Antisynthetase syndrome is an autoimmune condition that manifests clinically through signs and symptoms, such as interstitial lung disease, myositis, Raynaud’s phenomenon, fever, hyperkeratotic fingertips (mechanic’s hands), and arthritis. It is associated with antibodies against aminoacyl tRNA synthetase enzyme, the most common autoantibody being the anti-Jo-1. An 18-year-old girl presented with weakness of both the upper and lower limb, swelling and generalized body pain, difficulty in swallowing. MRI of the thigh was highly suggestive of myositis with symmetrical bilateral involvement. Based on proximal muscle weakness, elevated creatine phosphokinase (CPK), and lactate dehydrogenase (LDH), strongly positive anti-nuclear antibodies human epithelial cell type-2 (ANA-HEp2), and a normal nerve conduction velocity test with precise MRI findings, a diagnosis of polymyositis was made. She was given bolus intravenous methylprednisolone for five days, followed by oral methylprednisolone with subcutaneous methotrexate weekly. She reported a 50% improvement in muscle weakness; however, partial bulbar weakness persisted at the time of discharge. On her next follow-up, her blood investigations for auto-antibodies were done. The autoantibodies anti-Jo-1 (3+), Ro-52 (2+), and Mi-2β (2+) were found to be positive. These investigations, coupled with the clinical features she was presenting, finally led us to conclude that it was a case of polymyositis complicated by the antisynthetase syndrome.

Systemic lupus erythematosus (SLE) is a multisystemic autoimmune disease that can affect almost every organ in the body. Its complications can often be fatal. The fatal complications include lupus cerebritis, lupus nephritis, and cardiac manifestations such as pericardial effusion. In this report, we discuss the case of a 23-year-old female who presented with complaints of high-grade fever, seizures, and altered mental state (AMS) and was found to have generalized lymphadenopathy (LAP). Various blood and urine analyses and radiological findings (chest X-ray, MRI of the head) were suggestive of lupus nephritis, lupus cerebritis, massive pericardial effusion, and thrombocytopenia. Her anti-double stranded DNA (anti-dsDNA) antibody was positive, and her pericardial fluid was positive for anti-nuclear antibodies (ANAs). She was administered IV glucocorticoids and phenytoin. She reported improvements in her symptoms gradually for a few days but eventually succumbed to the disease. Although generalized LAP is a rare initial presentation of SLE, it should be included in the differential diagnosis of the disease.

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Background: Aluminium phosphide (AlP) is a common suicidal poison with a high mortality rate due to its cardiovascular impact and lack of antidote. The aim of the study was to describe the electrocardiographic changes and other cardio-vascular manifestations in acute AlP poisoning and evaluate its impact on survival outcomes.Methods: A prospective cross-sectional study was conducted in a tertiary care hospital including patients who presented with acute AlP ingestion in any form. Patients’ vitals and ECG at the time of admission were taken and outcomes of survival were identified. A descriptive study of echocardiography was also done. The clinical parameters were correlated with the survival outcomes.Results: Fifty patients were included with 30 males and 20 females. The consumption of AlP in tablet form caused more hemodynamic compromise (hypotension and high anion gap metabolic acidosis) as compared to the powder form. ECG changes were seen in 42% of the cases, the most common finding was prolonged QTc interval (26%). The mortality was 30%. Hypotension, bradycardia, and QRS widening were found to be significant predictors of mortality (p<0.05). Echocardiography was performed for 10 patients, of which, one had right ventricular dysfunction and two had left ventricular dysfunction.Conclusions: AlP tablets are more lethal and hemodynamically compromising than AlP powder. Hypotension, bradycardia, and QRS widening are significant predictors of mortality. Direct cardiotoxicity leads to ECG changes, of which, QTc prolongation is the most common.