chemical structure of quinidine
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Duraquin

Quinidine is a pharmaceutical agent that acts as a class I antiarrhythmic agent in the heart. It is a stereoisomer of quinine, originally derived from the bark of the cinchona tree. more...

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Like all other class I antiarrhythmic agents, quinidine primarily works by blocking the fast inward sodium current (INa). Quinidine's effect on INa is known as a use dependent block. This means that at higher heart rates, the block increases, while at lower heart rates the block decreases. The effect of blocking the fast inward sodium current causes the phase 0 depolarization of the cardiac action potential to decrease (decreased Vmax).

Quinidine also blocks the slowly inactivating tetrodotoxin-sensitive Na current, the slow inward calcium current (ICa), the rapid (IKr) and slow (IKs) components of the delayed potassium rectifier current, the inward potassium rectifier current (IKI), the ATP-sensitive potassium channel (IKATP) and Ito.

The effect of quinidine on the ion channels is to prolong the cardiac action potential, thereby prolonging the QT interval on the surface EKG.

The half life of oral quinidine is 6 to 8 hours, and it is eliminated by the cytochrome P450 system in the liver. About 20 percent is excreted unchanged via the kidneys.

Qunidine-induced thrombocytopenia (low platelet count) is mediated by the immune system, and may lead to thrombocytic purpura.

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Chemical photosensitivity: another reason to be careful in the sun - includes related article on tanning booths
From FDA Consumer, 5/1/96 by Craig D. Reid

Since childhood, my brother Blair always developed a dark tan without ever sunburning. Now a college soccer coach in Iowa, he is constantly outside practicing in the sun. Recently, Blair suffered a severe sunburn after only 45 minutes of sun exposure on a cool, partly sunny morning. Consulting his physician, he learned that the commonly prescribed colitis medication Azulfidine (sulfasalazine), which he was using at the time for a colon infection, was the cause of his problems.

Azulfidine is one of the many medications included in the Food and Drug Administration's most recent listing of medications that increase sensitivity to light and can cause a wide variety of health problems known as photosensitivity disorders. In some individuals, these medications can produce adverse effects when the person is exposed to sunlight and other types of ultraviolet (UV) light of an intensity or for a length of time that would not usually give the person problems. Some products are more likely to cause reactions than others. And not everyone who uses the products will be affected.

Photoreactions

Chemicals that produce a photoreaction (reaction with exposure to UV light) are called photoreactive agents or, more commonly, photosensitizers. After exposure to UV radiation either from natural sunlight or an artificial source such as tanning booths or even those "purple-lighted" mosquito zappers, these photosensitizers cause chemical changes that increase a person's sensitivity to light, causing the person to become photosensitized. Medications, food additives, and other products that contain photoreactive agents are called photosensitizing products.

FDA has also reported that photoreactive agents have been found in deodorants, antibacterial soaps, artificial sweeteners, fluorescent brightening agents for cellulose, nylon and wool fibers, naphthalene (mothballs), petroleum products, and in cadmium sulfide, a chemical injected into the skin during tattooing.

Photoreactive agents, such as Azulfidine, can cause both acute and chronic effects. Acute effects, from short-term exposure, include exaggerated sunburn-like skin conditions, eye burn, mild allergic reactions, hives, abnormal reddening of the skin, and eczema-like rashes with itching, swelling, blistering, oozing, and scaling of the skin. Chronic effects from long-term exposure include premature skin aging, stronger allergic reactions, cataracts, blood vessel damage, a weakened immune system, and skin cancer.

Widely used medications containing photoreactive agents include antihistamines, used in cold and allergy medicines; nonsteroidal anti-inflammatory drugs (NSAIDs), used to control pain and inflammation in arthritis; and antibiotics, including the tetracyclines and the sulfonamides, or "sulfa" drugs.

Sometimes this quality can be put to good medical use. For example, two well-known photoreactive chemicals, psoralens and coal-tar dye creams, are used together with UV lamps to treat psoriasis, a chronic skin condition characterized by bright red patches covered with silvery scales.

Pioneering Research

European scientists pioneered photosensitivity disorder research during the 1960s. In 1967, Danish researchers attributed strange skin lesions (any abnormal change on the skin) on women to perfumed soap. In 1967, British researchers discovered that sandalwood oil in sun-screens and facial cosmetics caused photoallergies and later reported that quindoxin, a food additive in animal feed also caused phototoxic erythemal skin patches on British farmers handling the feed.

Shortly thereafter, French scientists demonstrated that bergamot oil in sun-screens caused photosensitivity disorders. German researchers isolated photoreactive agents in colognes, perfumes and oral contraceptives.

In 1972, American scientists linked sunlight-activated aniline compounds (found in drugs, varnishes, perfumes, shoe polish, and vulcanized rubber) to hives and skin conditions such as dermatitis and dandruff.

Scientists were soon publishing laundry lists of photoreactive agents found in these substances as well as those in hair dyes, hair styling creams, and household items such as shoe polish and mothballs. Current research focuses on identifying what photoreactive agents are found in which medicinal products and how to control photosensitivity disorders.

