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Q:

Reviewed: February 24, 2020
10/10/2014
I have a 50 yo m who has recently been reacting to alcohol based drinks, with hives, angioedema of lips, flushing. Has happened with any alcohol based drink. He was fine all these years and now in the past 6-8 months having these issues. I have done screening labs including serum tryptase and screening lymphoma/leukemias labs (peripheral smear, LDH etc) and all the enzymes are fine. My question is- can you suddenly develop alcohol intolerance (the entity that we normally see) at this age without an underlying etiology. He has no venom allergy, has seasonal allergy to grass, mtn cedar and ragweed only, no food allergy- negative ige to an extensive panel (including 8 grains) and negative to red dye. What else should I be looking for?

A:

I would conclude that since the symptoms of alcohol intolerance developed later in life, this man is not of Asian ethnicity and does not suffer from flushing associated with alcohol due to abnormal metabolism of ethanol (deficiency of acetaldehyde dehydrogenase). This condition also would not cause angioedema or hives but may be confused with urticaria or allergic reactions (see below).

There are reports of ethanol reactions that resemble or may be IgE mediated reactions and anaphylaxis. Although compounds as small as ethanol or acetic acid should be too small to evoke an immune reaction, positive reactions to both have been described (see below).

Another thought would be aggravation of mast cell activation syndrome by alcohol ingestion. Although you indicated that the tryptase was not increased, I would encourage your review of the mast cell activation syndrome article that discusses a comparison of baseline and during episode tryptase to identify possible mast cell activation syndrome despite a baseline tryptase of less than 11 mcg/ml.

There have been several questions related to ethanol reactions that are in the archive of Ask the Expert. I have attached some of these but you can review others if you search the archive with the word “alcohol”.

Therefore, I would suggest obtaining the tryptase during an episode and compare to baseline. I would also follow the patient and consider repeat baseline tryptase in future to be sure the levels do not increase with time. I would also prescribe autoinjector epinephrine as the severity of the episodes seem to be increasing. I am not sure I would treat with chronic H1 and H2 inhibitors but might consider this if the patient insists on drinking ethanol, which I would recommend he avoids. You might consider prick testing with ethanol and acetic acid but be sure you do not use an irritating concentration.

7/19/2013
Safety of the ingestion of alcohol in patients with indolent systemic mastocytosis

Case Rep Dermatol. 2009 Apr 29;1(1):1-6.
Two Case Reports of Life-Threatening Ethanol-Induced Anaphylaxis.
Fernando SL1, Clarke LR.
Author information
1Departments of Allergy, Sydney, N.S.W., Australia.
Abstract
Adverse reactions to alcoholic beverages are common and diverse in aetiology. Ethanol-induced anaphylaxis, however, is a rare but often life-threatening condition that warrants careful evaluation in suspected individuals. We present the cases of two patients who developed urticaria, angioedema and throat constriction within minutes of consuming white wine. Both individuals demonstrated no adverse reaction to double-blind placebo-controlled challenges to metabisulphite or sodium salicylate. However, an open challenge to white wine elicited urticaria in both subjects. This reaction was reproduced with a double-blind placebo-controlled challenge to ethanol and was accompanied by a rise in serum total tryptase levels. Positive skin test responses to 2% acetic acid, a breakdown product of ethanol, were elicited from both patients but not from three normal controls. These two cases demonstrate the need for a systematic approach for the evaluation of allergic reactions to alcohol.

