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    "textoCompleto" => "<p class="elsevierStylePara"><span class="elsevierStyleBold">Dear Editor&#58;</span></p><p class="elsevierStylePara">Common variable immunodeficiency &#40;CVID&#41; is the most prevalent symptomatic primary antibody deficiency&#44; characterized by hypogamaglobulinemia&#44; normal or decreased B-cell numbers and impaired antibody response leading to chronic and recurrent infections&#44; mostly in the respiratory and gastrointestinal tracts<span class="elsevierStyleSup">1&#44;2</span>&#46; However&#44; a significant proportion of patients manifest features of immune dysregulation&#44; including polyclonal lymphocytic infiltration&#44; autoimmunity&#44; enteropathy and malignancy<span class="elsevierStyleSup">3</span>&#46;</p><p class="elsevierStylePara">Secondary amylodosis is an extremely rare complication of CVID<span class="elsevierStyleSup">4</span>&#44; mostly reported in middle aged males<span class="elsevierStyleSup">5-7</span>&#46; This manifestation refers to the extra-cellular tissue deposition of serum amyloid A &#40;SAA&#41; protein fibrils with &#946;-sheet structure&#44; which could be due to chronic and recurrent infections in this group of patients<span class="elsevierStyleSup">8</span>&#46; The self-assembly by amyloid proteins cannot progress in the soluble condition of dissembled precursor proteins alone&#44; while it is speeded up by seeding with preformed amyloid &#64257;brils<span class="elsevierStyleSup">9</span> which described as &#171;seeding mechanism&#187;&#46; Also&#44; enzyme inhibitory function against SAA proteins was confirmed in AA type of amyloid formation and deposition<span class="elsevierStyleSup">10</span>&#46; All reported CVID cases with amyloidosis had a sever status of infectious disease or underling complications like cor pulmonale&#44; congestive hepatomegaly&#44; bilateral bronchiectasis&#44; severe respiratory failure<span class="elsevierStyleSup">7</span> and tuberculosis<span class="elsevierStyleSup">6</span>&#46; Recurrent infections could be considered as the main cause of the amyloidosis development&#59; although recurrent infections could be as a consequence of inadequate IVIG therapy&#44; long delay diagnosis can also prone patient to chronic and recurrent infections<span class="elsevierStyleSup">7</span>&#46;</p><p class="elsevierStylePara">We report herein a 50-year old male with a history of recurrent respiratory tract infections and diarrhea from early childhood&#46; The diagnosis of amyloidosis was made for this patient based on histopathological findings of renal biopsy&#44; once he hospitalized due to edema and massive proteinuria at the age of 48 years&#46; Renal fine needle aspiration biopsy revealed deposition of amorphous pink hyaline eosinophilic material in glomerulus&#44; tubular basement membrane &#40;TBM&#41;&#44; interstitial area and vessel walls of arterioles&#59; it was documented by green appearance fibrils under polarized light which stained and bind with Congo red &#40;figure 1&#41;&#46; As the patient experienced several episodes of infections&#44; immunological studies were performed which showed significant decreased in all serum immunoglobulin levels&#44; compatible with diagnosis of CVID &#40;table 1&#41;&#46; Regular hypo-osmolar intravenous immunoglobulin was started in addition to prophylactic antibiotics and cholchicin&#44; which controlled his renal disease&#46; Moreover&#44; he has not experienced further episode of serious infection since last two years&#46;</p><p class="elsevierStylePara">The clinical manifestations of amyloidosis are widely dependent to the type of deposited protein and amount of amyloid deposition&#46; Variation in the clinical picture of amyloidosis is related to the type of precursor involved<span class="elsevierStyleSup">8&#44;11</span>&#46; Moreover&#44; the clinical features of amyloidosis vary by the organ affected&#59; the most common organ involvement in CVID patients&#44; which are complicated with amyloidosis&#44; is kidney<span class="elsevierStyleSup">5&#44;12</span>&#46; Gastrointestinal &#40;malabsorption&#44; perforation&#44; hemorrhage and obstruction&#41;<span class="elsevierStyleSup">6</span>&#44; joints &#40;arthropathy&#41;<span class="elsevierStyleSup">13</span>&#44; thyroid<span