Amounts of methylprednisolone in breastmilk are very low. No adverse effect have been reported in breastfed infants with maternal use of any corticosteroid during breastfeeding. With maternal intravenous doses of methylprednisolone 1 gram, fully breastfed infants would receive doses less than their daily cortisol output, and much less than a therapeutic dose on the day of infusion; accumulation of the drug does not occur in breastmilk with 3 consecutive daily doses. Avoiding breastfeeding during the infusion for as little as 2 hours after a 1 gram intravenous dose would markedly reduce infant exposure. Breastfeeding abstinence for 2 to 4 hours would further reduce the infant dose. Local injections, such as for tendinitis, would not be expected to cause any adverse effects in breastfed infants, but might occasionally cause temporary loss of milk supply.

Immune-mediated necrotizing myopathy is a very rare inflammatory disease affecting skeletal muscles. Immune-mediated necrotizing myopathy may be associated with myositis-specific autoantibodies including anti-single recognition particle and anti-3-hydroxy-3- methylglutaryl-coenzyme A reductase, infectious agents (HIV or hepatitis C), other connective tissue disorders (such as scleroderma), and malignancy. We reported a 28-year-old healthy woman presented with subacute onset ascending muscle weakness 2 weeks after an annual influenza vaccination. Cerebral Spinal Fluid study showed normal cell counts with elevated protein and nerve conduction study showed reduced diffuse compound muscle action potential amplitudes suggesting a diagnosis of Guillain-Barré syndrome. Despite treatment using intravenous immunoglobulin, her condition continued to get worse with new bulbar and respiratory muscle weakness. Eventually, the diagnosis of anti-single recognition particle-mediated necrotizing myopathy was made based on elevated creatine kinase, thigh magnetic resonance imaging, muscle biopsy, and positive antibody testing. Our patient responded to the combination of intravenous immunoglobulin, prednisone, and anti-CD20 monoclonal antibody, rituximab.

In order to explore a novel high efficacy drug delivery system for membranous glomerulonephritis (MGN), a complex chronic inflammation, methylprednisolone bovine serum albumin nanoparticles (ME BSA NPs) were designed. The nanoparticles were prepared by desolvation-chemical crosslinking method and its physicochemical characterizations were conducted. The experimental MGN rat models induced by cationic bovine serum albumin were established by a modified Border's method and applied in the pharmacodynamics study of ME BSA NPs. The results showed that the particle size, particle dispersion index, and entrapment efficiency of ME BSA NPs were 131.1 ± 3.4 nm, 0.159 ± 0.036, and 71.51 ± 1.74%, respectively. In addition, the image of transmission electron microscopy showed that the ME BSA NPs were the relatively uniform spherical particles. In the in vivo pharmacodynamics study, compared with saline group and SOLU-MEDROL® group, that the ME BSA NPs group was significantly reduced the levels of 24 h urinary protein (P < 0.01) and serum creatinine (P < 0.05). Consequently, these outcomes indicated that the nanoparticles we studied were a promising drug delivery system for the MGN disease, and it may be also useful for other complex chronic inflammations.

A new self-assembled formulation of methylprednisolone succinate (MPS) based on a carboxylated trifunctional block copolymer of ethylene oxide and propylene oxide (TBC-COOH) was developed. TBC-COOH and MPS associated spontaneously at increased concentrations in aqueous solutions to form almost monodisperse mixed micelles (TBC-COOH/MPS) with a hydrodynamic diameter of 19.6 nm, zeta potential of -27.8 mV and optimal weight ratio ∼1:6.3. Conditions for the effective formation of TBC-COOH/MPS were elucidated by comparing copolymers and glucocorticoids with different structure. The micellar structure of TBC-COOH/MPS persisted upon dilution, temperature fluctuations and interaction with blood serum components. TBC-COOH increased antiradical activity of MPS and promoted its intrinsic cytotoxicity in vitro attributed to enhanced cellular availability of the mixed micelles. Intracellular transportation and hydrolysis of MPS were analyzed using optimized liquid chromatography tandem mass spectrometry with multiple reaction monitoring which showed increased level of both MPS and methylprednisolone in neuronal cells treated with the formulated glucocorticoid. Our results identify TBC-COOH/MPS as an advanced in situ prepared nanoformulation and encourage its further investigation for a potential local glucocorticoid therapy.

Methylprednisolone sodium succinate (MPSS) has been suggested as a treatment for spinal cord injury (SCI), but its use has been limited due to its adverse effects. Erythropoietin (EPO) has been suggested as a promising candidate for limiting SCI in mammals. The aim of the present study was to investigate the effects of EPO in combination with MPSS on astrocytes following ischemic injury in vitro. Astrocytes were isolated from the cerebral cortex of postnatal day 3 Sprague‑Dawley rats and cultured in vitro. Astrocyte ischemic injury was induced by oxygen and glucose deprivation for 4 h, and reperfusion was simulated by subsequent culture under normoxic conditions. The effects of EPO and MPSS on the expression of aquaporin‑4 (AQP4) were investigated. Ischemic astrocytes were treated with EPO (10 U/ml), MPSS (10 µg/ml), or EPO (10 U/ml) in combination with MPSS (10 µg/ml) during reperfusion. The cell viability of astrocytes was assessed using an MTT assay. The mRNA and protein expression levels of AQP4 were determined using reverse transcription‑quantitative polymerase chain reaction and western blot analysis, respectively. The role of the protein kinase C (PKC) signaling pathway in the molecular mechanisms underlying the effects of EPO and MPSS was also investigated. The present results demonstrated that following treatment with EPO and MPSS, the mRNA expression levels of AQP4 were upregulated and cell viability was enhanced. EPO and MPSS effectively inhibited the oxygen and glucose deprivation‑mediated downregulation of AQP4 following reperfusion. In addition, the combined treatment with EPO and MPSS exhibited higher AQP4 expression levels and cell viability compared with each treatment alone. Finally, the effects of EPO and MPSS on AQP4 expression were partially reversed by pretreatment with the PKC inhibitor Ro 31‑8220. The present study indicated that EPO and MPSS had a synergistic effect on AQP4 expression following reperfusion, and suggest that they may be combined in the treatment of SCI.

Rapid improvement of tick-borne encephalitis after treatment with corticosteroids Tick-borne encephalitis (TBE) is a viral disease transmitted by ticks. The virus is divided into three subtypes named Western, Siberian and Far Eastern TBE virus (TBEV). Western TBEV is endemic in parts of Europe and Sweden and typically causes a biphasic illness with influenza-like symptoms followed by neurological symptoms ranging from mild meningitis to severe meningoencephalitis and death. Despite an effective vaccine, TBE is increasing in Sweden and Europe. The pathogenesis of TBE is poorly understood; direct infection of neurons as well as immunological reactions mediated by T-cells have been implicated. In some endemic areas, such as Lithuania, patients with TBE are given corticosteroids based on the clinical experience that it results in rapid improvement. However, existing retrospective studies have failed to show beneficial effects of corticosteroids compared to symptomatic treatment in patients with TBE. This case report describes how an elderly man with meningoencephalitis and cranial nerve palsy due to TBE  rapidly improved after administration of high dose corticosteroids.