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The Chronicles of Prednisone Uses

At times, steroids work for an individual, and at times they don’t. Corticosteroids, sometimes called adrenocorticosteroids or simply steroids, are essential hormones that are created by the adrenal cortex of the human body. Systemic corticosteroids (apart from dexamethasone and prednisone) and bisphosphonates weren’t permitted.

You should not quit using prednisone suddenly. As a corticosteroid, prednisone plays a crucial part in the normal physiology of the human body. It is a prednisone uses corticosteroid. It acts as a replacement for people with low levels of cortisol, one of the natural steroid hormones. It can be used on a short-term basis to treat hives. It is a type of drug known as a corticosteroid. It is used to treat a wide variety of medical conditions.

Both types of sinusitis usually have these symptoms connected with the infections. Repeated use can result in a rebound effect which can lead to even more headaches. There are lots of famous side effects to using the above-mentioned drugs so make certain you receive all the necessary information from your medical care provider beforehand. Amongst others, it’s essential in the control of salt and water balance within the body, together with in maintaining appropriate glucose, protein, and fat metabolism. Gastrointestinal difficulties and respiratory disorders are additional difficulties that may be solved with prednisone. The distinction is that I understand the secret. Be cautious about taking an excessive amount of tylenol since it can lead to liver problems at high dosages.

Tell your physician about any prednisone employs illness or infection you’ve had within prednisone 50 mg side effects the previous several weeks. The disease is far more common in smokers. Infections vary in duration because of differences in every man or woman and their private health conditions in addition to their surrounding living conditions and environment. The majority of the moment, based on the severity and if there’s an acute infection involved, the treatment involves inhalers and oxygen that might or might not be used daily or only as needed. Any infection can get worse so do ensure you steer clear of affected people when you’re under medication. Infection of the fallopian tubes, called salpingitis, is treated with antibiotics, also, sometimes several as a result of chance of distinct causes of infection. Antibiotics can be prescribed for women for a number of reasons.

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Your pharmacist might be in a position to counsel you on managing side effects. Your physician will be in a position to diagnose the problem from an easy video chat, which will give him all the information he’ll want to correctly advise you. A physician would simply tell you all the different steps that you must take as a way to relieve your symptoms. The physician might also opt to add new medicines to maintain a check on your side effects, and therefore do tell your health care provider if symptoms persist. Moreover, though a digital doctor can’t put in stitches, they can surely have a look at your cut to see whether you need them. To be able to do so, you want to understand a naturopathic doctor who knows about intestinal permeability.

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 long time, you might need to acquire regular eye exams. You may also spend the medicine directly with a glass of plain water. Any medicine turned out to work can just be called `medicine’. Another important consideration to remember in the timing of when you take the medication. Don’t attempt to crush or break the medicine whenever you have it.

Do check out the contents to ascertain if you’re allergic to the medication in any manner. Before you start using a medication, be certain to inform your doctor of any medical conditions or allergies you might have, any medications you’re taking, whether you’re pregnant or breast-feeding, and any other critical truth about your wellness. Steroid medication can weaken prednisone steroids your prednisone utilizes immune system, which makes it less difficult for you to find an infection.

If you aren’t certain what to do after missing a dose, speak to your physician or pharmacist for advice. The dose needs to be taken early morning by 9 if it’s a single dose. If it’s almost time for your next dose, skip the missed dose and return to your normal dosing schedule. Don’t use a household spoon as you may not receive the right dose.

Dosage needs to be decreased or discontinued gradually whenever the drug was administered for over a couple of days. Dosage of Apo-Prednisone needs to be individualized based on the seriousness of the disease and the response of the individual. For infants and kids, the suggested dosage needs to be governed by exactly the same considerations as opposed to 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.

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Prednisone Dosage

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Prednisone isn’t soluble in water, and so is unable to be given intravenously. It is a prodrug that is converted by the liver into prednisolone, which is the active drug and also a steroid. The medication Prednisone exists as a kind of glucocorticoid.

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Prednisone is called glucocorticoids, for the reason that they are armed. Along with its needed effects, it may cause some unwanted effects. Academy prednisone taper order destined to reside despite the grossest negligence is prednisone for dogs the very same as humans can likewise be excited by the movements of the individual.

