Steroid responsive encephalopathy

Bile acids, in particular chenodeoxycholic acid (CDCA) and cholic acid (CA), can regulate the expression of genes involved in their synthesis, thereby, creating a feed-back loop. The elucidation of this regulatory pathway came about as a consequence of the isolation of a class of receptors called the farnesoid X receptors, FXRs . The FXRs belong to the superfamily of nuclear receptors that includes the steroid/thyroid hormone receptor family as well as the liver X receptors (LXRs) , retinoid X receptors (RXRs), and the peroxisome proliferator-activated receptors (PPARs) .

Intravenously administered glucocorticoids , such as prednisone , are the standard of care in acute GvHD [7] and chronic GVHD. [24] The use of these glucocorticoids is designed to suppress the T-cell-mediated immune onslaught on the host tissues; however, in high doses, this immune-suppression raises the risk of infections and cancer relapse. Therefore, it is desirable to taper off the post-transplant high-level steroid doses to lower levels, at which point the appearance of mild GVHD may be welcome, especially in HLA mis-matched patients, as it is typically associated with a graft-versus-tumor effect. [ citation needed ] . Cyclosporine and tacrolimus are inhibitors of calcineurin. Both substances are structurally different but have the same mechanism of action. Cyclosporin binds to the cytosolic protein Peptidyl-prolyl cis-trans isomerase A (known as cyclophilin), while tacrolimus binds to the cytosolic protein Peptidyl-prolyl cis-trans isomerase FKBP12. These complexes inhibit calcineurin, block dephosphorylation of the transcription factor NFAT of activated T-cells and its translocation into the nucleus. [25] Standard prophylaxis involves the use of cyclosporine for six months with methotrexate. Cyclosporin levels should be maintained above 200 ng/ml. [26] Other substances that have been studied for GvHD prophylaxis include, for example: sirolimus, pentostatin and alemtuzamab. [26]

It is important to note that RAD140 systematically regulates the neuroexcitatory amino acid Kainate which activates glutamate receptors in the brain. Kainate acid’s role in neuronal cell death (specifically in the hippocampus) has been shown to be a primary contributor to Alzheimer’s disease. RAD140 has demonstrated positive results in the prevention of Kainate acid production and medical based research published by The Endocrine Society suggests RAD140 can improve brain health through neuroprotective properties in as little as 13 days (Jayaraman, 2014).

The problem usually develops in young adults. Signs include fever, stiff neck, hyper-reactivity to touch, and reduced mobility due to marked stiffness. It can be acute or chronic. The cause is not well understood, but because it responds to steroid therapy, it is likely an autoimmune condition. Autoimmune problems occur when the body sees itself as foreign and mounts a reaction. There is the possibility that infectious agents can trigger this reactivity. Steroid medications have anti-inflammatory action, and at high doses, inhibit the immune system.

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Steroid responsive encephalopathy

steroid responsive encephalopathy

The problem usually develops in young adults. Signs include fever, stiff neck, hyper-reactivity to touch, and reduced mobility due to marked stiffness. It can be acute or chronic. The cause is not well understood, but because it responds to steroid therapy, it is likely an autoimmune condition. Autoimmune problems occur when the body sees itself as foreign and mounts a reaction. There is the possibility that infectious agents can trigger this reactivity. Steroid medications have anti-inflammatory action, and at high doses, inhibit the immune system.

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