Five cases in which a depot steroid (hydrocortisone acetate and methylprednisolone acetate) was injected into the eye.
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Anti-Inflammatory Agents↗
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Bovine plasma and synovial fluid kinetics of methylprednisolone and methylprednisolone acetate after intra-articular administration of methylprednisolone acetate.
After an intra-articular administration of methylprednisolone acetate (MPA) in the cow, methylprednisolone (MP) was detected in the synovial fluid, at pharmacologically significant concentrations, during more than 3 months. From in vitro assay, it was shown that hydrolysis of MPA to MP was rapid both in blood (half-times from 11.8 to 21.7 min) and in synovial fluid (half-times from 45.6 to 130.3 min). After intra-articular administration of MPA as a suspension (200 mg in toto), both MP and MPA decline very rapidly and, 24 hr after injection, less than 1% of the dose was present in the synovial fluid, but systemic availability of MP during the first 24 hr was only 30% of the dose. Twenty-four hours postadministration, post-mortem examinations showed a significant quantity of MPA precipitated at the bottom of the synovial cavity. It was assumed that the relatively slow decline of MP synovial fluid concentration from 24 hr to 5 days postadministration was due mainly to a process of MP absorption. After this delay, the synovial fluid concentration decreased very slowly with an apparent half-time of 18 days. This has been tentatively explained in terms of a slow release of MP from MPA embedded in a fibrin-like deposit. Despite the fact that the quantity of MP absorbed each day was small, long-term systemic effects were observed. During 6 weeks, plasma hydrocortisone levels remained low or undetectable and the return to normal adrenal responsiveness to an adrenocorticotropic hormone test took 12 weeks.
Adrenal Glands↗
Synovial fluid and plasma kinetics of methylprednisolone and methylprednisolone acetate in horses following intra-articular administration of methylprednisolone acetate.
Synovial fluid and plasma kinetics of methylprednisolone acetate (MPA) and methylprednisolone (MP) after a single intra-articular administration of MPA at a therapeutic dose (111 mg in toto) was measured in five horses. MPA was detected in synovial fluid for two to six days post injection and MP, which results from synovial MPA hydrolysis, was present in pharmacologically significant concentrations for 4.8 to 39 days, depending on the horse. MPA synovial concentration was maximal (289 +/- 284 micrograms/ml) at the first sampling time (2 h after administration) and MP synovial concentration was maximal (from 58.9 to 379.5 micrograms/ml) at the first or second sampling time (2 to 10 h after administration). Thereafter, both MP and MPA declined rapidly. From time of administration to about five days later, MP synovial fluid concentration fell progressively with a half-time of 9.95 h. Subsequently, the MP synovial fluid concentration decreased more slowly with an apparent half-time of 115 h. During the first 24 h following MPA administration, trace amounts of MP (less than 5 ng/ml) were detected in plasma. Plasma hydrocortisone levels were depressed for three to four days after administration but adrenal responsiveness to adrenocorticotrophic hormone tests remained unaffected.
Adrenal Glands↗
Rectal and oral absorption of methylprednisolone acetate.
Rectal absorption of methylprednisolone acetate and oral absorption of methylprednisolone and methylprednisolone acetate were investigated in a single-dose 3-way crossover study of 12 normal male volunteers. The median value of bioavailability (relative to oral dose) of methylprednisolone acetate based on unchanged methylprednisolone plasma levels was 14.2% after rectal administration, suggesting that the drug exerts its therapeutic effect topically rather than systemically. In contrast, the median of total radioactivity in urine (as a percentage of rectal dose) was 34.3% (range, 4.52% to 58.8%), suggesting partial bacterial metabolism in the rectum prior to absorption. Mean bioavailability (relative to oral administration of methylprednisolone acetate) of methylprednisolone after oral administration was 89.9%, indicating somewhat better systemic availability of the ester than the alcohol. The average apparent elimination rate constant for methylprednisolone after oral administration of both ester and alcohol was 0.290 hr-1, corresponding to a half-life of 2.39 hr.
Absorption↗
Failure of methylprednisolone acetate to prolong the antinauseant effect of intravenous methylprednisolone sodium succinate in patients receiving chemotherapy.
The efficacy of intramuscular methylprednisolone acetate in maintaining the antinauseant effect of intravenous methylprednisolone sodium succinate was assessed in a prospectively-randomized, double-blind, crossover-design trial. Of 150 patients entered, 127 were evaluable. There was no statistically significant difference between methylprednisolone acetate and saline placebo, although patient preferences slightly favoured the methylprednisolone acetate for nausea, vomiting, and overall effectiveness.
Adult↗
Adrenocortical function and plasma biochemical values in dogs after subconjunctival treatment with methylprednisolone acetate.
