Systemic lupus erythematosus (SLE) is a chronic, inflammatory, autoimmune disorder involving multiple systems. A 18-year-old female patient presented with complaints of headache, weakness, and tingling sensation in the left upper limb and lower limb. On magnetic resonance imaging (MRI), acute nonhemorrhagic infarct in right thalamo-capsular region was seen. The patient gave a history of malar rash and intermittent joint pains for which she had taken nonspecific treatment. Antineutrophilic antibody (ANA) by innumoflourescence and ANA blot was suggestive of SLE. Hence, the patient had central nervous system vasculitis and stroke due to SLE. The patient was started on antiplatelet therapy, tablet prednisolone 40 mg once daily, and tablet warfarin 5 mg once daily. The patient was readmitted after 2 weeks with menorrhagia and deranged INR. Tablet Warfarin was with-held, fresh frozen plasma transfusions were given. Repeat MRI did not show any new changes. Patient was given tablet nicoumalone and three doses of injection cyclophosphamide 800 mg. Hemiplegia has improved by 90%, her menstrual cycles are now regular.

An 18-year-old female with Systemic Lupus Erythematosus (SLE) presented with bilateral thigh pain, fever, and diarrhea three days before admission. Diagnosed with SLE one month earlier, she reported prior symptoms, including joint pain, malar rash, hair loss, and hyperpigmented lesions. Initial investigations revealed elevated transaminase levels (AST 355, ALT 132), positive ANA, decreased complement levels (C3 68, C4 16.8), and raised creatine kinase (619). A muscle biopsy confirmed myositis. The patient was treated with immunosuppressant (a combination of steroids and hydroxychloroquine) and supportive therapy. By the eighth day of hospitalization, her symptoms, especially thigh pain, resolved. Electromyocardiography was done, and the results were normal, indicating therapeutic success. This case highlights the importance of prompt diagnosis and management of myositis as a rare SLE manifestation to achieve favorable outcomes.

Malar rash, also named a butterfly rash, is a common facial presentation of multiple disorders. characterized by an erythematous flat or raised rash across the bridge of the nose and cheeks, which usually spares nasolabial folds. It may be transient or progress to involve other areas of facial skin. This is mainly seen in patients with systemic lupus erythematosus. As per the American College of Rheumatology, Malar rash is one of the criteria for systemic lupus erythematosus (SLE); it may also be present with other types of lupus including discoid lupus and subacute cutaneous lupus. Differential diagnoses for malar rash are as follows: systemic lupus erythematosus, cellulitis, rosacea, erysipelas, dermatomyositis, and pellagra. Treatment starts with sun protection, including appropriate clothing, sunscreens, and behavior change and management of the underlying disease.

Photosensitive presentations of psoriasis are often under-recognized and may closely mimic other photodistributed dermatoses. We report the case of a 39-year-old male patient with no history of other photodermatoses who developed a progressive, non-pruritic rash, localized in sun-exposed skin areas, with marked exacerbation after phototherapy. Pronounced photosensitivity and atypical lesion distribution, involving the malar and nasal regions, complicated the initial differential diagnosis between photosensitive plaque psoriasis and cutaneous lupus erythematosus (CLE). Only further clinical evaluation, alongside histopathological analysis and immunological testing, helped to confirm the final diagnosis of photosensitive plaque psoriasis. Treatment with systemic and topical corticosteroids, vitamin D analogues, and calcineurin inhibitors resulted in gradual clinical improvement. This case report highlights photosensitive psoriasis as an important cause of photodistributed eruptions and a rare but significant mimic of CLE.

