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Oral Retinoid Treatment Of Psoriasis – Isotretinoin

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Oral Retinoid Treatment Of Psoriasis – Isotretinoin

Isotretinoin Causes Many Potential Side Effects

Isotretinoin side effects are very common, and sometimes the side effects can be devastating. An Irish man has spent more than 1million Euros taking on a pharmaceutical firm after his son committed suicide. Liam Grant is waging a battle with drugs giant Roche, claiming they are responsible for the death of his son, also called Liam.

In 1996, the 19-year-old started taking Roaccutane, a drug for acne, reports the Independent. He became withdrawn and reclusive and four months later, he hanged himself from a tree outside Dublin.

Since his son’s death, Grant, 61, has shelled out over 1 million fighting the drug’s Swiss manufacturer Roche. He is also pursuing regulators. A scientist hired by him to investigate Roaccutane found – despite studies suggesting a link with depression and suicide – few countries carry warnings on the drug. Roche denies it is to blame for deaths or severe mental health problems.

But Grant can celebrate a significant victory in his fight; he has won a ruling from the European Ombudsman that the European Medicines Agency must release details of all adverse reactions to medications under its rule. The move means for the first time patients will be able to access information on suspected negative reactions across Europe. “I did this out of utter anger,” Grant told the paper. “Roaccutane was licensed for the treatment of acne in 1982. Soon there were studies showing patients got depression within weeks of starting on it. “When I started investigating, I was looking at 20 to 30 published studies linking the drug to depression, psychosis and suicide. Why wasn’t Roche carrying out studies?” But Roche denies responsibility for Liam Grant’s suicide.

“Since 1982, over 15 million patients have been treated with Roaccutane,” said a spokesperson. “Although there have been very rare reports of suicides and suicidal ideation in patients with acne being treated with the medicine, the fact is that severe acne can cause some sufferers to become depressed and can also affect their mood and self esteem.” But the grieving father, whose wife, Loyola, died in 2007, has vowed to fight on. “I am not giving up now,” he added. “I have spent the last 30 years as a forensic accountant investigating some of the biggest frauds in the country and preparing reports for the courts. “That has allowed me to avoid getting involved emotionally and keep objective. It hasn’t dominated my life.”

Eric’s view: And I’m all for it, it’s about time somebody stood up and told pharmaceutical companies the real hard core facts. Noticed how many deaths that hit the media the past few years with regard to the Hollywood people that are pharmaceutical death related? Makes you kind of wonder how many tens of thousands more die you never hear of. I have had bad experiences with Isotretinoin in my clinic with several patients, there are much better ways to treat acne apart from prescribing toxic phramaceutical drugs. Isotretinoin is a synthetic version of Vitamin A. Why not use REAL Vitamin A for acne for goodness sakes?

New Zealanders, like most Westerners are sick to the back teeth of being “fobbed off” by companies such as Roche, just like Mr. Grant has been. Of course they deny responsibility, what is one death when billions of dollars of profits are at stake. The more money they make they more legal clout they have to call the shots and have the most powerful legal defense to defend their lies. Medicine has the nerve to call it “evidence” based medicine, I suppose illness and death related to a pharmaceutical drug is one way of viewing the evidence.

Accutane Lawsuits in 2009/2010 – Ulcerative Colitis

Approximately 5,000 personal injury lawsuits have been filed against Roche Pharmaceuticals, alleging that Accutane caused the onset of bowel problems. Additional lawsuits have been filed against Roche Pharmaceuticals for adverse reactions to Accutane including suicide, psychiatric side effects, and various gastrointestinal disorders.

Accutane Lawsuit 2009: In June of 2009, Roche Pharmaceuticals pulled Accutane from the U.S. market. While the company cited growing competition from generics as a key reason for the pull, Accutane sales had declined dramatically as Roche suffered harsh criticism and a string of lawsuits filed by plaintiffs who claimed the company did not provide proper warning about the dangers of the medication. Interesting fact that Roche ‘no longer make it’, and that in New Zealand Douglas Pharmaceuticals make it. Oh, another interesting fact is that in New Zealand you cannot take a drug company to court. Funny that.

Accutane Lawsuit 2010: In February of 2010, Roche was ordered to pay more than $25 million to a man who developed inflammatory bowel disease years after taking Accutane. The verdict was issued after an earlier decision forcing the company to pay the man $2.5 million was thrown out in a state appeals court.

Read more here: http://www.drugwatch.com/accutane/lawsuit.php

Eric’s Clinical Experiences With Isotretinoin

I do not like this drug and have seen many instances of patients who developed ulcerative colitis and also Crohn’s disease after a history of taking Roaccutane (Isotretinoin). Whenever a patient tells me they took this drug in the past, especially for several years, I begin to wonder if or how it is linked up with the complaints they present with when they see me for a consultation. Do you have psoriasis and take Isotretinoin or Acitretin? Why not take natural Vitamin A instead?

I’ve seen two patients who have complained of persistent dry eyes and/or a very dry tongue for many years after stopping this drug. And naturally, their doctor could see no connection. It’s absolutely amazing how many medical doctors prescribe drugs who have literally no idea about the potential side effects. My advice to you is to very carefully think about a chemical concoction you place in your mouth every day, because it may be causing you real harm, and even an entire new disease may develop that your medical doctor has ‘absolutely no idea’ of its cause.

