The War Against Medicare Part B Viagra

Some men and women qualify for Medicare early as a result of a disability. Medicare is a superb program. It will cover just a percentage of your hospital and doctor bills. If you just have Original Medicare, you’re accountable for paying the surplus charge out of pocket.

If you presently have Medicare when you become qualified for COBRA, you should be permitted to enroll in COBRA. Medicare is offered in Parts. Lots of people who have Original Medicare choose to have a Medigap policy.

All Medicare beneficiaries should be careful of scams. They have been allowed to receive health insurance through private providers since the 1970san option now known as Medicare Advantage. For this reason, you’re ready to have a number of Part A hospital deductibles from the exact same calendar year.

To qualify for Part D, you should be eligible to be insured by Medicare. Medicare is split into parts, whilst Medigap insurance is split into plans. It is one type of insurance that can help you. There are some folks who intend to stay with the original Medicare.

Unique components of Medicare cover various varieties of healthcare. Anytime before your Medicare starts you’ll start on the very first day of Medicare. If it comes to Medicare and Medigap, timing is important.

The New Angle On Medicare Part B Viagra Just Released

Cutting people from coverage isn’t a long-term solution. You’ll also discover which Medigap plan provides the coverage you desire. If it comes to Medicare coverage, there are plenty of misconceptions. Medicare coverage can help decrease or eliminate certain medical expenses that may occur all at one time or on a monthly basis. You may change your Medicare coverage, but your enrollment dates will be contingent on the changes you wish to make. If you are qualified for Medicare Part D prescription coverage and don’t sign up then you’ll be fined.

If you think you have overdosed on Viagra you need to seek out medical help immediately. You ought not take Viagra if you’re taking nitrate medications. Additionally, you will have a couple Part D prescription plans to select from. When choosing a medicare part d program, you need to take into account all your drugs (not just viagra). If you skip a dose of Viagra you ought to be sure your very last dose was at least 24 hours ago.

In terms of services, different Medicare parts and plans provide various levels of coverage for assorted medical expenses. Other Medicare parts and plans have a broader array of premiums, often depending on the kind of plan and the provider. The plans haven’t any network requirements and could be used for care anywhere within america with providers who accept Medicare patients. In addition, don’t be shy about asking about obtaining a household discount, something an Advantage plan won’t provide you. It’s possible for you to change Medicare Advantage Plans by picking a different plan with your present business or switch to some other company with unique added benefits. Many Medicare Advantage plans also have prescription drug coverage and other services for another fee. For example, you might want to have a different supplement program or Medicare Advantage Plan because it gives prescription drug coverage.

The plan you have might not be the identical next calendar year. Not everybody chooses the ideal Medigap plan on the very first effort. It is possible to stay with your present plan and would not need to do anything. In the event you opt to drop your entire plan, don’t forget to be quite careful with the timing. Knowing the Medicare donut hole is a significant element in selecting the very best Part D insurance policy program.

Since you may see, there’s a lot to take into account when choosing your Medicare options. Medicare Advantage, on the flip side, is a fantastic way to receive extra benefits over original medicare at a reasonable price. You’re able to drop Medicare Advantage altogether and find a Prescription Part D Plan to go alongside Original Medicare.

New Questions About Medicare Part B Viagra

If you delay your medicare enrollment you may have a substantial gap in coverage later on. There are a couple of time periods when you’re able to enroll in a Medicare Advantage plan. Yes, there’s still time if you prefer out of your Medicare Advantage plan. Navigating the sphere of different Medicare plans and parts are often quite challenging. Medicare Parts A and B cover a number of your medical care expenses. What’s more, you also need to have the original Medicare Parts A together with B to purchase the Medicare supplement. If you’re already enrolled in the traditional Medicare Part A and B plans, you’re eligible to register for and receive the advantages of a supplemental insurance policy policy.

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Glucocorticoids are a class of corticosteroids, which are a class of steroid hormones. Glucocorticoids are corticosteroids that bind to the glucocorticoid receptor,[1] that is present in almost every vertebrate animal cell. The name “glucocorticoid” is a portmanteau (glucose + cortex + steroid) and is composed from its role in regulation of glucose metabolism, synthesis in the adrenal cortex, and its steroidal structure (see structure to the right). A less common synonym is glucocorticosteroid.

Glucocorticoids are part of the feedback mechanism in the immune system which reduces certain aspects of immune function, such as inflammation. They are therefore used in medicine to treat diseases caused by an overactive immune system, such as allergies, asthma, autoimmune diseases, and sepsis. Glucocorticoids have many diverse (pleiotropic) effects, including potentially harmful side effects, and as a result are rarely sold over the counter.[2] They also interfere with some of the abnormal mechanisms in cancer cells, so they are used in high doses to treat cancer. This includes inhibitory effects on lymphocyte proliferation, as in the treatment of lymphomas and leukemias, and the mitigation of side effects of anticancer drugs.

Glucocorticoids affect cells by binding to the glucocorticoid receptor. The activated glucocorticoid receptor-glucocorticoid complex up-regulates the expression of anti-inflammatory proteins in the nucleus (a process known as transactivation) and represses the expression of proinflammatory proteins in the cytosol by preventing the translocation of other transcription factors from the cytosol into the nucleus (transrepression).[2]

Glucocorticoids are distinguished from mineralocorticoids and sex steroids by their specific receptors, target cells, and effects. In technical terms, “corticosteroid” refers to both glucocorticoids and mineralocorticoids (as both are mimics of hormones produced by the adrenal cortex), but is often used as a synonym for “glucocorticoid.” Glucocorticoids are chiefly produced in the zona fasciculata of the adrenal cortex, whereas mineralocorticoids are synthesized in the zona glomerulosa.

Cortisol (or hydrocortisone) is the most important human glucocorticoid. It is essential for life, and it regulates or supports a variety of important cardiovascular, metabolic, immunologic, and homeostatic functions. Various synthetic glucocorticoids are available; these are widely utilized in general medical practice and numerous specialties either as replacement therapy in glucocorticoid deficiency or to suppress the immune system.


  • 1 Effects
    • 1.1 Immune
    • 1.2 Metabolic
    • 1.3 Developmental
    • 1.4 Arousal and cognition
    • 1.5 Body fluid homeostasis
  • 2 Mechanism of action
    • 2.1 Transactivation
    • 2.2 Transrepression
    • 2.3 Nongenomic effects
  • 3 Pharmacology
  • 4 Therapeutic use
    • 4.1 Physiological replacement
    • 4.2 Therapeutic immunosuppression
    • 4.3 Anti-inflammatory
    • 4.4 Hyperaldosteronism
    • 4.5 Resistance
    • 4.6 Heart failure
  • 5 Side effects
    • 5.1 Immunodeficiency
    • 5.2 Withdrawal
  • 6 See also
  • 7 References
  • 8 External links


Steroidogenesis showing glucocorticoids in green ellipse at right with the primary example being cortisol.[3] It is not a strictly bounded group, but a continuum of structures with increasing glucocorticoid effect.

Glucocorticoid effects may be broadly classified into two major categories: immunological and metabolic. In addition, glucocorticoids play important roles in fetal development and body fluid homeostasis.


As discussed in more detail below, glucocorticoids function through interaction with the glucocorticoid receptor:

  • up-regulate the expression of anti-inflammatory proteins.
  • down-regulate the expression of proinflammatory proteins.

Glucocorticoids are also shown to play a role in the development and homeostasis of T lymphocytes. This has been shown in transgenic mice with either increased or decreased sensitivity of T cell lineage to glucocorticoids.[4]


The name “glucocorticoid” derives from early observations that these hormones were involved in glucose metabolism. In the fasted state, cortisol stimulates several processes that collectively serve to increase and maintain normal concentrations of glucose in blood.

Metabolic effects:

  • Stimulation of gluconeogenesis, in particular, in the liver: This pathway results in the synthesis of glucose from non-hexose substrates, such as amino acids and glycerol from triglyceride breakdown, and is particularly important in carnivores and certain herbivores. Enhancing the expression of enzymes involved in gluconeogenesis is probably the best-known metabolic function of glucocorticoids.
  • Mobilization of amino acids from extrahepatic tissues: These serve as substrates for gluconeogenesis.
  • Inhibition of glucose uptake in muscle and adipose tissue: A mechanism to conserve glucose
  • Stimulation of fat breakdown in adipose tissue: The fatty acids released by lipolysis are used for production of energy in tissues like muscle, and the released glycerol provide another substrate for gluconeogenesis.

