Anaphylactoid reactions to radiocontrast media.

As the role for diagnostic and therapeutic contrast-enhanced imaging increases, review of the epidemiology, mechanisms, risk factors, and pretreatment for radiocontrast-mediated anaphylactoid reactions becomes more and more pertinent. Ongoing research has failed to elucidate the precise mechanisms of both early and late reactions, though the current data point to a multifactorial pathogenesis. The risk of reactions has decreased over time as contrast media have evolved from ionic, high-osmolality to nonionic, low-osmolality formulations; however, the expense of the low-osmolality agents limit their universal use. Today, 1-12% of patients exhibit adverse responses ranging from mild to severe, with individual risk depending on the type of contrast administered and certain baseline patient characteristics. For those high-risk patients who must receive contrast, effective pretreatment guidelines have been established.     

Hypersensitivity reactions to radiocontrast media: The role of complement activation

Although intravenous use of radiocontrast media (RCM) for a variety of radiographic procedures is generally safe, clinically significant acute hypersensitivity reactions still occur in a significant percentage of patients. The mechanism of these anaphylactoid, or "pseudoallergic," reactions is complex, involving complement activation, direct degranulation of mast cells and basophils, and modulation of enzymes and proteolytic cascades in plasma. In this review, basic information on different RCMs and their reactogenicity is summarized and updated, and the prevalence, pathomechanism, prediction, prevention, treatment, and economic impact of hypersensitivity reactions are discussed. Particular attention is paid to the in vitro and in vivo evidence supporting complement activation as an underlying cause of RCM reactions.     

Reactions to radiocontrast media.

Adverse reactions to radiocontrast media (RCM) occur unexpectedly and may be life-threatening. This article describes an anaphylactoid reaction (AR) in one patient. The term AR refers to a syndrome clinically similar to anaphylaxis, but these reactions are independent of immunoglobulin E antibody-mediated mast cell or basophil degranulation. This article briefly reviews the literature regarding RCMs and types of reactions to RCM. The risk factors for AR to RCM infusions will be discussed along with current concepts of the pathogenesis of RCM-induced ARs. This article also describes the therapeutic management of patients who have had a previous adverse reaction to RCM and provides an approach to patients who have breakthrough reactions despite adequate premedication, but require additional radiographic studies.     

Anaphylactoid reactions and late skin reactions to iodinated contrast media: present state of the question--idea development]

PURPOSE: Adverse reactions to iodinated contrast media (ICM) share various mechanisms. Anaphylactoid reactions are among the most serious reactions when they are characterized by the elevation of seric tryptase. Pretreatment with corticosteroids and anti-H1 or the use of non-ionic contrast media do not prevent anaphylaxis. Late skin reactions could be mostly related to delayed hypersensitivity. Previous reactions to contrast media, cardiovascular disorders, beta-blockers, asthma, and atopy are risk factors. Female gender and age increase the severity. CURRENT KNOWLEDGE AND KEY POINTS: Anaphylaxis can be demonstrated by intradermal tests and the identification of specific IgEs. Delayed hypersensitivity is shown by the results of epicutaneous tests and the immunohistology of the skin. FUTURE PROSPECTS AND PROJECTS: Allergologic tests are advised in the case of previous reactions. In case of emergency, gadopentetate dimeglumine can be alternatively used. The other risk factors lead to the combination of pretreatment and use of non-ionic monomeric contrast media. Immediate hypersensitivity to iodinated media might increase in the near future with the use of divalent molecules.     

Anaphylactoid reaction to angiographic contrast media: Recurrence despite pretreatment with corticosteroids

A case who developed severe and potentially fatal reaction to an angiographic contrast medium despite adequate pretreatment with steroids for 2 weeks is reported. This is the second such case reported in the English literature.     

Prophylaxis against repeated radiocontrast media reactions in 857 cases. Adverse experience with cimetidine and safety of beta-adrenergic antagonists

Eight hundred fifty-seven radiocontrast media (RCM) procedures were performed from 1974 to 1984 in 743 patients who previously had experienced an immediate generalized (anaphylactoid) reaction to RCM. During the 695 intravascular infusions of RCM, prednisone-diphenhydramine hydrochloride pretreatment of 415 essential repeated RCM procedures from 1974 to 1980 resulted in 45 (10.8%) reactions during which transient hypotension occurred in three (0.7%) patients. From 1980 to 1983, prednisone-diphenhydramine-ephedrine sulfate pretreatment of 180 procedures was associated with only nine reactions (5.0%) (chi 2 = 5.195). The addition of cimetidine hydrochloride in 1983 to 1984 was not useful in that 14 reactions occurred during 100 procedures (14.0%). The 21 patients who had been receiving beta-adrenergic antagonist therapy were protected as well as those who were not, in that none of 11 patients receiving the three-drug regimen had a repeated reaction and only one of ten patients receiving the four-drug regimen reacted.     

