prednisolone
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Prednisolone represents one of the most versatile and potent synthetic glucocorticoids in clinical practice, essentially serving as the active metabolite of prednisone following hepatic conversion. This immediate bioavailability makes it particularly valuable in acute settings where rapid anti-inflammatory and immunosuppressive effects are critical. Unlike many newer biologic agents, prednisolone remains the workhorse for managing everything from severe asthma exacerbations to autoimmune flares, bridging the gap between emergency intervention and long-term disease control.
I remember when we first started using prednisolone regularly in our rheumatology department back in the early 2000s - we had this 68-year-old patient, Margaret, with giant cell arteritis who presented with jaw claudication and visual disturbances. The standard protocol then was high-dose prednisone, but her liver function tests were concerning, so we opted for prednisolone instead. The speed of her response surprised even our most experienced consultants - within 48 hours, her symptoms had significantly improved, and we avoided the vision loss that often accompanies delayed treatment in temporal arteritis.
Prednisolone: Potent Anti-inflammatory and Immunosuppressive Therapy - Evidence-Based Review
1. Introduction: What is Prednisolone? Its Role in Modern Medicine
Prednisolone is a synthetic glucocorticoid medication that mimics the effects of cortisol, the body’s primary stress hormone. Unlike its precursor prednisone, prednisolone doesn’t require hepatic activation, making it particularly valuable for patients with liver impairment or those needing immediate therapeutic effects. The fundamental question of what prednisolone is used for spans numerous clinical domains - it serves as first-line therapy for acute inflammatory conditions, autoimmune disorders, allergic reactions, and various hematologic malignancies.
In hospital settings, we often joke that prednisolone is our “medical duct tape” - it temporarily holds together inflammatory processes while we work on definitive treatments. But that analogy undersells its sophistication. The benefits of prednisolone extend beyond simple suppression of inflammation; it modulates immune cell function, affects vascular permeability, and influences countless cellular processes through genomic and non-genomic mechanisms.
2. Key Components and Bioavailability of Prednisolone
The composition of prednisolone centers around its corticosteroid structure, specifically as a synthetic analogue of hydrocortisone with additional fluorine atom and double bond between C1 and C2 positions. This molecular configuration significantly enhances its glucocorticoid potency while minimizing mineralocorticoid effects compared to endogenous cortisol.
The release forms of prednisolone include:
- Oral tablets (1mg, 5mg, 20mg)
- Oral solution (5mg/5mL, 15mg/5mL)
- Ophthalmic suspensions
- Rectal formulations
Bioavailability of prednisolone approaches 80-90% following oral administration, with peak concentrations occurring within 1-2 hours. Unlike prednisone, which requires conversion in the liver, prednisolone is active immediately upon absorption - this becomes crucial in patients with hepatic dysfunction or those requiring rapid onset of action. The protein binding characteristics (approximately 90-95% to transcortin and albumin) and relatively short half-life (2-4 hours) allow for flexible dosing regimens while maintaining therapeutic control.
We had this interesting case last year - a 45-year-old woman with autoimmune hepatitis and concurrent acute alcoholic hepatitis. Her liver enzymes were through the roof, and standard prednisone therapy wasn’t cutting it. When we switched to prednisolone, her inflammation markers started trending downward within days. The hepatology team initially questioned the switch, but the pharmacokinetic profile made all the difference - sometimes the subtle differences in drug metabolism really do change clinical outcomes.
3. Mechanism of Action of Prednisolone: Scientific Substantiation
Understanding how prednisolone works requires examining both genomic and non-genomic pathways. The primary mechanism involves diffusion across cell membranes and binding to cytoplasmic glucocorticoid receptors. This receptor-ligand complex then translocates to the nucleus, where it modulates gene transcription by binding to glucocorticoid response elements (GREs). This genomic effect leads to:
- Upregulation of anti-inflammatory proteins (lipocortin-1, IL-10)
- Downregulation of pro-inflammatory cytokines (IL-1, IL-2, IL-6, TNF-α)
- Inhibition of phospholipase A2, reducing prostaglandin and leukotriene synthesis
The non-genomic effects occur within minutes and include:
- Membrane stabilization through interaction with phospholipids
- Reduced vascular permeability
- Inhibition of inflammatory mediator release from mast cells and basophils
The scientific research behind prednisolone’s effects on the body reveals why it remains indispensable despite its side effect profile. It doesn’t just mask symptoms - it fundamentally alters the inflammatory cascade at multiple levels. I’ve seen patients with severe contact dermatitis go from miserable to functional within hours of initiation, not because the allergen disappeared, but because prednisolone interrupted the cellular conversation that perpetuates inflammation.