Systemic lupus erythematosus (SLE) is a quintessential illustration of an autoimmune disease. It results from complex interactions that include impaired apoptotic clearance, increased activity of both the innate and adaptive immune systems, complement activation, the development of immune complexes, and ensuing tissue inflammation, which collectively contribute to a sustained autoimmune response. We present a case relating to a 37-year-old female patient (from Ardabil, Iran) who received a diagnosis of SLE and antiphospholipid syndrome (APS), in accordance with established diagnostic criteria. She is currently admitted to the hospital due to a recurring pyoderma gangrenosum ulcer, accompanied by pain and swelling in her left leg. The patient tested positive for ANA, lupus anticoagulant, anti-beta2-glycoprotein I (anti-beta2GPI), and anti-Ro antibodies. These results, along with her clinical manifestations such as spontaneous abortion, stroke, malar rash, photosensitivity, and pyoderma gangrenosum ulcers, confirm a diagnosis of SLE associated with APS according to the relevant criteria. After appropriate medical treatment, she was identified as experiencing a lupus flare and multifocal osteonecrosis in the knee, hip, and shoulder.

Systemic lupus erythematosus (SLE) is a chronic autoimmune disease with heterogeneous manifestations, often overlapping with other conditions and complicating diagnosis. Oral lesions, though less common than cutaneous involvement, may offer important diagnostic clues. We report a 51-year-old female with rosacea, who developed persistent oral ulcers initially linked to a dental prosthesis. Lesions worsened despite adjustments and corticosteroid therapy, and the first biopsy was inconclusive. A second biopsy showed features of lupus erythematosus, including basal layer degeneration, subepithelial lymphocytic infiltrate, and PAS-positive basement membrane thickening. Serology revealed low-titter ANA (1:160) without additional autoantibodies. The coexistence of rosacea and lupus-like lesions delayed diagnosis, highlighting the need for clinicopathological correlation. Over 2 years of multidisciplinary follow-up, the patient achieved remission of oral and cutaneous lesions despite persistently low ANA titters. This case underscores the diagnostic complexity of overlapping dermatologic conditions and reinforces the importance of interdisciplinary management and long-term follow-up in suspected SLE.

Arboviral infections, notably those caused by West Nile virus (WNV), Dengue virus (DENV), Zika virus (ZIKV), and Chikungunya virus (CHIKV), represent a growing global health concern due to their expanding geographic distribution and evolving clinical spectrum. While systemic and neurologic complications are well recognized, cutaneous manifestations are frequently overlooked despite their diagnostic and prognostic value. These viruses, transmitted primarily by Aedes or Culex mosquitoes, share overlapping symptoms such as fever, headache, arthralgia, myalgia, and malaise but can often be distinguished by specific dermatologic features. WNV may present with a subtle truncal exanthem; DENV is characterized by flushing, petechiae, and the 'white islands in a sea of red' pattern; ZIKV typically is associated with a fine, pruritic maculopapular rash with palmar-plantar involvement, edema and erythema of the malar region of the face, and conjunctival injection; CHIKV frequently shows an asymptomatic or pruritic macular or maculopapular rash that can result in pigmentary changes mostly on the face and mucocutaneous involvement. Other arboviral infections such as Usutu virus (USUV) and Toscana virus (TOSV) more rarely exhibit cutaneous signs. These include transient macular or urticarial rashes, conjunctivitis, and aphthous-like ulcers on the palate during early or prodromal phases. This review synthesizes current clinical, virologic, and pathophysiologic insights into these cutaneous presentations, highlighting their diagnostic relevance, underlying mechanisms, and implications for dermatologic and interdisciplinary care. Recognizing these dermatologic signs can significantly aid early diagnosis and improve patient management in endemic and outbreak settings.