Allergol Int. 2006 Dec;55(4):411-4.
Urticarial reaction caused by ethanol.
Nakagawa Y1, Sumikawa Y, Nakamura T, Itami S, Katayama I, Aoki T.
Author information
1Osaka Kouseinenkin Hospital, Osaka-city, Japan.
Abstract
Background: We report a case of an urticarial reaction after drinking alcohol beverages. The patient was a 47-year-old man suffering urticarial and anaphylactoid reaction to alcohol for two years. These reactions were observed at every alcohol beverages intake.
Case Summary: We performed a prick test with diluted ethanol, alcohol beverages and their metabolites (acetaldehyde, acetic acid). Only acetic acid showed a positive result. Oral challenge test with diluted-ethanol caused pruritus and swelling of his lips. An oral challenge test with 8% diluted Shochu (Japanese distilled alcohol from rice or wheat) caused wheals on his upper back.
Discussion: Only acetic acid, a metabolite of alcohol, induced a positive prick test in the patient with alcohol-induced urticaria. This result was not observed in normal volunteers. An oral challenge test with diluted-alcohol or Shochu showed a positive wheal reaction in a dose dependent-manner which suggests that urticaria seen in this patient might be induced by alcohol-intolerance. However possible allergic reaction to acetaldehyde could not be excluded.

J Hematol Oncol. 2011 Mar 22;4:10. doi: 10.1186/1756-8722-4-10.
Mast cell activation disease: a concise practical guide for diagnostic workup and therapeutic options.
Molderings GJ1, Brettner S, Homann J, Afrin LB.
Author information
1Institute of Human Genetics, University Hospital of Bonn, Germany.
Abstract
Mast cell activation disease comprises disorders characterized by accumulation of genetically altered mast cells and/or abnormal release of these cells' mediators, affecting functions in potentially every organ system, often without causing abnormalities in routine laboratory or radiologic testing. In most cases of mast cell activation disease, diagnosis is possible by relatively non-invasive investigation. Effective therapy often consists simply of antihistamines and mast cell membrane-stabilising compounds supplemented with medications targeted at specific symptoms and complications. Mast cell activation disease is now appreciated to likely be considerably prevalent and thus should be considered routinely in the differential diagnosis of patients with chronic multisystem polymorbidity or patients in whom a definitively diagnosed major illness does not well account for the entirety of the patient's presentation.

Clin Exp Allergy. 2011 Dec;41(12):1777-83. doi: 10.1111/j.1365-2222.2011.03848.x. Epub 2011 Sep 1.
An increase in serum tryptase even below 11.4 ng/mL may indicate a mast cell-mediated hypersensitivity reaction: a prospective study in Hymenoptera venom allergic patients.
Borer-Reinhold M1, Haeberli G, Bitzenhofer M, Jandus P, Hausmann O, Fricker M, Helbling A, Müller U.
Author information
1Allergiestation, Medizinische Klinik, Spital Netz Bern Ziegler, Bern, Switzerland.
Abstract
Background: During a systemic hypersensitivity reaction (SR), an increase in serum tryptase compared to the baseline value is an indicator of mast cell activation, most often due to an IgE-mediated mechanism.
Objective: To study the relevance of an increase in serum tryptase below the upper normal value of 11.4 ng/mL.
Methods: Serum tryptase levels were measured in 35 patients with Hymenoptera venom hypersensitivity before and during venom exposure. Of these, 20 developed SR to stings or following venom injections during immunotherapy (reactors), while 15 tolerated reexposure to stings or venom injections during immunotherapy without SR (non-reactors). Serum tryptase was estimated at 2, 5 and 24 h after exposure and was compared to a baseline value obtained before or at least 72 h after exposure.
Results: Considering circadian variation of serum tryptase, a relative increase to =135% of the baseline value (relative delta bound) was defined to indicate mast cell activation. Such an increase was observed in 17 of 20 reactors (85%), but none of 15 non-reactors. A serum tryptase of =11.4 ng/mL following venom exposure was observed in eight of the 20 reactors (40%) and 2 (13.3%) of the 15 non-reactors. Both these non-reactors also had an elevated baseline serum tryptase.
Conclusions and Clinical Relevance: Serum tryptase values obtained during a suspected hypersensitivity reaction must always be compared to a baseline value. A relative tryptase increase to =135% of the baseline value during a suspected hypersensitivity reaction indicates mast cell activation even below 11.4 ng/mL.

