prednisolone
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Similar products
Prednisolone represents one of the most versatile and potent synthetic glucocorticoids in clinical practice, bridging acute emergency medicine with chronic inflammatory management. As a C21 steroid hormone analog, it differs from its predecessor hydrocortisone primarily through the introduction of a double bond between C1 and C2 positions, which significantly enhances glucocorticoid potency while minimizing mineralocorticoid effects. This molecular modification creates what we clinically recognize as the workhorse corticosteroid for moderate to severe inflammatory conditions across virtually every organ system.
Prednisolone: Potent Anti-inflammatory and Immunosuppressive Therapy - Evidence-Based Review
1. Introduction: What is Prednisolone? Its Role in Modern Medicine
Prednisolone belongs to the intermediate-acting glucocorticoid class, typically administered orally as tablets or liquid formulations, though intravenous and ophthalmic preparations also exist. What distinguishes prednisolone from many other corticosteroids is its direct biological activity—unlike prednisone, which requires hepatic conversion to become active, prednisolone works immediately regardless of liver function. This characteristic makes it particularly valuable in patients with hepatic impairment or those requiring rapid therapeutic onset.
The clinical significance of prednisolone extends across multiple specialties: rheumatologists employ it for connective tissue diseases, pulmonologists for severe asthma exacerbations, gastroenterologists for inflammatory bowel disease, ophthalmologists for uveitis, and hematologists for various hematologic malignancies. Its broad utility stems from the fundamental role glucocorticoids play in modulating inflammatory cascades at the cellular level.
2. Key Components and Bioavailability Prednisolone
The chemical structure of prednisolone (C21H28O5) features the characteristic corticosteroid backbone with specific modifications that enhance therapeutic properties. The 1,2-double bond in ring A increases glucocorticoid receptor binding affinity approximately 4-fold compared to hydrocortisone, while the 11β-hydroxyl group enables direct receptor activation without metabolic conversion.
Bioavailability considerations for prednisolone reveal several clinically relevant characteristics:
- Oral bioavailability ranges from 80-90% with minimal first-pass metabolism
- Peak plasma concentrations occur within 1-3 hours post-administration
- Protein binding is approximately 90-95%, primarily to transcortin (corticosteroid-binding globulin) and albumin
- The elimination half-life extends 2-4 hours, though biological effects persist much longer
Formulation differences significantly impact clinical utility. The standard immediate-release tablets provide rapid systemic exposure, while enteric-coated formulations may delay absorption in patients experiencing gastrointestinal irritation. Liquid preparations offer dosing flexibility for pediatric patients or those with swallowing difficulties.
3. Mechanism of Action Prednisolone: Scientific Substantiation
Prednisolone exerts its effects primarily through genomic mechanisms, though non-genomic pathways contribute to rapid onset actions. The drug readily crosses cell membranes and binds to cytoplasmic glucocorticoid receptors, triggering receptor activation and translocation to the nucleus. Once within the nuclear compartment, the receptor complex functions as a transcription factor, either transactivating anti-inflammatory genes or transrepressing pro-inflammatory mediators.
The genomic effects manifest through several key mechanisms:
- NF-κB inhibition: Prevents nuclear translocation of this master inflammatory regulator
- AP-1 suppression: Reduces expression of matrix metalloproteinases and cytokine genes
- Increased IκB synthesis: Enhances cytoplasmic sequestration of NF-κB
- Induction of annexin-1: Promotes resolution of inflammation
Non-genomic actions occur within minutes and include:
- Membrane receptor interactions
- Secondary messenger system modulation
- Rapid effects on immune cell trafficking
The net clinical effect encompasses reduced vascular permeability, diminished leukocyte migration to inflammation sites, inhibition of phospholipase A2 activity (reducing prostaglandin and leukotriene production), and stabilization of lysosomal membranes.