4. Indications for Use: What is Prednisolone Effective For?
Prednisolone for Rheumatologic Conditions
The anti-inflammatory properties make prednisolone foundational in managing rheumatoid arthritis, polymyalgia rheumatica, and giant cell arteritis. In our clinic, we typically start with 15-20mg daily for PMR, tapering gradually over 6-12 months based on symptom control and inflammatory markers.
Prednisolone for Respiratory Diseases
From acute asthma exacerbations to COPD flares, prednisolone rapidly reduces airway inflammation and bronchial hyperresponsiveness. The standard dose of 40mg daily for 5-10 days often prevents hospitalizations in moderate to severe exacerbations.
Prednisolone for Dermatologic Conditions
Severe eczema, psoriasis flares, and contact dermatitis respond remarkably well to short courses of prednisolone. We usually prescribe 20-30mg daily for 1-2 weeks with a subsequent taper to avoid rebound inflammation.
Prednisolone for Hematologic Disorders
In autoimmune hemolytic anemia and immune thrombocytopenia, prednisolone at 1mg/kg daily often produces rapid improvement in blood counts by reducing antibody-mediated destruction of blood cells.
Prednisolone for Gastrointestinal Diseases
Inflammatory bowel disease flares, particularly ulcerative colitis, frequently require prednisolone for induction of remission when mesalamine preparations prove insufficient.
Prednisolone for Allergic Conditions
Severe allergic reactions that don’t respond adequately to antihistamines alone often benefit from short-term prednisolone therapy to suppress the delayed hypersensitivity response.
I’ll never forget James, a 32-year-old chef who developed severe contact dermatitis from handling certain seafood. His hands were so swollen and painful he couldn’t work. After a 10-day course of prednisolone starting at 30mg daily with a 2-week taper, he was back in the kitchen. The dramatic turnaround always surprises patients - they expect gradual improvement, not near-complete resolution within days.
5. Instructions for Use: Dosage and Course of Administration
The instructions for use of prednisolone vary dramatically based on indication, severity, and patient factors. Here are common dosing strategies:
| Condition | Initial Dose | Tapering Schedule | Duration | Administration Notes |
|---|---|---|---|---|
| Asthma exacerbation | 40mg daily | None needed if course ≤7 days | 5-7 days | Single morning dose with food |
| Rheumatoid arthritis | 5-10mg daily | Slow taper over months | Long-term | Lowest effective dose, calcium/vitamin D supplementation |
| Autoimmune hepatitis | 30mg daily | Reduce by 5mg every 1-2 weeks | 6-24 months | Monitor liver enzymes closely |
| Contact dermatitis | 20-30mg daily | Reduce by 5mg every 3-7 days | 2-3 weeks | Must complete full taper to prevent rebound |
| ITP | 1mg/kg daily | Slow taper once platelets >50,000 | Weeks to months | Frequent platelet monitoring |
How to take prednisolone correctly involves several key principles:
- Morning administration mimics natural cortisol rhythm
- Always take with food to minimize GI irritation
- Never stop abruptly after more than 1-2 weeks of use
- Monitor for side effects throughout treatment
The course of administration requires careful planning - too rapid tapering risks disease flare, while too prolonged use increases adverse effects. We individualize every taper based on clinical response rather than rigid protocols.
6. Contraindications and Drug Interactions with Prednisolone
The contraindications for prednisolone include:
- Systemic fungal infections (unless life-threatening situation)
- Live virus vaccinations during immunosuppressive doses
- Known hypersensitivity to prednisolone or components
- Active peptic ulcer disease (relative contraindication)
Significant drug interactions with prednisolone require careful management:
- NSAIDs: Increased risk of GI ulceration
- Anticoagulants: Altered anticoagulant effect
- Antidiabetic agents: Reduced hypoglycemic efficacy
- CYP3A4 inducers (rifampin, phenytoin): Reduced prednisolone levels
- Potassium-depleting diuretics: Enhanced hypokalemia risk
The question of whether prednisolone is safe during pregnancy deserves special attention. While generally avoided in first trimester, the benefits may outweigh risks in serious maternal conditions. We recently managed a pregnant woman with severe asthma exacerbation at 28 weeks - the maternal and fetal benefits of adequate oxygenation outweighed the theoretical risks of short-term prednisolone use.
Side effects of prednisolone correlate with dose and duration:
- Short-term: Insomnia, mood changes, hyperglycemia, fluid retention
- Long-term: Osteoporosis, adrenal suppression, cataracts, weight gain
Our endocrinology team constantly reminds us that the most dangerous side effect isn’t what we see, but what we don’t see - the silent bone loss and adrenal suppression that can persist long after discontinuation.