3/15/2013
I saw a 20 yo college student in Nov. 2012 for angioedema of face that began in assoc. with consumption of large amount of alcohol including vodka, bourbon and tequila. Work up otherwise was negative. IgE only 15. Subsequently did well until recently when he had urticaria on 2 occasions that seemed to be associated with 1.5 shots of bourbon on one occasion and one shot of vodka in cranberry juice on another. He has not consumed any beer or wine in a long time. I am writing re: workup. I have read the “Expert” section of website, but was not sure how far to go. I cannot find a lab where I can obtain acetaldehyde dehydrogenase 2 levels. The pt. is not Asian. What about testing with ethanol (? what dilutions) or the individual alcoholic drinks? What about a challenge with beer or wine or the beverages in question? What about testing with acetic acid as mentioned in one study? I could tell pt. not to consume alcohol again, but I am sure he would not do this. Any additional suggestions?

A:
I am sending your question to Dr. Carmen Vidal, who does research in IgE-mediated reactions to carbohydrates, and has published extensively in regards to alcohol-related reactions. As soon as we receive her response, we will forward it to you.

Thank you again for your inquiry.

Sincerely,
Phil Lieberman, M.D.

Response from Dr. Carmen Vidal:
Well, first of all, it is important to know the composition of these beverages. As you know, alcoholic drinks differ in their composition (beer, for instance, can be made of barley...). I do not know the composition of these kind of spirits, perhaps some fruits or something like this.

The best option should be to perform an oral controlled challenge test in order to see the nature of the reaction. First of all, prick-prick tests with those drinks should be advisable. If positive, and knowing the exact composition, more prick tests should be performed. If negative, oral challenge test with increasing doses of the drinks should be performed. This patient seems to react against one kind of drink but tolerates others. That should be enough to rule out alcohol per se hypersensitivity.

Typical clinical picture of acetaldehyde dehydrogenase misfunction includes flushing but not angioedema.

Best Regards,
Carmen Vidal

Urticaria, facial swelling after beer/alcohol
Is there any reason why a patient of mine would have sudden onset of itchy hives on hands and facial swelling after consumption of beer and/or alcohol?

A:
There are a number of reports of reactions to alcohol in general, and to beer specifically in the literature. There are various explanations for these reactions including IgE-mediated reactions to the content of the drink involved, for example, hops in beer, as well as deficiencies in the acetaldehyde dehydrogenase enzyme. This question has been posed to our website on a number of occasions, and I am copying for you below a fairly recent response in this regard. In essence, nothing has changed since this response was placed on the website in 2008. There is also, at the bottom of this response, a fairly complete reading list which can give you more details of these types of reactions should you wish to research them further.

3/4/2008
I would like to know if there has ever been a case of a patient being allergic to beer, wine, and rum – all three. And if so, please email the information and outcome.

Answer:
There are a number of case reports of urticarial and anaphylactic reactions as well as flush and asthma to alcohol. A number of different mechanisms have been suggested regarding the production of these events. The flush and wheeze syndrome, which can be confused with an anaphylactic event, is well known and especially common in those of Asian descent. It is due to a defective metabolism of alcohol resulting from the deficient activity of acetaldehyde dehydrogenase-2, the enzyme that metabolizes acetaldehyde, a byproduct of alcohol metabolism. When acetaldehyde accumulates in the blood, mast cells degranulate and histamine levels rise. Patients can exhibit flush and urticarial type reactions, as well as wheezing.

Other mechanisms involved in anaphylactic and urticarial reactions to alcohol ingestion have also been described. Sensitization to both alcohol and acetic acid has been reported.

The reference list below will give you an adequate panorama of the types of reports detailing patients experiencing anaphylactic and other immediate hypersensitivity-like reactions to the ingestion of alcohol.