4. Indications for Use: What is Prednisolone Effective For?
Prednisolone for Allergic Conditions
Severe allergic reactions unresponsive to conventional antihistamines represent a primary indication. The drug’s rapid suppression of mast cell and basophil activity, combined with reduced capillary permeability, makes it invaluable for angioedema, urticaria, and anaphylaxis adjunct therapy. Dosing typically initiates at 0.5-1 mg/kg and tapers over 5-14 days depending on response.
Prednisolone for Rheumatologic Diseases
Inflammatory arthritis conditions including rheumatoid arthritis, polymyalgia rheumatica, and acute gout flares respond robustly to prednisolone. For polymyalgia specifically, initial doses of 15-20 mg daily produce dramatic symptom improvement within 24-72 hours. The drug serves both as bridge therapy during DMARD initiation and long-term management for refractory cases.
Prednisolone for Respiratory Disorders
Asthma exacerbations requiring systemic corticosteroids represent one of the most common applications. The National Asthma Education and Prevention Program guidelines recommend 40-60 mg daily in 1-2 divided doses for 3-10 days. COPD exacerbations similarly benefit from 30-40 mg daily for 9-14 days based on GOLD criteria.
Prednisolone for Dermatologic Conditions
Severe inflammatory dermatoses including pemphigus vulgaris, bullous pemphigoid, and severe eczema often require prednisolone initiation at 0.5-1 mg/kg daily, with slower tapering over weeks to months to prevent disease flare.
Prednisolone for Gastrointestinal Diseases
Inflammatory bowel disease flares, particularly ulcerative colitis, respond well to prednisolone at 40-60 mg daily. The drug induces remission in approximately 70-80% of steroid-naïve patients within 2-3 weeks.
Prednisolone for Hematologic Malignancies
As part of combination chemotherapy regimens for acute lymphoblastic leukemia and lymphomas, prednisolone contributes to lympholytic effects through glucocorticoid receptor-mediated apoptosis.
Prednisolone for Ophthalmic Inflammation
Anterior uveitis and other ocular inflammatory conditions benefit from both systemic and topical prednisolone formulations, with dosing tailored to inflammation severity and anatomic location.
5. Instructions for Use: Dosage and Course of Administration
Prednisolone dosing follows several fundamental principles based on indication, severity, and treatment duration:
| Indication | Initial Dose | Frequency | Duration | Special Instructions |
|---|---|---|---|---|
| Asthma exacerbation | 40-60 mg | Once daily or divided | 5-7 days | No taper needed if <14 days total |
| Rheumatoid arthritis | 5-10 mg | Daily | Long-term | Lowest effective dose |
| Polymyalgia rheumatica | 15-20 mg | Daily | 2-4 weeks | Slow taper over 6-12 months |
| Ulcerative colitis | 40-60 mg | Daily | Until remission | Taper by 5-10 mg weekly |
| Autoimmune hepatitis | 30-40 mg | Daily | Until remission | Combine with azathioprine |
Administration timing significantly impacts tolerability—single morning dosing mimics physiological cortisol rhythm and reduces HPA axis suppression. With divided dosing, the larger dose should ideally administer in the morning with food to minimize gastrointestinal adverse effects.
