We sought to elucidate the risk profiles of patients with Kawasaki disease who developed coronary artery abnormalities through a retrospective analysis with special reference to steroid treatment. Demographics of the patients were obtained from medical records, and characteristics of the coronary artery abnormalities were evaluated by echocardiography and coronary angiography, which included number, location, size, and length of coronary artery abnormalities (we evaluated by cardiac catheterisation with the American Heart Association classification with segments). We divided the patients into two groups based on steroid use and compared their characteristics and the complications of coronary artery abnormalities and cardiac events. A total of 29 patients were diagnosed with coronary artery abnormalities by echocardiography and coronary angiography during the study period (24 male; median age, 24 months [range: 2–84 months]). Eighteen patients were treated with aspirin and intravenous immunoglobulin (63%, non-steroid group), whereas 11 received aspirin and intravenous immunoglobulin plus steroids (37%, steroid group). No significant differences were found in the number and location of coronary artery abnormalities between the steroid and non-steroid groups. However, the size and number of segments for coronary artery abnormalities were significantly larger and shorter, respectively, in the steroid group (z-score: non-steroid group 6.3 versus steroid group 8.7; p < 0.01). The coronary artery abnormality segments under steroid use were also shorter (non-steroid group versus steroid group, two segments versus one segment; p = 0.02). Coronary artery abnormality size was larger in patients who used steroids than that of non-steroids. This study showed that steroid use significantly affected coronary artery abnormality size in patients with Kawasaki disease. However, cardiac complications from coronary artery abnormalities and cardiac events were comparable between the steroid and non-steroid groups. Further prospective, multicentre studies are needed to confirm these findings.

Recent evidence shows that subcutaneous immunoglobulin (SCIG) is as efficacious as intravenous immunoglobulin (IVIG) and has a better safety profile and acceptance rate among patients with neuromuscular disorders who require maintenance IVIG treatment. Awareness of the practical aspects of patient selection, enrollment, dose calculation, administration, and follow-up would help physicians coordinate a smooth and seamless transition from IVIG to SCIG. SCIG is ideally offered to patients having intolerable side effects during IVIG or wearing-off effect and in those keen for treatment autonomy. The weekly dose of SCIG is calculated by multiplying the maintenance dose of IVIG by the dose adjustment factor and dividing by the interval between IVIG in weeks and is initiated 1 week after the last dose of IVIG. The physician places the order for the SCIG and the clinic nurse or the physician refers the patient to the home care nursing program for further education and training. The necessary supplies are dispatched to the patient who would also collect the SCIG from the transfusion center of the nearest hospital. The patient is educated on assembling and administering the infusion, and home visits are continued until the patient or caregiver is confident. Regular follow-up with the patient is maintained to assess treatment response and side effects if any. With a smooth transition, most patients have excellent tolerance to SCIG and in our experience seldom request switching back to IVIG. Transitioning patients from IVIG to SCIG offers several advantages and thus, in general, is preferable for multiple stakeholders.

A 12-year-old girl presented with fever and signs of systemic inflammation, and was found to have junctional tachycardia. She was subsequently diagnosed with Multisystem Inflammatory Syndrome in Children and treated with intravenous immunoglobulin and steroids, which led to resolution of the arrhythmia.

The past decade has seen a surge of reports and investigations into cases of autoimmune-mediated encephalitis. The increasing recognition of these disorders is especially of relevance to the fields of neurology and psychiatry. Autoimmune encephalitis involves antibodies against synaptic receptors, neuronal cell surface proteins and intracellular targets. These disorders feature prominent symptoms of cognitive impairment and behavioural changes, often associated with the presence of seizures. Early in the clinical course, autoimmune encephalitis may manifest as psychiatric symptoms of psychosis and involve psychiatry as an initial point of contact. Although commonly associated with malignancy, these disorders can present in the absence of an inciting neoplasm. The identification of autoimmune encephalitis is of clinical importance as a large proportion of individuals experience a response to immunotherapy. This review focuses on the current state of knowledge on n-methyl-d-aspartate (NMDA) receptor-associated encephalitis and limbic encephalitis, the latter predominantly involving antibodies against the α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptor, the γ-aminobutyric acid (GABA)B receptor and leucine-rich glioma-inactivated 1 (LGI1) protein. In addition, we briefly describe anti-dopamine D2 receptor encephalitis. A summary of the literature will focus on common clinical presentations and course, diagnostic approaches and response to treatment. Since a substantial proportion of patients with autoimmune encephalitis exhibit symptoms of psychosis, the relevance of this disorder to theories of psychosis and schizophrenia will also be discussed.

Rheumatic carditis is a major manifestation of acute rheumatic fever. Conventional therapy includes the use of salicylates and steroids. To date, however, such therapy has not been proven to have a clear benefit in reducing valvar heart disease. We report the use of high-dose intravenous immunoglobulin in two chidlren with acute rheumatic carditis in whom we have been able to document the beneficial effect.