The effects of subconjunctivally administered methylprednisolone acetate on adrenocortical function and blood composition were studied in five dogs. Two 10 mg doses of methylprednisolone acetate were injected at an interval of 21 days. Plasma cortisol concentrations (COR), ACTH-stimulated cortisol concentrations and other blood components were determined regularly. The normal plasma COR (5.7 +/- 2.62 ng/ml) was one of the lowest reported in the literature for the dog, possibly because of the specificity of the high performance liquid chromatographic assay and the experimental environment. Plasma COR was depressed only after the first administration of methylprednisolone acetate. ACTH stimulated COR was significantly depressed nine and 20 days after the first and second subconjunctival injection respectively. Otherwise blood composition was unchanged.
Adrenal Cortex↗
Dangers from methylprednisolone acetate therapy by intraspinal injection.
Clinical trials first began in 1960 with methylprednisolone acetate (Depo-Medrol) administered intrathecally, in an attempt to treat both disk disease and multiple sclerosis. After a few reports of salubrious results, there began an outpouring of contradictory data, which continues in 1988. During this time span, researchers who cautiously tested the different theses of improvement began to publish serious warnings of many complications. For ten years prior to the intraspinal use of methylprednisolone acetate, basic scientists in anesthesiology and neurochemistry had published the following facts: (1) Methylprednisolone acetate's content of polyethylene glycol raises the risks of using it near the central nervous system. (2) Deleterious effects follow the use of glycols when they are placed into or near the neuraxis. (3) Methylprednisolone acetate contains approximately 30 mg of polyethylene glycol per milliliter. (4) When that glycol, which is both alcohol and detergent, is injected intraspinally, sterile meningitis, arachnoiditis, or pachymeningitis will occur. It has also been recognized since the 1960s that the epidural space is not wholly separate from the subdural and/or subarachnoid space. Many thousands of arachnoid villi subtend all the membranes from the intrathecal space, and many of these end in the large epidural veins. Therefore, the various spaces and membranes are not only contiguous, but continuous. It follows that an injection of methylprednisolone acetate into the epidural space does not guarantee that it will remain isolated there. Finally, the inadvertency of injections by the epidural route occurs with the following frequency: 40% of injections can be inadvertently made into interspinous ligaments, and 2.5% into the subarachnoid space.
Demyelinating Diseases↗
Observations on the action of prednisolone tertiary buryl acetate (Codelcortone TBA) and methylprednisolone acetate (depomedrone) on normal soft tissues.
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Angiography↗
Pharmacokinetics of methylprednisolone, methylprednisolone sodium succinate, and methylprednisolone acetate in dogs.
The absolute bioavailability and pharmacokinetic parameters of two methylprednisolone formulations (methylprednisolone sodium succinate and methylprednisolone acetate) were determined in five dogs. Plasma concentrations of methylprednisolone, methylprednisolone sodium succinate, and methylprednisolone acetate were measured by sensitive and specific high-performance liquid chromatographic methods. After intravenous methylprednisolone sodium succinate administration, methylprednisolone was released rapidly but the extent of availability was rather low (43.6%). This has been tentatively explained in terms of its subsequent single-pass metabolism in the liver, i.e., hepatic hydrolysis of methylprednisolone sodium succinate followed by immediate hepatic elimination of the released methylprednisolone. After intramuscular administration of methylprednisolone acetate, its absorption was slow (half-time of absorption, 69.04 h) and the availability of the released methylprednisolone was low (42.7%). Therapeutic implications of these results are discussed, especially those which are relevant to shock therapy.
Animals↗
Observations on the action of intraarticularly administered prednisolon tertiary butyl acetate (Codelcortone TBA) and methylprednisolon acetate (Depomedrone) in the normal rabbit knee joint. A vital microscopic and histologic study.
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Animals↗
Histologic changes in the intervertebral disc after intradiscal injections of methylprednisolone acetate in rabbits.
STUDY DESIGN: Histologic changes in the intervertebral disc were evaluated by light and electron microscopy after an intradiscal injection of methylprednisolone acetate. OBJECTIVE: To evaluate the histologic changes that occur in the disc after an intradiscal injection of cortico steroids. SUMMARY OF BACKGROUND DATA: Several orthopedic surgeons have managed lumbar disc herniation with intradiscal steroid injection. Few studies have addressed the histologic changes after this treatment. METHODS: Thirty rabbits were surgically treated. Rabbits were divided into two groups. Group A: 25 rabbits underwent intradiscal steroid injections. Methylprednisolone acetate was injected into the L3-L4 disc, whereas methylprednisolone sodium succinate was injected into the L4-L5 disc. Physiologic saline was injected into the L5-L6 disc as a control. Groups of five rabbits were killed 1 day, 1, 4, 12, and 24 weeks after the injection and subjected to microscopic evaluation. Group B: Another five rabbits underwent an injection of polyethylene glycol 4000, a vehicle for methylprednisolone acetate, into the L3-L4 and L4-L5 discs. All five rabbits were killed 24 weeks after the injection and subjected to microscopic evaluation. RESULTS: Group A: Light microscopic evaluation showed tissue in the nucleus pulposus, and the inner layer of the anulus fibrosus had degenerated in the methylprednisolone acetate group killed 24 weeks after the injection. Matrix vesicles, an indication of primary tissue calcification, were observed by electron microscopy. In the methylprednisolone sodium succinate group and saline group, however, no histologic changes were observed. Group B: Degeneration of the nucleus pulposus and primary tissue calcification were observed in the discs of all rabbits. CONCLUSIONS: Methylprednisolone acetate and its vehicle polyethylene glycol cause degeneration and primary calcification in discs.