class="elsevierStyleSup">7</span>&#44; and gum were other sites which could be affected by secondary amyloidosis in CVID&#46; Kidney organ function does not change with small amounts of AA amyloid deposition&#44; while the prognosis of excessive deposition of AA renal amyloidosis is generally poor and potentially fatal<span class="elsevierStyleSup">14</span>&#46;</p><p class="elsevierStylePara">It is considerable that renal AA amyloidosis in CVID patients commonly presented with asymptomatic proteinuria&#44; whilst nephrotic syndrome is present in more than one fourth of patients at the time of diagnosis<span class="elsevierStyleSup">15</span>&#46; Also&#44; red blood cells count in urinary sediments and microscopic haematuria may present in CVID patients with the AA type&#44; which more prominent than primary amyloidosis &#40;AL type&#41;<span class="elsevierStyleSup">15</span>&#46;</p><p class="elsevierStylePara">The incidence of AA amyloidosis could be increased with duration of the underlying disease condition and associated factors such as long delay diagnosis&#46; The mean duration of inflammation before the diagnosis of amyloidosis is estimated about 8&#8211;14 years<span class="elsevierStyleSup">15</span>&#46; CVID patients usually experience several episodes of infections since childhood&#59; it is expected that the patients had a history of many years inflammation without appropriate treatment&#44; which is enough for progression of AA amyloidosis&#46; The average age of reported CVID patients with renal secondary amyloidosis was 40&#46;7 &#177; 10&#46;9 years<span class="elsevierStyleSup">5-7</span>&#44; which is much lower than the age of other renal amyloidosis population &#40;70&#46;7 &#177; 12&#46;0 years&#41;<span class="elsevierStyleSup">15</span>&#46;</p><p class="elsevierStylePara">Glomerular deposition of amyloid substances in CVID patients had a significant differentiation from other individuals with renal amyloidosis&#46; In these patients&#44; immunoglobulins are not accompanied in intraglomerular deposition&#44; while in other diseases associated with renal amyloidosis&#44; deposition of IgG and C3 occurred at a rate of 60&#37; and 45&#37;&#44; respectively&#46; Furthermore&#44; IgA deposition can be seen in 50-60&#37; of cases with AA type<span class="elsevierStyleSup">9</span>&#46;</p><p class="elsevierStylePara">Control of the underlying inflammatory disease is the preferred therapy of AA amyloid&#44; but patients who have diagnostic criteria of CVID should receive immunoglobulin replacement therapy&#46; Administration of IVIG could dramatically reduce recurrent infections and subsequent complications in the patients with antibody deficiency<span class="elsevierStyleSup">1&#44;2</span>&#46; Although the usual initial dosage for IVIG therapy is 300-400 mg&#47;kg per month&#44; higher doses of 600-800 mg&#47;kg may be needed in subgroup of patients&#44; especially in patients with bronchiectasis or chronic sinusitis&#46; Nonetheless&#44; IVIG may induce renal damage&#44; especially in patients with preexisting renal insufficiency&#46; Increased level of sucrose&#44; blood viscosity and deposition of immune complex in renal tissue are the main causes of renal damage due to IVIG&#46; Therefore treatment of CVID patients with amyloidosis is a subject of debate&#46; However&#44; high dosage of hypo-osmolar IVIG without sucrose &#40;such as Gummunex or Octagam&#41; is recommended for prevention of renal damage in addition with adjustment of dosage of antibiotics and colchicines&#46; It is expected that new therapeutic strategies in addition to IVIG should be commenced in CVID-amyloidosis patients<span class="elsevierStyleSup">15</span>&#46; The biological agents such as tumor necrosis factor alpha &#40;TNF-&#945;&#41; blocker&#44; Etanercept&#44; Iododoxorubicin and low-molecular-weight sulfates &#40;Fbrilex&#41; have been shown to be effective in treatment of AA-type renal amyloidosis<span class="elsevierStyleSup">9</span>&#44; which should be tried in CVID-amyloidosis patients as well&#46;</p><p class="elsevierStylePara"><a href="grande&#47;10280&#95;108&#95;1593&#95;en&#95;10280&#95;t1&#95;copy1&#46;jpg" class="elsevierStyleCrossRefs"><img src="10280_108_1593_en_10280_t1_copy1.jpg" alt="Patients laboratory finding"></img></a></p><p class="elsevierStylePara">Table 