Related Experiment Video
Updated: Jul 10, 2026

12:04
The bm12 Inducible Model of Systemic Lupus Erythematosus (SLE) in C57BL/6 Mice
Published on: November 1, 2015
Active necrotizing cerebral vasculitis in systemic lupus erythematosus
Deepa Goel1, S Rajashekhar Reddy, Challa Sundaram
1Department of Pathology, Nizam's Intstitute of Medical Sciences, Hyderabad, Andhra Pradesh, India.
Summary
Systemic lupus erythematosus (SLE) can cause rare, fatal necrotizing vasculitis in brain and kidney vessels. This case highlights active necrotizing vasculitis as a severe complication of SLE.
Area of Science:
- Rheumatology
- Neurology
- Pathology
Background:
- Systemic lupus erythematosus (SLE) is a complex autoimmune disease with diverse clinical presentations.
- Neuropathological findings in SLE commonly include focal cortical brain infarcts and central nervous system (CNS) infections.
Observation:
- A 32-year-old woman experienced recurrent strokes over five years.
- She presented with polyarthritis, oral ulcers, high antinuclear antibody (ANA) titers, and high double-stranded DNA (dsDNA) antibody levels, leading to an SLE diagnosis.
Findings:
- Despite immunosuppressive treatment (azathioprine, cyclophosphamide), the patient died from a brainstem stroke.
- Autopsy revealed multiple cerebral cortical and brainstem infarcts with fibrinoid necrosis of vessel walls.
- Renal infarction with healed vasculitis and systemic vasculitis of small vessels were observed, but extensive thrombosis was absent.
Implications:
- Active necrotizing vasculitis affecting cerebral and renal vessels is a rare but critical complication of SLE.
- This case underscores the potential for severe, life-threatening vasculitic complications in SLE, even with treatment.
Related Concept Videos
Encephalitis ll: Pathophysiology
Encephalitis is inflammation of the brain parenchyma caused by direct viral invasion or immune-mediated mechanisms triggered by infections or tumors. Both processes lead to neuronal injury, disrupted neurotransmission, and diverse neurological symptoms, often with overlapping clinical and pathological features.Autoimmune EncephalitisIn autoimmune encephalitis, antibodies target neuronal antigens on cell surfaces, synapses, or within neurons. A key example is anti-NMDAR encephalitis, which can...
Cytotoxic Edema: Pathophysiology
Cytotoxic edema is a form of cerebral edema characterized by intracellular swelling of neurons, astrocytes, and other glial cells. It develops when the mechanisms responsible for maintaining ionic gradients across the cell membrane become impaired. Under normal physiological conditions, the sodium–potassium ATPase actively transports sodium ions out of the cell and potassium ions into the cell, preserving osmotic balance and enabling electrical signaling. This pump requires a continuous supply...
Encephalitis l: Introduction
Encephalitis is inflammation of the brain parenchyma, most often due to infections or autoimmune processes. It presents with neuropsychiatric features such as fever, altered mental status, behavioral changes, cognitive dysfunction, seizures, focal deficits, and sometimes autonomic instability. In some cases, the meninges are also involved, resulting in meningoencephalitis.Infectious CausesInfectious encephalitis is most commonly viral but can also result from bacterial, fungal, or parasitic...
Endocarditis II: Clinical Features of Infective Endocarditis
Endocarditis can present various clinical features depending on the causative organism and the patient's underlying health conditions. Initially, the clinical features of infective endocarditis develop gradually, presenting with nonspecific symptoms that can be easily mistaken for other illnesses.General SymptomsEarly symptoms of infective endocarditis are fever, chills, weakness, malaise, fatigue, and weight loss. These symptoms reflect the systemic nature of the infection and the body's...
Cellular Injury IV: Necrosis
Necrosis is a form of irreversible cell death caused by severe injury such as ischemia, toxins, or trauma. Unlike programmed cell death, it is an uncontrolled, pathological process that typically provokes inflammation in surrounding tissues.Pathophysiologic ChangesNecrosis begins when cells sustain critical damage, leading to swelling of organelles, particularly mitochondria, and rapid ATP depletion. As energy levels decline, membrane ion pumps fail, leading to calcium influx and eventually,...
Hemorrhagic Stroke ll: Pathophysiology
A hemorrhagic stroke develops when a cerebral blood vessel ruptures, allowing blood to escape into the surrounding brain tissue, as in intracerebral hemorrhage (ICH), or into the subarachnoid space, as in subarachnoid hemorrhage (SAH). Because the skull is a rigid compartment, the sudden presence of extravascular blood rapidly increases intracranial pressure and compresses adjacent neural structures, leading to immediate tissue injury and impaired cerebral perfusion.Mass Effect and Primary...
