Immunological and serological examinations yielded no abnormalities&#46; An ultrasound-guided kidney biopsy was performed that showed extended deposits of type AA proteinic amyloid material &#40;immunohistochemistry technique&#41; &#40;fig&#46; 2&#41;&#46; With the diagnosis of secondary renal amyloidosis &#40;AA&#41; the etiological study was undertaken&#46; The bone biopsy aspirate was normal&#46; The abdominal CT disclosed a retroperitoneal mass 6 x 5 x 6 cm adjacent to the inferior vena cava together with several retroperitoneal lymphadenopathies&#46; The mass was excised by laparoscopy&#46; The pathological examination revealed a lymphadenopathic structure with nodular proliferation of dendritic cells and hyaline appearance&#44; typical of Castleman&#180;s disease &#40;CD&#41;&#44; as well as deposits of type AA amyloid material&#46; Nephrotic syndrome remained despite the surgical removal of the lymphadenopathic mass&#46; Colchicine was initiated together with symptomatic medical treatment with no response&#44; and the clinical picture evolved to chronic end-stage renal failure&#44; which 9 months after required replacement treatment&#46; Six years later&#44; the patient received a kidney transplant from a cadaver donor and the course has been good to date &#40;serum creatinine&#58; 110 &#956;mol&#47;L&#44; plasma albumin&#58; 37 g&#47;L&#44; proteinuria&#58; 0&#46;2 g&#47;day&#41;&#46;</p><p class="elsevierStylePara"><span class="elsevierStyleBold">DISCUSSION OF CASE 2</span></p><p class="elsevierStylePara">Giant lymph node hyperplasia or Castleman&#191;s disease &#40;CD&#41; is a heterogeneous clinicopathological entity included in the group of atypical lymphoproliferative diseases&#46; Castleman et al&#46; described the disease for the first time in 1956 as a big lymphadenopathic mass&#44; localized in the mediastinum and with a benign behavior&#46; Other studies have demonstrated that the disease can also localize outside the mediastinum&#46;<span class="elsevierStyleSup">29</span> The classical pathological patterns of CD are vascular hyaline in 80&#37;-90&#37; of the cases&#44; and the plasma cell type&#44; in 10&#37;-20&#37;&#46; The vascular hyaline variant originates from capillary proliferation inside the germinal center of the lymph follicles&#46; It has a hyaline appearance&#44; with only one&#44; frequently mediastinal localization&#44; and a benign course after its removal&#46; The less frequent plasma cell variant is characterized by follicular hyperplasia with plasma cells&#44; often multicentric&#44; and can present as a clinical picture resembling a systemic inflammatory syndrome&#46; The prognosis is worse than that of vascular hyaline type&#44; and progression to lymphoma is not an exception&#46; The multicentric form is frequently associated to HIV infection&#44; as well as infection or co-infection by HHV 8&#46;<span class="elsevierStyleSup">30</span> Antiviral therapy can be useful to achieve disease regression&#46;<span class="elsevierStyleSup">31</span> Some mixed forms have also been described&#46; <br></br></p><p class="elsevierStylePara">Few cases of Castleman&#191;s disease associated to amyloidosis have been reported in the literature&#46; Only 9 out of 17 cases presented with nephrotic syndrome secondary to renal amyloidosis&#46;<span class="elsevierStyleSup">32</span> Other renal conditions have also been described in CD&#58; minimal changes nephropathy&#44; membranous and membranoproliferative nephropathy&#46;<span class="elsevierStyleSup">33</span> The pathogenesis of the amyloidosis AA associated to CD is not clear&#46; Some authors have pointed out cytokine IL-6&#44; present in great amounts inside the germinal centers of the lymph nodes&#44; as a possible factor responsible for the release of acute phase reactants that promote the formation of amyloid deposits &#40;PCR&#44; SAA&#41;&#46;<span class="elsevierStyleSup">34&#44; 35</span> Some authors have shown that lymphoid mass resection leads to CD healing&#44; and consequently to amyloid deposits regression with disappearance of the associated nephrotic syndrome&#46;<span class="elsevierStyleSup">36&#44; 37</span> However&#44; others