When you’re on prednisone, your skin will usually clear up inside a few days. Prednisone is a steroid that’s utilized to prevent inflammation. It is a type of oral corticosteroids that is used to reduce inflammation.

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Prednisone was know to result in long-term effects which itas advisable to completely understand to give you the absolute most informed decision when looking at using the drug. It can also be used to treat sarcoid rash, but it may cause the thinning of the skin. It should only be given by the right people who know what they are doing (which is, most of the times, your veterinarian) and for just the right amount of time, or else serious side effects will take place. Prednisone should only be given by the most suitable individuals who are aware of what they are doing (which is, the majority of the times, your veterinarian) and for just the correct quantity of time, or else significant prednisone side effects in dogs will occur.

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Carprofen

A 100 mg Rimadyl pill approximately 19 mm (0.75 in) wide and 8.6 mm (0.34 in) thick, sold in the United States

Carprofen, marketed under many brand names worldwide,[1] is a nonsteroidal anti-inflammatory drug (NSAID) that veterinarians prescribe as a supportive treatment for various conditions in animals.[2] It provides day-to-day treatment for pain and inflammation from various kinds of joint pain as well as post-operative pain.[2] Carprofen reduces inflammation by inhibition of COX-1 and COX-2; its specificity for COX-2 varies from species to species.[2]

Contents

  • 1 Use in dogs
  • 2 Adverse effects
  • 3 Human use
  • 4 Equine use
  • 5 Brands and dosage forms for veterinary use
  • 6 References

Use in dogs[edit]

Adverse effects[edit]

Most dogs respond well to carprofen use, but like all NSAIDs, it may cause gastrointestinal, liver and kidney problems in some patients.

After introduction, significant anecdotal reports of sudden animal deaths from its use arose. To date[when?], the FDA has received more than 6,000 adverse reaction reports about the drug (manufactured by Pfizer). As a result, the FDA requested that Pfizer advise consumers in their advertising that death is a possible side effect.[3] Pfizer refused and pulled their advertising; however, they now include death as a possible side effect on the drug label. Plans call for a “Dear Doctor” letter to advise veterinarians, and a safety sheet attached to pill packages.

Adverse effects include:

  • Loss of appetite
  • Vomiting
  • Diarrhea
  • Increase in thirst
  • Increase in urination
  • Fatigue and/or lethargy (drowsiness)
  • Loss of coordination
  • Seizures
  • Liver dysfunction: jaundice (yellowing of eyes)
  • Blood or dark tar-like material in urine or stools
  • Lethargy.
  • Staggering, stumbling, weakness or partial paralysis, full paralysis.[4]
  • Change in skin (redness, scabs, or scratching)
  • Change in behavior (such as decreased or increased activity level, seizure or aggression).[5]

Effects of overdose include gastritis and ulcer formation.[6]

In healthy dogs given carprofen, no perioperative adverse effects on the cardiovascular system have been reported at recommended dosages.[7] [8] Perioperative administration of carprofen to cats did not effect postoperative respiratory rate nor heart rate.[9]

Carprofen should not be administered concurrently with steroids, as this can cause ulcers in the stomach. Dogs should be taken off carprofen for three full days before ingesting a steroid (such as prednisolone). Carprofen should not be given at the same time with other types of medications such as other NSAIDs (aspirin, etodolac, deracoxib, meloxicam, tepoxalin) or steroids such as dexamethasone, triamcinolone, cortisone or prednisone.

Carprofen must be used with caution within the supervision of a veterinarian in dogs with liver or kidney disease, dehydration, bleeding deficits, or other health problems. It is not recommended for use in dogs with bleeding disorders (such as Von Willebrand’s disease), as safety has not been established in dogs with these disorders.[10] It has not been established whether carprofen can be safely used in pregnant dogs, dogs used for breeding purposes, or in lactating female dogs.

