Consider the rare side effects of allergy/anaphylaxis when prescribing sumatriptan or any other triptan. Although the full extent of cross-reactivity between triptan drugs is not known, caution should be exercised with other triptans when a patient has had a reaction to a triptan.

Sumatriptan is an effective and well-tolerated medication used for the acute relief of migraines. It blocks nociceptive neurotransmission by binding onto 5-HT1b and 5-HT1d-like serotonin receptors and vasoconstricting cerebral and dural blood vessels.1 It contains a sulfonamide chemical group and hence is considered a sulfa drug. We report a rare report of skin test-proven sumatriptan anaphylaxis in an 18-year-old female.

Cryoglobulins precipitate out of serum at temperatures lower than 37°C and can have serious clinical manifestations. They may be associated with haematological malignancies, chronic infections and autoimmune diseases. Traditional typing of cryoglobulins use the Brouet classification, depending on the presence or not of rheumatoid factor activity: type I (monoclonal immunoglobulin with no rheumatoid factor), type II (mixed cryoglobulin with monoclonal rheumatoid factor) and type III (mixed cryoglobulin with polyclonal rheumatoid factor). Current methods used to type cryoglobulins include electrophoresis and immunofixation. We describe a novel, streamlined workflow of cryoglobulin analysis using mass spectrometry (MS) to characterise the proteomic signatures [heavy chain complementarity-determining region 3 (HCDR3) regions] of cryoglobulins. This provides an extension to traditional immunochemical methods of analysis and offers increased sensitivity; monitoring capacity by HCDR3 regions at the amino acid level; and clinical applications. Outstandingly, MS analysis offers predictive value by detecting the presence of pathogenic clonotypes before the onset of clinical manifestations. We highlight its applicability and benefits through clinical cases, demonstrating the greater ability to molecularly characterise cryoprecipitates in a similar turn-around time to current methodology. Work to establish clinically relevant libraries of antibody clonotypes is currently underway.

Medication allergy is a significant cause of morbidity and mortality and proper evaluation and management by an allergy service is of paramount importance. We audited all adult medication allergy outpatient referrals received by a tertiary allergy/clinical immunology service for completeness. A 6‐month prospective audit of all medication allergy referrals was undertaken at a tertiary public hospital in South Australia. Each referral was assessed against the Australasian Society for Clinical Immunology and Allergy (ASCIA) medication allergy referral template. A total of 73 medication allergy referrals were received. There was an overall poor level of adherence to all criteria (44.7%) and general practitioner (GP) referrals were generally more detailed than internal referrals. Inadequately detailed referrals may have the knock‐on effect of inappropriate triaging of referrals. Future studies are required to identify barriers to doctors providing sufficiently detailed referrals, and investigate appropriate interventions to improve this.

A 75-year-old, nonatopic man had been experiencing a gastroenteritis-like illness for the last 24 hours characterized by diarrhea and malaise. He decided to take, for the first time, 4 mg of loperamide hydrochloride to assist with symptom relief. Within 30 minutes, he developed severe anaphylaxis with widespread urticaria, presyncope, and acute worsening of diarrhea and vomiting. He was transported by ambulance to the hospital, where his initial blood pressure was 82/50 mm Hg. He was successfully resuscitated with 2 doses of intramuscular epinephrine (1 mg total) and intravenous saline.