1&#46; Patients laboratory finding</p><p class="elsevierStylePara"><a href="grande&#47;10280&#95;108&#95;1594&#95;en&#95;10280&#95;new&#95;f1&#46;jpg" class="elsevierStyleCrossRefs"><img src="10280_108_1594_en_10280_new_f1.jpg" alt="Renal glomerule with deposition of amorphous pink material proved to be amyloid by Hematoxyline&#44; Eosin staining &#40;A&#46; X400&#41; and special reacting to Congo-red stain &#40;B&#46; X400&#41;&#46;"></img></a></p><p class="elsevierStylePara">Figure 1&#46; Renal glomerule with deposition of amorphous pink material proved to be amyloid by Hematoxyline&#44; Eosin staining &#40;A&#46; X400&#41; and special reacting to Congo-red stain &#40;B&#46; X400&#41;&#46;</p>"
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Renal amyloidosis in common variable immunodeficiency
Renal amyloidosis in common variable immunodeficiency
A.. Aghamohammadia, A.. Shafieia, H.. Abolhassania, R.. Sherkatb, F.. Mahjouba, N.. Rezaeia
a Research Group for Immunodeficiencies, Pediatrics Center of Excellence, Children's Medical Center, Tehran University of Medical Sciences, Tehran, Iran,
b Infectious Diseases and Tropical Medicine Research Center, Isfahan University of Medical Sciences, Isfahan, Iran,
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    "textoCompleto" => "<p class="elsevierStylePara"><span class="elsevierStyleBold">Dear Editor&#58;</span></p><p class="elsevierStylePara">Common variable immunodeficiency &#40;CVID&#41; is the most prevalent symptomatic primary antibody deficiency&#44; characterized by hypogamaglobulinemia&#44; normal or decreased B-cell numbers and impaired antibody response leading to chronic and recurrent infections&#44; mostly in the respiratory and gastrointestinal tracts<span class="elsevierStyleSup">1&#44;2</span>&#46; However&#44; a significant proportion of patients manifest features of immune dysregulation&#44; including polyclonal lymphocytic infiltration&#44; autoimmunity&#44; enteropathy and malignancy<span class="elsevierStyleSup">3</span>&#46;</p><p class="elsevierStylePara">Secondary amylodosis is an extremely rare complication of CVID<span class="elsevierStyleSup">4</span>&#44; mostly reported in middle aged males<span class="elsevierStyleSup">5-7</span>&#46; This manifestation refers to the extra-cellular tissue deposition of serum amyloid A &#40;SAA&#41; protein fibrils with &#946;-sheet structure&#44; which could be due to chronic and recurrent infections in this group of patients<span class="elsevierStyleSup">8</span>&#46; The self-assembly by amyloid proteins cannot progress in the soluble condition of dissembled precursor proteins alone&#44; while it is speeded up by seeding with preformed amyloid &#64257;brils<span class="elsevierStyleSup">9</span> which described as &#171;seeding mechanism&#187;&#46; Also&#44; enzyme inhibitory function against SAA proteins was confirmed in AA type of amyloid formation and deposition<span class="elsevierStyleSup">10</span>&#46; All reported CVID cases with amyloidosis had a sever status of infectious disease or underling complications like cor pulmonale&#44; congestive hepatomegaly&#44; bilateral bronchiectasis&#44; severe respiratory failure<span class="elsevierStyleSup">7</span> and tuberculosis<span class="elsevierStyleSup">6</span>&#46; Recurrent infections could be considered as the main cause of the amyloidosis development&#59; although recurrent infections could be as a consequence of inadequate IVIG therapy&#44; long delay diagnosis can also prone patient to chronic and recurrent infections<span class="elsevierStyleSup">7</span>&#46;</p><p class="elsevierStylePara">We report herein a 50-year old male with a history of recurrent respiratory tract infections and diarrhea from early childhood&#46; The diagnosis of amyloidosis was made for this patient based on histopathological findings of renal biopsy&#44; once he hospitalized due to edema and massive proteinuria at the age of 48 years&#46; Renal fine needle aspiration biopsy revealed deposition of amorphous pink hyaline eosinophilic material in glomerulus&#44; tubular basement membrane &#40;TBM&#41;&#44; interstitial area and vessel walls of arterioles&#59; it was documented by green appearance fibrils under polarized light which stained and bind with Congo red &#40;figure 1&#41;&#46; As the patient experienced several episodes