Several laboratory studies and clinical trials have been conducted to establish the safety of using Carprofen. Clinical studies were conducted in nearly 300 dogs, coming from different breeds. The dogs were treated with Rimadyl at the recommended dose for 2 weeks. According to these studies, the drug was clinically well tolerated and the treated dogs did not have a greater incidence of adverse reactions when compared to the control group.[11]

A number of factors that may contribute to the high incidence of adverse reports received for carprofen by the Center for Veterinary Medicine in the late 1990s. These include:

  • The type of drug;
  • Wide use;
  • Duration of use. While the side effects from carprofen are known to occur within a short period of time after administration, it is believed that long-term use may actually result in a higher risk for adverse reactions[citation needed];
  • Senior dog use. Older dogs are generally more prone to side effects caused by carprofen.

Human use[edit]

Carprofen was used in humans for almost 10 years, starting in 1988. It was used for the same conditions as in dogs, viz., joint pain and inflammation. Side effects tended to be mild, usually consisting of nausea or gastro-intestinal pain and diarrhea. Carprofen was available only by prescription in 150 to 600 mg doses.[12] Dosage over 250 mg was only for relieving pain after severe trauma, such as post-surgery inflammation. 150 mg doses were commonly used to relieve the pain of arthritis, while 200 mg doses were commonly prescribed in cases of severe arthritis or severe inflammation pain. The drug was taken orally. Pfizer voluntarily removed it from the market for human use on commercial grounds.[12]

Equine use[edit]

Carprofen may be administered intravenously to horses.[13] A single dose has been shown to reduce prostaglandin E2 production and inflammatory exudate for up to 15 hours,[14] although there was less effect on eicosanoid production when compared to the effects produced by NSAIDs such as phenylbutazone or flunixin.[15] Prostaglandin E2 and inflammatory exudate are also reduced and leukotriene B4 is inhibited. Carprofen can also be given orally, but intramuscular use may produce muscle damage.[16]

Brands and dosage forms for veterinary use[edit]

It is marketed under many brand names including: Acticarp, Austiofen, Bomazeal, Canidryl, Carporal, Carprieve , Carprocow, Carprodolor, Carprodyl, Carprofelican, Carprofen, Carprofène, Carprofeno, Carprofenum, Carprogesic, Carprosol, Carprotab, Carprox, Comforion, Dolagis, Dolocarp, Dolox, Eurofen, Kelaprofen, Librevia, Norocarp, Norodyl, Novocox, Prolet, Reproval, Rimadyl, Rimifin, Rofeniflex, Rycarfa, Scanodyl, Tergive, Vetprofen, and Xelcor.[1]

Veterinary dosage forms include 25 mg, 75 mg, and 100 mg tablets, and 50 mg per mL injectable form.[17]

References[edit]