Anaphylactoid reaction to zomepirac

Circulatory collapse and respiratory arrest occurred in a young woman shortly after taking 200 mg of zomepirac for relief of headache. She had no history of drug hypersensitivity and had tolerated zomepirac without adverse effects 18 months prior to this reaction. The patient was successfully treated and suffered no sequelae.     

Anaphylactoid reaction to goat's milk

We report on one young adult male patient who had severe anaphylactoid reaction after eating cheese made from goat's milk. This allergy to goat and sheep's milk, known by the patient, gave mainly rise to oral pruritus. Cow's milk and cheese were always eaten without any incident. Labial test and specific IgE antibodies confirm goat and sheep's milk allergy without cow's milk allergy.     

Anaphylactoid Reactions to Vitamin K

Anaphylactoid reactions in patients receiving intravenously administered vitamin K have been reported in the literature. To summarize the known data on anaphylactoid reactions from administration of vitamin K, we reviewed all published and unpublished reports of this adverse reaction. Published reports were obtained through medline (1966–1999) and EMBASE (1971–1999) searches of the English language literature and review of references from identified case reports. Unpublished reports were obtained using the Spontaneous Reporting System Adverse Reaction database of the United States Food and Drug Administration (FDA) between August 1968 and September 1997. All adverse drug reactions to vitamin K were categorized by route of drug administration, dose and standard adverse reaction code. In the FDA reports, we defined anaphylactoid reactions as any adverse drug reaction coded as either anaphylaxis, allergic reaction, apnea, dyspnea, death, heart arrest, hypotension, shock or vasodilatation. Additionally, all fatal and life-threatening FDA reported reactions were reviewed to determine if they could represent an anaphylactoid reaction missed by the above definition.The literature review uncovered a total of 23 cases (3 fatal) of anaphylactoid reactions from intravenous vitamin K. The FDA database contained a total of 2236 adverse drug reactions reported in 1019 patients receiving vitamin K by all routes of administration. Of the 192 patients with reactions reported for intravenous vitamin K, 132 patients (69%%) had a reaction defined as anaphylactoid, with 24 fatalities (18%%) attributed to the vitamin K reaction. There were 21 patients with anaphylactoid reactions and 4 fatalities reported with doses of intravenous vitamin K of less than 5[emsp4 ]mgs. For the 217 patients with reactions reported due to vitamin K via a non-intravenous route of administration, 38 patients had reactions meeting the definition of anaphylactoid (18%%), with 1 fatality (3%%) attributed to the drug.The absolute risk of an anaphylactoid reaction to intravenous vitamin K cannot be determined by this study, but the relatively small number of documented cases despite widespread use of this drug suggest that the reaction is rare. Anaphylactic reactions and case fatality reports were found even when intravenous vitamin K was given at low doses by slow dilute infusion. The pathogenesis of this reaction is unknown and may be multifactorial with etiologies including vasodilation induced by the solubilizing vehicle or immune-mediated processes. We conclude that use of intravenous vitamin K should be limited to patients with serious hemorrhage due to a coagulopathy that is secondary to a relative or absolute deficiency of vitamin K.     

Prophylactic hemodialysis after radiocontrast media in patients with renal insufficiency is potentially harmful.