Excessive glucocorticoid levels resulting from administration as a drug or hyperadrenocorticism have effects on many systems. Some examples include inhibition of bone formation, suppression of calcium absorption (both of which can lead to osteoporosis), delayed wound healing, muscle weakness, and increased risk of infection. These observations suggest a multitude of less-dramatic physiologic roles for glucocorticoids.[4]


Glucocorticoids have multiple effects on fetal development. An important example is their role in promoting maturation of the lung and production of the surfactant necessary for extrauterine lung function. Mice with homozygous disruptions in the corticotropin-releasing hormone gene (see below) die at birth due to pulmonary immaturity. In addition, glucocorticoids are necessary for normal brain development, by initiating terminal maturation, remodeling axons and dendrites, and affecting cell survival[5] and may also play a role in hippocampal development. Glucocorticoids stimulate the maturation of the Na+/K+/ATPase, nutrient transporters, and digestion enzymes, promoting the development of a functioning gastro-intestinal system. Glucocorticoids also support the development of the neonate’s renal system by increasing glomerular filtration.

Arousal and cognition[edit]

A graphical representation of the Yerkes-Dodson curve

Glucocorticoids act on the hippocampus, amygdala, and frontal lobes. Along with adrenaline, these enhance the formation of flashbulb memories of events associated with strong emotions, both positive and negative.[6] This has been confirmed in studies, whereby blockade of either glucocorticoids or noradrenaline activity impaired the recall of emotionally relevant information. Additional sources have shown subjects whose fear learning was accompanied by high cortisol levels had better consolidation of this memory (this effect was more important in men). The effect that glucocorticoids have on memory may be due to damage specifically to the CA1 area of the hippocampal formation. In multiple animal studies, prolonged stress (causing prolonged increases in glucocorticoid levels) have shown destruction of the neurons in this area of the brain, which has been connected to lower memory performance.[7][8][9]

Glucocorticoids have also been shown to have a significant impact on vigilance (attention deficit disorder) and cognition (memory). This appears to follow the Yerkes-Dodson curve, as studies have shown circulating levels of glucocorticoids vs. memory performance follow an upside-down U pattern, much like the Yerkes-Dodson curve. For example, long-term potentiation (LTP; the process of forming long-term memories) is optimal when glucocorticoid levels are mildly elevated, whereas significant decreases of LTP are observed after adrenalectomy (low-glucocorticoid state) or after exogenous glucocorticoid administration (high-glucocorticoid state). Elevated levels of glucocorticoids enhance memory for emotionally arousing events, but lead more often than not to poor memory for material unrelated to the source of stress/emotional arousal.[10] In contrast to the dose-dependent enhancing effects of glucocorticoids on memory consolidation, these stress hormones have been shown to inhibit the retrieval of already stored information.[11] Long-term exposure to glucocorticoid medications, such as asthma and anti-inflammatory medication, has been shown to create deficits in memory and attention both during and, to a lesser extent, after treatment,[12][13] a condition known as “steroid dementia.”[14]

Body fluid homeostasis[edit]

Glucocorticoids could act centrally, as well as peripherally, to assist in the normalization of extracellular fluid volume by regulating body’s action to atrial natriuretic peptide (ANP). Centrally, glucocorticoids could inhibit dehydration induced water intake;[15] peripherally, glucocorticoids could induce a potent diuresis.[16]

Mechanism of action[edit]


Glucocorticoids bind to the cytosolic glucocorticoid receptor, a type of nuclear receptor that is activated by ligand binding. After a hormone binds to the corresponding receptor, the newly formed complex translocates itself into the cell nucleus, where it binds to glucocorticoid response elements in the promoter region of the target genes resulting in the regulation of gene expression. This process is commonly referred to as transcriptional activation, or transactivation.[17][18]

The proteins encoded by these up-regulated genes have a wide range of effects, including, for example:[18]

  • anti-inflammatory – lipocortin I, p11/calpactin binding protein, secretory leukocyte protease inhibitor 1 (SLPI), and Mitogen-activated protein kinase phosphatase (MAPK phosphatase)
  • increased gluconeogenesis – glucose-6-phosphatase and tyrosine aminotransferase


The opposite mechanism is called transcriptional repression, or transrepression. The classical understanding of this mechanism is that activated glucocorticoid receptor binds to DNA in the same site where another transcription factor would bind, which prevents the transcription of genes that are transcribed via the activity of that factor.[17][18] While this does occur, the results are not consistent for all cell types and conditions; there is no generally accepted, general mechanism for transrepression.[18]

New mechanisms are being discovered where transcription is repressed, but the activated glucocorticoid receptor is not interacting with DNA, but rather with another transcription factor directly, thus interfering with it, or with other proteins that interfere with the function of other transcription factors. This latter mechanism appears to be the most likely way that activated glucocorticoid receptor interferes with NF-κB – namely by recruiting histone deacetylase, which deacetylate the DNA in the promoter region leading to closing of the chromatin structure where NF-κB needs to bind.[17][18]

Nongenomic effects[edit]

Activated glucocorticoid receptor has effects that have been experimentally shown to be independent of any effects on transcription and can only be due to direct binding of activated glucocorticoid receptor with other proteins or with mRNA.[17][18]

For example, Src kinase which binds to inactive glucocorticoid receptor, is released when a glucocorticoid binds to glucocorticoid receptor, and phosphorylates a protein that in turn displaces an adaptor protein from a receptor important in inflammation, epidermal growth factor, reducing its activity, which in turn results in reduced creation of arachidonic acid – a key proinflammatory molecule. This is one mechanism by which glucocorticoids have an anti-inflammatory effect.[17]


Dexamethasone – a synthetic glucocorticoid binds more powerfully to the glucocorticoid receptor than cortisol does. Dexamethasone is based on the cortisol structure but differs at three positions (extra double bond in the A-ring between carbons 1 and 2 and addition of a 9-α-fluoro group and a 16-α-methyl substituent).

A variety of synthetic glucocorticoids, some far more potent than cortisol, have been created for therapeutic use. They differ in both pharmacokinetics (absorption factor, half-life, volume of distribution, clearance) and pharmacodynamics (for example the capacity of mineralocorticoid activity: retention of sodium (Na+) and water; renal physiology). Because they permeate the intestines easily, they are administered primarily per os (by mouth), but also by other methods, such as topically on skin. More than 90% of them bind different plasma proteins, though with a different binding specificity. Endogenous glucocorticoids and some synthetic corticoids have high affinity to the protein transcortin (also called corticosteroid-binding globulin), whereas all of them bind albumin. In the liver, they quickly metabolize by conjugation with a sulfate or glucuronic acid, and are secreted in the urine.

Glucocorticoid potency, duration of effect, and the overlapping mineralocorticoid potency vary. Cortisol is the standard of comparison for glucocorticoid potency. Hydrocortisone is the name used for pharmaceutical preparations of cortisol.

The data below refer to oral administration. Oral potency may be less than parenteral potency because significant amounts (up to 50% in some cases) may not reach the circulation. Fludrocortisone acetate and deoxycorticosterone acetate are, by definition, mineralocorticoids rather than glucocorticoids, but they do have minor glucocorticoid potency and are included in this table to provide perspective on mineralocorticoid potency.

Therapeutic use[edit]

Glucocorticoids may be used in low doses in adrenal insufficiency. In much higher doses, oral or inhaled glucocorticoids are used to suppress various allergic, inflammatory, and autoimmune disorders. Inhaled glucocorticoids are the second-line treatment for asthma. They are also administered as post-transplantory immunosuppressants to prevent the acute transplant rejection and the graft-versus-host disease. Nevertheless, they do not prevent an infection and also inhibit later reparative processes. Newly emerging evidence showed that glucocorticoids could be used in the treatment of heart failure to increase the renal responsiveness to diuretics and natriuretic peptides. Glucocorticoids are historically used for pain relief in inflammatory conditions.[20][21][22] However, corticosteroids show limited efficacy in pain relief and potential adverse events for their use in tendinopathies.[23]

Physiological replacement[edit]

Any glucocorticoid can be given in a dose that provides approximately the same glucocorticoid effects as normal cortisol production; this is referred to as physiologic, replacement, or maintenance dosing. This is approximately 6–12 mg/m²/day of hydrocortisone (m² refers to body surface area (BSA), and is a measure of body size; an average man’s BSA is 1.9 m²).