have showed that the amyloid deposits persist after surgery&#46;<span class="elsevierStyleSup">38&#44; 39</span></p><p class="elsevierStylePara">In the present case it is possible that the amount of amyloid material in the kidneys was too big to disappear&#44; even after the elimination of the causative stimulus&#46;</p><p class="elsevierStylePara"><span class="elsevierStyleBold">CONSIDERATIONS</span></p><p class="elsevierStylePara">It is well known that the presence of type AAamyloid in a tissue sample obliges to discard a possible underlying chronic inflammatory disease as the cause of the deposit&#46; The two reported cases illustrate that benign proliferations are also to be taken into account together with other more frequent conditions as the possible cause of secondary amyloidosis&#46; It is important to note that early recognition of these entities can lead to healing of secondary amyloid disease&#44; and therefore to avoidance of the multiorgan parenchymal injury that can be a feature of the disease&#46; In the two cases&#44; the amyloid insult to the kidney&#44; which presented as nephrotic syndrome&#44; did not regress despite the elimination of the causative stimulus&#46; The first patient presented severe complications after the surgical procedure with hemodynamic collapse&#44; which probably prevented the potential renal function recovery&#46; The second patient had such extensive deposits of amyloid material in all renal compartments&#44; mainly within the glomeruli and the vessels&#44; that their elimination was impossible despite the disappearance of the primary stimulus&#46; However&#44; the favorable clinical renal and extrarenal evolution for both patients two years receiving a kidney transplant point out that systemic amyloid disease is resolved&#46;</p><p class="elsevierStylePara">Amyloidosis AA is a systemic disease and cardiac injury has a special relevance regarding the vital prognosis as well as the possible indication for kidney transplantation&#46; In the formerly commented cases&#44; ultrasonic myocardial assessment revealed no functional abnormalities&#44; both at diagnosis and before the transplantation&#44; and it was assumed that there was no cardiac affectation&#46; It can be concluded that once the causative stimulus for the amyloid disease disappears&#44; renal transplantation is indicated with excellent clinical outcome&#46;<br></br></p>"
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        "resumen" => "La amiloidosis se caracteriza por el dep&#243;sito de prote&#237;nas de caracter&#237;sticas ultraestructurales fibrilares&#44; con plegamiento &#946; en capas e insolubles&#44; que se depositan mayoritariamente a nivel de los espacios extracelulares de &#243;rganos y tejidos&#46; Se clasifica t&#237;picamente seg&#250;n la naturaleza bioqu&#237;mica de la prote&#237;na fibrilar&#44; y seg&#250;n su distribuci&#243;n en el organismo podr&#225; ser sist&#233;mica o localizada&#46; La amiloidosis sist&#233;mica m&#225;s frecuente en la pr&#225;ctica cl&#237;nica es la denominada AL &#40;idiop&#225;tica primaria o asociada a mieloma m&#250;ltiple&#41; cuyas fibrillas est&#225;n formadas por cadenas ligeras&#46; En cambio&#44; la amiloidosis AA &#40;secundaria&#44; reactiva o adquirida&#41; es aquella que se desarrolla t&#237;picamente como complicaci&#243;n de una enfermedad inflamatoria cr&#243;nica&#44; destacando entre las m&#225;s habituales&#59; enfermedades de origen reumatol&#243;gico &#40;artritis reumatoide&#44; espondilitis anquilopoy&#233;tica&#44; artritis psori&#225;sica&#41;&#44; la fiebre mediterr&#225;nea familiar&#44; la enfermedad inflamatoria intestinal&#44; as&#237; como infecciones cronificadas &#40;tuberculosis&#44; osteomielitis&#41;&#46; No obstante&#44; otras causas responsables de su desarrollo y en muchas ocasiones infravaloradas&#44; son las tumoraciones benignas&#46; Algunas de estas entidades&#44; tambi&#233;n tendr&#225;n capacidad de actuar como est&#237;mulo responsable de la formaci&#243;n de estas prote&#237;nas&#44; que finalmente se depositar&#225;n en diferentes tejidos del organismo&#46; Es importante resaltar&#44; que el diagn&#243;stico precoz as&#237; como el tratamiento eficaz de la enfermedad subyacente ha permitido disminuir su incidencia&#44; as&#237; como en algunos casos incluso revertirla&#46; Aqu&#237;&#44; presentamos dos casos cl&#237;nicos paradigm&#225;ticos de tumoraciones benignas&#44; adenoma hep&#225;tico y Enfermedad de Castlemann&#44; que desarrollaron posteriormente amiloidosis AA con afectaci&#243;n renal principalmente en forma de s&#237;ndrome Nefr&#243;tico&#46;"
