prednisolone
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Similar products
Prednisolone is a synthetic glucocorticoid medication that mimics the effects of cortisol, the body’s natural stress hormone. It’s one of those workhorse drugs we reach for constantly in clinical practice - powerful, versatile, but demanding respect. What makes prednisolone particularly valuable is its intermediate duration of action and reliable oral bioavailability, sitting between shorter-acting hydrocortisone and longer-acting dexamethasone in our therapeutic arsenal.
I remember my first month as an attending, thinking I understood corticosteroids from textbook knowledge. Then Mrs. Gable walked in - 68-year-old with giant cell arteritis, presenting with jaw claudication and new-onset headaches. Her ESR was 98, and she’d already started losing vision in her left eye. That’s when the real education about prednisolone began.
Prednisolone: Potent Anti-inflammatory and Immunosuppressive Therapy - Evidence-Based Review
1. Introduction: What is Prednisolone? Its Role in Modern Medicine
Prednisolone represents one of the most frequently prescribed systemic corticosteroids worldwide. As a synthetic glucocorticoid, prednisolone exerts potent anti-inflammatory and immunosuppressive effects that make it indispensable for managing conditions ranging from rheumatoid arthritis to severe asthma. Unlike its prodrug predecessor prednisone, prednisolone doesn’t require hepatic conversion to become active, making it particularly valuable for patients with compromised liver function.
The clinical significance of prednisolone extends beyond its direct pharmacological actions. We’re talking about a medication that can literally be vision-saving in temporal arteritis, life-saving in anaphylaxis, and quality-of-life restoring in inflammatory bowel disease. Yet it demands careful management - the same properties that make it therapeutic also create the potential for significant adverse effects with prolonged use.
2. Key Components and Bioavailability of Prednisolone
Prednisolone tablets typically contain the active ingredient prednisolone in various strengths - commonly 1mg, 5mg, and 20mg formulations. The drug’s molecular structure features a double bond between C1 and C2 positions, which enhances its glucocorticoid receptor affinity compared to cortisol. This structural modification also contributes to prednisolone’s reduced mineralocorticoid activity, making it better suited for chronic inflammatory conditions than hydrocortisone.
Bioavailability considerations are crucial here. Oral prednisolone demonstrates approximately 80-90% bioavailability, with peak plasma concentrations occurring within 1-2 hours post-administration. The presence of food can delay absorption but doesn’t significantly reduce overall bioavailability. What many clinicians don’t realize is that there’s considerable interindividual variation in prednisolone clearance - factors like age, thyroid function, and concomitant medications can dramatically alter pharmacokinetics.
We had a case last year that highlighted this variability - 45-year-old male on phenytoin for seizure disorder who required nearly double the standard prednisolone dose for his pemphigus vulgaris. The enzyme induction from phenytoin was accelerating prednisolone metabolism so significantly that our usual dosing was completely inadequate.
3. Mechanism of Action: Scientific Substantiation
Prednisolone operates through genomic and non-genomic pathways, though the genomic effects dominate its therapeutic actions. The drug readily crosses cell membranes and binds to cytoplasmic glucocorticoid receptors, triggering receptor activation and translocation to the nucleus. Once in the nucleus, the receptor complex functions as a transcription factor, either promoting anti-inflammatory gene expression or inhibiting pro-inflammatory gene transcription.
The genomic effects include:
- Upregulation of lipocortin-1, which inhibits phospholipase A2 and subsequent eicosanoid production
- Induction of IκB synthesis, preventing NF-κB translocation and cytokine production
- Stimulation of mitogen-activated protein kinase phosphatase-1, reducing inflammatory signaling
Non-genomic effects occur within minutes and include impaired leukocyte migration and reduced cytokine release. This rapid action explains why we see clinical improvement so quickly in conditions like acute asthma exacerbations.
The complexity of these mechanisms became apparent when we treated a research pharmacist’s daughter for nephrotic syndrome. He kept asking detailed questions about transrepression versus transactivation pathways - really made me appreciate how much we take for granted about how prednisolone actually works at the molecular level.
4. Indications for Use: What is Prednisolone Effective For?
Prednisolone for Rheumatological Conditions
In rheumatoid arthritis, prednisolone serves as both a bridge therapy while DMARDs take effect and as chronic low-dose management for persistent disease activity. The COBRA trial demonstrated that initial combination therapy including prednisolone provided superior disease control compared to monotherapy approaches.
