• Immunodeficiency
• subcutaneous immunoglobulin therapy
• SCIg
• immunoglobulin
• hyaluronidase
• peripheral neuropathies

Following the introduction of immunoglobulin (Ig) replacement therapy in a boy with agammaglobulinaemia by Bruton in 1952,1 this now forms the mainstay of treatment for patients with primary antibody deficiencies. The initial use of intramuscular immunoglobulin (IMIg) which was limited by volume and pain was followed by the development of intravenous immunoglobulin preparations (IVIg), with the advantage that much greater volumes could be given maintaining physiological blood levels of immunoglobulin using doses of around 0.4 g/kg/month. In addition immunoglobulin could be used at high dose (hdIVIg) for immunomodulation in a range of autoimmune and inflammatory settings. Subsequently, with the demonstration that immunoglobulin could be administered subcutaneously using portable syringe drivers,2 this route (SCIg) has become increasingly popular with rapid infusion rates of 35 ml/h. Intravenous regimes involve a large dose being given every third or fourth week, while subcutaneous regimes usually involve weekly dosing to one or more sites. This results in more stable trough IgG concentrations which are more physiological than the peaks and troughs associated with intravenous administration.

A 28-year-old Caucasian woman presented in 2003 with severe asthma and recurrent chest and sinus infections. The serum IgG concentration was low at 1.99 g/l (normal range 6–16 g/l), with IgA 0.39 g/l (0.9–3.4 g/l) and IgM 0.9 g/l (0.48–1.9 g/l). She had normal …