Allergies to Alcohol and Drugs
ALLERGIES TO ALCOHOL AND DRUGS
In addition to Alcohol, Opiates, and Barbiturates, some street drugs have been reported to induce allergic reactions. These allergic phenomena are most frequently mediated by reactions of the immune system known as immediate hypersensitivity and delayed hypersensitivity. Immediate hypersensitivity is mediated by the serum protein immunoglobulin E(IgE), whereas delayed hypersensitivity is mediated by thymus-derived lymphocytes (the white blood cells called T cells).
The symptoms and signs associated with IgE-mediated immune reactions are urticaria (hives); bronchospasm that produces wheezing; angioedema (swelling) of face and lips or full-blown anaphylaxis (a combination of all the above symptoms and lowering of blood pressure). Abdominal pain and cardiac arrhythmias (irregular heartbeat) may also occur with anaphylaxis. Any or all of these symptoms occur when IgE, which has previously been synthesized by a sensitized lymphocyte, fixes to mast cells or basophils in the skin, bronchial mucosa, and intestinal mucosa. This cell-fixed IgE then binds the antigen that triggers the release of the following—the histamine, the slow-reacting substance of anaphylaxis (SRSA), the bradykinin, and the other mediators that induce these symptoms. Examples of this type of allergic reaction are the allergic responses to either bee stings or to penicillin.
Similar symptoms may also occur when mediators are released by mast cells in response to chemical or physical stimuli. This is called an anaphylactoid reaction. In this instance, the mast cell or basophil is directly activated by the chemical to release mediators without having to bind to IgE. Examples of this type of reaction are responses to intravenous contrast material, such as IVP dye, or the hives induced by exposure to cold.
Reactions occur when antigenic chemicals stimulate T lymphocytes and induce their proliferation. T effector cells are then recruited into the tissue site. These effector cells bind the antigen and subsequently release effector molecules, such as the interleukins, the chemotactic factors, and the enzymes. These effector molecules induce an inflammatory response in the area and may also induce formation of granuloma (a mass of inflamed tissue) by macrophages and inflammatory cells. Symptoms of delayed hyper-sensitivity reactions are skin rashes, which may be red, pruritic (itchy), or bullous (blistered) in nature. Granulomas can cause lymph node enlargement and nodules in the skin or in organs. Examples of this response are poison ivy, cosmetic allergies, Erythema Nodosum or Sarcoidosis.
ALLERGIC RESPONSE TO ALCOHOL
True anaphylactic or anaphylactoid reactions to Alcohol (ethanol) are rare. Most reactions to ingested alcoholic beverages are secondary to other chemicals in the beverage such as yeasts, metabisulfite, papain, or dyes. However, there are reports of true allergic reactions in which the offending agent was shown to be the ethanol itself.
Symptoms of anaphylaxis have been reported to occur in several subjects following ingestion of beer and/or wine, and these symptoms were reproduced in one patient by administration of 95 percent ethanol. Hives have been reported with ethanol ingestion, and hives on contact with ethanol have been reported for some Asian patients. Bronchospasm was precipitated in some asthmatic patients by administration of ethanol, and contact hypersensitivity to 50 percent ethanol solution was produced in 6 percent of subjects tested. These allergic responses differ from the "flush" reaction exhibited in individuals (especially Asians) with acetaldehyde dehydrogenase abnormalities.
ALLERGIES TO OPIATES, BARBITURATES, AND STREET DRUGS
There have been reports of Morphine-induced hives in some people, and studies show that morphine can cause histamine release directly from cells without binding to specific receptors on cells. Anaphylaxis may also occur with either morphine or Codeine, and IgE antibodies against morphine and codeine have been found in patients experiencing anaphylaxis. Thus, the Opiates can mediate allergic reaction by either mechanism, and the antagonist drug Naloxone will not reverse these reactions. There are also reports of Heroin causing bronchospasm.
Some instances of anaphylaxis associated with the medical administration of opiates or local anesthesia during surgery are due to the often included preservative methylparaben, rather than to the opiate itself. Anaphylaxis may occur with more than one local anesthetic and/or analgesic compound in the same patient because of the methylparabens.
Numerous reports exist for anaphylactoid reactions following the use of Barbiturates for the induction of anesthesia. The drugs themselves may induce histamine release. This may also be mediated through a true allergic IgE mediated response in some patients. Skin rashes also occur frequently following barbiturate usage. This may be a hyper-sensitivity reaction, or it may be a pseudo-allergic reaction.
Street drugs have been reported to induce asthma and or anaphylaxis. Bronchospasm may occur in patients smoking Cocaine or in those injecting heroin. This may occur more often in patients who have a previous history of asthma. The asthma may persist after the subjects have stopped smoking cocaine. Pulmonary edema (fluid in the lungs) may also occur with Freebasing cocaine. These side effects are not likely to be mediated by the immune system. However, a hypersensitivity pneumonitis to cocaine has been described and is associated with elevated levels of IgE. Marijuana does not appear to increase the incidence of either asthma or anaphylaxis.
(See also: Complications )
Ettinger, N. A., & Albin, R. J. (1989). A review of the respiratory effects of smoking cocaine. American Journal of Medicine, 87, 664.
Fakuda, T., & Dohi, S. (1986). Anaphylactic reaction to fentanyl or preservative. Canadian Anesthetists' Society Journal, 33, 826.
Hicks, R. (1968). Ethanol, a possible allergen. Annals of Allergy, 26, 641.
Karvoren, J., & Hannuksela, M. (1976). Urticaria from alcoholic beverages. Acta Allergan, 31, 167.
Kelso, J., et al. (1990). Anaphylactoid reaction to ethanol. Annals of Allergy, 64, 452.
Mc Lelland, J. (1986). The mechanism of morphine induced urticaria. Archives of Dermatology, 122, 138.
Przybilla, B., & Ring, J. (1983), Anaphylaxis to ethanol and sensitization to acetic acid. Lancet, 1, 483.
Rebhun, J. (1988). Association of asthma and freebase smoking. Annals of Allergy, 60, 339.
Rilbet, A., Hunziker, N., & Braun, R. (1980) Alcohol contact urticaria syndrome. Dermatologica, 161, 361.
Rubin, R., & Neugarten, J. (1990). Codeine associated asthma. American Journal of Medicine, 88, 438.
Seto, A., et al., (1978). Biochemical correlates of ethanol-induced flushing in Orientals. Journal in the Studies of Alcohol, 39, 1.
Shaikh, W. A. (1970). Allergy to heroin. Allergy, 45, 555.
Shanaban, E. C., Marshall, A.G., & Garrett, C.P.U. Adverse reactions to intravenous codeine phosphate. Anesthesia, 38, 40.
Ting, S., et al. (1988). Ethanol induced urticaria: A case report. Ann. Allergy, 60, 527.
Wilkins, J.K., & Fortner, G. (1985). Ethnic contact urticaria to alcohol. Contact Dermatology, 12, 118.