Here is the information you will find in a doctor’s guide regarding this drug:

ROACCUTANE

Isotretinoin 10mg and 20mg capsules

Retinoid for systemic treatment of acne (but also used for psoriasis by many doctors and dermatologists)

COMPOSITION

Active Ingredient

isotretinoin; 13-cis retinoic acid.

Excipients

Both forms of the capsule contain the excipients soya oil, yellow beeswax, hydrogenated soya bean oil, partially hydrogenated soya bean oil, gelatin, glycerol 85%, sorbitol, mannitol, hydrogenated hydrolysed starch, titanium dioxide, canthaxanthin, shellac (refined) and black iron oxide.

Appearance

Isotretinoin 10mg capsules are reddish violet, opaque, oval, imprinted in black ROA 10, length 9.7mm and diameter 7.0mm.

Isotretinoin 20mg capsules are reddish violet opaque (half) and white opaque (half), oval, imprinted in black ROA 20, length 13.0mm and diameter 8.2mm.

PROPERTIES AND EFFECTS

Mechanism of Action

Isotretinoin, the active ingredient of Roaccutane, is a stereoisomer of all-trans retinoic acid (tretinoin). The exact mechanism of action of Roaccutane has not yet been elucidated in detail, but it has been established that the improvement observed in the clinical picture of severe acne is associated with suppression of sebaceous gland activity and a histologically demonstrated reduction in the size of the sebaceous glands. Furthermore, a dermal anti-inflammatory effect of isotretinoin has been established.

Efficacy

Hypercornification of the epithelial lining of the pilosebaceous unit leads to shedding of corneocytes into the duct and blockage by keratin and excess sebum. This is followed by formation of a comedone and, eventually, inflammatory lesions. Roaccutane inhibits proliferation of sebocytes and appears to act in acne by re-setting the orderly programme of differentiation. Sebum is a major substrate for the growth of Propionibacteriumacnes so that reduced sebum production inhibits bacterial colonisation of the duct.

PHARMACOKINETICS

Since the kinetics of isotretinoin and its metabolites are linear, its plasma concentrations during therapy can be predicted from single dose data. This property also provides some evidence that the activity of hepatic drug metabolising enzymes is not induced by isotretinoin.

Absorption

The absorption of isotretinoin from the gastro-intestinal tract is variable; the absolute bioavailability of isotretinoin has not been determined, since the compound is not available as an intravenous preparation for human use, but extrapolation from dog studies would suggest a fairly low and variable systemic bioavailability. In acne patients at steady state, peak blood concentrations (Cmax) of 310 ng/mL (range: 188-473 ng/mL) were observed 2-4 hours after dosing with 80 mg/day isotretinoin under fasting conditions. Plasma concentrations of isotretinoin are about 1.7 times those of blood concentrations due to poor penetration of isotretinoin into red blood cells.

When isotretinoin is taken with food, the bioavailability is doubled relative to fasting conditions.

Distribution

Isotretinoin is extensively bound to plasma proteins, mainly albumin (≥ 99.9%); therefore the free (= pharmacologically active) fraction of isotretinoin is less than 0.1% over a wide range of therapeutic concentrations.

The volume of distribution of isotretinoin in man has not been determined since isotretinoin is not available as an intravenous preparation for human use.

Steady state blood concentrations (Cmin,ss) of isotretinoin in patients with severe acne treated with 40 mg b.i.d. ranged from 120-200 ng/mL; the concentration of 4-oxo-isotretinoin in these patients was

2-5 times higher than the isotretinoin concentrations. In humans little information is available on the distribution of isotretinoin into tissue. Concentrations of isotretinoin in the epidermis are only half of those in serum.

Metabolism

After oral administration of isotretinoin, three major metabolites have been identified in plasma: 4-oxo-isotretinoin, tretinoin (all-trans retinoic acid), and 4-oxo-tretinoin. The major metabolite is 4-oxo- isotretinoin with plasma concentrations at steady state that are 2.5 times higher than those of the parent compound are. Other minor metabolites have been detected but are not completely identified, which also includes glucuronide conjugates.

Isotretinoin metabolites have shown biological activity in several in-vitro tests. Thus the observed clinical profile in patients could be the result of the pharmacological activity of isotretinoin and its metabolites.

Since isotretinoin and tretinoin (all-trans retinoic acid) are reversibly metabolised (= interconverted), the metabolism of tretinoin is linked with that of isotretinoin. It has been estimated that 20-30% of an isotretinoin dose is metabolised by isomerization.

Enterohepatic circulation may play a significant role in the pharmacokinetics of isotretinoin in man.

In vitro metabolism studies have demonstrated that several CYP enzymes are involved in the metabolism of isotretinoin to 4-oxo-isotretinoin and tretinoin. No single isoform appears to have a predominant role. CYP2C8, CYP2C9, CYP2B6, and possibly CYP3A4 appear to have the greatest contributions in the metabolism of isotretinoin to 4-oxo-isotretinoin. CYP2C9, CYP2B6, and possibly CYP2C8, CYP3A4, CYP2A6, and CYP2E1 contribute to the metabolism of isotretinoin. CYP 26 is also known to metabolize retinoids.