  • ^ a b Drugs.com International brand names for Carprofen Page accessed October 4, 2017
  • ^ a b c Carprofen/Rimadyl (Carprofen) prescribing instructions
  • ^ “Update On Rimadyl, FDA’s Center for Veterinary Medicine, December 1, 1999”. 
  • ^ “A Review of Signs of a Potentially Life-threatening Reaction to Rimadyl”. Retrieved 2010-05-20. 
  • ^ “Dog Owner Information About Rimadyl (carprofen)”. Retrieved 2010-05-20. 
  • ^ “Generic Dog Rimadyl Online”. Retrieved 2010-05-20. 
  • ^ Boström, IM; Nyman, GC; Lord, PE; Häggström, J; Jones, BE; Bohlin, HP (May 2002). “Effects of carprofen on renal function and results of serum biochemical and hematologic analyses in anesthetized dogs that had low blood pressure during anesthesia”. American journal of veterinary research. 63 (5): 712–21. doi:10.2460/ajvr.2002.63.712. PMID 12013473. 
  • ^ Frendin, JH; Boström, IM; Kampa, N; Eksell, P; Häggström, JU; Nyman, GC (December 2006). “Effects of carprofen on renal function during medetomidine-propofol-isoflurane anesthesia in dogs”. American journal of veterinary research. 67 (12): 1967–73. doi:10.2460/ajvr.67.12.1967. PMID 17144795. 
  • ^ Höglund, Odd V; Dyall, Barbara; Gräsman, Victoria; Edner, Anna; Olsson, Ulf; Höglund, Katja (22 November 2017). “Effect of non-steroidal anti-inflammatory drugs on postoperative respiratory and heart rate in cats subjected to ovariohysterectomy”. Journal of Feline Medicine and Surgery: 1098612X1774229. doi:10.1177/1098612X17742290. 
  • ^ “Rimadyl (Carprofen)”. Retrieved 2010-05-20. 
  • ^ “Rimadyl [package insert]. New York, NY: Pfizer Animal Health, 2007” (PDF). Retrieved 2014-08-13. 
  • ^ a b Committee for Veterinary Medicinal Products: Carprofen, European Agency for the Evaluation of Medicinal Products
  • ^ McIlwraith CW, Frisbie DD, Kawcak CE. Nonsteroidal Anti-Inflammatory Drugs. Proc. AAEP 2001 (47): 182-187.
  • ^ Lees, P; McKellar, Q; May, SA; Ludwig, B (May 1994). “Pharmacodynamics and pharmacokinetics of carprofen in the horse”. Equine veterinary journal. 26 (3): 203–8. doi:10.1111/j.2042-3306.1994.tb04370.x. PMID 8542839. 
  • ^ Lees, P; Ewins, CP; Taylor, JB; Sedgwick, AD (1987). “Serum thromboxane in the horse and its inhibition by aspirin, phenylbutazone and flunixin”. The British veterinary journal. 143 (5): 462–76. doi:10.1016/0007-1935(87)90024-8. PMID 3119142. 
  • ^ McKellar, QA; Bogan, JA; von Fellenberg, RL; Ludwig, B; Cawley, GD (July 1991). “Pharmacokinetic, biochemical and tolerance studies on carprofen in the horse”. Equine veterinary journal. 23 (4): 280–4. doi:10.1111/j.2042-3306.1991.tb03718.x. PMID 1915228. 
  • ^ Carprofen (Veterinary—Systemic) The United States Pharmacopeial Convention, 2007
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    See also
    Receptor/signaling modulators
    Leukotriene signaling modulators
    Nuclear receptor modulators


    Source: https://en.wikipedia.org/wiki/Carprofen

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    Azathioprine

    <h1>Azathioprine</h1>

    Azathioprine (AZA), sold under the brand name Imuran among others, is an immunosuppressive medication.[2] It is used in rheumatoid arthritis, granulomatosis with polyangiitis, Crohn’s disease, ulcerative colitis, and in kidney transplants to prevent rejection.[2][3][4] It is taken by mouth or injected into a vein.[2]

    Common side effect include bone marrow suppression and vomiting.[2] Bone marrow suppression is especially common in people with a genetic deficiency of the enzyme thiopurine S-methyltransferase.[2] Other serious risk factors include an increased risk of lymphoma.[2] Use during pregnancy may result in harm to the baby.[2] Azathioprine is in the purine analogue and antimetabolite family of medication.[2][5] It works via 6-thioguanine to disrupt the making of RNA and DNA by cells.[2][5]

    Azathioprine was first made in 1957.[5] It is on the World Health Organization’s List of Essential Medicines, the most effective and safe medicines needed in a health system.[6] The wholesale cost in the developing world is about 7.63 to 17.19 USD a month.[7] The wholesale cost in the United States is about 35.34 USD per month.[8]

    Contents

    • 1 Medical uses
      • 1.1 Transplantation
      • 1.2 Rheumatoid arthritis
      • 1.3 Inflammatory bowel disease
      • 1.4 Others
    • 2 Adverse effects
      • 2.1 Pharmacogenetics
      • 2.2 Cancers
        • 2.2.1 Skin cancers
    • 3 Overdose
    • 4 Interactions
    • 5 Pregnancy and breastfeeding
    • 6 Pharmacology
      • 6.1 Pharmacokinetics
      • 6.2 Mechanism of action
    • 7 Chemistry
    • 8 History
    • 9 References
    • 10 External links

    Medical uses[edit]

    Azathioprine is used alone or in combination with other immunosuppressive therapy to prevent rejection following organ transplantation, and to treat an array of autoimmune diseases, including rheumatoid arthritis, pemphigus, systemic lupus erythematosus, Behçet’s disease, and other forms of vasculitis, autoimmune hepatitis, atopic dermatitis, myasthenia gravis, neuromyelitis optica (Devic’s disease), restrictive lung disease, and others.[9] It is also an important therapy and steroid-sparing agent for inflammatory bowel disease (such as Crohn’s disease and ulcerative colitis) and for multiple sclerosis.[10]