7. Clinical Studies and Evidence Base for Prednisolone
The clinical studies on prednisolone span decades and thousands of patients. Landmark trials include:
The MRC Early Rheumatoid Arthritis Study demonstrated that low-dose prednisolone (7.5mg daily) significantly reduced radiographic joint damage over two years compared to NSAIDs alone. This finding revolutionized our approach to early RA management.
In respiratory medicine, the Cochrane systematic review of prednisolone for COPD exacerbations showed clear reduction in treatment failure and earlier improvement in lung function compared to placebo.
For giant cell arteritis, multiple trials have established prednisolone as first-line therapy, with initial doses of 40-60mg daily preventing vision loss in over 90% of patients when initiated promptly.
The scientific evidence supporting prednisolone extends beyond these large trials to countless clinical experiences. I remember reviewing the charts of our first 100 rheumatology patients on long-term low-dose prednisolone - the preservation of joint function and quality of life was undeniable, despite our careful monitoring for adverse effects.
8. Comparing Prednisolone with Similar Products and Choosing Quality Therapy
When comparing prednisolone with similar corticosteroids, several distinctions emerge:
Prednisolone vs. Prednisone: The key difference lies in hepatic conversion - prednisone requires 11-beta-hydroxysteroid dehydrogenase activation, while prednisolone is immediately active. This makes prednisolone preferable in liver disease.
Prednisolone vs. Methylprednisolone: Methylprednisolone has slightly greater glucocorticoid potency milligram-for-milligram and less mineralocorticoid effect, but clinical differences are often minimal.
Prednisolone vs. Dexamethasone: Dexamethasone has longer half-life and greater potency, making it suitable for conditions requiring sustained suppression but increasing HPA axis suppression risk.
Which prednisolone product is better often comes down to formulation reliability and manufacturer consistency. We’ve noticed variation in bioavailability between generic versions, particularly with the oral solution formulations.
How to choose the right corticosteroid involves considering:
- Onset of action required
- Patient comorbidities (especially hepatic function)
- Duration of therapy planned
- Monitoring capabilities
- Cost and insurance coverage
9. Frequently Asked Questions (FAQ) about Prednisolone
What is the recommended course of prednisolone to achieve results?
The course varies by condition - acute conditions may require 5-14 days, while chronic diseases need gradual tapering over months. Never stop abruptly after more than 1-2 weeks of therapy.
Can prednisolone be combined with other medications?
Yes, but requires careful monitoring for interactions, particularly with NSAIDs, anticoagulants, and diabetic medications. Always inform your doctor of all medications.
How quickly does prednisolone work for inflammation?
Anti-inflammatory effects begin within hours, with peak effect in 1-2 days. Immunosuppressive effects may take longer to manifest fully.
What monitoring is needed during prednisolone therapy?
Baseline and periodic monitoring should include blood pressure, weight, blood glucose, electrolytes, and bone density assessment for long-term use.
Can prednisolone cause weight gain?
Yes, through increased appetite, fluid retention, and fat redistribution. The characteristic “moon face” and central obesity typically occur with prolonged use.
Is there a best time of day to take prednisolone?
Morning administration (before 9 AM) mimics natural cortisol rhythm and may reduce sleep disturbances.
10. Conclusion: Validity of Prednisolone Use in Clinical Practice
The risk-benefit profile of prednisolone remains favorable when used judiciously for appropriate indications. Despite newer biologic agents, prednisolone maintains its essential role as both bridge therapy and primary treatment for numerous inflammatory and autoimmune conditions. The key to successful prednisolone use lies in matching intensity and duration to disease severity while implementing aggressive preventive strategies against adverse effects.
Looking back over twenty years of prescribing prednisolone, I’m struck by how this “old” medication continues to save lives and preserve function when used wisely. We recently discharged Sarah, a 28-year-old with lupus nephritis who had failed multiple immunosuppressants. A carefully titrated course of prednisolone, combined with mycophenolate, finally achieved the remission she needed. At her six-month follow-up, her renal function had stabilized, and she was planning her wedding - moments like these remind us why we tolerate prednisolone’s challenging side effect profile.
The longitudinal follow-up of our chronic prednisolone users reveals both the successes and challenges - the rheumatoid arthritis patients maintaining functional independence for decades, balanced against the osteoporotic fractures we work tirelessly to prevent. One of my longest-term patients, Robert, now 72, has been on 5mg daily for his PMR for eight years. At his last visit, he thanked me for “giving him back his golden years” despite our constant monitoring and preventive measures. That gratitude, coupled with the clinical evidence, validates prednisolone’s enduring place in our therapeutic arsenal.