Elimination

After oral administration of radiolabeled isotretinoin approximately equal fractions of the dose were recovered in urine and faeces. Following oral administration of isotretinoin, the terminal elimination half-life of unchanged medicine in patients with acne has a mean value of 19 hours. The terminal elimination half-life of 4-oxo-isotretinoin is longer, with a mean value of 29 hours.

Isotretinoin is a physiological retinoid and endogenous retinoid concentrations are reached within approximately two weeks following the end of Roaccutane therapy.

Pharmacokinetics in Special Populations

Since isotretinoin is contraindicated in patients with hepatic impairment, limited information on the kinetics of isotretinoin is available in this patient population.

INDICATIONS

Severe forms of nodulo-cystic acne which are resistant to therapy, particularly cystic acne and acne conglobata, especially when the lesions involve the trunk.

Roaccutane should only be prescribed by doctors who are experienced in the use of systemic retinoids, preferably dermatologists, and understand the risk of teratogenicity if Roaccutane is used during pregnancy.

DOSAGE AND ADMINISTRATION

Standard Dosage

The therapeutic response to Roaccutane and its adverse events are dose-related and varies between patients. This necessitates individual dosage adjustment during therapy. Roaccutane therapy should be started at a dose of 0.5 mg/kg daily. For most patients the dose ranges from 0.5-1.0 mg/kg per day. Patients with very severe disease or with truncal acne may require higher daily doses up to 2.0 mg/kg.

A cumulative dose of 120 mg/kg per treatment has been documented to increase remission rates and prevent relapse. The therapy duration in individual patients therefore varies as a function of the daily dose. Complete remission of the acne is often achieved by a therapy course of 16-24 weeks. In patients who show severe intolerance to the recommended dose, treatment may be continued at a lower dose with the consequence of a longer therapy duration.

In the majority of patients complete clearing of the acne is obtained with a single treatment course. In case of a definite relapse, a renewed course of Roaccutane therapy should be given with the same daily dose and cumulative treatment dose as previously. Since further improvement of the acne can be observed up to 8 weeks after discontinuation of treatment, retreatment should not be initiated until after this period.

The capsules should be taken with food once or twice daily.

Special Dosage Instruction

Patients with renal impairment

In patients with severe renal insufficiency treatment should be started at a lower dose (e.g. 10 mg/day) and afterwards individually adjusted according to tolerability.

CONTRAINDICATIONS

Roaccutane is contraindicated in:

pregnancy (in women who are pregnant or who may become pregnant while undergoing treatment; see section on pregnancy), hepatic insufficiency, pre-existing hypervitaminosis A, patients with excessively elevated blood lipid values, known hypersensitivity to Roaccutane and any of its components.

WARNINGS

It is recommended that clinically significant serum triglyceride elevations be controlled, since levels in excess of 800 mg/dL are sometimes associated with acute pancreatitis, which is known to be potentially fatal (see Undesirable Effects). Hence, Roaccutane should be discontinued if uncontrolled hypertriglyceridaemia or symptoms of pancreatitis occur.

PRECAUTIONS

Roaccutane should only be prescribed by doctors who are experienced in the use of systemic retinoids and understand the risk of teratogenicity associated with isotretinoin therapy (see Pregnancy, Nursing Mothers).

Depression, psychosis and suicidal attempts have been reported with Roaccutane. Particular care needs to be taken in patients with a history of depression, and all patients should be monitored for signs of depression and referred for appropriate treatment if necessary. Although no mechanism of action for these events has been established, discontinuation of therapy may be insufficient and further evaluation by a psychiatrist may be necessary.

Donation of blood by patients should be avoided during and within 1 month after cessation of Roaccutane treatment to prevent an accidental exposure.

Liver function should be checked before and 1 month after the start of treatment, and subsequently at 3 month intervals. Transitory and reversible increases in liver transaminases have been reported. In many cases these changes have been within the normal range and values have returned to baseline levels during treatment. However, when transaminase levels exceed the normal levels, reduction of the dose or discontinuation of treatment may be necessary.

Serum lipids (fasting value) should also be checked, before and one month after the start of therapy, and also at the end of treatment. The serum lipid values usually return to normal on reduction of the dose or discontinuation of treatment. The changes in serum lipids may also resolve in response to dietary measures.

Bone changes, including premature epiphyseal closure, have occurred after several years of administration at high doses for treating disorders of keratinization. Therefore, a careful evaluation of the risk/benefit ratio should be carried out in every patient.

Myalgia and arthralgia may occur and may be associated with reduced tolerance to vigorous exercise (see Undesirable Effects). Isolated instances of raised serum CPK values have been reported in patients receiving Roaccutane, particularly those undertaking vigorous physical activity.

Microdosed progesterone preparations (minipills) may be an inadequate method of contraceptive during Roaccutane therapy.

Aggressive dermabrasion should be avoided in patients on Roaccutane and for a period of 5-6 months after treatment because of the risk of hypertrophic scarring in atypical areas. Wax epilation should be avoided during therapy and at least for a period of 6 months thereafter due to the possibility of scarring or dermatitis.

Decreased night vision has occurred during Roaccutane therapy and in rare instances has persisted after discontinuation of therapy (see Undesirable effects). Because the onset in some patients was sudden, patients should be advised of this potential problem and warned to be cautious when driving or operating any vehicle at night. Visual problems should be carefully monitored.

