OR14-001 – Tocilizumab in autoinflammation and AA amyloidosis

Lane, Thirusha; Gillmore, JD; Wechalekar, AD; Stewart, N.M.; Gilbertson, JA; Sachchithanantham, Sajitha; Rowczenio, DM; Banypersad, Sanjay M.; Pinney, Jennifer H.; Mahmood, Shameem; Lachmann, HJ; Hawkins, PN

doi:10.1186/1546-0096-11-s1-a268

Cited by 4 publications

(6 citation statements)

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“…For example, seven patients, who were treated with etanercept, adalimumab, or rituximab, improved and had SAA suppression after tocilizumab therapy, and one patient, who was treated with a TNF inhibitor and tocilizumab, achieved remission with abatacept. [30,42] This suggests that biologic agents need to be replaced to suppress the progression of AA amyloidosis secondary to RA, depending on the patient. The limitations of this review are that it may contain publication bias, and consists only of case reports, as large, well-controlled studies comparing the effectiveness of each biologic are currently lacking.…”

Section: Discussionmentioning

confidence: 99%

“…[20] Tocilizumab is also effective in patients with renal AA amyloidosis, which manifests as proteinuria, hematuria, and renal failure. [19,[24][25][26][27][28][29][30][31] Miyagawa et al reported four patients with RA and secondary AA amyloidosis who were treated with tocilizumab, and three had GI tract involvement with proteinuria. [28] Three patients had decreased proteinuria after 2 months, no progression to other organs, and normalized inflammatory markers, except for one patient who had low SAA levels before tocilizumab therapy.…”

Section: 2mentioning

confidence: 99%

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Biologic therapy for amyloid A amyloidosis secondary to rheumatoid arthritis treated with interleukin 6 therapy

Jung

Kim

et al. 2021

Medicine

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Introduction: Secondary amyloidosis is a rare complication of rheumatoid arthritis (RA) that is histologically characterized by the deposition of amyloid fibrils in target organs, such as the kidneys and gastrointestinal tract. Controlling the inflammatory response is essential to prevent organ dysfunction in amyloid A (AA) amyloidosis secondary to RA, and no clear treatment strategy exists. Patient Concerns and Diagnosis: A 66-year-old woman with RA, who had been treated with disease-modifying anti-rheumatic drugs for 1 year, presented with recurrent abdominal pain and prolonged diarrhea. Endoscopy showed chronic inflammation, and colon tissue histology confirmed AA amyloidosis. Interventions and Outcomes: After tocilizumab therapy was begun, her diarrhea and abdominal pain subsided, and articular symptoms improved. Biologic drugs for RA have been used in patients with secondary AA amyloidosis, including tumor necrosis factor and Janus kinase inhibitors, interleukin 6 blockers, and a T cell modulator. Here, we systematically review existing case reports and compare the outcomes of RA-related AA amyloidosis after treatment with various drugs. Conclusion: The data indicate that biologic drugs like tocilizumab might be treatments of choice for AA amyloidosis secondary to RA.

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Section: Discussionmentioning

confidence: 99%

Section: 2mentioning

confidence: 99%

Biologic therapy for amyloid A amyloidosis secondary to rheumatoid arthritis treated with interleukin 6 therapy

Jung

Kim

et al. 2021

Medicine

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“…As part of the immunosuppressive regimen, prednisone was maintained. Because of complications due to secondary amyloidosis produced by the chronically inflammatory status, based on current reviews (Okuda et al ;4 Lane et al ;5 Courties et al 6) and the support of the rheumatologists with its experience of tocilizumab in inflammatory diseases, we started with the use of this anti-IL6 adjusted to cytopenias (anaemia and thrombocytopenia) which was able to be used at full doses after their recovery.…”

Section: Treatmentmentioning

confidence: 99%

Accelerated silicosis with bone marrow, hepatic and splenic involvement in a patient with lung transplantation

et al. 2019

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Chronic silicosis is an entity widely described in literature. However, other types such as accelerated, acute, complicated and extrapulmonary silicosis are little documented. We present a case of accelerated extrapulmonary silicosis in a lung transplant patient in whom the diagnosis of systemic silicosis was made incidental to non-respiratory complications that occurred during follow-up. The appearance of cytopenia and liver failure led to diagnostic tests that documented the presence of silicotic granulomas in those locations. Taking into account the intensity, time of exposure, onset and development of the disease, we found a highly atypical case of accelerated extrapulmonary silicosis in which inorganic particles (presumably silica) were documented inside granulomas and macrophages of the bone marrow. With these findings, we reflect on the lack of consideration of these entities within clinical practice, their probable under diagnosis and the need to study other pathophysiological mechanisms of acquisition and dissemination of silicosis.