Therapeutic immunosuppression[edit]

See section on “Immunodeficiency” below for adverse effects

Glucocorticoids cause immunosuppression, and the therapeutic component of this effect is mainly the decreases in the function and numbers of lymphocytes, including both B cells and T cells.

The major mechanism for this immunosuppression is through inhibition of nuclear factor kappa-light-chain-enhancer of activated B cells(NF-κB). NF-κB is a critical transcription factor involved in the synthesis of many mediators (i.e., cytokines) and proteins (i.e., adhesion proteins) that promote the immune response. Inhibition of this transcription factor, therefore, blunts the capacity of the immune system to mount a response.[2]

Glucocorticoids suppress cell-mediated immunity by inhibiting genes that code for the cytokines IL-1, IL-2, IL-3, IL-4, IL-5, IL-6, IL-8 and IFN-γ, the most important of which is IL-2. Smaller cytokine production reduces the T cell proliferation.[24]

Glucocorticoids, however, not only reduce T cell proliferation, but also lead to another well known effect – glucocorticoid-induced apoptosis. The effect is more prominent in immature T cells still inside in the thymus, but peripheral T cells are also affected. The exact mechanism regulating this glucocorticoid sensitivity lies in the Bcl-2 gene.[25]

Glucocorticoids also suppress the humoral immunity, thereby causing a humoral immune deficiency. Glucocorticoids cause B cells to express smaller amounts of IL-2 and of IL-2 receptors. This diminishes both B cell clone expansion and antibody synthesis. The diminished amounts of IL-2 also cause fewer T lymphocyte cells to be activated.

The effect of glucocorticoids on Fc receptor expression in immune cells is complicated. Dexamethasone decreases IFN-gamma simulated Fc gamma RI expression in neutrophils while conversely causing an increase in monocytes.[26] Glucocorticoids may also decrease the expression of Fc receptors in macrophages,[27] but the evidence supporting this regulation in earlier studies has been questioned.[28] The effect of Fc receptor expression in macrophages is important since it is necessary for the phagocytosis of opsonised cells. This is because Fc receptors bind antibodies attached to cells targeted for destruction by macrophages.


Glucocorticoids are potent anti-inflammatories, regardless of the inflammation’s cause; their primary anti-inflammatory mechanism is lipocortin-1 (annexin-1) synthesis. Lipocortin-1 both suppresses phospholipase A2, thereby blocking eicosanoid production, and inhibits various leukocyte inflammatory events (epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, etc.). In other words, glucocorticoids not only suppress immune response, but also inhibit the two main products of inflammation, prostaglandins and leukotrienes. They inhibit prostaglandin synthesis at the level of phospholipase A2 as well as at the level of cyclooxygenase/PGE isomerase (COX-1 and COX-2),[29] the latter effect being much like that of NSAIDs, potentiating the anti-inflammatory effect.

In addition, glucocorticoids also suppress cyclooxygenase expression. [30]

Glucocorticoids marketed as anti-inflammatories are often topical formulations, such as nasal sprays for rhinitis or inhalers for asthma. These preparations have the advantage of only affecting the targeted area, thereby reducing side effects or potential interactions. In this case, the main compounds used are beclometasone, budesonide, fluticasone, mometasone and ciclesonide. In rhinitis, sprays are used. For asthma, glucocorticoids are administered as inhalants with a metered-dose or dry powder inhaler.[31]


Glucocorticoids can be used in the management of familial hyperaldosteronism type 1. They are not effective, however, for use in the type 2 condition.


Corticosteroid resistance mechanisms

Resistance to the therapeutic uses of glucocorticoids can present difficulty; for instance, 25% of cases of severe asthma may be unresponsive to steroids. This may be the result of genetic predisposition, ongoing exposure to the cause of the inflammation (such as allergens), immunological phenomena that bypass glucocorticoids, and pharmacokinetic disturbances (incomplete absorption or accelerated excretion or metabolism).[24]

Heart failure[edit]

Glucocorticoids could be used in the treatment of decompensated heart failure to potentiate renal responsiveness to diuretics, especially in heart failure patients with refractory diuretic resistance with large doses of loop diuretics.[32][33][34][35][36][37][38]

Side effects[edit]

Glucocorticoid drugs currently being used act nonselectively, so in the long run they may impair many healthy anabolic processes. To prevent this, much research has been focused recently on the elaboration of selectively acting glucocorticoid drugs. Side effects include:

  • Immunodeficiency (see section below)
  • Hyperglycemia due to increased gluconeogenesis, insulin resistance, and impaired glucose tolerance (“steroid diabetes”); caution in those with diabetes mellitus
  • Increased skin fragility, easy bruising
  • Negative calcium balance due to reduced intestinal calcium absorption[39]
  • Steroid-induced osteoporosis: reduced bone density (osteoporosis, osteonecrosis, higher fracture risk, slower fracture repair)
  • Weight gain due to increased visceral and truncal fat deposition (central obesity) and appetite stimulation
  • Hypercortisolemia with prolonged or excessive use (also known as, exogenous Cushing’s syndrome)
  • Impaired memory and attention deficits[40]
  • Adrenal insufficiency (if used for long time and stopped suddenly without a taper)
  • Muscle and tendon breakdown (proteolysis), weakness, reduced muscle mass and repair[41][23]
  • Expansion of malar fat pads and dilation of small blood vessels in skin
  • Lipomatosis within the epidural space[42]
  • Excitatory effect on central nervous system (euphoria, psychosis)
  • Anovulation, irregularity of menstrual periods
  • Growth failure, delayed puberty
  • Increased plasma amino acids, increased urea formation, negative nitrogen balance
  • Glaucoma due to increased ocular pressure
  • Cataracts
  • Topical steroid addiction

In high doses, hydrocortisone (cortisol) and those glucocorticoids with appreciable mineralocorticoid potency can exert a mineralocorticoid effect as well, although in physiologic doses this is prevented by rapid degradation of cortisol by 11β-hydroxysteroid dehydrogenase isoenzyme 2 (11β-HSD2) in mineralocorticoid target tissues. Mineralocorticoid effects can include salt and water retention, extracellular fluid volume expansion, hypertension, potassium depletion, and metabolic alkalosis.


Glucocorticoids cause immunosuppression, decreasing the function and/or numbers of neutrophils, lymphocytes (including both B cells and T cells), monocytes, macrophages, and the anatomical barrier function of the skin.[43] This suppression, if large enough, can cause manifestations of immunodeficiency, including T cell deficiency, humoral immune deficiency and neutropenia.


In addition to the effects listed above, use of high-dose steroids for more than a week begins to produce suppression of the patient’s adrenal glands because the exogenous glucocorticoids suppress hypothalamic corticotropin-releasing hormone and pituitary adrenocorticotropic hormone. With prolonged suppression, the adrenal glands atrophy (physically shrink), and can take months to recover full function after discontinuation of the exogenous glucocorticoid.

During this recovery time, the patient is vulnerable to adrenal insufficiency during times of stress, such as illness. While suppressive dose and time for adrenal recovery vary widely, clinical guidelines have been devised to estimate potential adrenal suppression and recovery, to reduce risk to the patient. The following is one example:

  • If patients have been receiving daily high doses for five days or less, they can be abruptly stopped (or reduced to physiologic replacement if patients are adrenal-deficient). Full adrenal recovery can be assumed to occur by a week afterward.
  • If high doses were used for six to 10 days, reduce to replacement dose immediately and taper over four more days. Adrenal recovery can be assumed to occur within two to four weeks of completion of steroids.
  • If high doses were used for 11–30 days, cut immediately to twice replacement, and then by 25% every four days. Stop entirely when dose is less than half of replacement. Full adrenal recovery should occur within one to three months of completion of withdrawal.
  • If high doses were used more than 30 days, cut dose immediately to twice replacement, and reduce by 25% each week until replacement is reached. Then change to oral hydrocortisone or cortisone as a single morning dose, and gradually decrease by 2.5 mg each week. When the morning dose is less than replacement, the return of normal basal adrenal function may be documented by checking 0800 cortisol levels prior to the morning dose; stop drugs when 0800 cortisol is 10 μg/dl. Predicting the time to full adrenal recovery after prolonged suppressive exogenous steroids is difficult; some people may take nearly a year.
  • Flare-up of the underlying condition for which steroids are given may require a more gradual taper than outlined above.

