scholarly journals Myeloradiculitis with lupus-like autoimmunity following Sinovac COVID-19 vaccination

2021 ◽  
Vol 26 (4) ◽  
pp. 869-870
Author(s):  
Yew Long Lo ◽  
J J H Lam ◽  
L L Chan
Keyword(s):  
Antinuclear Antibody ◽  
Cauda Equina ◽  
Transverse Myelitis ◽  
Viral Antigens ◽  
Double Stranded Dna ◽  
Systemic Manifestations ◽  
Autoimmune Pathogenesis

We report a 67 year old man with features in keeping with transverse myelitis, lumbar root and cauda equina involvement suggestive of delayed autoimmune pathogenesis after the Sinovac COVID-19 vaccination previously observed  in vaccines  containing viral antigens. Grossly elevated antinuclear antibody and anti-double-stranded DNA are in line with observations in lupus myelitis despite the lack of systemic manifestations.

Rapid-Onset Weakness and Numbness in a Patient With Systemic Lupus Erythematosus

2021 ◽  
pp. 120-121
Author(s):  
Floranne C. Ernste
Keyword(s):  
Systemic Lupus Erythematosus ◽  
Cerebrospinal Fluid ◽  
Lupus Erythematosus ◽  
White Blood Cells ◽  
Cauda Equina ◽  
Transverse Myelitis ◽  
Lower Extremities ◽  
Systemic Lupus ◽  
Neuropsychiatric Manifestation ◽  
Fluid Analysis

A 33-year-old woman with systemic lupus erythematosus, diagnosed 2 years prior and treated with hydroxychloroquine, sought care for a 4-week history of pain and paresthesias in her low back and lower extremities. She described a bandlike sensation of numbness starting in her midback which descended to both legs. Her symptoms progressed to constipation and inability to urinate adequately. She reported difficulty with ambulation. Over the course of 1 week of hospitalization, urinary and fecal incontinence developed. On examination, she was alert and appropriately oriented. She had a malar rash and swelling of the metacarpophalangeal joints consistent with bilateral hand synovitis. Neurologic examination indicated hyperreflexia with brisk patellar and Achilles tendon reflexes bilaterally. She had trace motor weakness of the hip flexors, quadriceps, and hamstrings. She had loss of pinprick and temperature sensation in the lower extremities, extending beyond the saddle area to the T12 dermatome. Vibration perception and proprioception were preserved. She had a positive Babinski sign in the left foot. Her cerebellar examination showed slowing of rapid alternating movements in the left hand. Magnetic resonance imaging of the lumbosacral spine indicated subtle T2 signal change of the intramedullary conus and enhancement of the cauda equina nerve roots. Cerebrospinal fluid analysis showed an increased protein concentration. Two white blood cells/µL were found in the cerebrospinal fluid. The serum antinuclear antibody was strongly positive, and the anti–double-stranded DNA antibody level was greater than 1,000 IU/mL. The serum complement levels were low. Lupus anticoagulant, beta-2 glycoprotein antibodies, and antiphospholipid antibodies were increased, at greater than twice the upper limits of normal. Electromyography indicated multiple sacral radiculopathies. The patient was diagnosed with autoimmune myeloradiculitis as a neuropsychiatric manifestation of systemic lupus erythematosus (neuropsychiatric systemic lupus erythematosus). The patient received methylprednisolone followed by prednisone, with a gradual taper. Her hospital course was complicated by the development of deep venous thromboses in the bilateral lower extremities. She was started on heparin and transitioned to warfarin therapy. She started mycophenolate mofetil. Hydroxychloroquine was continued. At a 24-month follow-up visit, the patient remained in neurologic remission. Neuropsychiatric systemic lupus erythematosus events consist of a heterogeneous array of neurologic and psychiatric disorders including intractable headaches, cognitive dysfunction, psychosis, seizure disorders, transverse myelitis, aseptic meningitis, cranial neuropathies, and acute inflammatory demyelinating polyneuropathy.

