Refractory neurosarcoidosis responding to infliximab

Abstract

We read with interest the study of Sachdev et al., 1 who reported an association between elevated homocysteine levels and brain atrophy in healthy elderly subjects. To our knowledge, this observation is the second report about a linkage between increased homocysteine levels and brain volume reduction. Recently, radiologic evidence of temporal atrophy progression in patients with AD has been found to be significant greater among those patients with higher plasma homocysteine levels. 2 In addition to these findings we would like to emphasize the influence of elevated homocysteine levels in chronic alcoholism on alcoholism-related brain shrinkage. Chronic alcohol consumption leads, among other lesions, to cortical and subcortical cerebral atrophy (e.g., cerebral white matter, corpus callosum, hippocampal area, cerebellar vermis). 3 However, the precise mechanisms on which the alcohol-related brain tissue changes are based have yet to be fully explained. There is evidence that chronic alcoholism is associated with hyperhomocysteinemia. 4 In a recent volumetric MRI study including 52 chronic alcoholics we observed that pathologic raised levels of plasma homocysteine showed the most significant correlation to brain volume reduction. 5 These results further support the abovementioned observations. The decrease in homocysteine possibly may explain why brain atrophy no longer progresses during abstinence, taking into account that homocysteine levels steadily decrease during alcohol withdrawal. 4 Therefore, increased levels of homocysteine in patients with brain atrophy may have important implications for understanding the pathogenesis of neurodegenerative disorders. The results of these studies highlight the need for further research on whether neuroprotection against elevated homocysteine levels (e.g., NMDA antagonists) or the lowering of homocysteine (e.g., fortification) will protect patients from neuronal cell loss or brain atrophy. The relationship between increased homocysteine levels, their causes (e.g., common genetic polymorphisms such as methylenetetrahydrofolate reductase mutations) and neurotoxicity warrants further study.

Long-term outcomes of refractory neurosarcoidosis treated with infliximab

“…The efficacy of infliximab has also been studied in small series and case reports of patients with neurosarcoidosis( Table 2). [3,4,10,11,[14][15][16][17][18][19][20] those from studies which did not focus on neurosarcoidosis). Infliximab has been shown to demonstrate short-term efficacy in these patients, even in case of previous immunosuppressive drugs failure, as we observed in our study.…”

Treatment of refractory neurosarcoidosis with Infliximab

“…Other potential adverse effects include infusion reactions and the development of antibodies 18. Considerable caution in its use is therefore required; histological confirmation of the diagnosis is important, as is screening for tuberculosis.…”

Sarcoidosis of the nervous system

“…77,78 Infliximab (a monoclonal antibody against TNF-a) in particular has a growing body of literature supporting its effectiveness, and appears to be a safe treatment with good steroid sparing effects. [79][80][81][82][83] The long-term complications of these cytotoxic agents should not be underestimated, with awareness for the effects of immunocompromise. Infections such as toxoplasmosis, tuberculous and cryptococcal meningitis may occur, and also lymphoproliferative disorders, which may be overlooked as some features of these diseases may themselves mimic sarcoidosis.…”