    In the United States, it is currently approved by the Food and Drug Administration (FDA) for use in kidney transplantation from human donors, and for rheumatoid arthritis.[11]

    Transplantation[edit]

    Azathioprine is used to prevent rejections of kidney or liver allografts, usually in conjunction with other therapies including corticosteroids, other immunosuppressants, and local radiation therapy.[12][13] The administration protocol starts either at the time of transplantation or within the following two days.[11]

    Rheumatoid arthritis[edit]

    Being a disease-modifying antirheumatic drug (DMARD), azathioprine has been used for the management of the signs and symptoms of adult rheumatoid arthritis.[14] Nonsteroidal anti-inflammatory drugs (NSAIDs) and corticosteroids may be combined or continued (if they were already in use) with azathioprine, but the combination with other DMARDs is not recommended.[11]

    Inflammatory bowel disease[edit]

    Azathioprine has been used in the management of moderate to severe chronically active Crohn’s disease,[15] to maintain clinical remission (absence of disease activity) in corticosteroid-dependent patients,[16] and to provide benefit in people with fistulizing Crohn’s disease.[17] The onset of action is slow and it may require several months to achieve clinical response.[15]

    Azathioprine treatment is associated with an increased risk of lymphoma, but it is unclear if this is due to the drug or a predisposition related to Crohn’s disease.[18] Lower doses of azathioprine are used as a therapy in children with refractory or corticosteroid-dependent Crohn’s disease, without causing many side effects.[19]

    In Crohn’s disease, treatment with azathioprine shortly after diagnosis was no more likely to result in corticosteroid-free remission than standard care or placebo.[20]

    It may also be used to prevent flares in those with ulcerative colitis.[21]

    Others[edit]

    Azathioprine is sometimes used in systemic lupus erythematosus patients who require a maintenance dose of 15 mg or higher of prednisone and those who experience recurrent flares.[22]

    It is used as an add on therapy when steroid therapy is given by mouth for pemphigus and myasthenia gravis, as a “steroid-sparing” agent.[9][23][24] Azathioprine is also used to maintain remission in people who have granulomatosis with polyangiitis.[4]

    It was shown to be very effective in eczema and atopic dermatitis in researches, even though it is not commonly used.[9] The British National Eczema Society lists it as a third-line treatment for severe to moderate cases of these skin diseases.[25]

    It was widely used for the treatment of multiple sclerosis until the first half of the 1990s. Concerns about increased risk of malignancy has led to a decreased use, yet it is still used in maintenance treatment for patients who frequently relapse.[26]

    A widely used therapy for idiopathic pulmonary fibrosis was azathioprine in combination with prednisone and N-acetylcysteine. A 2012 study showed that there were worse outcomes with this combination than with placebo.[27]

    Adverse effects[edit]

    Two generic azathioprine oral tablets, 50 mg each

    Nausea and vomiting are common adverse effects, especially at the beginning of a treatment. Such cases are met with taking azathioprine after meals or transient intravenous administration. Side effects that are probably hypersensitivity reactions include dizziness, diarrhea, fatigue, and skin rashes. Hair loss is often seen in transplant patients receiving the drug, but rarely occurs under other indications. Because azathioprine suppresses the bone marrow, patients can develop anaemia and will be more susceptible to infection; regular monitoring of the blood count is recommended during treatment.[11][28] Acute pancreatitis can also occur, especially in patients with Crohn’s disease.[29]

    Under FDA rules, like many other immunosuppressants, the use of this drug excludes eligibility for blood donation.[30]

    It is listed by the International Agency for Research on Cancer as a group 1 carcinogen (carcinogenic to humans).[31]

    Pharmacogenetics[edit]