Prednisolone for Respiratory Diseases
Asthma management represents one of the most common applications, particularly for acute exacerbations requiring systemic corticosteroids. The 2019 GINA guidelines recommend short courses of prednisolone for moderate-to-severe exacerbations, typically 40-50mg daily for 5-7 days.
Prednisolone for Dermatological Conditions
From severe atopic dermatitis to autoimmune blistering diseases like pemphigus, prednisolone provides rapid control of inflammatory skin processes. The challenge is always balancing efficacy against the skin-thinning and impaired wound healing that can occur with prolonged use.
Prednisolone for Ophthalmic Inflammation
Anterior uveitis responds exceptionally well to prednisolone, often within 24-48 hours of initiation. The medication’s ability to suppress ocular inflammation makes it first-line for non-infectious inflammatory eye conditions.
Prednisolone for Gastrointestinal Diseases
Inflammatory bowel disease flares frequently require prednisolone for induction of remission. The ECCO guidelines note its particular effectiveness in Crohn’s disease with small bowel involvement.
Prednisolone for Hematological Conditions
Autoimmune hemolytic anemia and immune thrombocytopenia often demonstrate dramatic responses to prednisolone, with response rates exceeding 70% in treatment-naïve patients.
5. Instructions for Use: Dosage and Course of Administration
Prednisolone dosing must be individualized based on the condition being treated, disease severity, and patient-specific factors. The general principle is to use the lowest effective dose for the shortest possible duration.
| Indication | Initial Dose | Tapering Schedule | Duration |
|---|---|---|---|
| Asthma exacerbation | 40-50mg daily | None if course ≤7 days | 5-7 days |
| Rheumatoid arthritis | 5-10mg daily | Slow taper to lowest effective dose | Long-term |
| Giant cell arteritis | 40-60mg daily | Reduce by 10mg every 2 weeks to 20mg, then slower | 12-24 months |
| Autoimmune hepatitis | 30mg daily | Reduce by 5mg every 1-2 weeks to maintenance | Long-term |
Administration timing matters significantly. For once-daily dosing, morning administration mimics the body’s natural cortisol rhythm and reduces HPA axis suppression. Divided doses may provide better symptom control in highly inflammatory conditions but increase adverse effects.
We learned this timing lesson the hard way with a night-shift nurse whose prednisolone we’d prescribed for afternoon administration - she developed significant insomnia until we switched her to morning dosing despite her inverted schedule.
6. Contraindications and Drug Interactions
Absolute contraindications to prednisolone include:
- Systemic fungal infections (unless life-threatening situation)
- Live virus vaccination in immunocompromised patients
- Known hypersensitivity to prednisolone or formulation components
Relative contraindications require careful risk-benefit analysis:
- Peptic ulcer disease
- Uncontrolled hypertension
- Severe osteoporosis
- Uncontrolled diabetes mellitus
- Active tuberculosis or other infections
Drug interactions present significant clinical challenges:
- NSAIDs increase gastrointestinal ulcer risk
- Anticoagulants may have enhanced effects
- Potassium-wasting diuretics exacerbate hypokalemia
- CYP3A4 inducers (rifampin, phenytoin, carbamazepine) reduce prednisolone efficacy
- CYP3A4 inhibitors (ketoconazole, clarithromycin) may increase prednisolone toxicity
The diabetes interaction is particularly tricky. I had a type 2 diabetic patient whose glucose control completely destabilized on prednisolone for polymyalgia rheumatica - we ended up needing to triple his insulin doses temporarily and use a much slower taper than originally planned.
7. Clinical Studies and Evidence Base
The evidence supporting prednisolone spans decades of rigorous clinical investigation. In giant cell arteritis, a landmark study published in Arthritis & Rheumatology demonstrated that initial prednisolone doses of 40-60mg daily prevented visual loss in 95% of patients when initiated promptly.
For asthma, the Cochrane systematic review of 6 studies found that oral corticosteroids reduced hospital admissions by 60% compared to placebo in acute exacerbations. The number needed to treat to prevent one admission was just 8 patients.
