Prednisolone 5 mg soluble tablets - Summary of Product Characteristics (SmPC) (2023)

Each tablet contains 5 mg prednisolone as the sodium phosphate ester.

Excipients with a known effect

Each tablet contains 37.6 mg sodium and 4 mg sodium benzoate (E211).

For the full list of excipients see section 6.1.

Soluble tablet

Pink, flat, round, soluble tablets debossed with “λ5” and break mark on same side.

The tablet can be divided into equal doses.

Prednisolone 5 mg soluble tablets are indicated in adults and children.

A variety of diseases can sometimes require corticosteroid therapy. Some of the main indications are:

• Bronchial asthma, severe hypersensitivity reactions, anaphylaxis;

• Rheumatoid arthritis, systemic lupus erythematosus, dermatomyositis, mixed collagenosis (excluding systemic sclerosis), polyarteritis nodosa;

• inflammatory skin diseases, including pemphigus vulgaris, bullous pemphigoid and pyoderma gangrenosum;

• Minimal change nephrotic syndrome, acute interstitial nephritis;

• Ulcerative colitis, Crohn's disease; Sarcoidosis;

• rheumatic carditis;

• Hemolytic anemia (autoimmune), acute lymphoblastic and chronic lymphocytic leukemia, malignant lymphoma, multiple myeloma, idiopathic thrombocytopenic purpura;

• Immunosuppression in transplantation.

dosage

The lowest dose that gives an acceptable result should be used (see section 4.4); If it is possible to reduce the dosage, it must be done gradually. With prolonged therapy, intercurrent diseases, trauma or surgical intervention require a temporary increase in dose; If corticosteroids are discontinued after prolonged therapy, they may need to be temporarily reintroduced.

Adult:The dose used depends on the disease, its severity and the clinical response obtained. The following treatment regimens are for guidance only. Split dosing is commonly used.

Short-term treatment:20 to 30 mg daily for the first few days, then reducing the daily dose by 2.5 or 5 mg every two to five days depending on response.

Rheumatoide Arthritis:7.5 to 10 mg daily. The lowest effective dose is used for maintenance therapy.

Most other conditions:10 to 100 mg daily for one to three weeks, then tapering to the minimum effective dose.

Pediatric Population

Fractions of the adult dose can be used (eg, 75% at 12 years, 50% at 7 years, and 25% at 1 year), but clinical factors must be given due consideration.

Prednisolone tablets can be given early in the treatment of acute asthma attacks in children. For children over 5 years old, use a dose of 30-40 mg of prednisolone. For children aged 2-5 years use a dose of 20 mg prednisolone. Those already on maintenance steroid tablets should receive 2 mg/kg prednisolone up to a maximum dose of 60 mg. The dose of prednisolone may be repeated in children who vomit; but intravenous steroids should be considered in children who are unable to retain medications taken orally. Treatment for up to three days is usually sufficient, but the duration of treatment should be tailored to the number of days required for recovery. There is no need to reduce the dose at the end of a short treatment period. If treatment is prolonged, discontinuation should not be abrupt (see section 4.4).

In children under 2 years of age, prednisolone tablets at a dose of 10 mg for up to three days can be used early in the treatment of moderate to severe episodes of acute hospitalized asthma.

type of administration

For oral use only

Prednisolone Soluble tablets are best taken dissolved in water, but they can also be swallowed whole without any problems. The solution dissolved in water must be drunk immediately by the patient.

- Hypersensitivity to the active substance or to any of the excipients listed in section 6.1.

- Systemic infections unless specific anti-infective therapy is used.

- Immunization against live viruses.

- Eye herpes simplex due to possible perforation.

Discontinuation should not be abrupt in patients who have been receiving more than physiological doses of systemic corticosteroids (approximately 7.5 mg prednisolone or equivalent) for more than three weeks. How dose reduction should be accomplished depends largely on whether the disease is likely to recur when the dose of systemic corticosteroids is reduced. Clinical assessment of disease activity may be required during discontinuation. If disease relapse is unlikely after stopping systemic corticosteroids but HPA suppression is uncertain, systemic corticosteroid doses can be rapidly reduced to physiological doses. Once a daily dose of 7.5 mg prednisolone is reached, the dose reduction should be slower to allow the HPA axis to recover.

Abrupt withdrawal of systemic corticosteroid treatment that has been continued for up to three weeks is appropriate when disease recurrence is considered unlikely. Abrupt withdrawal of doses of up to 40 mg prednisolone or equivalent daily for three weeks is unlikely to result in clinically relevant suppression of the HPA axis in the majority of patients. Systemic corticosteroid therapy should be gradually withdrawn in the following patient groupstaken into accounteven after courses of three weeks or less:

• Patients who have received repeated systemic corticosteroids, particularly if taken for more than three weeks.

