D. Gillis

Role of local immunoglobulin E production in the pathophysiology of noninvasive fungal sinusitis

Objectives/Hypothesis: Immunoglobulin (Ig)E‐mediated hypersensitivity to fungi has been postulated to explain allergic fungal sinusitis (AFS). Not all patients suspected to have AFS demonstrate systemic evidence of allergy. Locally produced IgE might explain those patients with no systemic evidence of allergy but clinical features of AFS. The aim was to determine whether fungal‐specific IgE could be demonstrated in sinus mucin in patients with eosinophilic mucin rhino‐sinusitis.

Aspirin-sensitive asthma

Abstract

Improvement in intestinal permeability precedes morphometric recovery of the small intestine in coeliac disease

It is often difficult to assess small bowel recovery in adults with coeliac disease on a gluten-free diet (GFD). This prospective study compares changes in intestinal permeability with changes in intestinal biopsy at various intervals after commencing a GFD. Intestinal permeability was measured by lactulose/rhamnose absorption from 1 week to 24 months after commencing a GFD. Intestinal morphometry was measured by villus area, crypt length and mitotic count per crypt at diagnosis and after commencing a GFD. Median intestinal permeability values decreased from 0.47 (n = 35) at diagnosis to 0.25 (n = 17) after 1 week and to 0.16 (n = 18) after 2 months of a GFD. Rhamnose absorption improved significantly at an early stage, from 6.6% (untreated) to 15.4% at 3 months of a GFD, whereas the decrease in lactulose permeation took longer: from 3.4% (untreated) to 0.8% after 12 months of a GFD. Mean villus area (n = 29) was reduced to 16% of control values at diagnosis, and improved to a maximum of 48% after 6 months on a GFD, but did not change thereafter. Mean crypt length and mitotic count per crypt were increased by 222% and 356% respectively at diagnosis, and these parameters remained elevated at 172% and 216% above control values after 6 months of a GFD. We conclude that intestinal permeability improves within 2 months after starting a GFD, but that measurable intestinal biopsy improvement requires ingestion of a GFD for at least 3-6 months, and even then remains incomplete.

Rituximab use in systemic lupus erythematosus pneumonitis and a review of current reports

Rituximab is a chimeric monoclonal antibody specific for human CD20 that causes selective transient depletion of the CD20+ B‐cell subpopulation. We report the first case of systemic lupus erythematosus (SLE) pneumonitis resistant to conventional treatments that responded well to rituximab and review current reports on the use of rituximab in SLE.

Radiocontrast anaphylaxis with failure of premedication

Radiocontrast media (RCM) is used commonly in clinical practice, and can be associated with significant adverse effects. We report a patient who experienced severe anaphylaxis after being given multiple drugs. Challenge testing established allergy to both RCM and ceftriaxone. Premedication did not prevent recurrence of anaphylaxis on repeat challenge with RCM. The haemodynamic and serum tryptase consequences of the challenges are discussed, and a summary of RCM allergy is provided. (Intern Med J 2005; 35: 58−60)

Chronic urticaria: the autoimmune paradigm

Chronic urticaria is a disease consisting of spontaneous pruritic welts, present on all or most days for more than 6u2003weeks. It is commonly supposed to be allergic in origin, although allergy is not the cause in the majority of cases, and it has therefore been termed ‘chronic idiopathic urticaria’. Recent evidence indicates that at least a subset of patients in whom no extrinsic or internal cause can be identified are in fact autoimmune in origin. This is based mainly on the detection of pathogenic autoantibodies to the high‐affinity immunoglobulin E receptor FcɛR1, which are thought to activate cutaneous mast cells. In this article, we review the evidence that has given rise to this autoimmune ‘paradigm’ and its impact on diagnosis and management.

Anti-Ro52 antibodies, antisynthetase antibodies, and antisynthetase syndrome

We present a case of antisynthetase syndrome manifesting with interstitial lung disease, mechanic’s hands, nailfold abnormalities, and subclinical myositis, in the presence of antibodies to the aminoacyl tRNA synthetase PL-12 and also to Ro52. Antibodies to Ro52 have been recently associated with idiopathic inflammatory myositis, but there have only been occasional reports of this antibody occurring in association with aminoacyl tRNA synthetases, including PL-12. Our case adds to the descriptions of the concurrence of antibodies to PL-12 and Ro52. The mechanism for the coupling of antibody response remains elusive but is likely to play a fundamental role in disease pathogenesis.

Angioedema, lymphoproliferative disorder and angiotensin‐converting enzyme inhibitors: masking of diagnosis by corticosteroids

Angioedema is a relatively common clinical disorder. Although most cases are idiopathic, the use of angiotensin‐converting enzyme inhibitors is a well recognized cause of angioedema and a further rare but important diagnostic consideration is acquired C1 inhibitor deficiency. We discuss the diagnosis of C1 inhibitor deficiency in angioedema, with reference to a case in which the diagnosis was initially masked by the use of corticosteroids, which normalized the C1 inhibitor level.