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5 Spheres of Application of Prednisolone

Prednisolone is a synthetic corticosteroid, a dehydrated analogue of hydrocortisone. It takes anti-inflammatory, anti-allergic, immune-suppressive action, boosts sensitivity of beta-adrenergic receptors to endogenous catecholamines. Prednisolone interacts with specific cytoplasmic receptors (receptors for glucocorticosteroids are present in all tissues, especially in liver) with formation of complex inducing production of proteins (including enzymes regulating vital processes in cells).

Proteometabolism: Prednisolone decreases the number of globulins in blood plasma, increases the synthesis of albumins in liver and kidneys (with the increase of albumin/globulin rate), reduces synthesis and enhances catabolism in muscular tissue.

Lipid metabolism: Prednisolone increases synthesis of higher fatty acids and triglycerides, redistributes fat (fat accumulation occurs mainly in the area of thoracic girdle, face and stomach), leads to development of hypercholesterolemia.

Carbohydrate metabolism: Prednisolone increases absorption of carbonhydrates from gastro-intestinal tract; boosts activity of glucose 6-phosphatase (enhancement of glucose transfer from liver to blood); increases activeness of phosphoenolpyruvatecarboxylase and synthesis of aminotransferases (activation of gluconeogenesis); promotes development of hyperglycemia.

Water-electrolyte metabolism: Prednisolone detains sodium and water in organism, stimulates clearance of potassium (mineralocoid activeness), reduces absorption of calcium from gastro-intestinal tract, and decreases mineralization of bone tissue.

Anti-inflammatory effect of Prednisolone is connected with inhibition of inflammation mediators release by eosinophils and labrocytes; inducement of lipocortins formation and number of labrocytes reduction; decrease of capillary permeability; stabilization of cellular membranes (especially lysosomal) and organelle membranes. Prednisolone influences all stages of inflammatory process: inhibits synthesis of prostaglandins on the level of eicosatetraenoic acid (lipocortin inhibits phospholipase A2, blocks liberation of eicosatetraenoic acid and inhibits biosynthesis of leukotrienes promoting the process of inflammation, allergy, etc.), synthesis of anti-inflammatory “pro-inflammatory cytokines”; boosts resistance of cellular membrane to action of different damaging factors.

Immune-suppressive effect is explained by involution of adenoid tissue, inhibition of proliferation of lymphocytes, blockage of B-cells migration and interaction of T- and B-lymphocytes, slowing down release of cytokines from lymphocytes and macrophages and decrease of antibody formation. Anti-allergic effect gets developed resulting from the decrease of synthesis and secretion of allergy mediators, slowing down of release from sensitized labrocytes and other biologically active substances, decrease of the number of circulating basophiles. In case of obstructive diseases of respiratory tracts, Prednisolone action lies mainly in slowing down of inflammatory processes, prevention or decrease of degree of swollen mucosa, decrease of eosinophilic infiltration of submucous membrane of bronchial epithelium and accumulation of circulating immunte complexes in bronchial mucosa, as well as slowing down of erosion and desquamation of mucosa.

Treatment of Auto-Immune Conditions

Auto-immune diseases are human disorders that show themselves as a consequence of an excessively high activity of organism immune system in regards to its own cells. Immune system perceives its tissues as xenogenic elements and starts destroying them. These diseases are called systemic, since damage of a particular system of organism occurs, and sometimes the entire organism gets damaged. For modern medical experts, causes and occurrence mechanism of such conditions remain unclear. Thus, it is considered that stress, traumas, hypothermia, and infections of all sorts may cause auto-immune disorders.

Diseases that belong to this group of disorders include rheumatoid arthritis and a number of auto-immune diseases of thyroid body. Also, mechanism of 1-type diabetes, multiocular sclerosis, and systemic lupus erythematosus development is considered to be auto-immune. There are particular syndromes that are of auto-immune nature. Nowadays, treatment of auto-immune conditions is conducted quite successfully thanks to constant research studies of specialists. While prescribing medicinal products, a doctor must take into account the fact that immunity is a crucial factor that influences negatively all organs and systems. Therefore, the character of therapy in case of auto-immune diseases is immune-suppressive and immunomodulating.

Immuno-suppresives oppressively influence the functioning of immune system. This group of medications includes cytostatic agents, competitive antagonists, corticosteroid hormones, some antibiotics, etc. After the intake of such medications, function of immune system gets gradually inhibited, and the process of inflammation stops. Anyway, during the therapy of such disorders by means of the afore-mentioned medicines, it should be taken into account that these agents provoke occurrence of side-effects. These medicinal products do not act locally: their action gets spread on the entire human organism.

Due to their administration, hematogenesis gets inhibited, inner organs are damaged, and organism becomes vulnerable for infections. After the intake of some medications of this group, inhibition of cells division process occurs that may result in intensive hair loss. In case a patient is treated by means of hormonal medications, Cushing syndrome may become their side-effect. This condition is characterized by high blood pressure, obesity and gynecomastia in men. Therefore, therapy with such medicines is conducted only after a complete confirmation of diagnosis and under the control of experienced physician.