of infections&#44; immunological studies were performed which showed significant decreased in all serum immunoglobulin levels&#44; compatible with diagnosis of CVID &#40;table 1&#41;&#46; Regular hypo-osmolar intravenous immunoglobulin was started in addition to prophylactic antibiotics and cholchicin&#44; which controlled his renal disease&#46; Moreover&#44; he has not experienced further episode of serious infection since last two years&#46;</p><p class="elsevierStylePara">The clinical manifestations of amyloidosis are widely dependent to the type of deposited protein and amount of amyloid deposition&#46; Variation in the clinical picture of amyloidosis is related to the type of precursor involved<span class="elsevierStyleSup">8&#44;11</span>&#46; Moreover&#44; the clinical features of amyloidosis vary by the organ affected&#59; the most common organ involvement in CVID patients&#44; which are complicated with amyloidosis&#44; is kidney<span class="elsevierStyleSup">5&#44;12</span>&#46; Gastrointestinal &#40;malabsorption&#44; perforation&#44; hemorrhage and obstruction&#41;<span class="elsevierStyleSup">6</span>&#44; joints &#40;arthropathy&#41;<span class="elsevierStyleSup">13</span>&#44; thyroid<span class="elsevierStyleSup">7</span>&#44; and gum were other sites which could be affected by secondary amyloidosis in CVID&#46; Kidney organ function does not change with small amounts of AA amyloid deposition&#44; while the prognosis of excessive deposition of AA renal amyloidosis is generally poor and potentially fatal<span class="elsevierStyleSup">14</span>&#46;</p><p class="elsevierStylePara">It is considerable that renal AA amyloidosis in CVID patients commonly presented with asymptomatic proteinuria&#44; whilst nephrotic syndrome is present in more than one fourth of patients at the time of diagnosis<span class="elsevierStyleSup">15</span>&#46; Also&#44; red blood cells count in urinary sediments and microscopic haematuria may present in CVID patients with the AA type&#44; which more prominent than primary amyloidosis &#40;AL type&#41;<span class="elsevierStyleSup">15</span>&#46;</p><p class="elsevierStylePara">The incidence of AA amyloidosis could be increased with duration of the underlying disease condition and associated factors such as long delay diagnosis&#46; The mean duration of inflammation before the diagnosis of amyloidosis is estimated about 8&#8211;14 years<span class="elsevierStyleSup">15</span>&#46; CVID patients usually experience several episodes of infections since childhood&#59; it is expected that the patients had a history of many years inflammation without appropriate treatment&#44; which is enough for progression of AA amyloidosis&#46; The average age of reported CVID patients with renal secondary amyloidosis was 40&#46;7 &#177; 10&#46;9 years<span class="elsevierStyleSup">5-7</span>&#44; which is much lower than the age of other renal amyloidosis population &#40;70&#46;7 &#177; 12&#46;0 years&#41;<span class="elsevierStyleSup">15</span>&#46;</p><p class="elsevierStylePara">Glomerular deposition of amyloid substances in CVID patients had a significant differentiation from other individuals with renal amyloidosis&#46; In these patients&#44; immunoglobulins are not accompanied in intraglomerular deposition&#44; while in other diseases associated with renal amyloidosis&#44; deposition of IgG and C3 occurred at a rate of 60&#37; and 45&#37;&#44; respectively&#46; Furthermore&#44; IgA deposition can be seen in 50-60&#37; of cases with AA type<span class="elsevierStyleSup">9</span>&#46;</p><p class="elsevierStylePara">Control of the underlying inflammatory disease is the preferred therapy of AA amyloid&#44; but patients who have diagnostic criteria of CVID should receive immunoglobulin replacement therapy&#46; Administration of IVIG could dramatically reduce recurrent infections and subsequent complications in the patients with antibody deficiency<span class="elsevierStyleSup">1&#44;2</span>&#46; Although the usual initial dosage for IVIG therapy is 300-400 mg&#47;kg per month&#44; higher doses of 600-800 mg&#47;kg may be needed in subgroup of patients&#44; especially in patients with bronchiectasis or chronic sinusitis&#46; Nonetheless&#44; IVIG may induce renal damage&#44; especially in patients with preexisting renal insufficiency&#46; Increased level of