Animals↗
Intraspinal therapy using methylprednisolone acetate. Twenty-three years of clinical controversy.
The intraspinal use of methylprednisolone acetate (Depo-Medrol, Upjohn Company, Kalamazoo MI) began in 1960, followed 10 years later by reports of complications. In 1960, methylprednisolone acetate was first injected by the epidural route to treat low-back syndromes. Then in 1961, the intrathecal route was more widely used to treat arachnoiditis and multiple sclerosis. Epidural therapy again came into general use in 1980 for the treatment of the failed-back syndrome because intrathecal therapy was virtually abandoned after 10 years of spirited scientific controversy. Epidural steroid therapy is now employed extensively, and there are many sanguine reports of its efficacy in treating chronic pain secondary to the failed-back syndrome, but there have also been reports of complications. This review was prompted by recent manufacturer warnings, as well as by an ongoing heated controversy in Australia regarding its use epidurally. During the last 30 years, one can define 5 instructive historical parallels between intrathecal and epidural steroid therapy, and this historicity points up several principles that should govern any further epidural therapy with methylprednisolone acetate. This critical chronologic review surveys neurosurgical use from 1960 to 1970, neurologic use from 1970 to 1980, and anesthesiology use from 1980 to present.
Anesthesiology↗
Structure and development of parietal podocytes in renal glomerular cysts induced in rabbits with methylprednisolone acetate.
Newborn rabbits were injected with methylprednisolone acetate to induce polycystic kidneys. Two major types of cysts were observed: tubular cysts formed by the dilation of collecting tubules and glomerular cysts formed by the dilation of Bowman's capsular space. We examined the structure and developmental changes of the glomerular cysts of rabbits aged 2 to 75 days. Two types (I and II) of fully developed glomerular cysts were observed. Most were type I, having one small glomerulus and a parietal layer composed entirely of podocytes. Type II had one or several small glomeruli and a parietal layer composed partially of podocytes. In both types I and II cysts, the podocytes in the parietal layer were connected to various structures surrounding the cysts by a basal lamina. These cysts were first detected in the early postnatal stages. During the S-shaped body stage, the presumptive parietal layer was composed of simple columnar cells in contrast to the flat cells of normal S-shaped bodies. In the following stages, Bowman's capsular space was dilated, and podocytes were in the process of differentiation. The sequence of differentiation of the parietal podocytes was similar to that in the visceral layer in normal conditions. These data indicate that the differentiation and maturation of podocytes are not dependent upon the endothelial capillary factors. We hypothesized that an inhibitory factor that stabilizes the phenotype of the parietal cells under normal conditions is absent under conditions that cause glomerular cyst formation.
Animals↗
The systemic and local effects of an intramedullary injection of methylprednisolone acetate in growing rabbits.
Intramedullary injection of methylprednisolone acetate (Depo-Medrol) is successful in the treatment of children with unicameral cysts, but its mechanism of action remains obscure. Using a rabbit model, methylprednisolone was injected into the intramedullary canal of the left proximal tibia. Normal saline was injected into the right proximal tibia as a control. Venous blood samples following injection revealed that corticosteroid was rapidly cleared from bone. Serum methylprednisolone levels rose rapidly, giving a dose-response curve similar to that after an intramuscular injection in humans. Rabbits were killed and analyzed histologically for local changes. There was no fibroblastic proliferation, neovascularization, or other histologic change secondary to injection.
Animals↗
Clinical and endocrine side-effects of methylprednisolone acetate as used in hay-fever.
Eight patients were treated with two 80-mg. doses of methylprednisolone acetate (Depo-Medrone), given at an interval of two weeks. Pituitary-adrenal function was assessed before, during, and after treatment.Plasma cortisol levels were depressed maximally 72 hours after each injection of methylprednisolone acetate, and then gradually returned to normal. The adrenocortical response to administered corticotrophin was similarly affected; in seven patients normal values were again recorded three weeks after the second injection of methylprednisolone acetate. One patient whose adrenal function had returned to normal still showed some degree of pituitary suppression eight weeks after his second injection. Several side-effects were noted, and clinically the patients fared less well than a larger series studied during the previous year.