The main aim of immune-modulating medications application is achieving of balance between various components of immune system. Medications of this type are prescribed during therapy by immuno-suppresives in capacity of remedies for infectious complications prophylaxis.  Immune-modulating medicinal products are agents that mainly have natural origin. Such medicines contain biologically active substances that promote restoration of balance between various types of lymphocytes.

Also, complex therapy of auto-immune diseases includes specially developed and balanced complexes of minerals and vitamins. Nowadays, active research studies of new therapy methods of auto-immune disorders are conducted. One of the most prospective methods is gene therapy – method aimed at replacement of defective gene in organism. This therapy method is still under development. Also, medical experts elaborate medicines the basis of which is constituted by antibodies that can stand any attacks of immune system that are aimed at their own tissues.

Crohn’s Disease and Prednisolone

Crohn’s disease is non-specific inflammation of different divisions of gastro-intestinal tract with pre-eminent damage of small and large intestines that is characterized by relapsing progression with formation of inflammatory infiltrates and deep lateral ulcers. The latter get aggravated with bleeding, perforation, formation of external and internal fistula, coarctations and perianal abscesses. Etiology of the disease is unknown. Auto-immune mechanism plays main role in pathogenesis.

Crohn’s disease is treated in accordance with the following program:

  1. Therapeutic nourishment;
  2. Therapy of malabsorption syndrome, correction of metabolic impairments, and electrolyte and polyvitaminic imbalance.
  3. Basic pathogenic therapy: treatment with medications containing 5-aminosalicylic acid; therapy with glucocorticoids and non-hormonal immunosuppressant drugs.
  4. Disease-management therapy.
  5. Surgery.

The basis of medicamentous therapy is constituted by Salazosulfapyridine and corticosteroids. Salazosulfapyridine is prescribed in case of slight activeness of inflammatory process 1g per 3 times a day during 2 weeks. As long as inflammation decreases, the dose of the medicine is reduced to 1g per day. In case of expressed activity (more than 150 scores) and in case of effect absence after therapy with Salazosulfapyridine, Prednisolone is prescribed. Initial dose of the medicine is equal to 30-40mg per day. After 3-4 weeks of administration, the dose of Prednisolone is reduced up to 5mg per week. The relapse occurrence is prevented by means of intravenous introduction of hydrocortisone on a daily basis during the first 3-5 days of regular decrease of Prednisolone dosage.

Therapy with Salazosulfapyridine and Prednisolone may be long-term and continues after patient’s release from the hospital under the control of a physician. Minimal doses of medications include 1,5-1g of Salazosulfapyridine and 5-10mg of Prednisolone. Patients may take them during a couple of months, especially in case they cannot avoid withdrawal syndrome.

Corticosteroids for Bell’s Palsy

Bell’s palsy implies sudden weakness and palsy of one facial part due to the trauma of seventh cranial nerve. Exact cause of Bell’s palsy is still unclear. It is supposed that in case of irritation, seventh cranial nerve swells. Since facial nerve passes through narrow areas in skull, it becomes clenched resulting in paralytic stroke. Medical experts consider that nerve inflammation may cause herpes virus, which in turn leads to Bell’s palsy. Lyme disease and other infections may also become a cause of facial muscles weakness. This condition may be caused by the following factors: injuries of face or head; tumors; diabetes; cancer or infection in spinal fluid (liquor); apoplectic attack; abscess; HIV; infection; auto-immune diseases; pharmaceutical therapy; hereditary disorders; and other facts that cause facial palsy.

Corticosteroids are indicative to treatment of Bell’s palsy, but they are not effective for single agent therapy. Generally, a doctor prescribes 60-80mg of Prednisolone once a day during 1 week. Therapy with corticosteroids is to be started as soon as possible. Combination of corticosteroids and antiviral mediations unlikely has any synergetic effect; therefore this combination is not recommended for routine administration. Nevertheless, severe cases (such as damage of facial muscles of 4-5 degree according to House–Brackmann score) require application of combination of Prednisolone with Valacyclovir (1g 3 times a day during 1 week), but this method improves the function of facial muscles by just 7%, though.  Patients are to be warned that improvement of such therapy method may be slight in this case. Nevertheless, side-effects of this therapy are minimal as well.

In 2009 a meta-analysis of 18 randomized controlled research studies was conducted. It involved 2786 patients and showed that monotherapy with corticosteroids improves the progression of Bell’s palsy – monotherapy with antiviral medications was no less effective than placebo. Effectiveness of combination of corticosteroids with antiviral medications is contradictory. Meta-analysis of 7 randomized controlled research studies showed minimal advantage of such combination efficiency in comparison with monotherapy by means of steroids. Effectiveness data on the combination barely surpassed the threshold of clinical efficiency.