Photosensitizers can cause either photoallergic or phototoxic reactions.

Photoallergies

In photoallergic reactions, which generally occur due to medications applied to the skin, UV light may structurally change the drug, causing the skin to produce antibodies. The result is an allergic reaction. Symptoms can appear within 20 seconds after sun exposure, producing eczema-like skin conditions that can spread to nonexposed parts of the body. But sometimes, photoallergic reactions can be delayed. For example, Yuko Kurumaji reported in the October 1991 issue of Contact Dermatitis that photoallergic sensitivity disorders to the topically applied NSAID Suprofen (not approved for use in the United States) took up to three months to develop.

Other regularly used products that can cause photoallergic reactions are cosmetics that contain musk ambrette, sandalwood oil, and bergamot oil; some quinolone antibacterials; and the over-the-counter (OTC) NSAID pain relievers Advil, Nuprin and Motrin (ibuprofen), and Aleve (naproxen sodium).

Phototoxicity

Phototoxic reactions, which do not affect the body's immune system, are more common than photoallergic reactions. These reactions can occur in response to injected, oral or topically applied medications.

In phototoxic reactions, the drug absorbs energy from UV light and releases the energy into the skin, causing skin cell damage or death. The reaction occurs from within a few minutes to up to several hours after UV light exposure. Though sunburn-like symptoms appear only on the parts of the body exposed to UV radiation, resulting skin damage can persist.

For example, Henry Lim, M.D., reported in the March 1990 issue of Archives of Dermatology that several patients previously exposed to photoallergens continued to have phototoxic skin eruptions up to 20 years after discontinuing medication use, even though they avoided further exposure to the photoallergens.

Frequently prescribed medications that cause phototoxic reactions include tetracycline antibiotics, NSAIDs, and Cordarone (amiodarone), used to control irregular heartbeats.

Because drug-induced photosensitivity disorder symptoms mimic sunburns, rashes and allergic reactions, many cases go unreported. Also, although research has shown that the numbers of photosensitized individuals may be high, most people do not associate the sun's light with the development of their skin eruptions.

Photophobia

Some medications can cause photophobia. Although literally, photophobia is fear of light, photophobic photosensitivity disorder patients avoid light not because they're afraid of it but because their eyes are painfully sensitive to it.

Some medications that induce photophobia include several drugs prescribed for irregular heartbeat, such as Crystodigin (digitoxin) and Duraquin (quinidine), and several drugs for diabetes, such as Tolinase (tolazamide) and Orinase (tolbutamide).

Who Gets a Reaction?

The degree of photosensitivity varies among individuals. Not everyone who uses medications containing photoreactive agents will have a photoreaction. In fact, a person who has a photoreaction after a single exposure to an agent may not react to the same agent after repeated exposures.

On the other hand, people who are allergic to one chemical may develop photosensitivity to another related chemical to which they would normally not be photosensitive. In such cross-reaction, photosensitivity to one chemical increases a person's tendency for photosensitivity to a second. For example, J.L. deCastro reported in the March 1991 issue of Contact Dermatitis that 17 patients allergic to the antiseptic thimerosal, used in some contact lens preparations, developed photosensitivity to the NSAID Feldene (piroxicam), yet none of them had had any previous photoreaction to Feldene.

Although those with fair skin are more susceptible to photosensitizing, it is not uncommon for dark-skinned individuals to have chronic photodermatitis.

What is termed a "photo-recall" can take place when a non-photoreactive product prompts the repeat of a previous reaction to a photoreactive agent.

Photoreactive products can also aggravate existing skin problems like eczema, herpes, psoriasis and acne, and can inflame scar tissue. They can also precipitate or worsen autoimmune diseases, such as lupus erythematosus and rheumatoid arthritis, in which the body's immune system mistakenly destroys itself.

Do Sunscreens Help?

Does using sunscreens help protect against photosensitivity? The answer is not clear. Sunscreens do lessen the effects of UV radiation, but some contain ingredients that themselves may cause photosensitivity in some people. Also, most sunscreens protect only from shortwave UV light (UVB), whereas most phototoxic compounds are activated by longer wavelengths of UV light (UVA). Sunscreens containing bergamot oil, sandalwood oil, benzophenones, PABA, cinnamates, salicylates, anthranilates, PSBA, mexenone, and oxybenzone can all cause photosensitivity reactions. Titanium dioxide is the least likely sun-screen to cause photosensitivity disorders.

Before going out in the sun, it's a good idea to check with your doctor to see if any of the medications you're taking is likely to cause problems and decide how to best avoid such reactions. Read the labels of OTC drugs and note if they may be photosensitizing.

If you get symptoms after being out in the sun, you may want to consider what drugs and chemicals you are using and contact your doctor immediately for advice.

COPYRIGHT 1996 U.S. Government Printing Office
COPYRIGHT 2004 Gale Group

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