Lupus, Latin for “wolf,” is a term used to describe many dermatologic conditions, some of which are related to underlying systemic lupus erythematosus, while others are distinct disease processes. Cutaneous lupus erythematosus includes a wide array of visible skin manifestations and can progress to systemic lupus erythematosus in some cases. Cutaneous lupus can be subdivided into three main categories: acute cutaneous lupus erythematosus, subacute cutaneous lupus erythematosus, and chronic cutaneous lupus erythematosus. Physical exam, laboratory studies, and histopathology enable differentiation of cutaneous lupus subtypes. This differentiation is paramount as the subtype of cutaneous lupus informs upon treatment, disease monitoring, and prognostication. This review outlines the different cutaneous manifestations of lupus erythematosus and provides an update on both topical and systemic treatment options for these patients. Other conditions that utilize the term “lupus” but are not cutaneous lupus erythematosus are also discussed.

The utilization and identification of biomarkers in rheumatoid arthritis (RA) to facilitate timely diagnosis and the optimal management of the disease is an area of active investigation. This review focuses on biomarkers available for routine clinical use, details potential investigational biomarkers, and raises outstanding clinical questions.

Systemic lupus erythematous (SLE) is a chronic autoimmune disease that can target any organ of the body. It may coexist with other autoimmune neurologic conditions such as neuromyelitis optica spectrum disorder (NMOSD). NMOSD, previously known as Devic’s disease, is an autoimmune inflammatory disorder of the central nervous system (CNS) that targets the spinal cord, optic nerves, and certain brain regions. Most current evidence suggests that NMOSD is best described as a CNS astrocytopathy. While these diseases share several immunosuppressive treatment options, timely diagnosis of NMOSD is critical as patients may benefit from treatment tailored specifically to NMOSD as opposed to SLE. Steroids, plasmapheresis, intravenous immunoglobulin, cyclophosphamide, azathioprine, mycophenolate mofetil, and rituximab are used to treat both SLE and NMOSD. However, there are several new therapies (inebilizumab, eculizumab, and satralizumab) recently approved specifically for use in NMOSD. In this case series, we report on three patients with coexisting SLE and NMOSD. We describe a 31-year-old woman who suffered an NMOSD flare after 11 years of clinical remission in the context of receiving an influenza vaccination; her SLE remained quiescent on hydroxychloroquine. Next, we describe a 52-year-old woman with emergence of neurologically devastating seropositive NMOSD in the setting of active treatment for SLE with intravenous cyclophosphamide, oral steroids, and hydroxychloroquine. Last, we describe a 48-year-old woman with emergence of seronegative NMOSD in the setting of SLE that was well-controlled on azathioprine and hydroxychloroquine. These cases illustrate the importance of accurate diagnosis and targeted treatment of NMOSD when coexisting with SLE.

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Raynaud phenomenon is an overactive vascular response to cold and emotional stress that results in cutaneous color changes and sensory symptoms in the digits. It can be idiopathic (primary) or secondary to another condition; the latter can be more severe and more apt to lead to ischemic complications such as digital ulceration and even loss of digits. If nonpharmacologic interventions prove inadequate, then vasodilator agents are used.