PATHOGENESIS OF IMMUNE COMPLEX GLOMERULONEPHRITIS OF NEW ZEALAND MICE

1971 ◽  
Vol 134 (3) ◽  
pp. 65-71 ◽  
Author(s):  
Frank J. Dixon ◽  
Michael B. A. Oldstone ◽  
Giorgio Tonietti
Keyword(s):  
New Zealand ◽  
Immune Complex ◽  
Antibody Formation ◽  
Antinuclear Antibody ◽  
Viral Infections ◽  
Antibody Responses ◽  
Viral Antigens ◽  
Chronic Viral Infections ◽  
Nuclear Antigens ◽  
Antigen Antibody

Observations based on elution of IgG from nephritic kidneys of NZ mice and absorption of the eluted IgG with selected antigens indicate that their immune complex nephritis involves at least two kinds of antigen-antibody complexes. Antibodies reactive with nuclear antigens account for nearly half of the IgG eluted from the kidneys while antibodies reactive with Gross viral antigens make up a significant but lesser amount. Superimposed chronic viral infections affect the nephritis of NZ mice in different ways. LCM and polyoma infections hasten and intensify the antinuclear antibody responses and glomerulonephritis of these mice while LDV infection appears to protect against both antinuclear antibody formation and development of nephritis.

scholarly journals Breaking Tolerance to Double Stranded DNA, Nucleosome, and Other Nuclear Antigens Is Not Required for the Pathogenesis of Lupus Glomerulonephritis

2004 ◽  
Vol 199 (2) ◽  
pp. 255-264 ◽  
Author(s):  
Samuel T. Waters ◽  
Marcia McDuffie ◽  
Harini Bagavant ◽  
Umesh S. Deshmukh ◽  
Felicia Gaskin ◽  
...  
Keyword(s):  
Lupus Erythematosus ◽  
Antinuclear Antibody ◽  
Early Mortality ◽  
Chromosome 1 ◽  
Chronic Glomerulonephritis ◽  
Chromosome 4 ◽  
Double Stranded Dna ◽  
Nuclear Antigens ◽  
Dsdna Antibody ◽  
Lupus Glomerulonephritis

In lupus-prone NZM2328 mice, a locus Cgnz1 on chromosome 1 was linked to chronic glomerulonephritis, severe proteinuria, and early mortality in females. A locus Adnz1 on chromosome 4 was linked to antinuclear antibody (ANA) and anti–double stranded DNA (dsDNA) antibody (Ab) production. In this investigation, two congenic strains, NZM2328.C57L/Jc1 (NZM.C57Lc1) and NZM2328.C57L/Jc4 (NZM.C57Lc4), were generated by replacing the respective genetic intervals containing either Cgnz1 or Adnz1 with those from C57L/J, a nonlupus-prone strain. The NZM.C57Lc1 females had markedly reduced incidence of chronic glomerulonephritis and severe proteinuria. NZM.C57Lc4 females had chronic glomerulonephritis and severe proteinuria without circulating ANA, anti-dsDNA, and antinucleosome Ab. These data confirm the linkage analysis. Unexpectedly, NZM.C57Lc1 females had little anti-dsDNA and related Ab, suggesting the presence of a second locus Adnz2 on chromosome 1. The diseased NZM.C57Lc4 kidneys had immune complexes by immunofluorescence and electron microscopy. The eluates from these kidneys did not contain ANA, anti-dsDNA, and antinucleosome Ab, indicative of the presence of non–anti-dsDNA nephritogenic Ab. Thus, breaking tolerance to dsDNA and chromatin is not required for the pathogenesis of lupus nephritis. These results reaffirm that anti-dsDNA and related Ab production and chronic glomerulonephritis are under independent genetic control. These findings have significant implications in the pathogenesis of systemic lupus erythematosus.

Neurobiology of Transverse Myelitis and Infectious Myelopathies

2017 ◽  
Author(s):  
Ivana Vodopivec ◽  
Tracey A Cho
Keyword(s):  
Spinal Cord ◽  
Epidural Space ◽  
Transverse Myelitis ◽  
Intervertebral Discs ◽  
Infectious Agents ◽  
Direct Invasion ◽  
Neural Tissues ◽  
Autoimmune Pathogenesis

Infectious agents cause spinal cord pathology by three different mechanisms: direct invasion/infection of neural tissues (i.e., infective myelitis), secondary inflammation and tissue bystander damage with or without autoimmune pathogenesis (parainfectious myelitis), or involvement of extra-axial structures (including the pia-arachnoid, the dura, the epidural space, or the adjacent spinal bones or intervertebral discs), resulting in compressive or ischemic myelopathy. This chapter describes the pathogenesis and treatment of these disorders.

scholarly journals 1409. Next-Generation Sequencing-based Detection of Angiostrongylus cantonensis (AC) Using Microbial Cell-free DNA Sequencing of Plasma in Atypical Cases of Rat Lungworm Meningitis Presenting with Ascending Paralysis