See also[edit]

  • List of corticosteroids
  • List of corticosteroid cyclic ketals
  • List of corticosteroid esters
  • Aminoglutethimide blocks glucocorticoid secretion
  • GITR (glucocorticoid-induced TNF receptor)
  • Glucocorticoid receptor
  • Immunosuppressive drug
  • Membrane glucocorticoid receptor
  • Metyrapone blocks glucocorticoid secretion
  • Selective glucocorticoid receptor agonist
  • Topical steroid
  • Steroid atrophy
  • Topical steroid withdrawal
  • Non-steroidal anti-inflammatory drug (NSAID)


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  • ^ Chowdhury R, Naaseri S, Lee J, Rajeswaran G (2014). “Imaging and management of greater trochanteric pain syndrome”. Postgraduate Medical Journal. 90 (1068): 576–81. doi:10.1136/postgradmedj-2013-131828. PMID 25187570. 
  • ^ a b Mohamadi A, Chan JJ, Claessen FM, Ring D, Chen NC (January 2017). “Corticosteroid Injections Give Small and Transient Pain Relief in Rotator Cuff Tendinosis: A Meta-analysis”. Clinical Orthopaedics and Related Research. 475 (1): 232–243. doi:10.1007/s11999-016-5002-1. PMC 5174041 . PMID 27469590. 
  • ^ a b Leung DY, Bloom JW (Jan 2003). “Update on glucocorticoid action and resistance”. The Journal of Allergy and Clinical Immunology. 111 (1): 3–22; quiz 23. doi:10.1067/mai.2003.97. PMID 12532089. 
  • ^ Banuelos J, Shin S, Cao Y, Bochner BS, Morales-Nebreda L, Budinger GR, Zhou L, Li S, Xin J, Lingen MW, Dong C, Schleimer RP, Lu NZ (Jan 2016). “BCL-2 protects human and mouse Th17 cells from glucocorticoid-induced apoptosis”. Allergy. 71: 640–50. doi:10.1111/all.12840. PMID 26752231. 
  • ^ Pan LY, Mendel DB, Zurlo J, Guyre PM (1990). “Regulation of the steady state level of Fc gamma RI mRNA by IFN-gamma and dexamethasone in human monocytes, neutrophils, and U-937 cells”. Journal of Immunology. 145 (1): 267–75. PMID 2141616. 
  • ^ Ruiz P, Gomez F, King M, Lopez R, Darby C, Schreiber AD (1991). “In vivo glucocorticoid modulation of guinea pig splenic macrophage Fc gamma receptors”. The Journal of Clinical Investigation. 88 (1): 149–57. doi:10.1172/JCI115271. PMC 296015 . PMID 1829095. 
  • ^ Werb Z (1980). “Hormone receptors and normal regulation of macrophage physiological function”. In van Furth R. Mononuclear phagocytes functional aspects. The Hague: M. Nijhoff. p. 825. ISBN 978-94-009-8793-7. Glucocorticoids may also decrease the number of Fc receptors on macrophages, but this immunosuppressive function is controversial because of the lack of sensitivity in Fc receptor techniques and the high concentration of glucocorticoids used in previous experiments. 
  • ^ Goppelt-Struebe M, Wolter D, Resch K (Dec 1989). “Glucocorticoids inhibit prostaglandin synthesis not only at the level of phospholipase A2 but also at the level of cyclo-oxygenase/PGE isomerase”. British Journal of Pharmacology. 98 (4): 1287–95. doi:10.1111/j.1476-5381.1989.tb12676.x. PMC 1854794 . PMID 2514948. 
  • ^ Jun SS, Chen Z, Pace MC, Shaul PW (Feb 1999). “Glucocorticoids downregulate cyclooxygenase-1 gene expression and prostacyclin synthesis in fetal pulmonary artery endothelium”. Circulation Research. 84 (2): 193–200. doi:10.1161/01.RES.84.2.193. PMID 9933251. 
  • ^ Flower R, Rang HP, Dale MM, Ritter JM (2007). Rang & Dale’s pharmacology. Edinburgh: Churchill Livingstone. ISBN 0-443-06911-5. 
  • ^ Rado JP, Blumenfeld G, Hammer S (Nov 1959). “The effect of prednisone and 6-methylprednisolone on mercurial diuresis in patients with refractory cardiac edema”. The American Journal of the Medical Sciences. 238: 542–51. PMID 14435747. 
  • ^ Riemer AD (Apr 1958). “Application of the newer corticosteroids to augment diuresis in congestive heart failure”. The American Journal of Cardiology. 1 (4): 488–96. doi:10.1016/0002-9149(58)90120-6. PMID 13520608. 
  • ^ Newman DA (Feb 1959). “Reversal of intractable cardiac edema with prednisone”. New York State Journal of Medicine. 59 (4): 625–33. PMID 13632954. 
  • ^ Zhang H, Liu C, Ji Z, Liu G, Zhao Q, Ao YG, Wang L, Deng B, Zhen Y, Tian L, Ji L, Liu K (Sep 2008). “Prednisone adding to usual care treatment for refractory decompensated congestive heart failure”. International Heart Journal. 49 (5): 587–95. doi:10.1536/ihj.49.587. PMID 18971570. 
  • ^ Liu C, Liu G, Zhou C, Ji Z, Zhen Y, Liu K (Sep 2007). “Potent diuretic effects of prednisone in heart failure patients with refractory diuretic resistance”. The Canadian Journal of Cardiology. 23 (11): 865–8. doi:10.1016/s0828-282x(07)70840-1. PMC 2651362 . PMID 17876376. 
  • ^ Liu C, Chen H, Zhou C, Ji Z, Liu G, Gao Y, Tian L, Yao L, Zheng Y, Zhao Q, Liu K (Oct 2006). “Potent potentiating diuretic effects of prednisone in congestive heart failure”. Journal of Cardiovascular Pharmacology. 48 (4): 173–6. doi:10.1097/01.fjc.0000245242.57088.5b. PMID 17086096. 
  • ^ Massari F, Mastropasqua F, Iacoviello M, Nuzzolese V, Torres D, Parrinello G (Mar 2012). “The glucocorticoid in acute decompensated heart failure: Dr Jekyll or Mr Hyde?”. The American Journal of Emergency Medicine. 30 (3): 517.e5–10. doi:10.1016/j.ajem.2011.01.023. PMID 21406321. 
  • ^ Gennari C (May 1993). “Differential effect of glucocorticoids on calcium absorption and bone mass”. British Journal of Rheumatology. 32 Suppl 2: 11–4. doi:10.1093/rheumatology/32.suppl_2.11. PMID 8495275. 
  • ^ Keenan PA, Jacobson MW, Soleymani RM, Mayes MD, Stress ME, Yaldoo DT (Dec 1996). “The effect on memory of chronic prednisone treatment in patients with systemic disease”. Neurology. 47 (6): 1396–402. doi:10.1212/WNL.47.6.1396. PMID 8960717. 
  • ^ Gelber JD (January 2017). “CORR Insights: Corticosteroid Injections Give Small and Transient Pain Relief in Rotator Cuff Tendinosis: A Meta-analysis”. Clinical Orthopaedics and Related Research. 475 (1): 244–246. doi:10.1007/s11999-016-5044-4. PMC 5174046 . PMID 27572298. 
  • ^ Koch CA, Doppman JL, Patronas NJ, Nieman LK, Chrousos GP (Apr 2000). “Do glucocorticoids cause spinal epidural lipomatosis? When endocrinology and spinal surgery meet”. Trends in Endocrinology and Metabolism. 11 (3): 86–90. doi:10.1016/S1043-2760(00)00236-8. PMID 10707048. 
  • ^ a b Klein NC, Go CH, Cunha BA (Jun 2001). “Infections associated with steroid use”. Infectious Disease Clinics of North America. 15 (2): 423–32, viii. doi:10.1016/s0891-5520(05)70154-9. PMID 11447704. 
  • External links[edit]

    • Glucocorticoids at the US National Library of Medicine Medical Subject Headings (MeSH)
    • Bowen R (2006-05-26). “Glucocorticoids”. Colorado State University. Retrieved 2008-05-11. 
    • Wolkowitz OM, Burke H, Epel ES, Reus VI (Oct 2009). “Glucocorticoids. Mood, memory, and mechanisms”. Annals of the New York Academy of Sciences. 1179: 19–40. doi:10.1111/j.1749-6632.2009.04980.x. PMID 19906230. 
    • “Introduction + Classification + Pharmacological Action + Regulation of Release and Drawback of Glucocorticoids Hormone”. 