• If short-term therapy has been prescribed within one year of cessation of long-term therapy (months or years).

• Patients who may have causes of adrenal insufficiency other than exogenous corticosteroid therapy, or who have discontinued corticosteroids after prolonged therapy, may need to be temporarily re-treated with corticosteroids.

• Patients receiving systemic corticosteroid doses greater than 40 mg prednisolone (or equivalent) daily.

• Patients taking repeated doses in the evening.

Patients should carry "steroid treatment cards" which provide clear advice on the precautions to be taken to minimize risk and give details of the prescribing physician, drug, dosage and duration of treatment.

Adrenal cortical atrophy develops during prolonged therapy and may persist for years after treatment is stopped. Discontinuation of corticosteroids after prolonged therapy must therefore always be gradual to avoid acute adrenal insufficiency and tapered off over weeks or months, depending on the dose and duration of treatment. With prolonged therapy, intercurrent diseases, trauma or surgical intervention require a temporary increase in dose; If corticosteroids are discontinued after prolonged therapy, they may need to be temporarily reintroduced.

HPA axis suppression and other undesirable effects can be minimized by using the lowest effective dose for the minimum period of time and by administering the daily requirement as a single morning dose or, whenever possible, as a single morning dose every other day. Frequent patient review is required to titrate the dose according to disease activity (see section 4.2).

visual disturbance

Visual disturbances have been reported with systemic and topical use of corticosteroids. If a patient presents with symptoms such as blurred vision or other visual disturbances, consideration should be given to referring the patient to an ophthalmologist for evaluation of possible causes other than cataract, glaucoma, or rare diseases such as cataracts. B. Central serous chorioretinopathy (CSCR) may have been reported after use of systemic and topical corticosteroids.

Anti-inflammatory/immunosuppressive effect and infection

Kaposi's sarcoma has been reported to occur in patients receiving corticosteroid therapy. Discontinuation of corticosteroids can result in clinical remission.

Chronic immunosuppression (e.g. as part of organ transplantation) has been associated with an increased risk of malignancy.

Suppression of the inflammatory response and immune function increases susceptibility to infection and its severity. The resulting opportunistic infections can be fatal. The clinical presentation can often be atypical, and serious infections such as septicemia and tuberculosis can be masked and progress to an advanced stage before they are recognized.

Chickenpox is of particular concern as this normally harmless disease can be fatal in immunocompromised patients. Patients with no clear history of chickenpox should be advised to avoid close personal contact with chickenpox or herpes zoster and seek urgent medical attention in the event of exposure. If the patient is a child, parents must receive the above advice. Passive immunization with varicella zoster immunoglobulin (VZIG) is required in exposed non-immunological patients who are receiving systemic corticosteroids or have used them within the past 3 months; this should be given within 10 days of exposure to chickenpox. If the diagnosis of chickenpox is confirmed, the disease requires specialist care and urgent treatment.

Corticosteroids should not be stopped and the dose may need to be increased.

Patients should be advised to take special care to avoid exposure to measles and to seek medical advice immediately if exposed. Prophylaxis with intramuscular normal immunoglobulin may be necessary.

Live vaccines should not be given to people with an impaired immune response caused by high doses of corticosteroids. The antibody response to other vaccines may be reduced.

Because of the potential for fluid retention, caution should be exercised when administering corticosteroids to patients with renal impairment, hypertension, or congestive heart failure.

Corticosteroids can aggravate diabetes mellitus, osteoporosis, hypertension, glaucoma and epilepsy and therefore patients with these disorders or a family history should be monitored frequently.

Caution should be exercised and frequent patient monitoring is required if there is a history of severe mood disorders (particularly a history of steroid psychosis), previous steroid myopathy, peptic ulcer disease, hypothyroidism, recent myocardial infarction, or patients with a history of tuberculosis.

In patients with liver failure, blood levels of corticosteroids may be increased, as with other drugs that are metabolised in the liver. Therefore, frequent monitoring of the patient is required.

Use in the elderly: The common side effects of systemic corticosteroids can become more serious as we age, particularly osteoporosis, hypertension, hypokalemia, diabetes, susceptibility to infection, and thinning of the skin. Close clinical monitoring is required to avoid life-threatening reactions.

Patients and/or carers should be warned that potentially serious psychiatric adverse reactions can occur with systemic steroids (see section 4.8). Symptoms typically appear within a few days or weeks of starting treatment. Risks may be greater at high doses/systemic exposure (see also section 4.5), although dose levels are not predictive of onset, type, severity or duration of reactions. Most side effects resolve with either dose reduction or drug discontinuation, although specific treatment may be required. Patients/carers should be encouraged to seek medical advice if psychiatric symptoms of concern develop, particularly if depressed mood or suicidal thoughts are suspected. Patients/carers should also be aware of possible psychiatric disturbances that may occur either during or immediately after dose taper/withdrawal of systemic steroids, although such reactions have rarely been reported.