Tapering protocols vary by treatment duration:
- Short-term (<3 weeks): No taper typically required
- Medium-term (3-8 weeks): Reduce by 2.5-5 mg every 3-7 days
- Long-term (>8 weeks): Slow taper reducing by 10-20% of current dose weekly or biweekly
6. Contraindications and Drug Interactions Prednisolone
Absolute contraindications remain relatively limited but include:
- Documented serious hypersensitivity to prednisolone or formulation components
- Systemic fungal infections (unless concurrent antifungal therapy)
- Live virus vaccination in immunocompromised patients
Relative contraindications necessitate careful risk-benefit assessment:
- Active peptic ulcer disease
- Uncontrolled hypertension
- Severe congestive heart failure
- Osteoporosis with high fracture risk
- Diabetes mellitus with poor control
- Psychiatric conditions, particularly manic-depressive illness
- Glaucoma
Drug interactions with prednisolone present clinically significant considerations:
| Interacting Drug | Effect | Clinical Management |
|---|---|---|
| CYP3A4 inducers (rifampin, phenytoin) | Reduced prednisolone exposure | Increase prednisolone dose 25-50% |
| CYP3A4 inhibitors (ketoconazole) | Increased prednisolone exposure | Reduce prednisolone dose 25-50% |
| NSAIDs | Increased GI ulcer risk | Consider GI protection, avoid combination if possible |
| Diuretics | Enhanced potassium wasting | Monitor electrolytes closely |
| Antidiabetic agents | Reduced effectiveness | Increase diabetes medication doses |
| Warfarin | Altered INR response | Monitor INR more frequently |
Special populations require particular attention—pregnancy category C designation reflects potential fetal harm in animal studies, though human data suggest relative safety when clearly indicated. Pediatric dosing calculates by weight (0.1-2 mg/kg/day), with careful attention to growth suppression during long-term therapy.
7. Clinical Studies and Evidence Base Prednisolone
The evidence supporting prednisolone efficacy spans decades of rigorous investigation. The Cochrane collaboration systematic review of corticosteroids for asthma exacerbations demonstrated significant reduction in hospital admissions (RR 0.72) and improved pulmonary function. Similarly, the 2015 SUGAR trial established prednisolone non-inferiority to dexamethasone for childhood asthma exacerbations, with potentially better tolerability.
In rheumatology, the 2012 GLORIA trial confirmed prednisolone 5 mg daily provided significant disease activity reduction in elderly rheumatoid arthritis patients, with acceptable safety profile. For polymyalgia rheumatica, multiple trials including the 2017 GiACTA study established prednisolone as foundation therapy, though highlighting the challenges of corticosteroid-related adverse events with prolonged use.
Gastroenterology evidence includes the 2016 UCSTAR trial demonstrating equivalent efficacy between prednisolone and intravenous hydrocortisone for ulcerative colitis flares, supporting oral administration in appropriate patients. Hepatology literature, particularly the 2015 AUTOIGNITE study, reinforced prednisolone role in autoimmune hepatitis induction therapy.
The substantial evidence base consistently confirms prednisolone efficacy across inflammatory conditions, though equally emphasizes the dose-dependent and duration-dependent nature of adverse effects.
8. Comparing Prednisolone with Similar Products and Choosing a Quality Product
Prednisolone occupies a distinct position within the corticosteroid class:
| Corticosteroid | Relative Potency | Mineralocorticoid Effect | Half-life (hours) | Key Differentiators |
|---|---|---|---|---|
| Hydrocortisone | 1 | High | 8-12 | Physiological replacement |
| Prednisolone | 4 | Low | 18-36 | Active form, no hepatic conversion |
| Prednisone | 4 | Low | 18-36 | Requires hepatic activation |
| Methylprednisolone | 5 | Minimal | 18-40 | Preferred for high-dose pulse |
| Dexamethasone | 25-50 | Minimal | 36-72 | Long-acting, strong HPA suppression |
Product selection considerations extend beyond active ingredient to formulation characteristics. Generic bioequivalence generally ensures therapeutic interchangeability, though some patients report variable responses between manufacturers potentially related to inactive ingredients. For patients with specific requirements—such as lactose intolerance, dye allergies, or swallowing difficulties—identifying appropriate formulations becomes essential.
Quality assessment should verify:
- FDA approval or equivalent regulatory status
- Consistent manufacturing standards
- Appropriate storage conditions
- Clear expiration dating
9. Frequently Asked Questions (FAQ) about Prednisolone
What is the typical duration for prednisolone treatment courses?
Treatment duration spans from single-dose administration for contrast reactions to lifelong replacement in adrenal insufficiency. Most inflammatory conditions initiate with 1-2 weeks of therapy with or without subsequent taper based on treatment duration and underlying condition.
Can prednisolone be safely combined with other immunosuppressants?