    The enzyme thiopurine S-methyltransferase (TPMT) is responsible for various activation and deactivation steps in azathioprine’s mechanism of action. The first metabolic step that azathioprine undergoes in the body is the conversion to 6-mercaptopurine (6-MP; see Pharmacokinetics), which is itself an immunosuppressant prodrug.[32][33] The TPMT enzyme is responsible, in part, for the methylation of 6-MP into the inactive metabolite 6-methylmercaptopurine – this methylation prevents 6-MP from further conversion into active, cytotoxic thioguanine nucleotide (TGN) metabolites.[32][34] Certain genetic variations within the TPMT gene can lead to decreased or absent TPMT enzyme activity, and individuals who are homozygous or heterozygous for these types of genetic variations may have increased levels of TGN metabolites and an increased risk of severe bone marrow suppression (myelosuppression) when receiving azathioprine.[35] In many ethnicities, TPMT polymorphisms that result in decreased or absent TPMT activity occur with a frequency of approximately 5%, meaning that about 0.25% of patients are homozygous for these variants.[35][36] However, an assay of TPMT activity in red blood cells or a TPMT genetic test can identify patients with reduced TPMT activity, allowing for the adjustment of azathioprine dose or avoidance of the drug entirely.[35][37] The FDA-approved drug label for azathioprine recommends testing for TPMT activity to identify patients at risk for myelotoxicity.[38] Indeed, testing for TPMT activity is currently one of the few examples of pharmacogenetics being translated into routine clinical care.[39] Missense SNP in NUDT15 (e.g., rs116855232, inducing R139C)) has been identified to be a causal factor for AZA-induced leukopenia through a genome wide association study (GWAS) in East Asians.[40]

    Cancers[edit]

    Azathioprine is listed as a human carcinogen in the 12th Report on Carcinogens by the National Toxicology Program of U.S. Department of Health and Human Services, asserting that it is “known to be a human carcinogen based on sufficient evidence of carcinogenicity from studies in humans.”[41] Since August 2009, the U.S. Food and Drug Administration has required warnings to be placed on packaging with respect to increased risks of certain cancers.[42]

    The risks involved seem to be related both to the duration and to the dosage used. People who have previously been treated with an alkylating agent may have an excessive risk of cancers if treated with azathioprine. Epidemiological studies by International Agency for Research on Cancer (IARC) have provided “sufficient” evidence of azathioprine carcinogenicity in humans (Group 1),[43] although the methodology of past studies and the possible underlying mechanisms are questioned.[44]

    The various diseases requiring transplantation may in themselves increase the risks of non-Hodgkin’s lymphoma, squamous cell carcinomas of the skin, hepatobiliary carcinomas, and mesenchymal tumours to which azathioprine may add additional risks. Those receiving azathioprine for rheumatoid arthritis may have a lower risk than those undergoing transplantation.[31]

    Cases of hepatosplenic T-cell lymphoma – a rare type of lymphoma – have been reported in patients treated with azathioprine. The majority occurred in patients with inflammatory bowel disease. Adolescents and young adult males were the majority of cases.[45] They presented with a very aggressive disease course and, with one exception, died of the lymphoma. The FDA has required changes to the labeling to inform users and clinicians of the issue.[46]

    Skin cancers[edit]

    In transplant patients, skin cancer is 50 to 250 times more common than in the general population, and between 60% and 90% of patients are affected 20 years after transplantation. The use of immunosuppressive medication including azathioprine in organ transplantation has been linked to increased rates of developing skin cancer.[47] Azathioprine causes the accumulation of 6-thioguanine (6-TG) in patients’ DNA, which might trigger cancer when the patient is later exposed to ultraviolet light. Patients taking azathioprine were found to be abnormally sensitive to UVA light.[48]

    Overdose[edit]

    Large single doses are generally well tolerated; a patient who took 7.5 g azathioprine (150 tablets) at once showed no relevant symptoms apart from vomiting, slightly decreased white blood cell count and marginal changes in liver function parameters. Main symptoms of long-term overdosing are infections of unclear origin, mouth ulcers and spontaneous bleeding, all of which are consequences of the bone marrow suppression.[28]

    Interactions[edit]