PURPOSE: Acute renal failure induced by contrast media is an important cause of hospital-acquired renal insufficiency. Preexisting renal failure and the dose of contrast media are known risk factors for the development of radiocontrast nephropathy. We performed a randomized trial to test whether radiocontrast nephropathy can be avoided by prophylactic hemodialysis immediately after the administration of contrast media in patients with impaired renal function. SUBJECTS AND METHODS: Renal function and other parameters, hemodialysis requirement, and relevant clinical events were recorded before and during the 6 days after administration of contrast media in 113 patients with a baseline serum creatinine level >200 microm/L (>2.3 mg/dL). Patients were randomly assigned to either hemodialysis (n = 55) or nonhemodialysis (n = 58) treatment after parenteral low-osmolality contrast media. RESULTS: The characteristics of the patients in the two groups were similar. Compared with baseline levels, the mean [+/- SD] serum creatinine level decreased at day 1 (277 +/- 95 microm/L), peaked at day 4 (353 +/- 126 microm/L), and returned to baseline at day 6 (327 +/- 119 microm/L, P <0.05 by analysis of variance) after administration of contrast media in the hemodialysis group, whereas in the nonhemodialysis group, no significant changes in mean serum creatinine level were observed. Eleven patients required 1 or more hemodialyses (8 in the hemodialysis group and 3 in the nonhemodialysis group, P = 0.12), 6 of whom (4 vs. 2, P = 0.44) required 3 or more hemodialyses. Clinically relevant events included pulmonary edema (1 vs. 4 patients, P = 0.36), myocardial infarction (2 vs. 2), stroke (2 vs. 0, P = 0.24), and death (1 vs. 1). CONCLUSIONS: The strategy of performing hemodialysis immediately after the administration of low-osmolality contrast media in all patients with a reduced renal function did not diminish the rate of complications, including radiocontrast nephropathy.     

非离子型碘造影剂的过敏样反应

目的:对临床使用的非离子型碘造影剂的过敏样反应进行总结和分析。方法:回顾性总结2004年4月至2006年6月期间,在我院进行冠状动脉(冠脉)造影和(或)介入治疗的患者群中,接受非离子型碘造影剂血管内注射后1小时之内发生的过敏样反应病例,参照美国放射学会的诊断标准,根据患者的临床表现分为轻、中、重度三型;针对性别、年龄、冠脉病变程度、造影剂品种等变量因素进行分析和统计学处理。结果:在17033例患者中计有217例发生过敏样反应(发生率1.28%),轻、中、重度过敏样反应的发生率分别为0.22%、0.80%和0.26%,死亡3例(死亡率0.018%);男性患者的过敏样反应发生率高于女性患者(1.37%vs0.98%,P<0.05),在冠脉病变程度、不同造影剂品种等因素的分析中未检出性别之间存在显著性差异;过敏样反应发生率随年龄增加呈下降的趋势,经多元回归分析呈线性关系,男性患者尤为明显;过敏样反应的发生率与冠脉病变程度无显著相关性;年龄、不同造影剂品种对于过敏样反应的三型构成比无显著影响,在女性患者、冠脉多支病变患者尤其是病变累及左主干的患者人群中发生重度过敏样反应的比例较高。结论:非离子型碘造影剂在临床应用中安全性良好,过敏样反应发生率为1.28%,男性患者的过敏样反应发生率高于女性患者,过敏样反应发生率随患者年龄增加而呈下降趋势,在女性患者、冠脉多支病变尤其是病变累及左主干的患者人群中发生重度过敏样反应的比例较高。     

Anaphylactoid reactions in two patients after omalizumab administration after successful long-term therapy.

Anti-IgE therapy with omalizumab, a recombinant humanized monoclonal antibody, has anti-inflammatory effects in allergic asthma and rhinitis. Although omalizumab has been exceptionally safe, reactions after its administration have been reported. The goal of this study was to assess two patients who experienced apparent anaphylaxis after omalizumab administration. Two cases of apparent anaphylaxis after omalizumab administration are reported with diagnostic evaluation using skin testing and unique IgE and IgG anti-omalizumab serological assays. At the time of evaluation, both atopic asthmatic patients had total (free and bound) serum IgE levels of 199 kIU/L (100% free) and 200 kIU/L (80% free and 20% bound), respectively. Epicutaneous skin tests to omalizumab were negative at 150 mg/mL of omalizumab in both subjects and the nonexposed negative control subject. Intradermal skin tests were positive at 0.15 mg/mL in subject 1 and negative at 1.5 mg/mL of omalizumab in subject 2 and the control subject. Intradermal testing to polysorbate produced significant wheal/flare reaction in subject 2 but not in the negative control subject. Serological assays for IgE or IgG antibodies reactive with omalizumab were negative. The in vitro and in vivo immunologic data support the conclusion that the adverse reactions experienced by two patients after omalizumab administration after more than a year of successful omalizumab therapy for asthma were likely anaphylactoid in nature. Polysorbate, an excipient in omalizumab, is known to cause similar reactivity to other medicines and is the most likely cause of these reactions.