Sickle cell disease (SCD) is an inherited disorder, which occurs due to a single gene mutation. It has multisystemic manifestations, affecting millions of people worldwide. The effect of SCD on joints and musculature can overlap with clinical features of autoimmune disease (AD). It is therefore difficult for clinical haematologists and physicians treating SCD patients to discriminate between these two conditions clinically. A delay in diagnosis leads to untreated symptoms and treatment differs considerably. An accurate knowledge of clinical findings and laboratory results of AD and SCD can help physicians avoid this. In the review that follows, we examine the existing literature on SCD and AD, and describe the features that may distinguish SCD and autoimmune disease such as systemic lupus erythematosus and rheumatoid arthritis. We aim to guide clinical haematologists and physicians towards a more rapid diagnosis of AD in sickle cell anaemia patients, by correct interpretation of the clinical assessment and commonly available diagnostics.

The development of hyponatremia due to syndrome of inappropriate antidiuretic hormone secretion (SIADH) is well recognised in multiple myeloma (MM). SIADH, due to either MM or Bortezomib can be hazardous as severe hyponatremia may develop if large volumes of hypotonic intravenous fluid are used as an adjunct to chemotherapy. We report a case of Bortezomib-induced SIADH, in whom the use of tolvaptan, a vasopressin receptor-2 antagonist, permitted the continuation of triple combination anti-MM therapy with lenalidomide, Bortezomib and dexamethasone (RVD) in a female with aggressive disease, without the development of hyponatremia. Our patient had a rapid relapse, in which the use of Bortezomib as part of an RVD regimen was life-saving. The use of tolvaptan allowed continuation of therapy that is usually halted in other similarly reported cases. This case highlights the possible use of vaptans, which allows an aquaresis to occur by blocking the antidiuretic effects of vasopressin, as a treatment for Bortezomib-induced hyponatremia.

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