    Other purine analogues such as allopurinol inhibit xanthine oxidase, the enzyme that breaks down azathioprine, thus increasing the toxicity of azathioprine.[49] On the other hand, low doses of allopurinol have been shown to safely enhance the efficacy of azathioprine, especially in inflammatory bowel disease non-responders.[50][51][52] This may still lead to lower lymphocyte counts and higher rates of infection, therefore the combination requires careful monitoring.[53][54]

    Azathioprine decreases the effects of the anticoagulant warfarin and of non-depolarizing muscle relaxants, but increases the effect of depolarizing muscle relaxants.[28] It can also interfere with niacin (vitamin B3), resulting in at least one case to pellagra and fatal medullary aplasia.[55] It has also been reported to cause vitamin B12 deficiency.[56]

    Pregnancy and breastfeeding[edit]

    Azathioprine can cause birth defects.[57][58][59] A 2003 population-based study in Denmark showed that the use of azathioprine and related mercaptopurine resulted in a seven-fold incidence of fetal abnormalities as well as a 20-fold increase in miscarriage.[60] Birth defects in a child whose father was taking azathioprine have also been reported.[61] Although no adequate and well-controlled studies have taken place in humans, when given to animals in doses equivalent to human dosages, teratogenesis was observed.[62] Transplant patients already on this drug should not discontinue on becoming pregnant. This contrasts with the later-developed drugs tacrolimus and mycophenolate, which are contraindicated during pregnancy.[57]

    Traditionally, as for all cytotoxic drugs, the manufacturer advises not to breastfeed whilst taking azathioprine. However, the “Lactation Risk Category” reported by Thomas Hale in his book “Medications and Mothers’ Milk” lists azathioprine as “L3”, termed “moderately safe”.[63]

    Pharmacology[edit]

    Pharmacokinetics[edit]

    Metabolic pathway for azathioprine (AZA).[64][65] Active metabolites are highlighted.

    • XO: xanthine oxidase
    • 6-MP: 6-mercaptopurine
    • TPMT: thiopurine methyltransferase
    • 6-MMP: 6-methylmercaptopurine
    • HPRT: hypoxanthine-guanine phosphoribosyltransferase
    • TIMP: thioinosine monophosphate, thioinosinic acid
    • MeTIMP: methyl-thioinosine monophosphate
    • TGTP: thioguanosine triphosphate
    • TdGTP: thio-deoxyguanosine triphosphate

    Azathioprine is absorbed from the gut to about 88%. Bioavailability varies greatly between individual patients, between 30 and 90%, because the drug is partly inactivated in the liver. Highest blood plasma concentrations, counting not only the drug itself but also its metabolites, are reached after one to two hours; and the average plasma half-life is 26 to 80 minutes for azathioprine and three to five hours for drug plus metabolites. 20 to 30% are bound to plasma proteins while circulating in the bloodstream.[9][28][66][67]

    Azathioprine is a prodrug, a substance that is not an active drug itself but is activated in the body. This happens in several steps; at first it is slowly and almost completely converted to 6-mercaptopurine (6-MP) by reductive cleavage of the thioether (–S–). This is mediated by glutathione and similar compounds in the intestinal wall, the liver and on red blood cells, without the aid of enzymes. 6-MP is metabolized analogously to natural purines, giving thioguanosine triphosphate (TGTP) and thio-deoxyguanosine triphosphate (TdGTP) via thioinosine monophosphate (TIMP) and several further intermediates. On a second path, the sulfur atom of 6-MP and TIMP is methylated. The end products of azathioprine metabolism are thiouric acid (38%) and various methylated and hydroxylated purines, which are excreted via the urine.[36][66][67]

    Mechanism of action[edit]

    Azathioprine inhibits purine synthesis. Purines are needed to produce DNA and RNA. By inhibiting purine synthesis, less DNA and RNA are produced for the synthesis of white blood cells, thus causing immunosuppression.

    Azathioprine is converted within tissues to 6-mercaptopurine (6-MP). Some 6-MP is converted in turn to 6-thioguanine by the addition of an amino group. Both 6-MP and 6-thioguanine are conjugated with ribose, and then phosphorylated to form the nucleotides thioinosinic acid and thioguanylic acid respectively.[10] These nucleotides masquerade, respectively, as inosinic acid and guanylic acid: the former is the starting point for purine nucleotide biosynthesis, while the latter is one of the building blocks of DNA and RNA.