Dry eyes, corneal opacities, decreased night vision and keratitis usually resolve after discontinuation of therapy. Due to the possible occurrence of keratitis, patients with dry eyes should be monitored. Patients experiencing visual difficulties should be referred for an expert ophthalmological examination and withdrawal of Roaccutane considered.

Rare cases of benign intracranial hypertension (pseudotumor cerebri) have been reported, some of which involved concomitant use of tetracyclines (see Interactions).

Roaccutane has been associated with inflammatory bowel disease (including regional ileitis) in patients without a prior history of intestinal disorders. Patients experiencing severe (haemorrhagic) diarrhoea should discontinue Roaccutane immediately.

Anaphylactic reactions have been rarely reported and only after previous topical exposure to retinoids. Allergic cutaneous reactions are reported infrequently. Serious cases of allergic vasculitis, often with purpura (bruises and red patches) of the extremities and extracutaneous involvement have been reported. Severe allergic reactions necessitate interruption of therapy and careful monitoring.

Precautions for Special Patient Groups

In high risk patients (with diabetes, obesity, alcoholism or lipid metabolism disorder) undergoing treatment with Roaccutane, more frequent checks of serum values for lipids (see Warnings) and/ or blood glucose may be necessary.

In known or suspected diabetics, frequent determination of blood glucose levels is recommended. Elevated fasting blood sugars have been reported, and new cases of diabetes have been diagnosed during Roaccutane therapy.

PREGNANCY, NURSING MOTHERS

Isotretinoin is highly teratogenic. There is an extremely high risk that a deformed infant will result if pregnancy occurs while taking oral isotretinoin in any amount even for short periods. Potentially all exposed foetuses can be affected.

Roaccutaneis contraindicated in women of childbearing potential unless the female patient meets all the following conditions:

She must have severe acne resistant to standard therapies. She must be reliable in understanding and carrying out instructions. She must be informed by her doctor of the hazards of becoming pregnant during and 1 month after treatment with Roaccutane. She must be warned of the possibility of contraception failure. She must confirm that she has understood the precautions. She must be capable of complying with the mandatory effective contraceptive measures. She must use effective contraception without any interruption for 1 month before beginning Roaccutanetherapy, during therapy and for 1 month following discontinuation of therapy (see Precautions). She must have a negative result from a reliable pregnancy test within 11 days prior to the start of therapy. Monthly pregnancy testing is strongly recommended. She must start Roaccutane therapy only on the 2nd or 3rd day of the next normal menstrual period. In the event of relapse treatment she must also use the same uninterrupted and effective contraceptive measures 1 month prior to, during, and for 1 month after Roaccutanetherapy and the same reliable pregnancy evaluations should be followed. She must fully understand the precautions and confirm her understanding and her willingness to comply with reliable contraceptive measures as explained to her.

Even female patients who normally do not employ contraception because of a history of infertility (except in the case of hysterectomy) or who claim absence of sexual activity must be advised to use effective contraceptive measures while taking isotretinoin, following the above guidelines.

Should pregnancy occur in spite of these precautions during treatment with Roaccutane or in the month following, there is a great risk of very severe malformation of the foetus (involving in particular the central nervous system, the heart and the large blood vessels). There is also an increased risk of spontaneous abortion. If pregnancy does occur, the doctor and patient should discuss the advisability of continuing the pregnancy.

Major human foetal abnormalities related to Roaccutane administration have been documented, including hydrocephalus, microcephalus, abnormalities of the external ear (micropinna, small or absent external auditory canals), microphthalmia, cardiovascular abnormalities, facial dysmorphia, thymus gland abnormalities, parathyroid gland abnormalities and cerebellar malformation.

As isotretinoin is highly lipophilic, the passage of isotretinoin into human milk is very likely. Because of the potential for adverse effects, the use of Roaccutane should be avoided in nursing mothers.

UNDESIRABLE EFFECTS

Most of the side effects of Roaccutane are dose-related. With the recommended dosage, the risk/benefit ratio is generally acceptable considering the severity of the disease.

Symptoms associated with hypervitaminosis A

The following symptoms are the most frequently reported undesirable effects with Roaccutane: dryness of the skin, dryness of the mucosae e.g. of the lips, the nasal mucosa (epistaxis), the pharynx (hoarseness), the eyes (conjunctivitis, reversible corneal opacities and intolerance to contact lenses).

Skin and appendages disorders

Exanthema, pruritus, facial erythema/dermatitis, sweating, pyogenic granuloma, paronychia, nail dystrophy, increased formation of granulation tissue, persistent hair thinning, reversible alopecia, acne fulminans, hirsutism, hyperpigmentation, photosensitivity, photoallergic reactions, skin fragility. Acne flare occurs at the start of treatment and persists for several weeks.

Musculo-skeletal system disorders

Myalgia (muscle pain) with or without elevated serum CPK values (see Precautions), arthralgia (joint pain), hyperostosis, arthritis, calcification of ligaments and tendon and other bone changes, tendinitis.

Psychiatric and central nervous system disorders

Behavioral disorders, depression (see Precautions), headache, increased intracranial pressure (pseudotumor cerebri), seizures.

Sensory disorders

Isolated cases of visual disturbances, photophobia, dark-adaptation disturbances (decreased night vision), rarely colour vision disturbances (reversible upon discontinuation), lenticular cataract, keratitis, impaired hearing at certain frequencies.