Adrenocorticotropic Hormone↗
The effect of posterior subtenon methylprednisolone acetate in the refractory diabetic macular edema: a prospective nonrandomized interventional case series.
BACKGROUND: To investigate the efficacy of posterior subtenon methylprednisolone acetate injection in treatment of refractory diffuse clinically significant diabetic macular edema (CSME). METHODS: In a prospective, nonrandomized, interventional case series, 52 eyes were diagnosed with CSME and treated with at least two sessions of laser photocoagulation according to Early Treatment Diabetic Retinopathy Study guidelines. At least 3 months after laser therapy, eyes with a residual central macular thickness were offered posterior subtenon injection of 40 mg methylprednisolone acetate. Main outcome measures were visual acuity, macular thickness and intraocular pressure. Potential complications were monitored, including intraocular pressure response, cataract progression and scleral perforation. RESULTS: Mean baseline visual acuity (in logMAR) improved significantly (p = 0.003) from 0.8 +/- 0.36 to 0.6 +/- 0.41 at 3 months. Mean foveal thickness decreased from 388 +/- 78 mum at baseline to 231 +/- 40 mum after 3 months (p < 0.0001). Visual acuity improvement in eyes with CSME with extrafoveal hard exudates was significant (p = 0.0001), but not significant in eyes with CSME with subfoveal hard exudates (p = 0.32). Intraocular pressure increased from 14.7 +/- 2.0 mmHg (range, 12-18 mmHg) to a maximum value of 15.9 +/- 2.1 mmHg (range, 12-20 mmHg) during the follow-up period. Complications in two eyes developed focal conjunctival necrosis at the site of injection. CONCLUSION: Posterior subtenon methylprednisolone acetate may improve early visual outcome in diffuse diabetic macular edema that fails to respond to conventional laser photocoagulation. Visual acuity improvement in eyes with CSME with extrafoveal hard exudates was significant; and this improvement is depends on location of hard exudates. Further study is needed to assess the long-term efficacy, safety, and retreatment.
Adult↗
Effects of sodium hyaluronate and methylprednisolone acetate on proteoglycan synthesis in equine articular cartilage explants.
OBJECTIVE: To determine effects of sodium hyaluronate (HA) on corticosteroid-induced cartilage matrix catabolism in equine articular cartilage explants. SAMPLE POPULATION: 30 articular cartilage explants from fetlock joints of 5 adult horses without joint disease. PROCEDURE: Articular cartilage explants were treated with control medium or medium containing methylprednisolone acetate (MPA; 0.05, 0.5, or 5.0 mg/mL), HA (0.1, 1.0, or 1.5 mg/mL), or both. Proteoglycan (PG) synthesis was measured by incorporation of sulfur 35-labeled sodium sulphate into PGs, and PG degradation was measured by release of radiolabeled PGs into the medium. Total glycosaminoglycan (GAG) content in media and explants and total explant DNA were determined. RESULTS: Methylprednisolone acetate caused a decrease in PG synthesis, whereas HA had no effect. Only the combination of MPA at a concentration of 0.05 mg/mL and HA at a concentration of 1.0 mg/mL increased PG synthesis, compared with control explants. Methylprednisolone acetate increased degradation of newly synthesized PGs into the medium, compared with control explants, and HA alone had no effect. Hyaluronate had no effect on MPA-induced PG degradation and release into media. Neither MPA alone nor HA alone had an effect on total cartilage GAG content. Methylprednisolone acetate caused an increase in release of GAG into the medium at 48 and 72 hours after treatment. In combination, HA had no protective effect on MPA-induced GAG release into the medium. Total cartilage DNA content was not affected by treatments. CONCLUSIONS AND CLINICAL RELEVANCE: Our results indicate that HA addition has little effect on corticosteroid-induced cartilage matrix PG catabolism in articular cartilage explants.
Animals↗
Effects of intra-articular administration of methylprednisolone acetate on normal equine articular cartilage.
The effects of the corticosteroid 6-alpha-methylprednisolone acetate on normal equine articular cartilage were evaluated, using the middle carpal joint in 4 clinically normal young horses. One middle carpal joint of each horse was injected 3 times with 100 mg of 6-alpha-methylprednisolone acetate, at 14-day intervals. The opposite middle carpal joint (control) was injected with 2.5 ml of lactated Ringer solution at the same intervals. Effects were studied until 8 weeks after the first injection. Evaluation included clinical and radiographic examination, and gross, microscopic, and biochemical evaluation of joint tissues. Horses remained clinically normal during the study, and significant radiographic changes were not observed. Safranin-0 matrix staining intensity and uronic acid content were significantly (P less than 0.05) lower and hydroxyproline content was significantly (P less than 0.05) higher in articular cartilage of corticosteroid-injected joints vs control joints.
Animals↗