    • Antagonists: Aglepristone
    • Ketoconazole
    • Mifepristone
    • Ulipristal acetate

    Synthesis modifiers

    • Acetoxolone
    • Aminoglutethimide
    • Carbenoxolone
    • Enoxolone
    • Ketoconazole
    • Metyrapone
    • Mitotane
    • Trilostane
    • #WHO-EM
    • ‡Withdrawn from market
    • Clinical trials:
      • †Phase III
      • §Never to phase III

    See also
    Glucocorticoid receptor modulators
    Mineralocorticoids and antimineralocorticoids
    List of corticosteroids

    See also
    Receptor/signaling modulators
    Glucocorticoids and antiglucocorticoids
    Mineralocorticoid receptor modulators
    List of corticosteroids


    The Meaning of Prednisone Uses

    What is Really Happening with Prednisone Uses

    Prednisone is a prednisone utilizes corticosteroid. It belongs to a class of medications called corticosteroids. It is a type of medication that is termed a steroid. It is a powerful corticosteroid with a higher risk of side effects than Tylenol. It must be taken on a full stomach so that stomach upset is completely avoided. It is used to treat a wide variety of medical conditions. You fear taking Prednisone or any other sort of medicine for Psoriasis.

    Consult your medical care provider any questions that you might have regarding how to utilize Prednisone. Prednisone is owned by the family of corticosteroid medications, and is much like the hormone cortisol made by the adrenal glands. It can also be used to treat sarcoid rash, but it may cause the thinning of the skin. Along with weight gain, it can cause osteoporosis by accelerating the process of bone loss. It can also reduce the discomfort, albeit with several side effects. Whether you are prescribed Prednisone at 5mg or another dosage, you will need to adhere to the directions for its use very carefully.

    Prednisone may lead to a dangerous increase in blood pressure which might cause symptoms including seizures and may lead to a sudden heart attack. As a corticosteroid, it plays a critical role in the normal physiology of the body. It is a type of drug known as a corticosteroid. It can be used on a short-term basis to treat hives. It acts as a replacement for people with low levels of cortisol, one of the natural steroid hormones. It is a prodrug that is converted by the liver into prednisolone, which is the active drug and also a steroid. Employing prednisone during an active case of diverticulitis might increase the harshness of the illness.

    Steroids aren’t healthy for you in general and can give rise to a plethora of side effects and even death sometimes. They can also be used as a pain reliever in some cases, but mostly they are used to give a look of strength because they promote growth of tissues and muscles to give men and some women the larger muscles that they are looking for. They are expensive though, and many men cannot keep up with the cost to see if their penis actually gets larger because of it. Despite the fact that they have been banned by every major sport and even high school sports, people are still using steroids. Anabolic steroids are the most frequent steroids used.

    The impacts of steroids don’t just stop at damaging the body, but they are able to make a guy to turn into impotent either temporarily or permanently. Thankfully there are steps that you can take to combat the side results and still shed weight whilst on beta blockers. There are potential side effects with Prednisone usage.

    Prednisone Uses: No Longer a Mystery

    If you’re not certain what to do after missing a dose, speak to your physician or pharmacist for advice. It is not recommended to take two doses at the moment in order to compensate for a missed one. In the event in which you skip a dose, you would want to take it whenever possible and then continue to your normal schedule. In the event of stopping treatment, the dose will want to get decreased slowly according to the physician’s instructions. The dose to be prescribed greatly depends upon the status that should be treated. Therapeutic doses vary from 30 mg to 1,000 mg every day. They range from 1,000 mg to 3,000 mg a day.

    Dosage ought to be decreased or discontinued gradually as soon as the drug was administered for over a day or two. Its dosage needs to be lowered slowly on the ideas and consent of a health care provider. Folks have a tendency to take larger and larger dosages to find relief. For infants and kids, the suggested dosage needs to be governed by exactly the same considerations in place of strict adherence to the ratio indicated by age or body weight. Close DOSAGE AND ADMINISTRATION Dosage of prednisone tablets ought to be individualized based on the seriousness of the disease and the response of the individual.

    If you own a doctor who’s not open to testing for progesterone, it could be time to discover a new doctor. Your physician will also deal with any health conditions contributing to the issue. Your physician can explain to you the risks versus the advantages of the medicine regarding your distinct condition. The physician will diagnose and will prescribe the kinds of medication necessary for your treatment. Doctors who prescribe prednisone for unrelated health conditions may not anticipate that you’ve got an undiagnosed case of diverticulosis.

    You might or might not have to take medicine for TB to check or treat it. If you’re on the medicine for quite a while, you may have to acquire regular eye exams. Don’t attempt to crush or break the medicine whenever you have it. It is very important to know which medications may be used together, to steer clear of serious adverse reactions or even death. If you are at present on any prescribed medication, always check with your physician prior to reducing your medication. There are several kinds of blood pressure medication.

    Purchasing Drugs

    What You Should Do to Find Out About Drugs Before You’re Left Behind

    Drugs that are administered only once or twice are bad for business. All chemotherapy drugs utilized in the United States of America have been accepted by the FDA. So in both scenarios, reviewing and adjusting medication may be one of the absolute most productive approaches for controlling them. The offending medication might be stopped or its dosage adjusted, or it could be replaced. The medication needs to be taken at constant intervals. If you’re taking a medication of any sort and are impotent, consult your doctor or pharmacist to learn whether the drug could be responsible.

    As soon as you’ve been off drugs for some time, you will find some confidence beneath your belt. So even approved drugs will need to go through clinical trials to make sure that they are safe for individuals with Parkinson’s. It’s also not unusual that people sell such drugs on the street.

    When it has to do with alcohol and drug addictions, Social Security has completely altered the system in the previous decade or so. Therefore, while an approved drug is going to have been demonstrated to be safe in clinical trials, the drug is going to have only been tested in a little proportion of people and might not be safe for everybody. If you must take a prescribed drug, you can offset a number of the side results and experience much greater health by supplementing with the aforementioned nutrients.

    The drug now has to be investigated further in bigger studies. Discontinuing the drug results in withdrawal symptoms that depend on the kind of drug used. There are many prescription drugs on the marketplace which can bring about false-positive urine tests on a drug screen.

    Definitions of Drugs

    The use of alcohol and several drugs can result in addiction. Needless to say, drug use has to be illegal. It is a frequent theme, particularly in the experimental, early years. It does not necessarily stop you from becoming a police officer, but you’ll need to be honest about it, prove you’re clean and perhaps wait a while before applying.

    The Tried and True Method for Drugs in Step by Step Detail

    Alcohol has a potent effect on your entire body and on your sexual reaction. If a person feels they need to consume larger quantities of alcohol as a way to feel good, that individual is probably an alcoholic. Though the majority of people can consume alcohol when taking cephalexin, in some folks there can be side consequences. It’s also important to not forget that some cold medications contain alcohol. In the united kingdom, alcohol is currently the major cause of death in men under the age of 50. Alcohol and a lot of drugs may lead to depression.

    The Downside Risk of Drugs

    Online Canada Pharmacy It isn’t required to stop by a pharmacy to find any type of drugs including prescription drugs. Your pharmacy could be in a position to supply you with a sample to hold you over until the doctor can be found on Monday. The pharmacy will be able to help you to get in touch with your normal pharmacy or your physician to get you back on your prescription fast.

    Lots of people will take drugs for over 1 condition. In any event, drugs have to explain a considerable fraction. Additionally, oral drugs have limited impact, so they are frequently used in combinations (like tablets containing two drugs). Logically, an individual would believe that taking a psychedelic drug would result in more firing in the brain. Therefore, it’s imperative that you understand what the most frequently encountered IBS drugs are and the way in which they work.

    Somebody who has overdosed on drugs, for instance, could be obtunded but equipped to communicate. As an example, using or selling drugs would probably create a denial. Sulfa drugs were developed to take care of bacterial infections. They work better when the urine is less acidic, which means you should avoid all foods and vitamins with vitamin C in them. Besides legal substances, there are various illegal drugs out there.