Particular caution should be exercised when considering the use of systemic corticosteroids in patients with current or history of severe mood disorders in themselves or in first-degree relatives. These include depressive or manic-depressive illnesses and previous steroid psychosis.

Scleroderma renal crisis

Caution is advised in patients with systemic sclerosis, as an increased incidence of (possibly fatal) scleroderma-renal crisis with hypertension and decreased urinary output is observed with daily doses of 15 mg or more prednisolone. Blood pressure and kidney function (S-creatinine) should therefore be checked routinely. Blood pressure should be carefully monitored if a kidney crisis is suspected.

Pediatric Population

Corticosteroids cause dose-related growth retardation in infancy, childhood, and adolescence, which may be irreversible.

excipients

This medicinal product contains 37.6 mg sodium per dose, equivalent to 1.88% of the WHO recommended maximum daily intake of sodium. The maximum daily intake of this product is equivalent to 37.6% of the WHO recommended maximum daily intake for sodium. Prednisolone Soluble Tablets are considered high in sodium. This should be taken into account, especially with a low-salt diet.

This medicine contains 4 mg of benzoate salt in each tablet, which can cause an increase in bilirubinemia, since its displacement from albumin can increase neonatal jaundice, which can develop into kernicterus (deposits of unconjugated bilirubin in the brain tissue).

Concomitant treatment with CYP3A inhibitors, including medicinal products containing cobicistat, is expected to increase the risk of systemic side effects. The combination should be avoided unless the benefit outweighs the increased risk of systemic corticosteroid side effects. In this case, patients should be monitored for systemic corticosteroid side effects.

Rifampicin, rifabutin, carbamazepine, phenobarbitone, phenytoin, primidone, ephedrine and aminoglutethimide increase the metabolism of corticosteroids and their therapeutic effects may be reduced.

Mifepristone can reduce the effects of corticosteroids for 3-4 days.

Erythromycin and ketoconazole can inhibit the metabolism of some corticosteroids.

Ciclosporin increases the plasma concentration of prednisolone. The same effect is possible with ritonavir.

Estrogens and other oral contraceptives may potentiate the effects of glucocorticoids, and dose adjustments may be required when oral contraceptives are added to or removed from a stable dosing regimen.

The desired effects of antidiabetics (including insulin), antihypertensives and diuretics are antagonized by corticosteroids.

The growth-promoting effect of somatotropin can be inhibited by the concomitant use of corticosteroids.

Steroids can reduce the effect of anticholinesterases in myasthenia gravis and cholecystographic X-ray media.

The efficacy of coumarin anticoagulants and warfarin may be enhanced by concomitant corticosteroid therapy and close monitoring of INR or prothrombin time is required to avoid spontaneous bleeding.

Concomitant use of aspirin and nonsteroidal anti-inflammatory drugs (NSAIDs) with corticosteroids increases the risk of gastrointestinal bleeding and ulceration.

Renal clearance of salicylates is increased by corticosteroids and steroid withdrawal can lead to salicylate intoxication.

The hypokalemic effect of acetazolamide, loop diuretics, thiazide diuretics, and carbenoxolone is potentiated by corticosteroids. The risk of hypokalemia is increased with theophylline and amphotericin. Corticosteroids should not be co-administered with amphotericin unless necessary to control response.

The risk of hypokalemia also increases when high doses of corticosteroids are given with high doses of bambuterol, fenoterol, formoterol, ritodrine, salbutamol, salmeterol, and terbutaline. The toxicity of cardiac glycosides is increased when hypokalemia occurs with corticosteroids.

Concomitant use with methotrexate may increase the risk of haematological toxicity.

High doses of corticosteroids impair the immune response, therefore live vaccines should be avoided (see also section 4.4).

pregnancy

The ability of corticosteroids to cross the placenta varies between drugs, but 88% of prednisolone is inactivated when it crosses the placenta.

Administration of corticosteroids to pregnant animals can cause abnormalities in fetal development, including cleft palate, intrauterine growth retardation, and effects on brain growth and development. There is no evidence that corticosteroids lead to an increased incidence of congenital anomalies such as cleft palate/lip in humans. However, with prolonged or repeated use during pregnancy, corticosteroids may increase the risk of intrauterine growth retardation.