Gastro-intestinal system disorders

Nausea, inflammatory bowel disease such as colitis, ileitis, and haemorrhage have been reported to occur. Patients treated with Roaccutane, especially those with high triglyceride levels, are at risk of developing pancreatitis. Fatal pancreatitis has been rarely reported (see Warnings).

Liver and biliary system disorders

Transitory and reversible increases in liver transaminases, some cases of hepatitis. In many such cases the changes have been within the normal range and values have returned to baseline levels during treatment. In other cases, however, it has been necessary to reduce the dose or discontinue treatment with Roaccutane.

Respiratory system disorders

Bronchospasm has been rarely reported; sometimes in patients with a pre-history of asthma.

Disorders of the blood

Decrease in white blood cell count, disorders of red blood cell parameters (such as decrease in red blood cell count and Haematocrit, elevation of sedimentation rate), increase or decrease in platelet count.

Laboratory findings

Increase in serum triglyceride and cholesterol levels, decrease in HDL hyperuricemia. Rare cases of elevated blood glucose have been reported, and new cases of diabetes have been diagnosed (see Precautions).

Resistance mechanism disorders

Local or systemic infections due to Gram positive microorganisms (Staphylococcus aureus).

Miscellaneous reactions

Lymphadenopathy, haematuria, and proteinuria, vasculitis (for example Wegener’s granulomatosis, allergic vasculitis), allergic responses, systemic hypersensitivity, glomerulonephritis.

INTERACTIONS

Concurrent therapy with Roaccutane and vitamin A must be avoided, as symptoms of hypervitaminosis A may be intensified.

Rare cases of benign intracranial hypertension ‘pseudotumor cerebri’ have been reported, some of which involved concomitant use of tetracyclines. Therefore, concomitant treatment with tetracyclines must be avoided (see Precautions).

OVERDOSAGE

Signs of hypervitaminosis A could appear in cases of overdose. Evacuation of the stomach may be indicated in the first few hours after overdosage.

STABILITY

Store below 25°C.

This medicine should not be used after the expiry date shown on the pack.

MEDICINE CLASSIFICATION

Prescription medicine

PACKS

Capsules 10 mg 30’s

Capsules 20 mg 30’s

DATE OF PREPARATION

8 July 2003

Oral Retinoids And Psoriasis – Acitretin

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What Are Oral Retinoids?

Oral retinoids are recommended for psoriasis, they are synthetic drugs derived from Vitamin A. There are two kinds of retinoids, isotretinion and acitretin. Isotretinoin contains an ingredient related to Vitamin A, and is used primarily to treat acne. I’ve found a link with isotretinoin and ulcerative colitis, amongst other side effects. These drugs can tend to have rather strong side-effects, and one day may be overtaken by biologic therapies for psoriasis, which are currently far too expensive to even contemplate for the average psoriasis patient.

Acitretin

Acitretin helps to slow the rapid growth of skin cells, thereby reducing the redness, thickness and scaling found in the skin of those who have psoriasis.

Acitretin is not unlike isotretinoin, but is prescribed by dermatologists primarily for psoriasis; it results in slow improvements over a period of several months and is targeted treatment for moderate to severe psoriasis that has failed to respond to topical treatments and phototherapy. Some patients may notice a temporary worsening of their condition before any improvements are noticed. Sometimes this drug will be used in combination with topical corticosteroids or calcipotriol.

This drug is well known to cause birth defects if given to pregnant women, so don’t be surprised if you are a female and your doctor requests a pregnancy test first. Pregnancy must be strictly avoided whilst on acitretin and for at least 2 years afterwards because it may cause birth deformities. Your doctor will also want complete blood tests performed, including kidney and liver function tests as well as a fasting blood lipid test to determine your cholesterol and triglyceride levels before prescribing this drug.

There are many precautions around taking this drug this drug, especially if you are a female, and the risk of side effects is significantly increased if you drink any alcohol, or take any minocycline, doxycycline, or tetracycline (antibiotics), methotrexate, cyclosporine, of dietary supplements like St. John’s Wort or real Vitamin A. Check with your doctor, because this not the complete list. The drug guide I was studying also mentioned not to have any cosmetic procedures performed on you skin while taking acitretin, because retinoids can increase your chance of scarring or skin inflammation.

Sun safety tips if you do take acitretin.

Wear protective clothing; especially long sleeves and a wide-brimmed hat. Use a broad-spectrum sunscreen with a high SPF rating. Look for the shade; don’t spend too much time in the sun! Avoid peak exposure, the sun is strongest between 10 A.M. and 3.00 P.M.

Reasons you would not want to take acitretin

You are pregnant or planning a pregnancy Nursing women Not wanting to use birth control Experiencing any liver or kidney health issues Experiencing moderate or high cholesterol/triglyceride elevation Experiencing leucopenia (low white blood cells)

Side effects of acitretin include chapped or dry lips, peeling palms and soles, thinning hair or hair loss, muscle pains, nose bleeds, dry mouth, dry or irritated eyes, pain behind the eyes or blurred vision, headaches, vomiting. Stop the drug at once and contact your doctor if you experience any of the these side effects.

Can Pharmaceutical Drugs Be Causing My Psoriasis?

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Can Pharmaceutical Drugs Be Causing My Psoriasis?