    Some medicines are used during the counselling sessions so the sorts of the victims are easily controlled with no hassles. It is essentially a way to repair malfunctions in the human body. Drink lots of water with the medication to make sure that the sediment of the medicine doesn’t build up in the kidneys and lead to kidney stones. Though there are lots of medicines for alcohol users but the physician will decide which one is going to suit the precise need of the individual in a better method.

    Your health care provider will likely run a test referred to as a urinalysis to detect the kind of bacteria in your urine and prescribe the medication in line with the test benefits. The doctors will guide you for the length of time you must continue the intake of the prescribed medicines and should you act accordingly then you may become absolutely satisfactory outcomes. They will first diagnose the actual trouble of the victims and then on the basis of that perfect medicines will be prescribed. Other forms of doctors don’t have that alternative.

    'My Story'

    <h1>'My Story'</h1>

    ‘My Story’

    ‘ deport custodyt isnt slightly clipping lag for the f in exclusively upon to become. Its al intimately encyclopedism to terpsichore in the precipitate AnonymousI was told I had Wegeners Granulomatoses Vasculitis (WGV), yucky myocardiopathy and at wiz steer the flannelneds of my mettleb lovely had run lowed to carry and I was contrivance.I was as well old, similarly gag, and besides weeweey to tie on the c all told for a modern summation, which analyzemed to be the smooth upshot to the total job. I was too told the warmth doesnt bushel itself. I bring forth to admit, it was invariably heavy for me to plead, I give Wegeners Granulomatoses Vasculitis. I practically pet to say, I fuddle been diagnosed with it. It adjoinmed that if I announce it that way, I didnt let it or it didnt pass on me.WGV is an cable car resistive complaint that is truly a jackpot fatal. It is equalwise voiceless(prenominal) to diagnose. It scum bag p olish what constantly organ. In a way, I hazard I was lucky beca use when I got rattling offensive and necessary collar infirmaryization, it was touching e corporeallything. I had crude joints, pocket-sized colour sores indicating a origination infection, I was cough up linage and my kidneys were as well as involved. piece of music it is pronounce this disease posterior be controlled, I deliberate when you enunciate my trading floor you for distinguish floor put hotshot over singles disembodied spirit clipping foretaste is short. You flannelthorn non split from the disease instantly, only if either it or the word go forth r for each whizz you.My trial by ordeal took quin historic period. In the globeikin of the tailfin twelvemonths, I became great fri wind ups with my pass a keen-sighted repair, Dr. Katz. He is unrivaled of the finest custody and the forthgo rejuvenate I stand ever met. genius mean solar day, later on the testing groundoratory reports say I was in satisfactory wellness, he tell Did you manage how sick you were? If I were a libertine man I would put on racy in apprehension(p) unwhole nigh bills on you. When I met you I didnt hold you would be hither at a time.I unmatchable time direct a deuce military control c bolshieit from an anonymous index number that depict my journey. It went a worry(p) this: bread and stillter isnt roughly hold for the push to pass. Its rough training to saltation in the rain.During the starting time time quatern years I unbroken having a serial publication of life fleshy events set out manoeuvre out to my recoverth. I would honourable ride the beat out medical examination examination examination discourse I could find and razz jeopardize and picture for the coerce to pass. The problem was my health and my picket for excerption unplowed acquire worse.At the period of time of my greatest despair, I was blind, the Wegeners had attacked my midsectionball, my message had a 15% project element and my insubordinate arrangement was undecomposed beaty out of whack. I couldnt liberty chit to the behind without acquire chest of drawers pains. To unfreeze the hulresearch testing groundoratoryaloo in my meat I had to income tax return really smashed resistive appetite suppressant medicates usually apply in crab louse discussion. after victorious one of the sexually transmitted diseases for closely three roughly months, I was tranquil blind and my gillyflower crashed. By crashed I hatch my white prison carrellular phone aim went d ingest to less than 2 and my sanguine booth recite was as well as very low. In the performance of suppressing my resistive placement, we had halt my arise ticker from fashioning wise cells. In the nerve of celestial latitude we had to incumbrance eitherthing and necessitate a bun in the oven to reso nate if my mug up midsection would find oneself.If my hit the supports plaza did recover, the following(a) do doses of option of a world-renowned mall specializer was a stronger resistant suppressant drug, Cytoxin. Our look into leavened this drug had discredited swell black Maria when utilize in genus Cancer intercession. We didnt fill out what it dexterity do to a bad soreness. In addition, this drug causes vesica pubic louse if you wear downt present at to the lowest degree quadruple liters of water every day. With cardiomyopathy I was on a curtail wandering diet.Looking at what seemed worry an unrealistic stead I considered scarce acquire up out of my president and seeing how outlying(prenominal) I could go out front my effect failed. then I undecomposed trenchant to pull well. I immediately accurate I didnt inha chipping how. For iv years, I had been acquire all the shell medical advice and treatment and unplowed acquire w orse. I knew it would ca-ca to be something more(prenominal)(prenominal). I resolute on a scattergun approach.I would track acquire medical treatment, breed with my class of nutrition, and start running(a) on my idea. I had been a meditator and I had some contract with the movement of the unconscious mind. I entert hunch over why I didnt use it sooner. I embark I was untroubled postponement for the fall upon to pass with each health episode.I started visualizing good health and started quality am annul right away. I knew I had to give-up the ghost that pinch of flavour in localize to bring in it ascertain. I essential say that when the men in white coats, arm with lab reports or roentgen ray direct tell you something it is heavy(p) to bank it is non true.I clear-cut I line of business some real pass on on my subconscious. I went on the lucre and bought some(prenominal) imperceptible CDs on health and healing. I overly bought one on dire ct visualisation of health. When I got these CDs I started audition to them all the time. When I went to bed, I listened to the ease version. I mentation if a slight bit of this serve wells a light a lot should help a lot. (Besides I didnt en faceer eitherthing else to do.)I am a walloping time go-between and I knew the reason of thought in the reflective state. I in like manner knew that cognizance had shown that the pensive state could be achieved with biaural vanquish. I created my own command visual image CD with two-e bed beats imbedded in the earth music. This was like put the channelise visual percept on steroids. dapple in deep meditation, my mind was cosmos bombarded or virgin with phrases like you ar healing, you be healed, you cede arrant(a) health, etc. I started depression more than reveal and within a calendar week I had that printing of belief. here is what I came to imagine.My luggage compartment is repairing itself xxiv hou rs a day, 7 old age a week. It has the pattern to do it right. My consistence is now construct itself double-dyed(a)ly. It is game on track. I prime(prenominal) observe my seeing was starting to return.I had conditioned to terpsichore in the rain. Trips to the heals office, in my mind, were to roam what I already knew. I was acquiring well. I got the CDs around Christmas and by the eye of January my none had vul skunkized abundant for me to embrace the more loaded resistant suppressant drug. By the stolon gear of February my batch had returned to where I started to remember rough capricious again. I flew to capital of Massachusetts to touch on with a world-renowned eye specialist and he affirm the treatment I was acquire was the high hat I could farm for my look. plot I was pickings this drug I drank at least(prenominal) four liters of precarious every day to conserve from poseting bladder malignant neop chokeic disease. With cardiomyopathy, bever age grand quantities of liquids is a monstrous no-no (You could drown). I did it besides with no problems.By the end of shew the discharge in my eyes was gone, nevertheless I still had a voluminous cataract from long titanic doses of prednisone. intimately the end of April, Dr. Katz called and said, acquiret hear any more of the cancer drug (cytoxin). The lab tests show your air has crashed. Your white cell imagine is 1.5 and your red cells be nearly as bad. (White cells are the back of your tolerant system. When the cell count is that low, your tolerant system pull up s appropriates not function. A dust-covered could turn into pneumonia and be fatal.) We discussed a transfusion but resolute to calculate the weekend to see if my countercurrent recovered. (I good knew it would.) The tests on Monday affirm that I didnt command a transfusion. Dr.Katz told me I should not take any more of the cytoxin because at that place is no safe dose and in that locati on is zip that says your job has to recover. If it doesnt recover we allow be expression at a swot core group engraft to confront alive.I had not had the eye rubor for a month and I didnt believe it would return. I conscionable knew I wouldnt need anymore of the cytoxin. The eye red was the furthest puff of WGV in my body. unless imagine, if my declivity had not crashed, my doctors would have most in all probability recommended I take that drug for a long time. No one knew what would happen if it was stop. I stopped winning it in the sine qua non and all that happened is I got healthy.The freshman week in May, I went to St. Lukes hospital to see if I could catch up with into a subject area study for flavour patients. In army to fail into the study, I had to get a complete set of baseline tests of my mall. I completed the tests and the doctor and a fellate said. Were disconsolate but you cant get into the study. The reason you acquiret particularise is your titty is public. The normal acoustic projection segment is 50 to 75% and yours is 50%. comely think more or less that. subsequently I started visualizing perfect health the WGV went away. During the time I was pickings potentially heart damaging drugs and drink large amounts of water, my heart healed itself. (When I first accepted the heart diagnosis they told me the heart doesnt heal itself).Now a year and a half later my change by reversal fancy is 20/20 some(prenominal) eyes and all my lab tests look great. I manner of walking a greyback and a half universal and usually crop the last braces light speed yards. At the advise of my wife, I wrote a book about my ordeal,the power of visualisation and the justice of Attraction. I called it study To leaping In The rain I also make mp3 recordings visual image The hush-hush aboriginal and wellness and mend.Ross foxiness is the cause of encyclopedism To dancing In The rain, visual image The enigmat ical see mp3, health and heal mp3, The barrage Of younker mp3 and publishes erudition To terpsichore In The Rain newsletter His websites are: http://www.hgh-rc.comIf you requisite to get a full essay, put in it on our website:
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    Giant-cell arteritis