The purpose of this audit was to review the 2 day Ultra-rush bee venom immunotherapy (VIT) protocols used at Flinders Medical Centre (FMC) to assess rate, dose, severity of reaction and treatment provided as well as cumulative/final dosing level achieved for each patient. A retrospective case note review of all patients undergoing Ultra-rush VIT at FMC, between July 2010 and June 2016 was conducted. Patient demographics, details of the initial reaction and reactions during the initial 2 days of immunotherapy, baseline tryptase, and bee venom specific IgE’s were recorded for analysis. A total of 36 patients commenced VIT during the review period. 19 of these undertook Ultra-rush VIT, all with prior grade 2–3 bee venom anaphylaxis (Brown scale, 2004). The age ranged from 2 to 17 years at commencement of treatment. There were 14 males and 5 females. Of the 19 patients, 3 (16%) had no reaction and 8 (42%) had injection site reactions. 2 patients (11%) developed urticaria. 6 patients (32%) had anaphylaxis on day 1 or 2, with one patient having anaphylaxis on both days. 4 patients reacted to the 20 mcg dose, 1 at 30mcgs and the final patient reacted at 10mcgs on day one and 30mcgs on day 2. 5 patients received IM adrenaline and another, with transient bronchospasm, responded promptly to salbutamol. 2 patients achieved a final single dose of ≥50mcg without reaction on day 2. The remaining 4 patients tolerated a final single dose between 20 and 40 mcg. Ultra-rush bee VIT continues to be a safe and effective treatment option in children with a history of bee venom anaphylaxis. A target single dose of ≥50 mcg was achieved in 15/19 (79%) patients. Future amendments of the ultra-rush protocol need to consider the 20mcg dose as a threshold for anaphylaxis.

We have recently reported the presence of an immunoglobulin G (IgG) autoantibody (Ab) in patients with narcolepsy with cataplexy that abolishes spontaneous colonic migrating motor complexes (CMMCs) and increases smooth muscle tension and atropine-sensitive phasic contractions in a physiological assay of an isolated colon. In this study, we used the cholinesterase inhibitor, neostigmine, to explore the mechanism of the narcoleptic IgG-mediated disruption of enteric motor function in four patients with narcolepsy with cataplexy and to identify a pharmacological mimic of the Ab. Neostigmine potentiated the narcoleptic IgG-mediated increase in smooth muscle resting tension and phasic smooth muscle contractions by an atropine-sensitive mechanism but exerted no effect on resting tension in the presence of control IgG. Decreased frequency of CMMCs mediated by IgG with anti-M3R activity was reversed by neostigmine. Therefore, a challenge with a cholinesterase inhibitor improves the specificity of the CMMC assay for narcoleptic IgG. Tetrodotoxin (TTX), a neuronal sodium channel blocker, also abolished CMMCs and increased resting tone, and a similar potentiation was observed with neostigmine; thus, TTX is a mimic of the functional effects of the narcoleptic IgG in this bioassay. These findings provide a link to pharmacological studies of canine narcolepsy and are consistent with a functional blockade of both excitatory and inhibitory motor neurons by the narcoleptic Ab, similar to the TTX mimic, presumably by binding to an autoantigenic target expressed in both populations of neurons.

Despite strong circumstantial evidence for the autoimmune hypothesis of narcolepsy, conventional immunological methods have failed to detect an autoantibody. This study investigated the real-time effects of narcoleptic immunoglobulins on a spontaneous colonic migrating motor complex (CMMC) preparation. IgG from patients with narcolepsy with cataplexy or healthy controls was added directly to isolated mouse colons undergoing CMMC activity to test for autoantibodies that disrupt colonic motility. The effect of immunoglobulins prepared for clinical intravenous treatment (IVIg) on autoantibody-mediated colonic disruption was also assessed. Narcoleptic IgGs markedly reduced the frequency of CMMCs or irreversibly abolished them. Abrogation of CMMCs was followed by an increase in the resting tension of the colon preparation and appearance of atropine-sensitive phasic smooth muscle contractions. IVIg partially neutralized the inhibitory effect of narcoleptic IgG on the CMMCs. The dramatic effect of narcoleptic IgG on CMMC generation is consistent with an autoantibody-mediated disruption of enteric neural pathways. The ex vivo whole-organ approach allows real-time examination of the physiological effects of the narcoleptic autoantibody and offers a new avenue for exploring the autoimmune basis of narcolepsy. The neutralizing effect of IVIg on the autoantibody provides a rationale for the reported clinical improvement in cataplexy when IVIg are given at disease onset.