References:
1. Haden JR and Khan DA. Remission of anaphylactoid reaction to alcohol. J Allergy Clin Immunol, February 2003; 111(1):S98-S99 (abstract).
2. Takao A, et al. Correlation between alcohol-induced asthma and acetaldehyde dehydrogenase-2 genotype. J Allergy Clin Immunol 1998; 101(5):576-580.
3. Ehlers I, et al. Ethanol as a cause of hypersensitivity reactions to alcoholic beverages. Clin and Expe Allergy 2002; 32(8):123-125.
4. Kelso JM, et al. Anaphylactoid reaction to ethanol. Annals of Allergy 1990; 64(5):452-454.
5. Ormerod AD and Holt PJA. Acute urticaria due to alcohol. Br J Derm 1983; 108:723-724.
6. Przybilla B and Ring J. Anaphylaxis to ethanol and sensitization to acetic acid. Lancet 1983; 483.
7. Sticherling M and Brasch J. Alcohol: Intolerance syndromes, urticarial and anaphylactoid reactions. Clin Dermatol 1999; 17(4):417-422.
8. Timg S. Anaphylactoid reaction to alcohol. Annals of Allergy 1992; 69(5):463.

Allergic-like reaction to white wine and beer
12/20/2011
A patient report a sensation of throat closing, increased salivation and on occasion a hoarse voice with certain beer and white wine ingestions. Guinness does not seem to bother him. He has an Epi-pen and when he experiences any of these symptoms he stops drinking the aforementioned beverages. No problem with liquor. He is Asian-no flushing no wheezing. He was tested for wheat, malt, barley, hops, white grape, botrytis and saccharomyces cerevisiae-which was the only positive Are there any other products that should be avoided besides beer and wine?

A:
I think that you have done relatively good due diligence, especially regarding the workup for the patient who has an allergic-like reaction to beer. However, wine is a far more complex culprit, and there are other putative agents in wine that have been incriminated. It is a very complex issue, and in my experience, one is very rarely able to identify any specific agent in patients such as the one you described. Also the history of reacting to white wine and beer, but not other alcoholic preparations is puzzling since I know of no allergen that would normally be shared between them.
Just to illustrate the complexity of the issue, I have copied below a number of abstracts along with a reference. We also have a couple of entries on the Academy’s Ask the Expert website that can be reviewed by simply typing “wine” into the search box.

In summary, it is very unlikely, at least in my experience, that you will be able to identify a culprit that is responsible for these reactions, especially one that would be common to both white wine and beer. However, it may be helpful for you, if for no other reason than to illustrate the difficulties involved, to peruse the references below and the previous website entries to the Ask the Expert website regarding these issues.

F. Borghesan Allergy to Wine Allergy Volume 59, Issue 10, pages 1135–1136, October 2004
Journal of Allergy and Clinical Immunology
Volume 111, Issue 2, February 2003, Pages 350-359 Mechanisms of Allergy
Identification of grape and wine allergens as an Endochitinase 4, a lipid-transfer protein, and a Thaumatin
Elide A. Pastorello MDa, Laura Farioli BScb, Valerio Pravettoni MDa, Claudio Ortolani MDc, Donatella Fortunato BScd, Maria Gabriella Giuffrida BScd, Lorenza Perono Garoffo BScd, Ambra Marianna Calamari MDa, Oreste Brenna PhDe, Amedeo Conti PhDd
From athe Allergy Center, First Division of General Medicine, Ospedale Maggiore IRCCS, Milan; bUOOML, CEMOC, I.C.P., Milan; cBizzozzero Division, Niguarda Ca' Granda Hospital, Milan; dNational Research Council, ISPA, Turin; and ethe Department of Food Science and Microbiology, University of Milan, Milan.
Received 9 April 2002; revised 20 May 2002; Available online 9 April 2003.
Abstract
Background: Few allergic reactions to grape are reported in the literature. In some cases an association with peach and cherry allergy was observed. No IgE-mediated reactions to wine have been described, and no grape major allergens have yet been identified.
Objective: We describe several severe reactions to grape or wine. We characterized the grape major allergens and tried to identify the allergen in wine. Methods: We collected documented histories of allergic reactions to grape and wine. Grape allergens were identified by means of SDS-PAGE and immunoblotting and purified by means of HPLC. Using amino acid sequencing and mass spectrometry, we identified the family of proteins to which the allergens belong. Cross-reactivity with peach and cherry was evaluated by means of cross-wise inhibition experiments.
Results: Eleven patients with reactions to grape and 3 with anaphylactic reactions to wine were recruited. The major allergens were an endochitinase 4A and a lipid-transfer protein (LTP) that was homologous to and cross-reactive with peach LTP. A 24-kd protein homologous to the cherry thaumatin-like allergen was a minor allergen. Endochitinase 4A is very likely the allergen in vino novello and in vino Fragolino.
Conclusions: Grape and wine might cause severe allergic reactions in sensitive patients. The major allergens of grape are endochitinase 4A, which is also the allergen of wine, and an LTP cross-reacting with the peach major allergen. (J Allergy Clin Immunol 2003;111:350-9.)