sucrose&#44; blood viscosity and deposition of immune complex in renal tissue are the main causes of renal damage due to IVIG&#46; Therefore treatment of CVID patients with amyloidosis is a subject of debate&#46; However&#44; high dosage of hypo-osmolar IVIG without sucrose &#40;such as Gummunex or Octagam&#41; is recommended for prevention of renal damage in addition with adjustment of dosage of antibiotics and colchicines&#46; It is expected that new therapeutic strategies in addition to IVIG should be commenced in CVID-amyloidosis patients<span class="elsevierStyleSup">15</span>&#46; The biological agents such as tumor necrosis factor alpha &#40;TNF-&#945;&#41; blocker&#44; Etanercept&#44; Iododoxorubicin and low-molecular-weight sulfates &#40;Fbrilex&#41; have been shown to be effective in treatment of AA-type renal amyloidosis<span class="elsevierStyleSup">9</span>&#44; which should be tried in CVID-amyloidosis patients as well&#46;</p><p class="elsevierStylePara"><a href="grande&#47;10280&#95;108&#95;1593&#95;en&#95;10280&#95;t1&#95;copy1&#46;jpg" class="elsevierStyleCrossRefs"><img src="10280_108_1593_en_10280_t1_copy1.jpg" alt="Patients laboratory finding"></img></a></p><p class="elsevierStylePara">Table 1&#46; Patients laboratory finding</p><p class="elsevierStylePara"><a href="grande&#47;10280&#95;108&#95;1594&#95;en&#95;10280&#95;new&#95;f1&#46;jpg" class="elsevierStyleCrossRefs"><img src="10280_108_1594_en_10280_new_f1.jpg" alt="Renal glomerule with deposition of amorphous pink material proved to be amyloid by Hematoxyline&#44; Eosin staining &#40;A&#46; X400&#41; and special reacting to Congo-red stain &#40;B&#46; X400&#41;&#46;"></img></a></p><p class="elsevierStylePara">Figure 1&#46; Renal glomerule with deposition of amorphous pink material proved to be amyloid by Hematoxyline&#44; Eosin staining &#40;A&#46; X400&#41; and special reacting to Congo-red stain &#40;B&#46; X400&#41;&#46;</p>"
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2024 Febrero 57 49 106
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2023 Diciembre 46 26 72
2023 Noviembre 58 35 93
2023 Octubre 55 42 97
2023 Septiembre 63 31 94
2023 Agosto 37 32 69
2023 Julio 86 28 114
2023 Junio 81 30 111
2023 Mayo 88 40 128
2023 Abril 57 19 76
2023 Marzo 45 31 76
2023 Febrero 43 29 72
2023 Enero 54 27 81
2022 Diciembre 76 42 118
2022 Noviembre 41 45 86
2022 Octubre 64 62 126
2022 Septiembre 62 52 114
2022 Agosto 48 74 122
2022 Julio 38 55 93
2022 Junio 39 40 79
2022 Mayo 66 44 110
2022 Abril 40 58 98
2022 Marzo 65 56 121
2022 Febrero 52 39 91
2022 Enero 63 45 108
2021 Diciembre 75 42 117
2021 Noviembre 76 49 125
2021 Octubre 53 54 107
2021 Septiembre 56 32 88
2021 Agosto 36 47 83
2021 Julio 118 41 159
2021 Junio 81 33 114
2021 Mayo 81 33 114
2021 Abril 117 61 178
2021 Marzo 87 27 114
2021 Febrero 59 27 86
2021 Enero 38 21 59
2020 Diciembre 40 12 52
2020 Noviembre 39 13 52
2020 Octubre 30 20 50
2020 Septiembre 37 15 52
2020 Agosto 33 13 46
2020 Julio 47 19 66
2020 Junio 55 15 70
2020 Mayo 56 18 74
2020 Abril 71 28 99
2020 Marzo 62 23 85
2020 Febrero 113 23 136
2020 Enero 50 16 66
2019 Diciembre 49 33 82
2019 Noviembre 42 22 64
2019 Octubre 26 17 43
2019 Septiembre 32 23 55
2019 Agosto 19 24 43
2019 Julio 39 31 70
2019 Junio 30 18 48
2019 Mayo 30 21 51
2019 Abril 52 31 83
2019 Marzo 31 22 53
2019 Febrero 26 17 43
2019 Enero 27 17 44
2018 Diciembre 74 39 113
2018 Noviembre 105 20 125
2018 Octubre 64 12 76
2018 Septiembre 53 18 71
2018 Agosto 48 19 67
2018 Julio 48 20 68
2018 Junio 45 14 59
2018 Mayo 50 14 64
2018 Abril 44 11 55
2018 Marzo 27 7 34
2018 Febrero 35 5 40
2018 Enero 41 8 49
2017 Diciembre 42 8 50
2017 Noviembre 23 13 36
2017 Octubre 23 3 26
2017 Septiembre 27 13 40
2017 Agosto 34 7 41
2017 Julio 26 8 34
2017 Junio 30 8 38
2017 Mayo 31 4 35
2017 Abril 18 10 28
2017 Marzo 24 5 29
2017 Febrero 9 4 13
2017 Enero 16 9 25
2016 Diciembre 52 4 56
2016 Noviembre 57 9 66
2016 Octubre 71 3 74
2016 Septiembre 97 3 100
2016 Agosto 151 8 159
2016 Julio 139 3 142
2016 Junio 92 0 92
2016 Mayo 128 0 128
2016 Abril 87 0 87
2016 Marzo 80 0 80
2016 Febrero 87 0 87
2016 Enero 89 0 89
2015 Diciembre 99 0 99
2015 Noviembre 75 0 75
2015 Octubre 77 0 77
2015 Septiembre 74 0 74
2015 Agosto 80 0 80
2015 Julio 82 0 82
2015 Junio 45 0 45
2015 Mayo 78 0 78
2015 Abril 19 0 19
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