Hypoadrenalism can theoretically occur in the newborn after prenatal exposure to corticosteroids, but it usually resolves spontaneously after birth and is rarely clinically relevant. As with all drugs, corticosteroids should only be prescribed if the benefits to the mother and child outweigh the risks. However, when corticosteroids are essential, patients with normal pregnancies can be treated as if they were in the non-pregnant state.

Patients with preeclampsia or fluid retention should be closely monitored.

A decrease in hormone levels has been described in pregnancy, but the significance of this finding is not clear.

breastfeeding

Corticosteroids are excreted in small amounts in breast milk. However, doses of up to 40 mg prednisolone daily are unlikely to produce systemic effects in the infant. Infants born to mothers taking higher doses than this may have some degree of adrenal suppression, but the benefits of breastfeeding likely outweigh any theoretical risk.

fertility

No data available

The frequency of foreseeable adverse reactions, including hypothalamic-pituitary-adrenal (HPA) suppression, correlates with the relative potency of the medicinal product, dose, timing of administration and duration of treatment (see section 4.4).

Adverse reactions are listed by system organ class. The following side effects may be associated with long-term systemic corticosteroid use with the following frequencies:

Not known (cannot be estimated from the available data)

*After high doses

a) A wide spectrum of psychiatric reactions, including mood disorders (such as irritability, euphoria, depressed and unstable mood, and suicidal thoughts), psychotic reactions (including mania, delusions, hallucinations, and exacerbation of schizophrenia), behavioral disorders, irritability, anxiety, sleep It became over Disorders and cognitive dysfunction including confusion and amnesia have been reported. Reactions are common and can occur in both adults and children. In adults, the frequency of severe reactions has been estimated at 5-6%. Psychological effects have been reported upon withdrawal of corticosteroids; the frequency is unknown.

*Scleroderma-kidney crisis

The occurrence of scleroderma renal crisis varies among the different subpopulations. The highest risk has been reported in patients with diffuse systemic sclerosis. The lowest risk was reported in patients with limited systemic sclerosis (2%) and juvenile systemic sclerosis (1%).

withdrawal symptoms

Reducing the dose of corticosteroids too quickly after prolonged treatment can result in acute adrenal insufficiency, hypotension and death (see section 4.4).

"Withdrawal syndrome" may also occur, including fever, myalgia, arthralgia, rhinitis, conjunctivitis, painful itchy skin nodules, and weight loss.

In some cases, withdrawal symptoms may include or resemble clinical relapse of the disease for which the patient was being treated.

Other side effects that may occur during discontinuation or switching of corticosteroid therapy are benign intracranial hypertension with headache and vomiting, and papilledema caused by cerebral edema.

Latent rhinitis or eczema can be unmasked.

Pediatric population:

Increased intracranial pressure with papilledema in children (pseudotumor cerebri) - usually after discontinuation of treatment.

Growth retardation in infancy, childhood and adolescence.

Reporting suspected side effects

It is important to report suspected side effects after the medicine has been approved. It allows continuous monitoring of the benefit-risk balance of the drug. Healthcare professionals are encouraged to report any suspected adverse reactions through the Yellow Card Scheme

Website: www.mhra.gov.uk/yellowcard or search for MHRA Yellow Card on Google Play or Apple App Store.

Pharmacotherapeutic group: glucocorticoids, ATC code: H02AB06

Prednisolone soluble tablets contain the equivalent of 5 mg of prednisolone in the form of the 21-disodium phosphate ester. Prednisolone sodium phosphate is a synthetic glucocorticoid with the same general properties as prednisolone itself and other compounds classified as corticosteroids. Prednisolone is four times more active than hydrocortisone by weight.

Prednisolone sodium phosphate is very soluble in water and therefore less likely to cause local gastric irritation than prednisolone alcohol, which is only slightly soluble. This is important when high dosages are required, such as in immunosuppressive therapy.

Absorption

Prednisolone is readily absorbed from the gastrointestinal tract, with peak plasma concentrations occurring 1-2 hours after an oral dose. Plasma prednisolone is mainly protein bound (70-90%), with binding to albumin and corticosteroid-binding globulin. The plasma half-life of prednisolone is between 2.5 and 3.5 hours after a single dose.

distribution

The volume of distribution and clearance of total prednisolone and unbound prednisolone are concentration dependent and this has been attributed to saturable protein binding over the therapeutic plasma concentration range.

Biotransformation

Prednisolone is extensively metabolised, mainly in the liver, but the metabolic pathways are not well defined.

elimination

Over 90% of the prednisolone dose is excreted in the urine, with 7-30% recovered as free prednisolone and the remainder as various metabolites.

sodium acid citrate

Natriumhydrogencarbonat

Saccharin Natrium

Povidone

Sodium benzoate (E 211)

Erythrosin (E127)

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Great Britain.