Food Addit Contam Part A Chem Anal Control Expo Risk Assess. 2011 Apr;28(4):408-16. Epub 2011 Feb 16.
Levels of histamine and other biogenic amines in high-quality red wines.
Konakovsky V, Focke M, Hoffmann-Sommergruber K, Schmid R, Scheiner O, Moser P, Jarisch R, Hemmer W.
Source
FAZ - Floridsdorf Allergy Centre, Franz Jonas Platz 8/6, A-1210 Vienna, Austria.
Abstract
Biogenic amines in wine may impair sensory wine quality and cause adverse health effects in susceptible individuals. In this study, histamine and other biogenic amines were determined by HPLC after amine derivatisation to dansyl chloride conjugates in 100 selected high-quality red wines made from seven different cultivars. Amine levels varied considerably between different wines. The most abundant amines were putrescine (median = 19.4 mg l(-1), range = 2.9-122), histamine (7.2 mg l(-1), 0.5-26.9), and tyramine (3.5 mg l(-1), 1.1-10.7), whereas lower levels were found for isoamylamine (median = 0.25 mg l(-1)), phenylethylamine (0.16 mg l(-1)), cadaverine (0.58 mg l(-1)), spermidine (1.8 mg l(-1)) and tryptamine (0.06 mg l(-1)). Positive correlations were observed between isoamylamine and phenylethylamine, and between histamine, putrescine and tyramine levels. Amine concentrations were similar in all wine cultivars except Pinot noir and St. Laurent wines, which showed significantly higher tryptamine and cadaverine levels. The results indicate that levels of histamine and other biogenic amines may vary considerably between red wines independent of grape variety and that high amounts can also be found in high-rated wines. Adopting a legal histamine threshold level of 10 mg l(-1) in the European Union, as formerly introduced in other countries, would have excluded 34% of the investigated wines from the market.

Curr Opin Allergy Clin Immunol. 2008 Jun;8(3):266-9.
Adverse reactions to wine: think outside the bottle.
Armentia A.
Source
Allergy Section, Río Hortega Hospital, Valladolid, Spain.
Abstract
Purpose of Review: Wine contains chemical and biological contaminants. Symptoms such as facial flushing, asthma and oral allergic swelling and burning (oral syndrome) have been attributed to these contaminants and food additives. Their clinical implications should be known.
Recent Findings: Recent studies have reported a high prevalence of hypersensitivity symptoms after intake of alcoholic drinks in the general population. Red wine was the most common beverage implicated. Wine contains many contaminants. Some of them come from Hymenoptera insects that fall into the wine when grapes are collected and pressed. We have found patients with allergic symptoms related to wine consumption who are sensitized to Hymenoptera venom without previous stings. The aim of this study is to assess the potential importance of their sensitization to Hymenoptera antigens as the cause of their symptoms and also to comment on other recent studies on wine hypersensitivity.
Summary: We found patients with allergic symptoms related to wine consumption who are sensitized to Hymenoptera venoms. Challenges were negative with sulfites, other additives and aging wines, but positive with young wines. Sera from all the patients detected Hymenoptera venom antigens. We report the first cases of sensitization to venom antigens by the oral route.

