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Aghamohammadi, A. Shafiei, H. Abolhassani, R. Sherkat, F. Mahjoub, N. Rezaei" "autores" => array:6 [ 0 => array:4 [ "Iniciales" => "A." "apellidos" => "Aghamohammadi" "email" => array:1 [ 0 => "aghamohammadi@sina.tums.ac.ir" ] "referencia" => array:1 [ 0 => array:2 [ "etiqueta" => "<span class="elsevierStyleSup">a</span>" "identificador" => "affa" ] ] ] 1 => array:3 [ "Iniciales" => "A." "apellidos" => "Shafiei" "referencia" => array:1 [ 0 => array:2 [ "etiqueta" => "<span class="elsevierStyleSup">a</span>" "identificador" => "affa" ] ] ] 2 => array:3 [ "Iniciales" => "H." "apellidos" => "Abolhassani" "referencia" => array:1 [ 0 => array:2 [ "etiqueta" => "<span class="elsevierStyleSup">a</span>" "identificador" => "affa" ] ] ] 3 => array:3 [ "Iniciales" => "R." "apellidos" => "Sherkat" "referencia" => array:1 [ 0 => array:2 [ "etiqueta" => "<span class="elsevierStyleSup">b</span>" "identificador" => "affb" ] ] ] 4 => array:3 [ "Iniciales" => "F." "apellidos" => "Mahjoub" "referencia" => array:1 [ 0 => array:2 [ "etiqueta" => "<span class="elsevierStyleSup">a</span>" "identificador" => "affa" ] ] ] 5 => array:3 [ "Iniciales" => "N." "apellidos" => "Rezaei" "referencia" => array:1 [ 0 => array:2 [ "etiqueta" => "<span class="elsevierStyleSup">a</span>" "identificador" => "affa" ] ] ] ] "afiliaciones" => array:2 [ 0 => array:3 [ "entidad" => "Research Group for Immunodeficiencies, Pediatrics Center of Excellence, Children's Medical Center, Tehran University of Medical Sciences, Tehran, Iran, " "etiqueta" => "<span class="elsevierStyleSup">a</span>" "identificador" => "affa" ] 1 => array:3 [ "entidad" => "Infectious Diseases and Tropical Medicine Research Center, Isfahan University of Medical Sciences, Isfahan, Iran, " "etiqueta" => "<span class="elsevierStyleSup">b</span>" "identificador" => "affb" ] ] ] ] "titulosAlternativos" => array:1 [ "en" => array:1 [ "titulo" => "Renal amyloidosis in common variable immunodeficiency" ] ] "textoCompleto" => "<p class="elsevierStylePara"><span class="elsevierStyleBold">Dear Editor:</span></p><p class="elsevierStylePara">Common variable immunodeficiency (CVID) is the most prevalent symptomatic primary antibody deficiency, characterized by hypogamaglobulinemia, normal or decreased B-cell numbers and impaired antibody response leading to chronic and recurrent infections, mostly in the respiratory and gastrointestinal tracts<span class="elsevierStyleSup">1,2</span>. However, a significant proportion of patients manifest features of immune dysregulation, including polyclonal lymphocytic infiltration, autoimmunity, enteropathy and malignancy<span class="elsevierStyleSup">3</span>.</p><p class="elsevierStylePara">Secondary amylodosis is an extremely rare complication of CVID<span class="elsevierStyleSup">4</span>, mostly reported in middle aged males<span class="elsevierStyleSup">5-7</span>. This manifestation refers to the extra-cellular tissue deposition of serum amyloid A (SAA) protein fibrils with β-sheet structure, which could be due to chronic and recurrent infections in this group of patients<span class="elsevierStyleSup">8</span>. The self-assembly by amyloid proteins cannot progress in the soluble condition of dissembled precursor proteins alone, while it is speeded up by seeding with preformed amyloid fibrils<span class="elsevierStyleSup">9</span> which described as «seeding mechanism». Also, enzyme inhibitory function against SAA proteins was confirmed in AA type of amyloid formation and deposition<span class="elsevierStyleSup">10</span>. All reported CVID cases with amyloidosis had a sever status of infectious disease or underling complications like cor pulmonale, congestive hepatomegaly, bilateral bronchiectasis, severe respiratory failure<span class="elsevierStyleSup">7</span> and tuberculosis<span class="elsevierStyleSup">6</span>. Recurrent infections could be considered as the main cause of the amyloidosis development; although recurrent infections could be as a consequence of inadequate IVIG therapy, long delay diagnosis can also prone patient to chronic and recurrent infections<span class="elsevierStyleSup">7</span>.</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. The diagnosis of amyloidosis was made for this patient based on histopathological findings of renal biopsy, once he hospitalized due to edema and massive proteinuria at the age of 48 years. Renal fine needle aspiration biopsy revealed deposition of amorphous pink hyaline eosinophilic material in glomerulus, tubular basement membrane (TBM), interstitial area and vessel walls of arterioles; it was documented by green appearance fibrils under polarized light which stained and bind with Congo red (figure 1). As the patient experienced several episodes of infections, immunological studies were performed which showed significant decreased in all serum immunoglobulin levels, compatible with diagnosis of CVID (table 1). Regular hypo-osmolar intravenous immunoglobulin was started in addition to prophylactic antibiotics and cholchicin, which controlled his renal disease. Moreover, he has not experienced further episode of serious infection since last two years.