Periocular and Orbital AmyloidosisClinical Characteristics, Management, and Outcome

Leibovitch, Igal; Selva, Dinesh; GOLDBERG, R; Sullivan, Thomas J.; Saeed, Perooz; Davis, G. H.; MCCANN, J; McNab, Alan A.; Rootman, Jack

doi:10.1016/j.ophtha.2006.03.052

Cited by 119 publications

(185 citation statements)

References 29 publications

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“…In patients with primary amyloid deposition in the lacrimal gland, involvement is usually unilateral, whereas in systemic cases the involvement tends to bilateral [6] as seen in our patient. Lacrimal gland amyloidosis is a rare phenomenon with few case reports in the available literature [5][6][7][8]. The majority of reported cases of lacrimal gland amyloidosis are primary and unilateral; bilateral lacrimal gland involvement is unusual.…”

supporting

confidence: 55%

“…This mechanism has been previously proposed to explain the relationship between sarcoidosis and lymphoid malignancies, such as Hodgkin's and non-Hodgkin's lymphoma, and it is possible that a similar mechanism may lead to the development of other hematologic malignancies including multiple myeloma. Polyclonal hypergammaglobulinemia is a common feature in sarcoidosis patients [6] and may be due to continuous stimulation of B cells by activated CD41 T cells. In addition, this chronic stimulation may result in prolonged B-cell and plasma cell half-lives that may increase the risk of genetic mutations, leading to the formation of a malignancy, such as multiple myeloma [14].…”

Section: Commentarymentioning

confidence: 99%

“…Although multiple myelomatous infiltration of the lacrimal glands is unusual, no reports have found bilateral amyloid infiltration of the lacrimal glands in patients with multiple myeloma prior to our patient. Only one patient had a mild plasma cell dyscrasia with systemic light chain amyloidosis [6].…”

Section: Commentarymentioning

confidence: 99%

“…Previous nomenclature has divided amyloidosis into either primary or secondary forms. In primary amyloidosis, immunoglobulin light chain fragments (either kappa or lambda) are precursors to the amyloid light forms of amyloidosis that are either idiopathic or related to light chain-producing monoclonal gammopathy, as in multiple myeloma [6][7][8]. Secondary amyloidosis, also referred to as amyloid associated, or reactive amyloidosis results from longstanding inflammation or infection derived from an acute phase protein known as amyloid A with deposition leading to hepatosplenomegaly and renal dysfunction.…”

Section: Commentarymentioning

confidence: 99%

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Multiple myeloma with lacrimal gland amyloidosis and sarcoidosis

et al. 2010

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supporting

confidence: 55%

Section: Commentarymentioning

confidence: 99%

Section: Commentarymentioning

confidence: 99%

Section: Commentarymentioning

confidence: 99%

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Multiple myeloma with lacrimal gland amyloidosis and sarcoidosis

et al. 2010

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“…This disturbance has been proposed to explain the relationship between sarcoidosis and lymphoid malignancies, and it is possible that a similar mechanism may lead to the development of other hematologic malignancies, including multiple myeloma [14]. Polyclonal hyper-gammaglobulinemia is a common feature in sarcoidosis patients [17] and may be due to continuous stimulation of B cells by activated CD4? T cells.…”

Section: Discussionmentioning

confidence: 99%

Atypical sarcoidosis diagnosed by bone marrow biopsy during renal workup for possible multiple myeloma

et al. 2012

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Sarcoidosis is a multi-organ disease of unknown etiology characterized by non-caseating granulomas. Here we report the case of a 78-year-old white male with a past medical history of diabetes mellitus, hypertension, and chronic kidney disease stage III with a baseline serum creatinine of 2.5 mg/dl. The patient had a prior admission history for acute kidney injury (AKI) attributed to dehydration and medication-induced nephro-toxicities. He presented to the renal clinic for follow-up with acute worsening of chronic kidney failure with a serum creatinine level of 3.5 mg/dl. Examination revealed that he was anemic and mildly hypercalcemic with suppressed parathyroid hormone and had proteinuria of 1.3 g per day. The computed tomography scan of the abdomen revealed right renal pelvic non-obstructing calculi. Serum protein electrophoresis revealed gammopathy with two distinct monoclonal peaks consisting of immunoglobulin G (IgG) kappa and IgG lambda, respectively. The kappa/lambda ratio was within normal limits, and urine protein electrophoresis showed no evidence of a monoclonal peak or Bence Jones proteins. Further workup for multiple myeloma, including bone marrow (BM) biopsy, revealed polyclonal plasma cells and B cells with no clonality. No morphological and immunephenotypic evidence of plasma cell dyscrasia was found, but BM biopsy did show numerous non-caseating granulomas consistent with sarcoidosis. Skin biopsy from non-scaly 6-mm skin colored papule also showed non-caseating granulomas. The patient had elevated angiotensinconverting enzyme levels (165 ug/l) and an erythrocyte sedimentation rate of 27 mm/h. Kidney biopsy did not show granulomas. The hypercalcemia, proteinuria, and AKI responded well after 2 weeks of 60 mg oral prednisone daily.

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