Podocyte infolding glomerulopathy is a rare glomerular lesion characterized by microtubular structures and microspheres in the glomerular basement membrane. While most reported cases are associated with autoimmune diseases such as systemic lupus erythematosus, pediatric cases are rarely reported. The patient was a 14-year-old Japanese girl with a 1-year history of proteinuria detected during a school urinary screening program. Five months prior to admission to our department, she was hospitalized at a regional hospital for acute abdominal pain. Although her symptoms resolved spontaneously, a renal biopsy was performed due to the presence of proteinuria, leukopenia and antinuclear antibody positivity. However, the diagnoses of systemic lupus erythematosus was not established at that time owing to negative IgG, IgA, IgM, C3 and C1q on immunofluorescence, negative anti-dsDNA and anti-Smith antibody as well as normal serum C3 and C4 levels. On admission to our department, she was diagnosed with systemic lupus erythematosus and lupus enteritis based on the presence of malar rash, fever, leukopenia, and proteinuria supported by the characteristic findings on abdominal enhanced computed tomography. Reassessment of the initial renal pathology revealed microtubular structures and microspheres within the glomerular basement membrane on electron microscopy, consistent with podocyte infolding glomerulopathy. Induction therapy with methylprednisolone pulse therapy improved her systemic symptoms and proteinuria promptly. This is the first report of podocyte infolding glomerulopathy in a pediatric patient with systemic lupus erythematosus. Clinicians should be aware of this unique glomerular lesion in pediatric-onset systemic lupus erythematosus.

The association between systemic lupus erythematosus (SLE) and multiple myeloma (MM) is rare, with fewer than 20 cases reported in the literature, raising questions about the link between chronic immune dysregulation and oncogenesis. We report the case of a 43-year-old Malagasy woman in whom a monoclonal β2-globulin spike, incidentally discovered during the workup of pneumonia, led to the diagnosis of MM. The diagnosis of SLE was straightforward, based on evocative clinical features (photosensitive malar rash, inflammatory arthralgia) and positive autoantibodies (antinuclear antibodies at 1:320, native anti-DNA at 861 IU/mL). Anemia (Hb at 10 g/dL), with a drop of more than 2 g/dL from baseline, and a high erythrocyte sedimentation rate (90 mm) prompted a bone marrow aspiration, which revealed 35% dystrophic clonal plasma cells. A diagnosis of kappa light chain MM was made, without bone lesions. This case highlights three major issues: (1) the diagnosis of MM in a young patient with atypical but fulfilled SLiM-CRAB criteria; (2) a pathophysiological mechanism suggesting chronic B-cell stimulation related to SLE, rather than an iatrogenic effect; (3) the potential role of autologous stem cell transplantation (ASCT) in modulating immune response in both conditions. It underscores the need for diagnostic vigilance, better access to advanced biomarkers, and a multidisciplinary approach.

Lupus podocytopathy (LP) is an increasingly recognised and histopathologically distinct entity within the spectrum of lupus nephritis (LN). It is defined by diffuse podocyte foot process effacement in the absence of subendothelial or subepithelial immune complex deposition and often mimics minimal change disease or focal segmental glomerulosclerosis. LP is typically observed at the onset of systemic lupus erythematosus (SLE) or in patients with known LN. We report a rare case of LP in a 28-year-old Japanese woman with a 12-year history of SLE and no prior renal involvement. She presented with fever, malar rash, arthralgia, and progressive bilateral lower extremity oedema. Laboratory studies revealed marked hypoalbuminemia (1.5 g/dl), nephrotic-range proteinuria (15 g/gCr), elevated anti-dsDNA antibody titers (>400 IU/ml), and hypocomplementemia. Renal biopsy revealed ISN/RPS 2018 class II LN, with mild mesangial hypercellularity and mesangial deposition of IgG, C3, and C1q, without subendothelial or subepithelial immune complexes. Electron microscopy confirmed extensive foot process effacement, establishing the diagnosis of LP. The coexistence of class II LN and LP accounted for the acute onset of nephrotic syndrome in the absence of proliferative changes. The patient was treated with methylprednisolone pulse therapy, high-dose corticosteroids, and intravenous cyclophosphamide, followed by oral cyclosporine. This regimen resulted in prompt clinical and immunological improvement, including near-complete resolution of proteinuria. She remained in remission throughout a 6-month follow-up. This case emphasises the need to consider LP in SLE patients with nephrotic syndrome, even in the absence of prior renal complications during long-term follow-up.