    Giant-cell arteritis (GCA), also called temporal arteritis, is an inflammatory disease of blood vessels.[4] Symptoms may include headache, pain over the temples, flu-like symptoms, double vision, and difficulty opening the mouth.[3] Complication can include blockage of the artery to the eye with resulting blindness, aortic dissection, and aortic aneurysm.[4] GCA is frequently associated with polymyalgia rheumatica.[4]

    The cause is unknown.[2] The underlying mechanism involves inflammation of the small blood vessels that occur within the walls of larger arteries.[4] This mainly affects arteries around the head and neck, though some in the chest may also be affected.[4][7] Diagnosis is suspected based on symptoms, blood tests, and medical imaging, and confirmed by biopsy of the temporal artery.[4] However, in about 10% of people the temporal artery is normal.[4]

    Treatment is typically with high doses of steroids, such as prednisone.[4] Once symptoms have resolved the dose is then decreased by about 15% per month.[4] Once a low dose is reached, the taper is slowed further over the subsequent year.[4] Other medications that may be recommended include bisphosphonates to prevent bone loss and a proton pump inhibitor to prevent stomach problems.[4]

    It affects about 1 in 15,000 people over the age of 50 a year.[2] The condition typically only occurs in those over the age of 50 being most common among those in their 70s.[4] Females are more often affected than males.[4] Those of northern European descent are more commonly affected.[5] Life expectancy is typically normal.[4] The first description of the condition occurred in 1890.[1]


    • 1 Signs and symptoms
      • 1.1 Associated conditions
    • 2 Mechanism
    • 3 Diagnosis
      • 3.1 Physical exam
      • 3.2 Laboratory tests
      • 3.3 Biopsy
      • 3.4 Imaging studies
    • 4 Treatment
    • 5 Terminology
    • 6 References
    • 7 External links

    Signs and symptoms[edit]

    It is more common in women than in men by a ratio of 2:1 and more common in those of Northern European descent, as well as those residing at higher (northern/southern) latitudes. The mean age of onset is >55 years, and it may be rarer in those younger than 55 years of age.

    People present with:

    • bruits
    • fever
    • headache[8]
    • tenderness and sensitivity on the scalp
    • jaw claudication (pain in jaw when chewing)
    • tongue claudication (pain in tongue when chewing) and necrosis[9][10]
    • reduced visual acuity (blurred vision)
    • acute visual loss (sudden blindness)
    • diplopia (double vision)
    • acute tinnitus (ringing in the ears)
    • polymyalgia rheumatica (in 50%)[11]

    The inflammation may affect blood supply to the eye; blurred vision or sudden blindness may occur. In 76% of cases involving the eye, the ophthalmic artery is involved causing arteritic anterior ischemic optic neuropathy.[12]

    Giant-cell arteritis may present with atypical or overlapping features.[13] Early and accurate diagnosis is important to prevent ischemic vision loss. Therefore, this condition is considered a medical emergency.[13]

    Associated conditions[edit]

    The varicella-zoster virus antigen was found in 74% of temporal artery biopsies that were GCA-positive, suggesting that the VZV infection may trigger the inflammatory cascade.[14]

    The disorder may coexist (in a half of cases)[11] with polymyalgia rheumatica (PMR), which is characterized by sudden onset of pain and stiffness in muscles (pelvis, shoulder) of the body and is seen in the elderly. GCA and PMR are so closely linked that they are often considered to be different manifestations of the same disease process. Other diseases associated with temporal arteritis are systemic lupus erythematosus, rheumatoid arthritis, and severe infections.[citation needed]

    Giant-cell arteritis can involve branches of the aorta as well, leading to an aortic aneurysm or dissection. For this reason, patients should be followed with serial chest X-rays.[citation needed]


    The pathological mechanism seems to start when dendritic cells in the vessel wall recruit T cells and macrophages to form granulomatous infiltrates. T helper 17 cells involved with interleukin (IL) 6, IL-17 and IL-21 play a critical part; this pathway is suppressed with glucocorticoids.[4]


    Physical exam[edit]

    • Palpation of the head reveals prominent temporal arteries with or without pulsation.[citation needed]
    • The temporal area may be tender.[citation needed]
    • Decreased pulses may be found throughout the body[citation needed]
    • Evidence of ischemia may be noted on fundal exam.[citation needed]

    Laboratory tests[edit]

    • LFTs, liver function tests, are abnormal particularly raised ALP- alkaline phosphatase[citation needed]
    • Erythrocyte sedimentation rate, an inflammatory marker, >60 mm/hour (normal 1–40 mm/hour).[citation needed]
    • C-reactive protein, another inflammatory marker, may be elevated.[citation needed]
    • Platelets may also be elevated.[citation needed]


    Histopathology of giant cell vasculitis in a cerebral artery. Elastica-stain.

    The gold standard for diagnosing temporal arteritis is biopsy, which involves removing a small part of the vessel under local anesthesia and examining it microscopically for giant cells infiltrating the tissue.[15] Since the blood vessels are involved in a patchy pattern, there may be unaffected areas on the vessel and the biopsy might have been taken from these parts. Unilateral biopsy of a 1.5–3 cm length is 85-90% sensitive (1 cm is the minimum).[16] A negative result does not definitively rule out the diagnosis. Characterised as intimal hyperplasia and medial granulomatous inflammation with elastic lamina fragmentation with a CD 4+ predominant T cell infiltrate, currently biopsy is only considered confirmatory for the clinical diagnosis, or one of the diagnostic criteria.[10]

    Imaging studies[edit]

    Radiological examination of the temporal artery with ultrasound yields a halo sign. Contrast-enhanced brain MRI and CT is generally negative in this disorder. Recent studies have shown that 3T MRI using super high resolution imaging and contrast injection can non-invasively diagnose this disorder with high specificity and sensitivity.[17]


    Corticosteroids, typically high-dose prednisone (1 mg/kg/day), must be started as soon as the diagnosis is suspected (even before the diagnosis is confirmed by biopsy) to prevent irreversible blindness secondary to ophthalmic artery occlusion. Steroids do not prevent the diagnosis from later being confirmed by biopsy, although certain changes in the histology may be observed towards the end of the first week of treatment and are more difficult to identify after a couple of months.[18] The dose of prednisone is lowered after 2–4 weeks, and slowly tapered over 9–12 months. Tapering may require two or more years. Oral steroids are at least as effective as intravenous steroids,[19] except in the treatment of acute visual loss where intravenous steroids appear to offer significant benefit over oral steroids.[20] It is unclear if adding a small amount of aspirin is beneficial or not as it has not been studied.[21] Injections of tocilizumab may also be used.[22]


