The significance of post mortem tryptase levels in supportinga diagnosis of anaphylaxis

After reading the case report regarding a lady who suffered a fatal anaphylactic reaction at induction (Konarzewski & De'Ath. Anaesthesia 2001; 56: 497–8) and reply (Girgis. Anaesthesia 2001; 56: 1016–17), we feel neither author emphasised the significance of such a vastly elevated serum tryptase level (185 μg.l−1, normal < 1 μg.l−1). In addition, we would like to reiterate that the absence of cutaneous and respiratory features of anaphylaxis does not preclude the diagnosis. Following death, body tissues undergo autolysis and therefore tryptase enzyme leaks from tissue mast cells. This results in elevated serum tryptase levels if blood samples are taken post mortem. This was shown by Randall et al. [1], and Edston and Van Hage-Hamsten [2]. The former found that 31 out of 49 autopsy cases had raised tryptase levels when there was no evidence of anaphylaxis. However, of the 31 cases, 24 had values of only 1–5 μg.l−1, two had values of 5–10 μg.l−1, five had values␣of␣> 10 μg.l−1 and one had a value of 106 μg.l−1 The figure of 185 μg.l−1is far in excess of any of Randall's 31 autopsy cases. Edston and van Hage-Hamsten [2] looked at 193 post mortem patients of known, unexplained and anaphylactic deaths. They found they required a significantly high cut-off tryptase value of 10 μg.l−1 to provide a specificity for anaphylaxis of 88%. This was increased to 93% if a cut-off of 20 μg.l−1 was used. We feel the main reasons for raised post mortem serum tryptase levels are: autolysis, trauma resulting in organ damage (one case had a reported tryptase level of 170 μg.l−1 following a car accident [2]) and anaphylaxis/anaphylactoid reactions. Autolysis is likely to give low to moderate tryptase levels, i.e. 1–10 μg.l−1[1], whereas trauma and anaphylaxis give much higher figures, i.e. > 20 μg.l−1[2]. Recent Advances in Histopathology [3] advise that post mortem tryptase levels should be interpreted with caution unless grossly elevated and supported by a suggestive clinical history. The absence of cutaneous and respiratory manifestations of anaphylaxis suggests a rapid onset, for example an intravenous allergen as opposed to an ingested allergen. Out of a series of 56 iatrogenic anaphylactic deaths, none demonstrated cutaneous manifestations, and only 13 demonstrated upper airway oedema and bronchial obstruction [3]. As we have a good case report history (also presented to Konarzewski and De'Ath's anaesthetic department), a tryptase level of 185 μg.l−1, and no autopsy evidence to dispute the diagnosis of anaphylaxis, we believe this lady died as a result of an anaphylactic reaction.