</p><p class="elsevierStylePara">The clinical manifestations of amyloidosis are widely dependent to the type of deposited protein and amount of amyloid deposition. Variation in the clinical picture of amyloidosis is related to the type of precursor involved<span class="elsevierStyleSup">8,11</span>. Moreover, the clinical features of amyloidosis vary by the organ affected; the most common organ involvement in CVID patients, which are complicated with amyloidosis, is kidney<span class="elsevierStyleSup">5,12</span>. Gastrointestinal (malabsorption, perforation, hemorrhage and obstruction)<span class="elsevierStyleSup">6</span>, joints (arthropathy)<span class="elsevierStyleSup">13</span>, thyroid<span class="elsevierStyleSup">7</span>, and gum were other sites which could be affected by secondary amyloidosis in CVID. Kidney organ function does not change with small amounts of AA amyloid deposition, while the prognosis of excessive deposition of AA renal amyloidosis is generally poor and potentially fatal<span class="elsevierStyleSup">14</span>.</p><p class="elsevierStylePara">It is considerable that renal AA amyloidosis in CVID patients commonly presented with asymptomatic proteinuria, whilst nephrotic syndrome is present in more than one fourth of patients at the time of diagnosis<span class="elsevierStyleSup">15</span>. Also, red blood cells count in urinary sediments and microscopic haematuria may present in CVID patients with the AA type, which more prominent than primary amyloidosis (AL type)<span class="elsevierStyleSup">15</span>.</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. The mean duration of inflammation before the diagnosis of amyloidosis is estimated about 8–14 years<span class="elsevierStyleSup">15</span>. CVID patients usually experience several episodes of infections since childhood; it is expected that the patients had a history of many years inflammation without appropriate treatment, which is enough for progression of AA amyloidosis. The average age of reported CVID patients with renal secondary amyloidosis was 40.7 ± 10.9 years<span class="elsevierStyleSup">5-7</span>, which is much lower than the age of other renal amyloidosis population (70.7 ± 12.0 years)<span class="elsevierStyleSup">15</span>.</p><p class="elsevierStylePara">Glomerular deposition of amyloid substances in CVID patients had a significant differentiation from other individuals with renal amyloidosis. In these patients, immunoglobulins are not accompanied in intraglomerular deposition, while in other diseases associated with renal amyloidosis, deposition of IgG and C3 occurred at a rate of 60% and 45%, respectively. Furthermore, IgA deposition can be seen in 50-60% of cases with AA type<span class="elsevierStyleSup">9</span>.</p><p class="elsevierStylePara">Control of the underlying inflammatory disease is the preferred therapy of AA amyloid, but patients who have diagnostic criteria of CVID should receive immunoglobulin replacement therapy. Administration of IVIG could dramatically reduce recurrent infections and subsequent complications in the patients with antibody deficiency<span class="elsevierStyleSup">1,2</span>. Although the usual initial dosage for IVIG therapy is 300-400 mg/kg per month, higher doses of 600-800 mg/kg may be needed in subgroup of patients, especially in patients with bronchiectasis or chronic sinusitis. Nonetheless, IVIG may induce renal damage, especially in patients with preexisting renal insufficiency. Increased level of sucrose, blood viscosity and deposition of immune complex in renal tissue are the main causes of renal damage due to IVIG. Therefore treatment of CVID patients with amyloidosis is a subject of debate. However, high dosage of hypo-osmolar IVIG without sucrose (such as Gummunex or Octagam) is recommended for prevention of renal damage in addition with adjustment of dosage of antibiotics and colchicines. It is expected that new therapeutic strategies in addition to IVIG should be commenced in CVID-amyloidosis patients<span class="elsevierStyleSup">15</span>. The biological agents such as tumor necrosis factor alpha (TNF-α) blocker, Etanercept, Iododoxorubicin and low-molecular-weight sulfates (Fbrilex) have been shown to be effective in treatment of AA-type renal amyloidosis<span class="elsevierStyleSup">9</span>, which should be tried in CVID-amyloidosis patients as well.</p><p class="elsevierStylePara"><a href="grande/10280_108_1593_en_10280_t1_copy1.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. Patients laboratory finding</p><p class="elsevierStylePara"><a href="grande/10280_108_1594_en_10280_new_f1.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, Eosin staining (A. X400) and special reacting to Congo-red stain (B. X400)."></img></a></p><p class="elsevierStylePara">Figure 1. Renal glomerule with deposition of amorphous pink material proved to be amyloid by Hematoxyline, Eosin staining (A. X400) and special reacting to Congo-red stain (B. X400).</p>" "pdfFichero" => "P1-E501-S2268-A10280.pdf" "tienePdf" => true "bibliografia" => array:2 [ "titulo" => "Bibliografía" "seccion" => array:1 [ 0 => array:1 [ "bibliografiaReferencia" => array:15 [ 0 => array:3 [ "identificador" => "bib1" "etiqueta" => "1" "referencia" => array:1 [ 0 => array:3 [ "referenciaCompleta" => "Cunningham-Rundles C, Bodian C. Common variable immunodeficiency: clinical and immunological features of 248 patients. 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año/Mes | Html | Total | |
---|---|---|---|
2024 Noviembre | 5 | 4 | 9 |
2024 Octubre | 55 | 33 | 88 |
2024 Septiembre | 54 | 25 | 79 |
2024 Agosto | 71 | 59 | 130 |
2024 Julio | 61 | 40 | 101 |
2024 Junio | 79 | 64 | 143 |
2024 Mayo | 74 | 32 | 106 |
2024 Abril | 85 | 47 | 132 |
2024 Marzo | 88 | 34 | 122 |
2024 Febrero | 57 | 49 | 106 |
2024 Enero | 42 | 23 | 65 |
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 |