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Nasopharyngeal rhabdomyosarcoma is a rare tumour of the paediatric age group that emerges from embryonal mesenchymal cells. Presented here is a case of a 54-year-old male of Asian ethnicity with a notable history of weight loss, lack of energy, anal fissure, and haematochezia. After the incidental finding of a lytic lesion following imaging, the patient underwent an extensive work-up to rule out malignancy and increased uptake on nasopharynx was found, which was biopsied to diagnose a poorly differentiated tumour, having desmin and myogenin positivity on immunohistochemistry. Metastatic work-up showed extensive bone marrow invasion apart from multiple lytic bone lesions throughout the body. The patient was started on vincristine, actinomycin D (dactinomycin), and cyclophosphamide (VAC) protocol chemotherapy and was followed-up until two cycles were completed, with no evidence of disease remission.

This case details a 33-year-old female who presented with a suggestive autoimmune history, arthralgias, and splenomegaly, and tested positive for Sjögren’s syndrome and anti-liver–kidney microsomal antibody. This was further validated by findings from a liver biopsy, confirming a very rare association with Type 2 autoimmune hepatitis. Primary Sjögren’s syndrome is a sporadic disease with a global prevalence of 61 per 100,000 people and a total prevalence of 0.4% for secondary Sjögren’s syndrome. The prevalence of autoimmune hepatitis in association with primary Sjögren’s syndrome is 4–47%. It is divided into two types, associated with characteristic antibodies. Type 2 autoimmune hepatitis is rarely reported with Sjögren’s syndrome; much of the association reported in the literature has been with Type 1 autoimmune hepatitis.

Haemophagocytic lymphohistiocytosis (HLH) is a rare but potentially aggressive and life-threatening syndrome of overactive histiocytes and lymphocytes that commonly affects infants; it is also observed in children and adults of all ages. The disease is differentiated into either primary or secondary causes. Primary HLH tends to be of genetic origin, while secondary HLH results from either infection, autoimmune disorders, or malignancies. Secondary HLH is most commonly associated with viral infections in immunocompromised patients. This paper presents a case of HLH in a tertiary care hospital, associated with adult-onset Still’s disease, diagnosed on both biochemical criteria and histopathologic examination of bone marrow smear.

Guillain–Barré syndrome (GBS) is a form of rapidly progressive, acute inflammatory demyelinating polyradiculopathy. Acute inflammatory demyelinating polyradiculopathy is the most common variant of GBS, especially in the western hemisphere. It is diagnosed without hesitation when it presents with its characteristic clinical features of ascending paralysis and areflexia. It is when an atypical presentation appears, with brisk or very brisk reflexes, that diagnosis becomes difficult. In this case, a patient who presented with progressive motor weakness, unilateral facial palsy, and hyperreflexia on examination is described in order to demonstrate a variant of GBS and its management. Keeping in mind that the management of the disease does not change with the variant, the diagnostic challenge that is put forward by those variants needs a focussed approach by physicians.

A 30-year-old Asian male with a significant history of deep vein thrombosis and family history positive for pulmonary embolism presented with complaints of fever, nonradiating epigastric pain, and a sense of abdominal fullness. After the initial workup, ultrasonography of the whole abdomen was carried out which showed thrombus formation in the portal vein. A CT scan of the abdomen was performed, which showed findings suggestive of mesenteric panniculitis. Keeping the significant family history and imaging findings in mind, the clotting and thrombin profiles were analysed and came back positive for the factor V Leiden gene (homozygous). A CT angiogram was performed to demonstrate extensive thrombosis throughout the abdominal vasculature with cavernous transformation. It is asserted that the chronic thrombosis on a background of factor V mutation led towards chronic inflammation of the mesentery. To the authors’ knowledge it is the first reported case of mesenteric panniculitis in a patient with factor V homozygous gene mutation.

Lupus panniculitis occurs in 1–3% of the patients diagnosed with systemic lupus erythematosus (SLE) and 10% of the patients diagnosed with discoid lupus erythematosus (DLE). It is a disorder of autoimmune origin, manifesting as deep erythematous plaques and nodules involving the trunk, breasts, buttocks, face, and proximal extremities. It does not commonly ulcerate. This report highlights the case of a 22-year-old Asian female with a history of coeliac disease and significant family history of antiphospholipid antibody syndrome (APS) who presented with fever, malaise, weight loss, and subcutaneous non-tender nodules over the forearm, back, bilateral thighs, and feet. Laboratory investigations revealed positive antinuclear antibodies, anti-Ro/SSA antibody, and lupus anticoagulant, resulting in a diagnosis of APS. Biopsies of lesions were consistent with findings of lupus panniculitis. Every case of SLE and DLE with discrete skin lesions should be reviewed for any distinct entity such as lupus panniculitis, as it may be associated with greater risk of flares and systemic involvement. The purpose of this case report is to emphasise that early diagnosis and prompt treatment is crucial to improving the prognosis of such patients.