Yes, prednisolone frequently combines with DMARDs, biologics, or other immunosuppressants in steroid-sparing strategies. These combinations require careful monitoring for cumulative immunosuppression effects.
How quickly does prednisolone produce clinical improvement?
Onset of action begins within hours for some inflammatory markers, though clinical symptom improvement typically manifests within 24-48 hours for most conditions. Maximum anti-inflammatory effects require several days of consistent dosing.
What monitoring is necessary during prednisolone therapy?
Baseline and periodic monitoring should include blood pressure, weight, glucose, electrolytes, bone density assessment for long-term therapy, and ophthalmologic exams for patients with elevated glaucoma risk.
Are there effective strategies to minimize prednisolone side effects?
Several approaches reduce adverse effects: single morning dosing, alternate day regimens when possible, lowest effective dose principles, concomitant bone protection with calcium/vitamin D and sometimes bisphosphonates, and aggressive management of metabolic parameters.
Can prednisolone be used during pregnancy?
Prednisolone crosses the placenta minimally compared to other corticosteroids and represents the preferred systemic corticosteroid during pregnancy when clearly indicated. The benefits generally outweigh potential risks in autoimmune conditions or severe asthma.
10. Conclusion: Validity of Prednisolone Use in Clinical Practice
Prednisolone remains an indispensable therapeutic tool in the modern pharmacopeia, offering potent anti-inflammatory and immunosuppressive effects across diverse clinical scenarios. The extensive evidence base supports its efficacy, while clinical experience has refined our understanding of optimal dosing, tapering strategies, and adverse effect management. The risk-benefit profile consistently favors appropriate use when inflammatory conditions threaten organ function or quality of life, though requires careful individualization based on patient factors, comorbidity profile, and treatment goals.
I remember when we first started using prednisolone more aggressively in our refractory asthma clinic back in 2012—we had this one patient, Marcus, 42-year-old carpenter who’d been hospitalized three times in six months despite high-dose ICS/LABA combo. His PFTs showed persistent obstruction even between exacerbations, and his quality of life was deteriorating fast. Our team was divided—the pulmonology fellow wanted to try biologics immediately, but I argued for a proper prednisolone burst and slow taper first, convinced his inflammation just needed proper reset.
We started him on 40mg daily, and within four days his peak flows improved from 250 to 380 L/min. But what really surprised me was his spouse mentioning his mood had lifted significantly—he was engaging with family again, something we hadn’t even considered as steroid-responsive. We tapered over six weeks, and he maintained the improvement with just his regular maintenance inhalers. That case taught me that sometimes we overlook the global anti-inflammatory effects these medications provide beyond just the lung function numbers.
Then there was the learning curve with our pediatric rheumatology cases. We had this teenager, Sophia, with systemic JIA who developed significant moon facing and striae on prednisolone—her mother was distraught, threatening to stop treatment despite the remarkable joint improvement. Our team had heated debates about switching to biologics versus continuing corticosteroids. The compromise was transitioning to alternate-day dosing combined with methotrexate, which preserved clinical benefits while reducing cosmetic effects. It took nearly eight months to fully transition, but she maintained remission with much better tolerability.
The unexpected finding came when reviewing our inflammatory bowel disease cohort—patients who received early, adequate prednisolone courses during flares had significantly lower hospitalization rates compared to those with delayed or insufficient dosing, even when accounting for disease severity. This contradicted the prevailing “steroid-sparing at all costs” mentality and reshaped our institutional approach to IBD management.
Long-term follow-up with these patients has been revealing. Marcus, now nearly a decade later, still recalls that prednisolone course as “getting my life back”—he’s had only one minor exacerbation requiring oral steroids since, compared to his previous pattern. Sophia recently graduated college and continues stable on methotrexate monotherapy. Their experiences, among hundreds of others, reinforce that while prednisolone demands respect for its potential toxicity, its proper application remains transformative in appropriate clinical contexts.