2019 ◽  
Vol 6 (Supplement_2) ◽  
pp. S513-S513 ◽  
Author(s):  
Marian Melish ◽  
Chanel Casamina ◽  
Rachael Merrifield ◽  
Keisuke Abe ◽  
Asim A Ahmed ◽  
...  
Keyword(s):  
Next Generation Sequencing ◽  
Cauda Equina ◽  
Transverse Myelitis ◽  
Response To Therapy ◽  
High Dose ◽  
Normal Brain ◽  
Next Generation ◽  
Lower Extremity Weakness ◽  
Rat Lungworm ◽  
Generation Sequencing

Abstract Background AC or Rat Lungworm meningitis usually presents as a self-limited illness with headache and sensory changes, rarely progressing to coma, death, or permanent brain damage. It is usually diagnosed by eosinophils in the CSF. Once limited to Asia and the tropical Pacific AC transmission via slugs and snails documented on US mainland in 2018. We describe 2 unusual, severe examples of AC infection in infants presenting with ascending paralysis and initial CSF without eosinophilia suggesting Guillain–Barre syndrome (GBS). Methods Conventional lab testing of serum and CSF, brain and spine MRI, AC PCR by Hawaii Department of Health, and mcfDNA next-generation sequencing (NGS) of plasma (Karius). Results Two infants, aged 8 and 11 months, presented with fever, lower extremity weakness, and ascending paralysis. An initial evaluation in both included normal brain/spine imaging and CSF with modest lymphocytic pleocytosis without eosinophils. Paralysis progressed despite IVIG. Case 1: 11-month male: Admitted on fever day 5. Paralysis progressed to respiratory failure requiring ventilation for 20 days. Illness day 16: MRI showed spinal cord swelling C3-C7, Brain normal. CSF#3: WBC 269 28% eos, ↑ protein. Visible 8 mm long young adult worms, PCR positive for AC. Rx high-dose corticosteroids, albendazole for >4 weeks. Day 29 illness MRI: Cerebral infarct L frontal lobe, worm tracks medulla, inflammation cauda equina. Slow improvement over 5 months. Case 2: 8-month-old female: Admitted fever day 8. Weakness progressed to arms and trunk. Day 10 illness: CSF #2: Visible worms present, WBC 84, 26% eos. PCR positive for AC. Rx: High-dose steroids and albendazole x4 weeks. MRI spine illness day 30: inflammation cauda equina. Weakness improved by illness day 37. McfDNA sequencing of plasma detected AC in acute stage peaks of 123 and 12 molecules/microliter in cases 1 and 2. Serial mcfDNA testing showed a decline in the AC DNA level in plasma which correlated with treatment and clinical response. Conclusion AC infection may mimic GBS or transverse myelitis. AC diagnosis may require repeat CSF testing. NGS detection of AC in plasma holds promise as rapid, noninvasive diagnosis and assessment of response to therapy. High-dose steroids with albendazole may be effective even in severe AC. Disclosures All authors: No reported disclosures.

scholarly journals Spontaneous soft tissue haemorrhage in systemic lupus erythematosus

Reumatismo ◽  
2016 ◽  
Vol 68 (4) ◽  
pp. 199 ◽  
Author(s):  
M.C. Abdulla
Keyword(s):  
Systemic Lupus Erythematosus ◽  
Soft Tissue ◽  
Lupus Erythematosus ◽  
Antinuclear Antibody ◽  
Low Grade ◽  
Systemic Lupus ◽  
Double Stranded Dna ◽  
Positive Antinuclear Antibody ◽  
Clinical Presentations ◽  
Retinal Haemorrhages

Diversity in clinical presentations and complications of systemic lupus erythematosus (SLE) make the diagnosis and management challenging. The mechanisms of haemorrhagic manifestations in SLE have not been well elucidated. A 47-year-old woman with no comorbidities was admitted after suffering fatigue and low grade fever for six months. She had bilateral soft tissue haemorrhage over the forearm and intra retinal haemorrhages. She was assessed and diagnosed as having SLE based on positive antinuclear antibody, strongly positive anti double stranded DNA, thrombocytopenia and low C3 and C4 levels. We describe a case of spontaneous bilateral soft tissue haemorrhage in SLE and discuss the various mechanisms causing bleeding in lupus.

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