ABSTRACT
We present a rare case of a 25-year-old woman who developed idiopathic portal hypertension and ascites four days after delivering a stillborn child at term. She had no previous liver illness or risk factors for portal vein thrombosis. Investigations revealed a dilated portal vein, esophageal varices, and high serum-albumin gradient ascites, all of which point to a presinusoidal etiology of portal hypertension. There was no indication of cirrhosis, hepatic or portal vein thrombosis, metabolic or autoimmune liver diseases, or persistent infections. She was treated with antibiotics, diuretics, and beta-blockers, and she underwent a therapeutic paracentesis. The etiology of her portal hypertension remains undetermined. Idiopathic portal hypertension is a rare condition of unknown etiology, characterized by portal hypertension without cirrhosis or thrombosis. It is linked to several risk factors and histological abnormalities, and it can be accompanied by portal hypertension consequences, such as variceal hemorrhage and ascites. The diagnosis is made using clinical criteria and the elimination of alternative causes of portal hypertension. Management is mostly symptomatic, intending to avoid and treat portal hypertension consequences. The prognosis varies according to the underlying etiology and presence of complications.
ABSTRACT
We describe a case of longitudinally extensive transverse myelitis (LETM), an uncommon and dangerous complication of systemic lupus erythematosus (SLE) that struck a 22-year-old woman with SLE. Chronic autoimmune illness (e.g., SLE) affects the skin, kidneys, joints, blood, and neurological system, among other organs. LETM is a condition where the spinal cord becomes inflamed and damaged, causing neurological problems, such as weakness, sensory loss, and bladder dysfunction. The patient presented with abdominal pain, vomiting, body aches, and fatigue, followed by shock, hypoxia, urinary retention, and constipation. Moreover, she had severe and asymmetric weakness, sensory loss, and areflexia in her limbs. She was diagnosed with LETM based on a nerve conduction study and MRI of the spine, which showed a motor neuron disease pattern and T2 hyperintense signals throughout the spinal cord gray and white matter. She responded well to immunoglobulins, plasma exchange, and high-dose steroids as treatment. Although her prognosis is favorable, there might be some lingering neurological issues or limitations. This instance highlights the significance of treating individuals with SLE as soon as possible after developing LETM.
