Steroid responsive

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]

A 14-year-old boy, without any preceding history of trauma, meningoencephalitis or seizures, was admitted in a comatose state. A similar episode of loss of consciousness 2 months prior with normal neuroimaging and electroencephalogram (EEG) had been followed by behavioral alterations. A year previously, during evaluation for increased appetite and poor weight gain, he was noted to have small goitre with thyroid-stimulating hormone (TSH) mIU/L, T3 nmol/L, and T4 nmol/L. Routine hemogram, blood biochemistry, thyroid function tests including free hormone levels, ultrasonography thyroid and magnetic resonance imaging were normal. EEG showed diffuse slowing of all waves. Cerebrospinal fluid showed no pleocytosis and electrophoresis showed oligoclonal band. Viral studies and serum N-methyl-D-aspartate receptor antibody levels were negative. Anti-thyroid peroxidase (Anti-TPO) antibodies were raised. Intervention was with intravenous dexamethasone 4 mg every 6 h for 1 week followed by tapering schedule of oral prednisolone over 6 months.

Steroid Responsive Meningitis - Samantha Goldberg BVSc MRCVS

Neck Pain and Fever in a Boxer--NAVA Clinician's Brief, November 2009
The Five Minute Veterinary Consult Page 388,
J AM Vet Med Assoc 201[10]:1553-8 Nov 15'92--Systemic Necrotizing Vasculitis in Nine Young Beagles.
J Vet Inter Med 4[2]:112 Mar/Apr'90 ACVIM 8th Annual Forum--Systemic Vasculitis {Canine Pain Syndrome} in young beagles
J Vet Intern Med 2[1]:26-35 Jan/Mar'88 123 Refs--Canine Meningitis:A Changing Emphasis
The Veterinary Record, June 17, 1978--Polyarteritis in a colony of beagles.
The Veterinary Record, April 7th 1973--Polyarteritis in the Dog: A Case Report   Dr. Roughie’s Questions and Answers- Steroid Responsive Meningitis-Vasculitis: The Disease With Many Names   Kasmin D. Bittle DVM   /images/Health/Dr-Roughie-ST-Column/
Neck Pain By Dr. J. E. Dillberger,  /images/Health/Dr-Roughie-ST-Column/

Steroid responsive

steroid responsive


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