Immune dysfunction attributed to hypogammaglobulinaemia is common in chronic lymphocytic leukaemia (CLL) and infection is a major contributor to morbidity and mortality. A higher incidence of multiple immunoglobulin and immunoglobulin G (IgG) subclass deficiency was associated with more advanced disease (P < 0·001 and P < 0·001, respectively) in a cohort of 147 CLL patients. Multiple immunoglobulin and IgG subclass deficiency were significantly associated with shorter treatment-free survival (TFS) (P < 0·001 and P = 0·006, respectively). The association between disease stage and immune dysfunction demonstrated by these data suggest aspects of immune deficiency correlate with disease severity and may be associated with shorter TFS in CLL.

Iron deficiency without anaemia is common. Patients may present with unexplained, non-specific symptoms.Iron studies will usually show a low ferritin and low transferrin saturation with a normal haemoglobin concentration. The cause of the iron deficiency should be identified and managed. Diagnosing iron deficiencyIron deficiency can occur secondary to inadequate dietary intake, increased requirements (e.g. pregnancy and breastfeeding), impaired absorption (e.g. coeliac disease, bariatric surgery), or blood loss (e.g. menstrual, blood donation, gastrointestinal). A drug history should be taken particularly regarding anticoagulants, over-thecounter non-steroidal anti-inflammatory drugs and antiplatelet drugs. The underlying cause of iron deficiency should always be sought and managed.

Whilst this may theoretically limit detection of small lesions in the pancreatic tail, it does not appear to have reduced the high sensitivity of 68 Ga-exendin-4 PET/CT in this case or published trials. 6 Recently updated scatter correction protocols have reduced this problem, but if observed it can be resolved through re-processing PET data without use of 'scatter correction'.In our patient initially reported to have a normal pancreas on CT, 68 Ga-exendin-4 PET/CT effectively localised an insulinoma at the splenic hilum enabling a curative laparoscopic resection. This case highlights the role of functional imaging with 68 Ga-exendin 4 PET/CT for preoperative insulinoma localisation. Delayed-onset heparin-induced thrombocytopenia complicated by arterial and venous thrombosesHeparin-induced thrombocytopenia (HIT) is an immune mediated adverse reaction caused by platelet-activating immunoglobulin G (IgG) antibodies reacting against platelet factor 4 (PF4) bound to heparin. 1,2 A more recently recognised atypical form, delayed-onset HIT, is due to high titre PF4/heparin antibodies which activate platelets even in the absence of heparin and cause thrombocytopenia and thrombosis weeks after heparin cessation. 3A 73-year-old female was diagnosed with delayedonset HIT 24-h after admission to our facility critically unwell with bilateral pulmonary emboli (PE). She was initially treated with tenecteplase followed by intravenous unfractionated heparin (IV UFH). Her platelet count prior to thrombolysis was 70 × 10 9 /L.A haematological consultation suggested the diagnosis of HIT syndrome, prompting her heparin infusion to be replaced with danaparoid. A screening test for antibodies to heparin/PF4 was positive. Over the next 4 days her platelet count fell to a nadir of 25 × 10 9 /L before gradually normalising over 2 weeks after heparin cessation. Her slow platelet count recovery caused the diagnosis of HIT to be questioned, but alternative diagnoses were excluded and serologic evidence of persisting high levels of antibodies supported the diagnosis of HIT. A functional whole blood impedance aggregometry assay was subsequently performed. Platelet aggregation occurred in the presence of low dose (0.5 IU/mL) heparin, but was abolished with high dose (100 IU/mL) thus demonstrating the platelet activating nature of the anti-PF4/heparin antibodies and confirming the diagnosis of HIT. 4,5 After 7 days of danaparoid therapy and confirmation of the diagnosis of HIT she was changed to rivaroxaban. She had three hospital admissions in the 2 months prior to presentation with PE and eventual HIT diagnosis. The first, a 5-day hospitalisation due to small-bowel obstruction, featured a normal platelet count while receiving daily enoxaparin as thromboprophylaxis. Five weeks later, she had a 2-day admission for elective shoulder replacement at which time she had a normal platelet count and received no thromboprophylaxis. One week after her orthopaedic surgery and 6 weeks after enoxaparin therapy she re-presented with an inferior ST-elevat...

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