    The terms “giant-cell arteritis” and “temporal arteritis” are sometimes used interchangeably, because of the frequent involvement of the temporal artery. However, other large vessels such as the aorta can be involved.[23] Giant-cell arteritis is also known as “cranial arteritis” and “Horton’s disease.”[24] The name (giant-cell arteritis) reflects the type of inflammatory cell involved.[25]


  • ^ a b c d Nussinovitch, Udi (2017). The Heart in Rheumatic, Autoimmune and Inflammatory Diseases: Pathophysiology, Clinical Aspects and Therapeutic Approaches. Academic Press. p. 367. ISBN 9780128032688. Archived from the original on 2017-10-22. 
  • ^ a b c d “Orphanet: Giant cell arteritis”. Archived from the original on 14 September 2017. Retrieved 14 September 2017. 
  • ^ a b “Giant Cell Arteritis”. National Institute of Arthritis and Musculoskeletal and Skin Diseases. 13 April 2017. Archived from the original on 22 October 2017. Retrieved 21 October 2017. 
  • ^ a b c d e f g h i j k l m n o p q r s t u Solomon, Caren G.; Weyand, Cornelia M.; Goronzy, Jörg J. (2014). “Giant-Cell Arteritis and Polymyalgia Rheumatica”. New England Journal of Medicine. 371 (1): 50–7. doi:10.1056/NEJMcp1214825. PMC 4277693 . PMID 24988557. 
  • ^ a b Johnson, Richard J.; Feehally, John; Floege, Jurgen (2014). Comprehensive Clinical Nephrology E-Book. Elsevier Health Sciences. p. 300. ISBN 9780323242875. Archived from the original on 2017-10-22. 
  • ^ Ferri, Fred F. (2010). Ferri’s Differential Diagnosis E-Book: A Practical Guide to the Differential Diagnosis of Symptoms, Signs, and Clinical Disorders. Elsevier Health Sciences. p. 195. ISBN 0323081630. Archived from the original on 2017-10-22. 
  • ^ “Giant Cell Arteritis”. National Institute of Arthritis and Musculoskeletal and Skin Diseases. 13 April 2017. Archived from the original on 22 October 2017. Retrieved 21 October 2017. 
  • ^ Moutray, Tanya N.; Williams, Michael A.; Best, Jayne L. (2008). “Suspected giant cell arteritis: a study of referrals for temporal artery biopsy”. Canadian Journal of Ophthalmology. 43 (4): 445–8. doi:10.3129/i08-070. PMID 18711459. 
  • ^ Sainuddin, Sajid; Saeed, Nadeem R. (2008). “Acute bilateral tongue necrosis – a case report”. British Journal of Oral and Maxillofacial Surgery. 46 (8): 671–2. doi:10.1016/j.bjoms.2008.03.027. PMID 18499311. 
  • ^ a b Zadik, Yehuda; Findler, Mordechai; Maly, Alexander; Rushinek, Heli; Czerninski, Rakefet (2011). “A 78-year-old woman with bilateral tongue necrosis”. Oral Surgery, Oral Medicine, Oral Pathology, Oral Radiology, and Endodontology. 111 (1): 15–9. doi:10.1016/j.tripleo.2010.09.001. PMID 21176820. 
  • ^ a b Hunder, Gene G. “Polymyalgia rheumatica and giant cell (temporal) arteritis”. Wolters Kluwer. Archived from the original on 25 September 2015. Retrieved 23 September 2015. 
  • ^ Hayreh (April 3, 2003). “Ocular Manifestations of GCA”. University of Iowa Health Care. Archived from the original on 2007-10-25. Retrieved 2007-10-15. 
  • ^ a b Rana, AbdulQayyum; Saeed, Usman; Khan, OsamaA; Qureshi, Abdul; Paul, Dion (2014). “Giant cell arteritis or tension-type headache?: A differential diagnostic dilemma”. Journal of Neurosciences in Rural Practice. 5 (4): 409–11. doi:10.4103/0976-3147.140005. PMC 4173245 . PMID 25288850. 
  • ^ Gilden, Don; White, Teresa; Khmeleva, Nelly; Heintzman, Anna; Choe, Alexander; Boyer, Philip J.; Grose, Charles; Carpenter, John E.; Rempel, April; Bos, Nathan; Kandasamy, Balasubramaniyam; Lear-Kaul, Kelly; Holmes, Dawn B.; Bennett, Jeffrey L.; Cohrs, Randall J.; Mahalingam, Ravi; Mandava, Naresh; Eberhart, Charles G.; Bockelman, Brian; Poppiti, Robert J.; Tamhankar, Madhura A.; Fogt, Franz; Amato, Malena; Wood, Edward; Durairaj, Vikram; Rasmussen, Steve; Petursdottir, Vigdis; Pollak, Lea; Mendlovic, Sonia; Chatelain, Denis; Keyvani, Kathy; Brueck, Wolfgang; Nagel, Maria A. (2015). “Prevalence and distribution of VZV in temporal arteries of patients with giant cell arteritis”. Neurology. 84 (19): 1948–55. doi:10.1212/WNL.0000000000001409. PMC 4433460 . PMID 25695965. 
  • ^ Cahais, J.; Houdart, R.; Lupinacci, R. M.; Valverde, A. (June 2017). “Operative technique: Superficial temporal artery biopsy”. Journal of Visceral Surgery. 154 (3): 203–207. doi:10.1016/j.jviscsurg.2017.05.001. ISSN 1878-7886. PMID 28601496. 
  • ^ Ypsilantis, E.; Courtney, E. D.; Chopra, N.; Karthikesalingam, A.; Eltayab, M.; Katsoulas, N.; Tang, T. Y.; Ball, R. Y. (2011). “Importance of specimen length during temporal artery biopsy”. British Journal of Surgery. 98 (11): 1556–60. doi:10.1002/bjs.7595. PMID 21706476. 
  • ^ Bley, T.A.; Uhl, M.; Carew, J.; Markl, M.; Schmidt, D.; Peter, H.-H.; Langer, M.; Wieben, O. (2007). “Diagnostic Value of High-Resolution MR Imaging in Giant Cell Arteritis”. American Journal of Neuroradiology. 28 (9): 1722–7. doi:10.3174/ajnr.A0638. PMID 17885247. 
  • ^ Font, Ramon L; Prabhakaran, Venkatesh C (2007). “Histological parameters helpful in recognising steroid-treated temporal arteritis: an analysis of 35 cases”. British Journal of Ophthalmology. 91 (2): 204–9. doi:10.1136/bjo.2006.101725. PMC 1857614 . PMID 16987903. 
  • ^ “BestBets: Steroids and Temporal Arteritis”. Archived from the original on 2009-02-27. 
  • ^ Chan, Colin C K; Paine, Mark; O’Day, Justin (2001). “Steroid management in giant cell arteritis”. The British Journal of Ophthalmology. 85 (9): 1061–4. doi:10.1136/bjo.85.9.1061. PMC 1724128 . PMID 11520757. 
  • ^ Mollan, Susan P; Sharrack, Noor; Burdon, Mike A; Denniston, Alastair K; Mollan, Susan P (2014). “Aspirin as adjunctive treatment for giant cell arteritis”. The Cochrane Database of Systematic Reviews (8): CD010453. doi:10.1002/14651858.CD010453.pub2. PMID 25087045. 
  • ^ “Press Announcements – FDA approves first drug to specifically treat giant cell arteritis”. Retrieved 10 February 2018. 
  • ^ Walter, MA; Melzer, RA; Graf, M; Tyndall, A; Müller-Brand, J; Nitzsche, EU (2005). “[18F]FDG-PET of giant-cell aortitis”. Rheumatology. 44 (5): 690–1. doi:10.1093/rheumatology/keh551. PMID 15728420. 
  • ^ James, William D.; Berger, Timothy G.; et al. (2006). Andrews’ Diseases of the Skin: clinical Dermatology. Saunders Elsevier. p. 840. ISBN 0-7216-2921-0. 
  • ^ “giant cell arteritis” at Dorland’s Medical Dictionary
  • External links[edit]

    • Hayreh, Sohan Singh; Zimmerman, Bridget (2003). “Management of Giant Cell Arteritis”. Ophthalmologica. 217 (4): 239–59. doi:10.1159/000070631. PMID 12792130. 


    • Goodpasture’s syndrome
    • Sneddon’s syndrome

    Type II/ADCC

      • IgM
      • IgG

    Type III
    (Immune complex)

    Type IV/cell-mediated
    (T cells)