Three multicenter randomized controlled trials with participation of 1500 adult patients compared various combinations of Prednisolone, antiviral medications and placebo. It was proven that monotherapy with Prednisolone was effective; Acyclovir addition had no effect, whereas addition of Valacyclovir had minimal positive effect. Double blind placebo-controlled randomized research study with participation of 497 patients with Bell’s palsy experienced positive effect of Prednisolone monotherapeutic administration within 72 hours. Combination Prednisolone-Acyclovir and monotherapy with Acyclovir had no effect. Conciliative instruction from American Academy of Neurology recommends warning patients of insignificant effect of combination Prednisolone-antiviral drug; meanwhile side-effects are generally minimal.

Can it Suppress Cluster Headaches?

Cluster headache is a variety of unpleasant feelings; it is characterized by high intensiveness. Generally, the pain is located in the area of eyes and occurs suddenly. This type of headache occurs in around 1 per cent of world population. Moreover, men are more often affected by cluster headaches than women. According to ICD, the disease is classified as G44. Therapy of this disorder is a complicated task and is divided into treatment of algesic cluster attack and prophylactic therapy preventing from development of cluster period.

Corticosteroids, including Prednisolone, are considered to be effective for preventive therapy of chronic form of cluster headache. This group of these medications supposedly decreases edema degree and reactive inflammation around cranial blood vessels allowing a patient to reduce stimulation of sympathetic plexus and impacts on trifacial nerve system. Besides, the data about alteraction of cellular and antibody-mediated protection in case of cluster cephalalgia confirm effectiveness and pathogenic direction of action of these medications. Generally, three-day course of Prednisolone is prescribed in the dose of 40-60 mg per day with gradual reduction of the dosage by 10mg each fourth day. Gradual withdrawal of the medication doesn’t induce any side-effects.

Treatment of Dermatomyositis

Dermatomyositis is a disease of systemic character that affects smooth and somatic musculature, as well as skin covering with formation of edema and erythema. In case a disease progresses without skin damage, it is called polymyosite. Dermatomyositis may develop in both men and women regardless of their age.

Dermatomyositis therapy is aimed at inhibition of the process in acute and sub-acute form and remission achievement in case of chronic disease progression. The main medicinal product that is applied for dermatomyositis is Prednisolone. At the initial stage lasting three months, Prednisolone is introduced in higher doses. Later on, the dosage is gradually decreased up to the maintenance dose which should last several years. Withdrawal of the medicine is possible only in case of steady absence of laboratory signs of the disorder. This medication is also applied for mixed connective tissue disease, pseudoxanthoma elasticum, Leber’s disease, etc.

In case of effect absence during dermatomyositis treatment with corticosteroids or in case of contraindications to them, a doctor may prescribe immune-suppressive agents. These medicines may be prescribed in combination with Prednisolone in case of necessity to reduce the dose of corticosteroids. Chronic forms of dermatomyositis require moderate Prednisolone doses at first stage. Along with decrease of Prednisolone decrease, salycylates are recommended for additional administration.

Possible Side-Effects

Medical trials stated interconnection between the intake of particular doses of Prednisolone and a number of occurring side-effects. The remedy taken in small dose during a long time provoked less adverse consequences in comparison with the use of considerable doses during a short period of time.

Patients were diagnosed the following side-effects after Prednisolone intake:

  • Hirsuties;
  • Hypopotassemia;
  • Glycosuria;
  • Hyperglycemia;
  • Impotency;
  • Depression;
  • Clouding of consciousness;
  • Delirium, hallucination;
  • Emotional instability.

Therapeutic course of the drug is generally a cause of enhanced weariness, weakness, drowsiness and insomnia. The decrease of functional activity of immune system leads to frequent relapses of chronic pathologies, viral and bacterial infectious diseases.

Recommendation: side-effects of Prednisolone may occur all at once, but more often they occur gradually. This condition must be reported to attending doctor. He will compare the severity level of side-effects with necessity of gluco-corticosteroid intake, discontinue a drug, or recommend continuing therapy.

Cardio-vascular system – long-term intake of high Prednisolone doses will provoke liquid accumulation in tissues. Such condition leads to narrowing of blood vessels diameter and raise of arterial blood pressure. Gradually, hypertension develops accompanied by steady cardiac failure. These pathologies of cardio-vascular system were diagnosed in more than 10% of patients taking glucocorticosteroid drug.

Endocrine system – Prednisolone intake is often a cause of addiction to glucose and increase of its content in blood serum. Persons with genetic predisposition or with underlying risk for development of diabetes are in risk group. Therefore, this endocrine pathology belongs to contraindications to glucocorticosteroid administration. It may be prescribed to those patients who require this medication according to vital indications. It is possible to prevent from decrease of functional activity of suprarenal capsule by means of gradual reduction of Prednisolone dose and decrease of its application frequency.

Gastro-intestinal tract – usage of Prednisolone in therapy of various pathologies is indicative to patients with peptic ulcer. Prednisolone long-term effect may lead to destructive-degenerative changes of mucous membranes and more deep layers of gastro-intestinal tract.


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