Can pharmaceutical drugs be causing my psoriasis? This is something many psoriasis patients may be thinking. The tragedy I have found is that a patient can sometimes experience many of the typical signs and symptoms of psoriasis, like itchy, dry, or cracked skin. There may even be patches of plaque forming that look just like psoriasis. This “mystery illness” may even lead the patient down the road of taking an over the counter drug; they may visit a doctor or chemist and buy a cream, ointment or a tablet on the advice of the pharmacist in the belief that they have developed a new illness, one that affects their skin and looks and behaves a lot like psoriasis.

Article of interest: What causes psoriasis?

What this patient may be unaware of is that he or she may well have in fact a drug-induced (iatrogenic) case of psoriasis. Yes, it actually happens, you can develop psoriasis from taking a pharmaceutical drug.

In some situations it can be tricky for psoriasis patients to take pharmaceutical drugs for other unrelated conditions, such as high blood pressure. It is most unfortunate that some people who actually have pre existing psoriasis may face a Catch-22 situation, when a drug they take for another condition may cause their red, scaly or itchy rashes to get far worse, or may even bring on a case of psoriasis for the very first time.

Certain drugs, particularly those for bipolar disorder, high blood pressure, and hepatitis, can provoke psoriasis for reasons doctors don’t yet “fully understand”, according to a leading medical website I just viewed. Well it’s pretty obvious to me what is occurring, the drug is causing a degree of liver and/or kidney toxicity, something Dr. John Pagano (Healing Psoriasis) discovered many years ago. Whenever a patient cleans up his or her diet and lifestyle, and undertakes a good detoxification program, their psoriasis almost disappears.

What doctors believe is that certain medications trigger or worsen psoriasis outbreaks in those who are genetically predisposed.

Here is a quote from The Journal of Clinical and Aesthetic Dermatology :

“Psoriasis is a commonly encountered dermatosis with a variety of internal and external paradoxical factors contributing to the clinical course of the disease. There are several drugs described in the literature that have been associated with the initiation, exacerbation, and aggravation of psoriasis. Understanding the pathophysiology can provide clues to treatment and management of drug-induced and drug-aggravated psoriasis, which may be indistinguishable from idiopathicpsoriasis. The clinical manifestations of drug-associated psoriasis can range from plaque-type psoriasis to severe erythroderma, thus warranting astute and sustained clinical observation”.

Psoriasis Patients May Take Other Drugs

Do you have psoriasis and another medical condition as well? Analysis of individuals with chronic psoriasis has revealed some interesting statistics2. Over one quarter of those with psoriasis have been diagnosed with high blood pressure (28.2%), diabetes (10.5%) and high cholesterol levels (12.5%). Bearing this in mind, many patients with psoriasis can be on multi-drug regimens; therefore a careful analysis of the various medications that can interact with each other as well as exacerbate psoriasis is very prudent.

Pharmaceutical drugs have several different ways in which they can affect a person’s susceptibility of developing psoriasis, including:

Stimulate the development of psoriasis in susceptible or in non-susceptible individuals.Exacerbate pre-existing psoriatic skin lesions.Induce lesions or lesions different to those experienced by psoriasis patients.Developing drug-resistant psoriatic lesions.

Sometimes a psoriasis patient may develop nail or scalp psoriasis after commencing a drug, or other psoriatic symptoms she may not have previously experienced. The drugs that appear to have the strongest casual relationship with psoriasis are the following:

NSAIDs (Non-Steroidal Anti-Inflammatory Drugs) such as aspirin, paracetamol, ibuprofen, etc.Beta-blockers (blood-pressure)Lithium (bipolar depression)Tetracyclines (antibiotics)Hydroxychloroquine (synthetic antimalarial drugs)

The Drugs Most Commonly Linked In Causing Psoriasis

NSAIDs. (Non-Steroidal Anti-Inflammatory Drugs) such as aspirin, paracetamol, ibuprofen, etc. I have seen many patients over the years that have come into my clinic complaining of psoriasis, who have previously not had psoriasis – until they started taking a NSAID drug regularly. Maybe this is you? Can you relate to having psoriasis since taking a common drug like Tylenol or Advil? Stop this drug and look for an alternative.Beta-Blockers. These are drugs commonly prescribed for high blood pressure and have been extensively studied, and have been found to exacerbate psoriasis patients in a quarter to a third of patients who take them. If you are unsure if your anti-hypertensive drugs are Beta-blockers, go to Google and do an online search. Psoriatic lesions or eruptions will appear in those susceptible from 1 to 18 months after the initiation of Beta blocker therapy, and they have even been implicated in those who have never had psoriasis before. Many different kinds of skin rashes have been implicated with this class of drug, so check it out carefully. Beta-blocker provoked psoriasis improves upon discontinuation of medication, but usually does not completely resolve.Lithium. Lithium is a drug used to control psychiatric illnesses like bipolar, also commonly termed manic depression. Lithium can provoke or aggravate psoriasis in almost half of psoriasis that take it. An interesting study conducted in 2003 revealed that when patients were given omega-3 at the same time, this reaction was diminished.Antibiotics. Drugs such as tetracycline, minocycline and amoxicillinand various other antibiotic drugs are known to cause skin reactions, ranging from mild to most severe, even anaphylactic skin reactions.Some antibiotics are known to cause photosensitization, which may result in predisposed patients with psoriasis to experience exacerbation through the “Koebner phenomenon” secondary to sun exposure. In one study, investigators reported that 4 percent of patients experienced exacerbation of psoriasis as a consequence of antibiotic use. It has also been suggested that tetracyclines should be avoided in patients with clinical evidence of psoriasis, as well as in healthy individuals with a genetic predisposition forpsoriasis.Anti Malarial Drugs. These drugs are used not only to treat malaria, but are also commonly prescribed in auto-immune conditions such as psoriasis, lupus and rheumatoid arthritis. Many have been known to cause acute flare-ups in those with psoriasis in as little as a few weeks after commencement of the drug.