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“…14,15 Of note, tocilizumab, a humanized anti-IL-6 receptor antibody, has been reported to have the ability to suppress the SAA level and reduce the deposition of amyloid fibrils, which indicates that IL-6 plays a critical role in the pathogenesis of SA. 16,17 Cases of more than 20 patients with severe EB including RDEB who developed SA have been reported to date, whereas patients with chronic inflammatory skin disorders such as atopic dermatitis and psoriasis vulgaris have been rarely reported to be complicated with SA. [18][19][20][21][22][23][24][25][26][27][28][29] Elevated serum levels of IL-6 have been reported in bullous pemphigoid and EB acquisita 30,31 ; however, there is currently no established link of SA with these diseases.…”

Section: Introductionmentioning

confidence: 99%

“…IL‐6 is a representative inflammatory cytokine that induces SAA expression via STAT3 in various types of cells including hepatocytes 14,15 . Of note, tocilizumab, a humanized anti‐IL‐6 receptor antibody, has been reported to have the ability to suppress the SAA level and reduce the deposition of amyloid fibrils, which indicates that IL‐6 plays a critical role in the pathogenesis of SA 16,17 . Cases of more than 20 patients with severe EB including RDEB who developed SA have been reported to date, whereas patients with chronic inflammatory skin disorders such as atopic dermatitis and psoriasis vulgaris have been rarely reported to be complicated with SA 18–29 .…”

Section: Introductionmentioning

confidence: 99%

Elevated expression of interleukin‐6 (IL‐6) and serum amyloid A (SAA) in the skin and the serum of recessive dystrophic epidermolysis bullosa: Skin as a possible source of IL‐6 through Toll‐like receptor ligands and SAA

Kawakami,

Kajita,

Hasui

et al. 2024

Experimental Dermatology

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The effect of persistent skin inflammation on extracutaneous organs and blood is not well studied. Patients with recessive dystrophic epidermolysis bullosa (RDEB), a severe form of the inherited blistering skin disorder, have widespread and persistent skin ulcers, and they develop various complications including anaemia, hyperglobulinaemia, hypoalbuminaemia and secondary amyloidosis. These complications are associated with the bioactivities of IL‐6, and the development of secondary amyloidosis requires the persistent elevation of serum amyloid A (SAA) level. We found that patients with RDEB had significantly higher serum levels of IL‐6 and SAA compared to healthy volunteers and patients with psoriasis or atopic dermatitis. Both IL‐6 and SAA were highly expressed in epidermal keratinocytes and dermal fibroblasts of the skin ulcer lesions. Keratinocytes and fibroblasts surrounding the ulcer lesions are continuously exposed to Toll‐like receptor (TLR) ligands, pathogen‐associated and damage‐associated molecular pattern molecules. In vitro, TLR ligands induced IL‐6 expression via NF‐κB in normal human epidermal keratinocytes (NHEKs) and dermal fibroblasts (NHDFs). SAA further induced the expression of IL‐6 via TLR1/2 and NF‐κB in NHEKs and NHDFs. The limitation of this study is that NHEKs and NHDFs were not derived from RDEB patients. These observations suggest that TLR‐mediated persistent skin inflammation might increase the risk of IL‐6‐related systemic complications, including RDEB.

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OR14-001 – Tocilizumab in autoinflammation and AA amyloidosis

Cited by 4 publications

References 0 publications

Biologic therapy for amyloid A amyloidosis secondary to rheumatoid arthritis treated with interleukin 6 therapy

Biologic therapy for amyloid A amyloidosis secondary to rheumatoid arthritis treated with interleukin 6 therapy

Accelerated silicosis with bone marrow, hepatic and splenic involvement in a patient with lung transplantation

Elevated expression of interleukin‐6 (IL‐6) and serum amyloid A (SAA) in the skin and the serum of recessive dystrophic epidermolysis bullosa: Skin as a possible source of IL‐6 through Toll‐like receptor ligands and SAA

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