Lisa Dunkley

IgG4-related disease presenting with raised serum IgG2-real timeline of IgG4-RD?

elevated (Fig. 1A). A chest CT scan confirmed right lowerand middle-lobe pneumonia (Fig. 1B). Blood cultures, pneumococcal and legionella antigen urine tests were negative. Sputum could not be collected in the absence of cough. Amoxicillin/clavulanate i.v. was started and the prednisone dose increased to 20 mg/day for 3 days. After 24 h, antibiotics were switched to oral therapy and continued for 14 days total. On the third day on antibiotics he developed a productive cough but generally felt much better. IL-6 normalized within 10 days. TCZ was discontinued and he remained asymptomatic and with normal CRP and ESR 12 weeks after the last TCZ dose. Pneumonic infiltrate was resolved 8 weeks later (Fig. 1C). According to post-marketing surveillance of TCZ in RA, patients >65 years of age with prednisone doses >5 mg and pre-existing pulmonary conditions were at highest risk for pneumonia [3]. GCA patients are older and exposed to high prednisone doses [7]. Community-acquired pneumonia may—like diverticulitis—present subtly in TCZ-treated patients. A surrogate marker for infection would thus be of value. Our case illustrates that IL-6 measurement may be useful in early detection and therapy monitoring in TCZtreated patients. Rising/high IL-6 with TCZ treatment irrespective of CRP/ESR should alert one to search for infection. Whether IL-6 elevation differentiates infection vs GCA relapse remains to be tested.

4. A challenging case of refractory BehÇet's disease in an adolescent with sight threatening uveitis

patient.Asignificantlyelevatedtroponinhowever,couldnotbeexplained bya tachyarrhythmiaalone.One hypothesis fordevelopinganacutecoronary syndrome, is the vasodilatation role of TNF in the maintenance of myocardial vascular perfusion through the induction of nitric oxide. It is also capable of inhibiting apoptosis of myocardiocytes and attenuation of cardiac stimulation by the sympathetic nervous system through breceptors. The administration of Infliximab, which is a potent anti-TNF antibody can neutralise both soluble and membrane-bound TNF which can suspend these homeostatic mechanisms, resulting in deprivation of first linedefencesandleadingtocoronaryvasoconstrictionandhypoperfusion. Why patients without prior cardiovascular disease develop such symptomsisstillunclearandmaybeafurtherscopeforresearch. KeyLearning Points:Potentanti-TNFagents have the theoretical ability of causing coronary vasoconstriction and hypoperfusion. Albeit rare, patients presenting with chest pain, during or after the infusion should have the appropriate coronary biochemistry and investigations performed.Youngpeoplewithnoriskofcardiovasculardiseasecandevelop transient acute coronary syndrome in response to potent anti-TNF agents. Doubling the frequency of infusion in attempt to regain control of disease after secondary failure should be done with caution and may increasetherisk. Disclosure: K.M. Achilleos: None. P. Bale: None. A. Shastri: None. N. Puvanachandra:None.K.Armon:None.