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        "resumen" => "Amyolidosis is a systemic disorder characterized by the extracelllular tissue deposition of insoluble&#44; toxic aggregates in bundles of &#946;- sheet fibrillar proteins&#46; These deposits are typically identified on the bases of their apple-green birrefringence under a polarized light microscope after staining with Congo red&#44; and by the presence of rigid&#44; nonbranching fibrils 8 to 10 nm in diameter on electron microscopy&#46; The type of amyloid fibril unit can be further defined by immunohistology or by immunoelectron microscopy&#46; It has been described at least 25 different human protein precursors of amyloid fibrils&#44; which will describe its corresponding amyloid disease&#46; The most common types of amyloidosis are AL &#40;primary&#41; and AA &#40;secondary&#41; types&#59; the former&#44; is the most frequent and is due to deposition of proteins derived from immunoglobulin light chain fragments&#44; occurring alone or in association with multiple myeloma&#46; The later &#40;AA&#41;&#44; is caused by deposition of fibrils composed of fragments of the acute phase reactant serum amyloid A &#40;SAA&#41; and complicates chronic diseases with ongoing or recurring inflammation&#44; namely&#59; rheumatoid arthritis &#40;RA&#41;&#44; juvenile chronic polyarthritis&#44; ankylosing spondylitis&#44; familial periodic fever syndromes &#40;Familial Mediterranean Fever&#41;&#44; chronic infections and furthermore&#44; some neoplasms &#40;mainly renal cell carcinoma and Hodking&#191;s disease&#41;&#46; Despite its less frequent association&#44; some benign neoplasms can subsequently complicate to AA amyloidosis&#44; therefore&#44; an early diagnose and successful treatment may lead indeed&#44; to regression of the amyloid disease&#46; Herein&#44; we present two cases of AA amyloidosis&#44; both of them caused by 2 different benign neoplasms&#58; 1&#46; A 34 year-old woman&#44; after chronic oral contraceptive use&#44; developed an hepatic adenoma &#40;fig&#46; 1&#41; which finally lead to AA amyloidosis with primary kidney presentation &#40;pure nephrotic syndrome&#41; &#40;table 1&#41;&#46; Post-surgical complications yield to acute renal failure from which unfortunately could not be recovered&#46; After being on hemodialysis therapy during 10 months she received a first renal allograft without any complication&#46; 2&#46; A 20 yearold woman&#44; was diagnosed of AA amyloidosis after a renal biopsy &#40;fig&#46; 2&#41; because of nephrotic syndrome &#40;table 1&#41;&#46; Further investigation lead to the finding of a hialyne-vascular type Castleman&#191;s disease located in the retroperotoneum &#40;fig&#46; 2&#41;&#46; Despite surgical resection and medical treatment &#40;colchicine&#41; she developed progressive renal failure requiring initialization of hemodialysis therapy&#46; After 6 years being on hemodialysis&#44; she received a first renal allograft which is currently functioning after one year of follow- up&#46; Although other chronic inflamatory diseases complicate more frequently to AA amyloidosis&#44; benign tumors have to be taken into account as a potential ethiological cause for secondary amyloidosis&#46;"
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                  "referenciaCompleta" => "Cosme A, Horcajada JP, Vidaur F, Ojeda E, Torrado J, Arenas JI. Systemic AA amyloidosis induced by oral contraceptive-associated hepatocellular adenoma: a 13-year follow up. Liver 15 (3): 164-7, 1995. <a href="http://www.ncbi.nlm.nih.gov/pubmed/7674844" target="_blank">[Pubmed]</a>"
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ISSN: 20132514
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