Disease relevance of methylprednisolone

• A case of Duchenne muscular dystrophy from an exceptionally young patient yielded a muscle culture that was myogenically stimulated by Mepd [1].
• During AII hypertension, chronic infusion of 5 or 10 mg/day of MP also resulted in a marked renal vasodilation, natriuresis, and reductions in sodium iothalamate space, while causing small reductions in MAP [2].
• These results indicate that, at least in rabbits, HC and MP, in contrast to indomethacin, have very weak anti-inflammatory actions on three complement- and neutrophil-mediated inflammatory responses, i.e., E. coli, ZAP (C5ades-arg) and reversed Arthus reactions [3].
• Moreover, the efficacy of MP in limiting lipid peroxidation and secondary spinal cord or motor nerve degeneration has also been duplicated by a nonglucocorticoid 21-aminosteroid, tirilazad mesylate (U-74006F), which suggests the independence of the antioxidant and glucocorticoid effects of MP [4].
• The effects of Res on edema, LDH, Na+, K+-ATPase, and MDA were determined at 1 h, 24 h, and 48 h after SCI compared with MPSS [5].

High impact information on methylprednisolone

• For in vitro MP studies, normal lymphocytes cultured with varying concentrations of MP were significantly less stimulated by phytohemagglutinin (PHA) and concanavalin A (Con A) [6].
• Addition of histamine (1 x 10(-3) M) as well as MP in vitro led to a further inhibition of proliferative responses of these cells in an additive pattern in cultures of all MP concentrations [6].
• Chronic infusion of MP at doses of 2--800 mg/day in four dogs maintained on low (5 mEq/day) or high sodium intakes (160--223 mEq/day) also caused increases in GFR and ERPF, as well as natriuresis and decreased sodium iothalamate space, while causing either no change or a slight reduction in MAP [2].
• RESULTS: Supplementing peritransplant alpha-CD3-IT treatment with a brief course of DSG and MP promoted rejection-free kidney allograft acceptance in 75% of macaques followed for up to 550 days [7].
• ALFR, MPR, and MPRAL show statistically significant immunological effects in LIU treatment [8].

Biological context of methylprednisolone

• The doses of MP that affect this improved recovery have been demonstrated to inhibit posttraumatic spinal cord lipid peroxidation (LP), which has been postulated to be a key event in the secondary injury-induced degenerative cascade [9].
• Increasing the concentration of EDS or MP resulted in a dose-dependent increase in the incidence of apoptosis that reached a maximum of 25% (EDS) or 12% (MP) of detached cells [10].
• The administration of anti-CD11a, anti-CD18, anti-lectin cell adhesion molecule-1 (anti-LECAM-1), and MP increased the survival rate to 70, 62, 64, and 100%, respectively; however, NMLA had no significant effect [11].
• But the effects of Res 50 and 100 mg/kg were stronger in improving the energy metabolism system and inhibiting the lipid peroxidation in the local injured spinal cord after SCI than MPSS at the dose of 100 mg/kg [5].

Anatomical context of methylprednisolone

• In contrast, HC and MP caused only a mild decrease in blood flow, without altering protein exudation or leukocyte influx [3].
• After 12 weeks of methylprednisolone (MP) administration, the rabbit femur heads displayed cartilage erosions, marked decrease of glycosaminoglycans (GAG) content, and narrowing of joint spaces [12].
• Different effects of DSG and MP were also observed on B cells [13].
• The 45 consecutively enrolled patients received methylprednisolone (mPSL) 1000 mg per body for 3 d (from day 1 to day 3), IFM 1000 mg/m(2) for 5 d (from day 1 to day 5), MTX 30 mg/m(2) on day 3 and day 10, VP-16 80 mg/m(2) for 3 d (from day 1 to day 3), and CBDCA 300 mg/m(2) on day 1, with granulocyte colony-stimulating factor every 21 d [14].
• The numbers of leucocytes, lymphocytes and monocytes, the percentages of T and B cells and the expression of the interleukin 2 receptor and the human leucocyte antigen DR locus (HLA-DR) were determined in blood from these patients and from patients treated with MP only [13].

Associations of methylprednisolone with other chemical compounds

• Their mechanisms of inhibition were studied in lymphocytes exposed to methylprednisolone (MP) both in vivo and in vitro [6].
• Either in vivo MP treatment or in vitro histamine incubation depressed lymphocyte responsiveness to mitogen stimulation [6].
• The glucocorticoid steroid methylprednisolone (MP) has been shown to enhance chronic recovery after human spinal cord injury when administered in a 24-hr high-dose regimen beginning within 8 hr [4].
• Histomorphologic scores suggest detrimental effects of METH, DMSO, and the experimental COX-2 inhibitor [15].

Gene context of methylprednisolone

• Treatment with i.v. methylprednisolone (MP) led to an increase of IL-4 mRNA and a significant decrease of IFN-gamma and TNF-alpha mRNA expression [16].
• Administration of anti-CD18 and MP reduced the level to 1.80 and 1.41 nmol/mg protein, respectively, whereas NMLA did not affect it [11].

Analytical, diagnostic and therapeutic context of methylprednisolone

• Increased analgesia (P < 0.05) was noted when a double dose of INM was used (Group II) or when 80 mg of MTP was given [17].
• Group III (82 patients) was treated by 2 epidural injections of MTP 80 mg [17].
• No difference was observed in both groups with respect to the incidence of CMV disease after antirejection therapy either with MP or with OKT3/ATG [18].

References