Reduction in the Free Radical Status and Clinical Benefit of Repeated Intrathecal Triamcinolone Acetonide Application in Patients With Progressive Multiple Sclerosis

Abstract

Repeat triamcinolone application improves dysfunction of upper and lower extremities even when administered 5 times only and in series every other day. The declined potential for free radical synthesis may be caused by the anti-inflammatory effect of triamcinolone. It may contribute to suppress the smoldering, chronic inflammation, particularly in spinal lesions of patients with progressive multiple sclerosis. The enhanced arm function hypothetically reflects the effect on cervical and brain lesions due to the hypobaric features of triamcinolone.

One-time intrathecal triamcinolone acetonide application alters the redox potential in cerebrospinal fluid of progressive multiple sclerosis patients: a pilot study

“…This decline generally precedes neuronal recovery. One may even hypothesize that changes of free radical metabolism may trigger the observed descent of RGMa concentrations in patients with an enhancement of MS symptoms during TCA treatment [Müller et al 2014[Müller et al , 2015. However, this hypothesis warrants further investigation in combination with repeat clinical evaluation of MS patients, and assessment of further metabolic CSF substrates that are responsible for regenerative processes according to a similar signal-transduction pathway as in the case of fibrinogen generation [Aiken et al 2011].…”

Intrathecal triamcinolone acetonide exerts anti-inflammatory effects on Lewis rat experimental autoimmune neuritis and direct anti-oxidative effects on Schwann cells

“…According to studies on MS patients, a potential effect of intrathecal TRIAM characterized in CSF is the reduction of repulsive guidance molecule A (RGMa), a cell death regulator [23]. Recurrent TRIAM applications induced a decreased concentration of RGMa fragments combined with a decline in free radical concentration, potentially improving neuronal regeneration [6, 7].…”

Polymorphism of Triamcinolone Acetonide Acetate and Its Implication for the Morphology Stability of the Finished Drug Product

“…Drugs with long-term therapy applications are prime candidates for polymorphism investigations, as many have no solid-state chemistry recorded in detail, especially those that undergo additional and significant changes during processing. Glucocorticoid drugs are a class of steroid hormones and are widely prescribed for asthma and connective-tissue diseases. − Several new polymorphic modifications for these compounds, such as triamcinolone acetonide, hydrocortisone, prednisolone, and bethamethasone valerate, were recently reported by Näther. − Triamcinolone acetonide acetate (TAA, Scheme ) is a long-term glucocorticoid clinically prescribed for the treatment of chronic inflammatory diseases such as asthma, rheumatoid arthritis, inflammatory bowel disease, and autoimmune diseases. , Especially for treatment of rheumatoid arthritis, TAA can obviously inhibit secretion of interleukin-1 and TNF-α from articular synovial tissue to reduce the proliferation of capillaries and fibroblasts . It belongs to a class II compound according to the Biopharmaceutics Classification System (BCS) with poor aqueous solubility (0.001 mg/mL) and high permeability (log P = 3.2). , TAA is officially listed in Chinese Pharmacopoeia as an intramuscularly injectable suspension for rheumatoid arthritis.…”

“…17−23 Triamcinolone acetonide acetate (TAA, Scheme 1) is a long-term glucocorticoid clinically prescribed for the treatment of chronic inflammatory diseases such as asthma, rheumatoid arthritis, inflammatory bowel disease, and autoimmune diseases. 24,25 Especially for treatment of rheumatoid arthritis, TAA can obviously inhibit secretion of interleukin-1 and TNF-α from articular synovial tissue to reduce the proliferation of capillaries and fibroblasts. 25 It belongs to a class II compound according to the Biopharmaceutics Classification System (BCS) with poor aqueous solubility (0.001 mg/mL) and high permeability (log P = 3.2).…”

“…24,25 Especially for treatment of rheumatoid arthritis, TAA can obviously inhibit secretion of interleukin-1 and TNF-α from articular synovial tissue to reduce the proliferation of capillaries and fibroblasts. 25 It belongs to a class II compound according to the Biopharmaceutics Classification System (BCS) with poor aqueous solubility (0.001 mg/mL) and high permeability (log P = 3.2). 26,27 TAA is officially listed in Chinese Pharmacopoeia as an intramuscularly injectable suspension for rheumatoid arthritis.…”