Good advice is to use as little of the medicine as you can get away with preferably, or ask your doctor if you can try an alternative drug. There is little point remaining on any drug that cases strong or uncomfortable side effects. Be sure to consult with your doctor or specialist before you reduce or consider discontinuation of any drug, it is the right and responsible thing to do.

 

Medical Treatment For Psoriasis

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Medical Treatment For Psoriasis

When considering medical treatment for psoriasis, your doctor will generally consider the following factors:

What kind of psoriasis you have, whether it is mild, moderate or severe. Your overall state of health. How much psoriasis affects the quality of your life.

Sometimes a medical doctor will get you to complete a questionnaire to see how much psoriasis is affecting your life. The mildest skin treatments are used first, and if these are not effective then a stronger treatment is recommended. With moderate to severe kinds of psoriasis, one of the five treatments on this page may be recommended. With certain cases, various combinations of treatment are recommended including ultraviolet light, injections, creams, ointments and tablets.

1 – Coal Tar

Coal tar and pine tar have been used for many years for psoriasis, it is an old therapy dating back to the 1920’s. Tar preparations are generally most useful for scalp psoriasis and chronic plaque form of psoriasis. It works by way of reducing the itching and inflammation, helping to thin down the rough lesions that develop.

I’m personally not a big fan of this kind of treatment, in its most effective form it is a messy and smelly treatment, most patients I know who have tried it have discontinued it due to the smell.

Refined coal tar is readily available in various cream, ointment, gel and stick bases. It isn’t suitable for everyone because it can sting or even aggravate the psoriasis. It tends to be messy to use and many patients dislike the smell. Some people combine it with Vaseline or other forms of petroleum jelly. Be careful NOT to apply coal tar preparations prior to going into the sun, as it may cause sunburn, because the ultraviolet light may cause contact photosensitivity dermatitis. If you are going to consider this therapy, please read the booklet – Psoriasis, What To Do With Your Skin, I wrote about Coal Tar in its natural form, from the pine tree.

2 – Dithranol

Dithranol (also called anthralin) is derived from synthetic drug Chrysarobin. This drug has been around for almost as long as Coal Tar, since the early 1930’s. It works by reducing the skin cell turn-over and can be even more effective than Coal Tar. Unfortunately, it too has a major drawn back as it also tends to be a messy preparation that stains skin, bath and clothing a purplish brown color that does not wash out easily.

It can be very irritating when used on unaffected skin and is unsuitable for those with fair skin. Dithranol should not be used on sensitive skin, the face or in the body’s folds or creases.

This product was originally designed to be left on overnight, and the affected parts that were treated were to be covered with bandages. Today we use if for less greater periods of time with equal effectiveness, and it is best used for very short periods of time only, i.e; “short contact”, for 10 to 60 minutes maximum.

3 – Topical Corticosteroids

Did you know that your body makes it own steroid hormones? The powerful steroid called cortisol is produced by your adrenal gland, and it helps to regulate an incredible amount of processes in your body, including your reaction to stress. Cortisol has a most profound effect of your white blood cells, it helps to activate and empower them.

Corticosteroids are a synthetic version of these naturally produced hormones, and are readily prescribed in creams, ointments and pills. There is no doubt, steroid creams do work and they are effective in many cases, they allow damaged skin to heal and can help to relieve symptoms. They are easy to use, are clean and don’t smell like those other preparations we mentioned before.

Psoriasis patients often prefer to use topical steroids as these are easy, clean, and have a soothing action. Steroidal drugs are useful for treating flexural forms of psoriasis, and have a rather limited action I find with plaque and scalp forms of psoriasis. They are also used frequently for psoriasis affecting the palms and soles. Topical steroid lotions may also be recommended by your doctor to be placed under affected nails for onycholysis (nail psoriasis).

For severe forms of plaque psoriasis, a dermatologist may even offer an intralesional steroid injection, a steroid injection used to reduce the thickened plaques of psoriasis.

You will find that weak topical steroids (often in combination with an antifungal drug) may improve flexural psoriasis but the plaque psoriasis and psoriasis that affects the palms and soles will require stronger topical steroids.

Stronger topical steroids need to be used with care, extreme care in fact. You will find that the most powerful of all topical steroid preparations are without a doubt the most effective, but these drugs also tend to have the highest risk of side effects.

They should be used with a great deal of caution, particularly on large areas of skin and preferably for limited periods because:

They can trigger other forms of psoriasis if stopped suddenly. They can result in long-term aggravation of psoriasis. They may thin the skin, causing broken capillaries and stretch marks. They are an incredible amount of side effects if used excessively.

You can reduce your risk of side effects if you apply them for no more than two weeks continuously out of every eight weeks, or use them for two consecutive days in each seven-day (weekly) cycle. Side effects are much more likely in the elderly and children, both who are particularly at risk from steroid overuse because their skin is thinner and more absorbent. Some experts feel that children should not receive steroids for asthma, eczema, psoriasis or other immune-mediated conditions because it may interfere with their growth and development.