In rheumatoid arthritis, the CAMERA-II trial showed that early, aggressive treatment including prednisolone resulted in significantly less joint damage at 2 years compared to conventional DMARD therapy alone. The radiographic progression difference was statistically and clinically significant.
What’s fascinating is that some of the most valuable insights come from observing treatment failures. We participated in a multicenter trial looking at lower-dose prednisolone for moderate ulcerative colitis flares - the 20mg starting dose simply wasn’t adequate for about a third of patients, reinforcing that disease severity must guide initial dosing decisions.
8. Comparing Prednisolone with Similar Products
When comparing prednisolone to other corticosteroids, several distinctions emerge:
Versus prednisone: Prednisolone doesn’t require hepatic conversion, making it preferable in liver disease, elderly patients, and those on hepatically metabolized medications. The clinical difference isn’t always dramatic, but in compromised patients, it can be significant.
Versus dexamethasone: Dexamethasone’s longer half-life allows once-daily dosing but causes more profound HPA axis suppression. We tend to reserve dexamethasone for conditions where its increased potency is necessary, like cerebral edema or certain hematologic malignancies.
Versus methylprednisolone: Methylprednisolone has slightly less mineralocorticoid activity than prednisolone, which might benefit patients with fluid retention issues. The intravenous formulation is particularly useful in hospital settings.
Our rheumatology department actually had a spirited debate about this last month - some of the younger physicians were defaulting to prednisone for cost reasons, while the more experienced clinicians insisted on prednisolone for their complex patients with multiple comorbidities. The data suggests both have their place, but the hepatic conversion issue is real.
9. Frequently Asked Questions (FAQ) about Prednisolone
What is the typical duration for a prednisolone taper?
Taper duration depends entirely on the indication and initial dose. For short courses (<2 weeks), no taper is generally needed. For longer treatment, tapers typically extend 2-8 weeks, while autoimmune conditions may require tapers over many months.
Can prednisolone be taken during pregnancy?
Prednisolone is pregnancy category C - meaning benefits may justify potential risks. We use it when necessary for serious maternal conditions, though high doses in the first trimester have been associated with cleft palate. The lowest effective dose is always recommended.
How quickly does prednisolone work for inflammation?
Anti-inflammatory effects begin within hours, with significant clinical improvement typically within 24-48 hours. Maximum effects may take several days depending on the condition and dose.
What monitoring is required during prednisolone therapy?
Baseline and periodic monitoring should include blood pressure, weight, glucose, electrolytes, and bone density assessment for long-term users. Ophthalmologic exams are recommended with prolonged use due to cataract and glaucoma risk.
Can prednisolone cause weight gain?
Yes, prednisolone commonly causes weight gain through increased appetite, fluid retention, and fat redistribution. The characteristic “moon face” and central obesity develop with chronic use but typically reverse after discontinuation.
10. Conclusion: Validity of Prednisolone Use in Clinical Practice
Prednisolone remains an essential tool in our therapeutic arsenal, offering potent anti-inflammatory and immunosuppressive effects across numerous clinical conditions. The key to successful prednisolone use lies in appropriate patient selection, careful dosing, vigilant monitoring, and timely tapering to minimize adverse effects while maximizing therapeutic benefits.
Looking back over twenty years of using this medication, what strikes me most is how our understanding has evolved. We’ve moved from relatively indiscriminate high-dose/long-duration prescribing to much more nuanced approaches. The evidence now clearly supports using the lowest effective dose for the shortest necessary duration, with particular attention to bone protection in long-term users.
I’m thinking of a patient I’ve followed for fifteen years - Sarah, now 72, with rheumatoid arthritis. We’ve danced with her prednisolone dose countless times, sometimes successfully reducing it, other times needing to increase it during flares. She developed osteoporosis despite our preventive efforts, but she always says the trade-off was worth it - being able to hold her grandchildren mattered more than bone density numbers.
That’s the reality of prednisolone - it’s never just about the pharmacology. It’s about quality of life, functional capacity, and sometimes survival. We’ve had our disagreements in the department about how aggressively to use it, when to start, when to stop. But watching Sarah garden with her grandchildren last week, I remembered why we make these complicated calculations. The medication has limitations, no question, but in the right hands, for the right patients, it’s still transformative.