Allergy. 1999 Jun;54(6):630-4.
Beer-induced anaphylaxis: identification of allergens.
Figueredo E, Quirce S, del Amo A, Cuesta J, Arrieta I, Lahoz C, Sastre J.
Source
Fundación Jiménez Díaz, Servicio de Alergología, Universidad Autónoma de Madrid, Spain.
Abstract
Background: We report on a 21-year-old atopic woman who developed urticaria, angioedema of the face, and wheezy dyspnea shortly after drinking beer and after eating a corn-made snack.
Methods: Skin prick tests and specific IgE determinations to beer ingredients and cereal extracts were performed. Immunoblotting inhibition assays were carried out to investigate possible common allergens shared by barley and malt with corn.
Results: Skin prick tests and specific IgE measurements with beer, barley, malt, wheat, corn, rye, rice, and oat flour were positive. Ten pollen-allergic patients showed negative skin tests to beer. Double-blind, placebo-controlled, oral challenge tests with sodium metabisulfite and wheat flour were negative. Immunoblotting demonstrated several IgE-binding bands at 31-56 kDa in malt and barley extracts, and a major band at 38 kDa in the beer extract. Immunoblot inhibition assays showed that malt extract was able to inhibit most of the IgE-binding bands in wheat and corn extracts, whereas corn did not produce significant inhibition to barley and malt extracts.
Conclusions: This patient developed type I hypersensitivity to barley/malt and corn. Although she also showed IgE reactivity to wheat and other cereals, no symptoms were elicited upon ingestion of these cereals, probably indicating latent sensitization to them.

Sincerely,
Phil Lieberman, M.D.

Ask The Expert
7/19/2013
Safety of the ingestion of alcohol in patients with indolent systemic mastocytosis

Case Rep Dermatol. 2009 Apr 29;1(1):1-6.
Two Case Reports of Life-Threatening Ethanol-Induced Anaphylaxis.
Fernando SL1, Clarke LR.
Author information
1Departments of Allergy, Sydney, N.S.W., Australia.
Abstract
Adverse reactions to alcoholic beverages are common and diverse in aetiology. Ethanol-induced anaphylaxis, however, is a rare but often life-threatening condition that warrants careful evaluation in suspected individuals. We present the cases of two patients who developed urticaria, angioedema and throat constriction within minutes of consuming white wine. Both individuals demonstrated no adverse reaction to double-blind placebo-controlled challenges to metabisulphite or sodium salicylate. However, an open challenge to white wine elicited urticaria in both subjects. This reaction was reproduced with a double-blind placebo-controlled challenge to ethanol and was accompanied by a rise in serum total tryptase levels. Positive skin test responses to 2% acetic acid, a breakdown product of ethanol, were elicited from both patients but not from three normal controls. These two cases demonstrate the need for a systematic approach for the evaluation of allergic reactions to alcohol.

Allergol Int. 2006 Dec;55(4):411-4.
Urticarial reaction caused by ethanol.
Nakagawa Y1, Sumikawa Y, Nakamura T, Itami S, Katayama I, Aoki T.
Author information
1Osaka Kouseinenkin Hospital, Osaka-city, Japan.
Abstract
Background: We report a case of an urticarial reaction after drinking alcohol beverages. The patient was a 47-year-old man suffering urticarial and anaphylactoid reaction to alcohol for two years. These reactions were observed at every alcohol beverages intake.
Case Summary: We performed a prick test with diluted ethanol, alcohol beverages and their metabolites (acetaldehyde, acetic acid). Only acetic acid showed a positive result. Oral challenge test with diluted-ethanol caused pruritus and swelling of his lips. An oral challenge test with 8% diluted Shochu (Japanese distilled alcohol from rice or wheat) caused wheals on his upper back.
Discussion: Only acetic acid, a metabolite of alcohol, induced a positive prick test in the patient with alcohol-induced urticaria. This result was not observed in normal volunteers. An oral challenge test with diluted-alcohol or Shochu showed a positive wheal reaction in a dose dependent-manner which suggests that urticaria seen in this patient might be induced by alcohol-intolerance. However possible allergic reaction to acetaldehyde could not be excluded.

