Thrombotic Thrombocytopenic Purpura in a Patient with Rheumatoid Arthritis Treated by Plasmapheresis

Baz, Elizabeth M. Kfoury; Mahfouz, Rami; Masri, Abdel Fattah

doi:10.1046/j.1526-0968.1999.00166.x

Cited by 15 publications

(3 citation statements)

References 8 publications

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“…Noteworthy points in our series include the presence of autoimmune illnesses in 3 of our cases; although TTP is not habitually associated with an underlying disorder [5], several reports imply a link between TTP and other immune systemaffected conditions [10][11][12][13][14][15][16][17][18][19][20]. Fatal TTP-related cardiogenic shock in the context of immune illnesses, without cardiac histological evidence of the underlying disorder, has been described [4,5].…”

Section: Discussionmentioning

confidence: 99%

Myocardial injury in thrombotic thrombocytopenic purpura: A frequent, perplexing complication

Perez

Ramappa

Guzmán

2008

International Journal of Cardiology

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Section: Discussionmentioning

confidence: 99%

Myocardial injury in thrombotic thrombocytopenic purpura: A frequent, perplexing complication

Perez

Ramappa

Guzmán

2008

International Journal of Cardiology

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“…None of the patients reviewed in the 14 published cases were treated with chloroquine before or at the time of TMA onset. There is one reported case, in a patient with rheumatoid arthritis, of TMA occurring after 18 months of treatment with glucocorticoids and chloroquine diphosphate and with no known precipitating factor [20]. It is possible that in our case chloroquine diphosphate may have been a co-factor for thrombocytopenia but it is not likely to have induced the TMA.…”

Section: Discussionmentioning

confidence: 70%

Thrombotic microangiopathy in adult-onset Still's disease: case report and review of the literature

Šalamon

Morović‐Vergles

2009

Wien Klin Wochenschr

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Coexistence of thrombotic microangiopathy and adult-onset Still's disease is extremely rare. There is increasing evidence that this association could be more than just coincidental. We report on the case of a 34-year-old male diagnosed with adult-onset Still's disease and successfully treated with intravenous glucocorticoids. Nine months after onset the patient exhibited the presence of asymptomatic thrombocytopenia during treatment with chloroquine. The physical status was unremarkable except for pallor of the skin and mucosa. Laboratory evaluation revealed profound thrombocytopenia and hemolytic anemia. Coombs' tests were negative; renal function tests were all normal. The peripheral blood smear showed frequent schistocytes. Based on the presence of thrombocytopenia and microangiopathic hemolytic anemia, and with the exclusion of other known causes, the patient was diagnosed with thrombotic microangiopathy and successfully treated with plasma exchange and intravenous glucocorticoids. We also review the literature on the association between adult-onset Still's disease and thrombotic microangiopathy; our case is the 15(th) report on such an association. The mean age at onset of adult Still's disease in these cases was 31.60 years and the interval between the diagnosis of Still's disease and the onset of thrombotic microangiopathy ranged from 3 days to 17 years, with a female/male ratio of 2 : 1. In more than half the patients thrombotic microangiopathy occurred within the first 6 months after the diagnosis of the Still's disease. Eleven of the 15 (73%) patients were treated with plasmapheresis in addition to glucocorticoid therapy: eight of 11 (73%) had complete remission, the other three had permanent visual impairment and/or digital ischemia. Of the four patients who were not treated with plasmapheresis, two died, one developed end-stage renal disease and one had complete remission. Awareness of the possible development of thrombotic microangiopathy in patients with adult-onset Still's disease is critical, so that treatment can be initiated early and the complications and recurrence of thrombotic microangiopathy prevented. Patients with adult-onset Still's disease should be closely monitored for signs and symptoms of thrombotic microangiopathy during the first six months after diagnosis of the Still's disease.

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“…Lastly, since our patient suffered from RA, secondary TMA associated with RA should be considered. Except for rheumatoid vasculitis only a few cases with RA were reported to be associated with systemic TMA not localized renal TMA [18, 19], all which were thought to be caused by severe deficiency of ADAMTS13 due to autoantibodies that alter its function [20]. Since there were no renal vasculitic lesions, RA-associated TMA was excluded in our patient.…”

Section: Discussionmentioning

confidence: 99%

A Case of Rheumatoid Arthritis Presenting with Renal Thrombotic Microangiopathy Probably due to a Combination of Chronic Tacrolimus Arteriolopathy and Severe Hypertension

Honma

Fujigaki

Nemoto

et al. 2019

Case Reports in Nephrology

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A 51-year-old woman with rheumatoid arthritis presented with mild hypertension 20 months after tacrolimus treatment and developing proteinuria 24 months after the treatment. Tacrolimus was discontinued 27 months after the treatment, followed by heavy proteinuria, accelerated hypertension, and deteriorating renal function without ocular fundus lesions as a clinical sign of malignant hypertension. Renal biopsy revealed malignant nephrosclerosis characterized by subacute and chronic thrombotic microangiopathy (TMA), involving small arteries, arterioles, and glomeruli. Focal segmental glomerulosclerosis, probably secondary to chronic TMA, was identified as a cause of heavy proteinuria. The zonal tubulointerstitial injury caused by subacute TMA may have mainly contributed to deteriorating renal function. The presence of nodular hyalinosis in arteriolar walls was indicative of tacrolimus-associated nephrotoxicity. Together with other antihypertensive drugs, administration of aliskiren stabilized renal function with reducing proteinuria. Owing to the preexisting proteinuria prior to severe hypertension and the complex renal histopathology, we postulated that chronic TMA, which was initially triggered by tacrolimus, was aggravated by severe hypertension, resulting in overt renal TMA.

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Thrombotic Thrombocytopenic Purpura in a Patient with Rheumatoid Arthritis Treated by Plasmapheresis

Cited by 15 publications

References 8 publications

Myocardial injury in thrombotic thrombocytopenic purpura: A frequent, perplexing complication

Myocardial injury in thrombotic thrombocytopenic purpura: A frequent, perplexing complication

Thrombotic microangiopathy in adult-onset Still's disease: case report and review of the literature

A Case of Rheumatoid Arthritis Presenting with Renal Thrombotic Microangiopathy Probably due to a Combination of Chronic Tacrolimus Arteriolopathy and Severe Hypertension

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