    • The nucleotides are incorporated into newly synthesized (but non-functional) DNA, halting replication.
    • The nucleotides act to inhibit glutamine-phosphoribosyl pyrophosphate amidotransferase (GPAT), one of the enzymes involved in purine biosynthesis, one of the earlier steps in the synthesis of DNA and RNA. They achieve GPAT inhibition through a form of negative feedback called product inhibition.[68] Because actively replicating cells (such as cancer cells and the T cells and B cells of the immune system) are most active in synthesizing purine making new DNA, these cells are most strongly affected. ].[69][9]
    • A portion of the nucleotides is additionally phosphorylated to the triphosphate forms. These bind to GTP-binding protein Rac1, blocking synthesis of the protein Bcl-xL and thus sending activated T cells and mononuclear cells into apoptosis (a kind of programmed cell death). Increased apoptosis of mononuclear cells is seen in inflammatory bowel disease patients treated with azathioprine.[69]

    Chemistry[edit]

    Azathioprine is a thiopurine linked to a second heterocycle (an imidazole derivative) via a thioether. It is a pale yellow solid with a slightly bitter taste and a melting point of 238–245 °C. It is practically insoluble in water and only slightly soluble in lipophilic solvents such as chloroform, ethanol and diethylether. It dissolves in alkaline aqueous solutions, where it hydrolyzes to 6-mercaptopurine.[66]

    Azathioprine is synthesized from 5-chloro-1-methyl-4-nitro-1H-imidazole and 6-mercaptopurine in dimethyl sulfoxide (DMSO).[70] The synthesis of the former starts with an amide from methylamine and diethyl oxalate, which is then cyclizised and chlorinated with phosphorus pentachloride;[71] the nitro group is introduced with nitric and sulfuric acid.

    History[edit]

    Azathioprine was synthesized by George Herbert Hitchings and Gertrude Elion in 1957 (named BW 57-322) to produce 6-mercaptopurine (6-MP) in a metabolically active but masked form, and at first used as a chemotherapy drug.[72][73][74]

    Robert Schwartz investigated the effect of 6-MP on the immune response in 1958 and discovered that it profoundly suppresses the formation of antibodies when given to rabbits together with antigens.[75] Following the work done by Sir Peter Medawar and Gertrude Elion in discovering the immunological basis of rejection of transplanted tissues and organs, and Schwartz’s researches on 6-MP, Sir Roy Calne, the British pioneer in transplantation, introduced 6-MP as an experimental immunosuppressant for kidney and heart transplants.[76] When Calne asked Elion for related compounds to investigate, she suggested azathioprine, which was subsequently found out to be superior (as effective and less toxic to the bone marrow) by Calne.[72][9] On 5 April 1962, with regimens consisting of azathioprine and prednisone, the transplantation of kidneys to unrelated recipients (allotransplantation) was successful for the first time.[9][77] For many years, this kind of dual therapy with azathioprine and glucocorticoids was the standard antirejection regimen, until ciclosporin was introduced into clinical practice (by Calne as well) in 1978.

    Ciclosporin has now replaced some of the azathioprine use due to a longer survival time, especially in heart-related transplantations.[78][79][80] Moreover, despite being considerably more expensive, mycophenolate mofetil is also increasingly being used in place of azathioprine in organ transplantation, as it is associated with less bone marrow suppression, fewer opportunistic infections, and a lower incidence of acute rejection.[13][81]

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  • External links[edit]

    • Imuran
    • Azasan (manufacturer’s website)
    • U.S. National Library of Medicine: Drug Information Portal – Azathioprine

    Intracellular
    (reception)

    Extracellular

    Polyclonal

    • Anti-thymocyte globulin
    • Anti-lymphocyte globulin

    -cept (Fusion)

    • CTLA-4
      • Abatacept
      • Belatacept
    • TNF inhibitor
      • Etanercept
      • Pegsunercept
    • Aflibercept
    • Alefacept
    • Rilonacept
    • Pharmacy and pharmacology portal
    • Medicine portal


    Source: https://en.wikipedia.org/wiki/Azathioprine

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