J Hematol Oncol. 2011 Mar 22;4:10. doi: 10.1186/1756-8722-4-10.
Mast cell activation disease: a concise practical guide for diagnostic workup and therapeutic options.
Molderings GJ1, Brettner S, Homann J, Afrin LB.
Author information
1Institute of Human Genetics, University Hospital of Bonn, Germany.
Abstract
Mast cell activation disease comprises disorders characterized by accumulation of genetically altered mast cells and/or abnormal release of these cells' mediators, affecting functions in potentially every organ system, often without causing abnormalities in routine laboratory or radiologic testing. In most cases of mast cell activation disease, diagnosis is possible by relatively non-invasive investigation. Effective therapy often consists simply of antihistamines and mast cell membrane-stabilising compounds supplemented with medications targeted at specific symptoms and complications. Mast cell activation disease is now appreciated to likely be considerably prevalent and thus should be considered routinely in the differential diagnosis of patients with chronic multisystem polymorbidity or patients in whom a definitively diagnosed major illness does not well account for the entirety of the patient's presentation.

Clin Exp Allergy. 2011 Dec;41(12):1777-83. doi: 10.1111/j.1365-2222.2011.03848.x. Epub 2011 Sep 1.
An increase in serum tryptase even below 11.4 ng/mL may indicate a mast cell-mediated hypersensitivity reaction: a prospective study in Hymenoptera venom allergic patients.
Borer-Reinhold M1, Haeberli G, Bitzenhofer M, Jandus P, Hausmann O, Fricker M, Helbling A, Müller U.
Author information
1Allergiestation, Medizinische Klinik, Spital Netz Bern Ziegler, Bern, Switzerland.
Abstract
Background: During a systemic hypersensitivity reaction (SR), an increase in serum tryptase compared to the baseline value is an indicator of mast cell activation, most often due to an IgE-mediated mechanism.
Objective: To study the relevance of an increase in serum tryptase below the upper normal value of 11.4 ng/mL.
Methods: Serum tryptase levels were measured in 35 patients with Hymenoptera venom hypersensitivity before and during venom exposure. Of these, 20 developed SR to stings or following venom injections during immunotherapy (reactors), while 15 tolerated reexposure to stings or venom injections during immunotherapy without SR (non-reactors). Serum tryptase was estimated at 2, 5 and 24 h after exposure and was compared to a baseline value obtained before or at least 72 h after exposure.
Results: Considering circadian variation of serum tryptase, a relative increase to =135% of the baseline value (relative delta bound) was defined to indicate mast cell activation. Such an increase was observed in 17 of 20 reactors (85%), but none of 15 non-reactors. A serum tryptase of =11.4 ng/mL following venom exposure was observed in eight of the 20 reactors (40%) and 2 (13.3%) of the 15 non-reactors. Both these non-reactors also had an elevated baseline serum tryptase.
Conclusions and Clinical Relevance: Serum tryptase values obtained during a suspected hypersensitivity reaction must always be compared to a baseline value. A relative tryptase increase to =135% of the baseline value during a suspected hypersensitivity reaction indicates mast cell activation even below 11.4 ng/mL.

I hope this information helps you in the care of your patient.

All my best.
Dennis K. Ledford, M.D., FAAAAI

Close-up of pine tree branches in Winter Close-up of pine tree branches in Winter