The big problem with topical corticosteroids is this, they don’t cure your psoriasis, they suppress the symptoms, and this symptom suppression comes at a cost. As soon as you stop taking these steroid drugs, the symptoms come back with vengeance, and in some cases the psoriasis may even come back as another kind or a more severe form of psoriasis.

There is a danger of using corticosteroids continuously for long periods of time. Because steroids reduce inflammation by blocking aspects of your immune system, they are also known to interfere with the body’s ability to heal itself, thus slowing down the skin’s innate healing response. This increases reliance on steroids and leaves the body wide open to infections. Corticosteroids are also drugs that consume Vitamin D, potassium and zinc, important nutrients the body requires to power up the immune system. Corticosteroids trick your body’s adrenal glands into producing less cortisol that help us cope with stress. And because we now know that stress is one of the leading psoriasis triggers, corticosteroid use is particularly damaging to the body.

Corticosteroid drugs have been linked with stomach ulcers, wasting of the muscles, thinning of the skin and many additional skin disorders, water retention, rapid and unwieldy weight-gain, bone disintegration (osteoporosis), a marked increase risk of viral, bacterial and fungal infections, loss or irregularity of menstrual periods, headaches, diabetes, growth retardation, manic depressive and other neurological, mental and psychological disturbances. Are you still interested in these kinds of drugs long term?

Because of these known side effects, steroids are generally only prescribed short term, but psoriasis users know from experience that when the steroids are stopped, that symptoms return, many will continue to use these corticosteroid applications for years, and indeed, and most always written repeat prescriptions for them. My recommendation is to never begin using topical corticosteroids in the first place, avoid them and use natural solutions on your skin instead, you can read all about them in my booklet entitled Psoriasis, What To Do With Your Skin.

4 – Vitamin D-Like Compounds

The most common form of a Vitamin D like compound used is Calcipotriol. The other name it is known as is Daivonex®. This nonsteroidal antipsoriatic cream or ointment is considered one of the safest topical solutions for those with more mild to moderate forms of plaque psoriasis, and is not generally recommended for the more severe and extensive forms. These drugs appear to work by slowing up the development of keratinocytes, the cells that make up the horny layer of epidermis.

Just like topical corticosteroids, calcipotriol does not smell, stain, and is very easy to use. But unlike steroids, long-term use does not seem to have such devastating consequences. Side effects do include local skin irritation and at times an exacerbation of psoriasis. The drug guide I researched stated not to use it on the face, skin folds to use it on the skin and then cover it. Extensively used treatments can increase serum (blood) calcium levels, it is recommended not to use it therefore for any longer than one year without a long break. Irritation is more likely to occur upon first using it (especially the ointment, which is more potent than cream or solution) but this usually lessens with continued use. If irritation does occur, reducing the frequency of application to every second day or less for a period of time usually allows continued use. Discontinue if you feel that the irritation is severe or does not go away after you have stopped it for some time.

Don’t use this ointment on your face; I had one patient complain of a facial rash for many months after she discontinued its use. No more than 100g should be used each week. I always question why doctors like to recommend “derivatives” or synthetic analogues of Vitamins, when they could be monitoring Vitamin D level in your blood. By doing so they can ensure Vitamin stays in the optimal range, so whey should you therefore have to take artificial forms of Vitamin D? It’s just plain crazy.

5 – Calcineurin inhibitors

These kinds of ointments and creams work by suppressing Interleukin 2 (IL-2) produced by your body’s T-Cells, white blood cells. They are also known as TIMs (topical immune-modulators), and powerfully suppress an inflammatory pathway designed by your immune system to counter inflammation in the body. These medications come with very powerful effects on reducing your immune system’s functioning, even more so than topical corticosteroids, and naturally, this come at a huge price, massive side-effects.

Tacrolimus ointment and pimecrolimus cream are both examples of calcineurin inhibitors and both are not registered for use in psoriasis in New Zealand, although this may be different in your country, they are have been registered to use for atopic dermatitis and eczema. They are sometimes used by dermatologists for psoriasis in thin-skinned areas such as face, skin folds and genital areas. For your information, I found this statement on Medscape.com about this class of drugs:

“Patients using calcineurin inhibitors can potentially experience many adverse effects. In general, the number and severity of adverse effects are related to the overall exposure, measured by length of therapy and blood drug concentration. Patients taking cyclosporine may develop high blood-pressure, tremor, kidney toxicity, high cholesterol levels, gum disease, and hirsutism (hair growth on face). Patients receiving tacrolimus may develop high blood-pressure, tremor, many and varied digestive disturbances, kidney toxicity, headaches, liver toxicity, abnormal blood sugar control (diabetes), skin itching, white blood cell toxicity, high potassium levels, and hypomagnesemia. Tacrolimus causes a greater number of and more severe adverse events than does cyclosporine. Dosage reduction may decrease toxicities; however, additional pharmaceutical drugs are often required to counteract the adverse effects of calcineurin inhibitor therapy. The kidney toxicity seen with cyclosporine and tacrolimus is particularly problematic in kidney transplant recipients and may negate a kidney transplant. Calcineurin inhibitor doses are often tapered postoperatively because of such toxicities.” .

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