Systemic Lupus Erythematosus Presenting as Anorexia Nervosa Ppt Powerpoint Presentation slides-Medical Slideshow Systemic lupus erythematosus,SLE. ?Systemic lupus erythema

Systemic Lupus Erythematosus Presenting as Anorexia Nervosa

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Slide 1 :

Systemic Lupus Erythematosus Presenting as Anorexia Nervosa Julia Rhiannon Sterling West March, 2007

Slide 2 :

Summary At CIS School of Autoimmune Disease in 3/2007 we presented a case illustrating an extremely rare manifestation of neuropsychiatric lupus, that of anorexia nervosa. This can not be reproduced here on the web as we are submitting it for publication. This has been described only twice before in the literature, but never in the context of initial presentation.

Slide 3 :

Case Report of Anorexia Nervosa in association with SLE Described a 13 year old girl with SLE presenting August 1984 with 2 months of sxs: Organ Systems Involved in her disease: +ANF and LE cell prep, with arthralgias, fever, malar rash, alopecia, amenorrhea, weakness, and a histologically-proven vasculitis. She responded completely and rapidly to oral prednisolone 100mg/day. By December 1984 she had developed truncal obesity and was taunted by her parents and siblings. She developed classic anorexia nervosa, which eventually responded to conventional multi-modal therapy including individual and family psychotherapy, physical and “dietary therapy”. Prednisolone was tapered down to 10mg per day and she had no further problems over the next year. Bambery B., et. al. Anorexia nervosa in a patient with systemic lupus erythematosus. Rheumatology International (1987) 7:177-179.

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Case Report #2 15 year old girl with SLE, lung and renal involvement. She was treated with prednisolone 60mg po daily and gained weight rapidly. She began to restrict her food intake over concerns for her body image. Her subsequent weight loss was attributed to SLE, but eventually classic anorexia was diagnosed. This responded to multimodal therapy (individual and family therapy, dietary therapy). During this time her steroids were tapered to a maintenance dose of 2mg prednisolone daily. Sloan D., et. al. Anorexia nervosa complicating systemic lupus erythematosus (SLE). Ir Med J. 1998 May-Jun;91(3):97.

Slide 5 :

Concerns The authors both acknowledge an “impressive interplay between psychosocial and cultural factors” in the onset of AN in these 2 patients. Of note, the AN did not surface in either case until AFTER weight gain 2/2 steroids had occurred. Bambery speculated that a minute hypothalamic lesion could have been responsible, but dismisses this since there was no other evidence of hypothalamic dysfunction, and since AN completely resolved during dose-reduction (not escalation) of steroids. We doubt these cases represent true neuropsychiatric SLE, but rather psychiatric complications of SLE.

Slide 6 :

Anorexia, NP-SLE, and our patient Anorexia nervosa is common in younger women with a certain psychological substrate, and is a recurrent phenomenon with an often gradually progressive onset. Our patient had no known episodes consistent with anorexia nervosa prior to this presentation. Once she gained weight on steroids, she exhibited no further residual body-image issues, in contrast to the prior cases, whose onset of AN corresponded to weight-gain from steroids. Our patient’s prednisone was tapered down to 5 mg po daily without any weight loss.

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Neuropsychiatric SLE Prevalence: 15-66% of SLE patients Central Nervous System: Diffuse (35-60%) Neurologic syndromes (6-45%) Cognitive dysfunction/dementia Acute confusional state: Delirium/coma Psychiatric (8-61%) Psychosis (12-30%) Organic mood/anxiety disorders

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NP-SLE Focal (10-35%) Cranial neuropathies (4-49%) Cerebrovascular disease (4-33%) Demyelinating syndromes Optic neuritis, ataxias, others Transverse myelitis (0-3%) Movement disorders (0-8%) Chorea/hemiballismus Seizure disorders (15-35%) Diffuse: grand mal Focal Temporal lobe Petit mal

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NP-SLE Complex presentation Diffuse, focal, and/or seizure symptoms Other Cognitive dysfunction—mild Headaches including migraines and benign intracranial hypertension Aseptic meningitis

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NP-SLE Peripheral Nervous System (4-46%) Peripheral neuropathy (10-20%) Symmetric polyneuropathy Motor, sensory, combined Asymmetric Mononeuropathy, single/multiplex Plexopathy Acute inflammatory demyelinating polyradiculoneuropathy (Guillain Barre) Chronic, relapsing polyneuropathy

Slide 11 :

NP-SLE Other Autonomic neuropathy Myasthenic syndromes Secondary (non-SLE) causes of neuropsychiatric dysfunction Infection, uremia, fever, endocrine, hematologic, embolic, medications, reactive depression, fibromyalgia

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Etiopathogenesis Vascular occlusion/ischemia Immune complex/complement injury Vasculitis Leukoagglutination Vasculopathy APLAS Other: Platelets, cytokines, plasma factors, immune complex/complement, endothelial cell adhesion molecules Clot APLAS Thrombosis Cardiac emboli Other as above

Slide 13 :

Etiopathogenesis Antineuronal antibodies Serum (brain has lymphatic drainage) Neural tissue specific: brain synapse (50kD), neurofilaments, GFAp, MAP-2, anti NMO Non-neural specific: gangliosides (GM-10), lymphocytotoxic, anti-RP, APLA, anti-DNA, anti NR2 (NMDA) CSF Serum anti-neuronal antibodies cross blood-brain barrier at sites of microinfarcts Intrathecal synthesis by activated lymphocytes Activated T cells, B cells, macrophages/monos can cross BBB APLA may be able to disrupt neuronal function directly at nerve terminals Presence in CSF correlates with diffuse sxs Cytokine effects Serum cytokines: IL-2, IL-10, IFN alpha and gamma elevated CSF cytokines: IL-1, IL-2, IL-6, IL-8, IL-10, TNFa, IFNa elevated

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Diagnostic evaluation Laboratory Tests: CBC, chemistries, C3/C4, DNA binding, APLA CSF glucose, protein, cx/gm/cell count, Q Albumin, IgG index, oligoclonal bands Imaging studies MRI with gadolinium for suspected hemorrhage/mass Angio/MRA for suspected vasculitis CNS neurologic function EEG Others: echocardiogram, carotid ultrasound, psychometric tests

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Treatment Six “Ps” and a “C” Platelet inhibitors Plaquenil Prozac or other SSRI Prednisone Powerful cytotoxics Focal presentation +/- seizures Severe neurologic diffuse presentations not responding to steroids Cerebral vasculitis Plasmapheresis Coumadin unless contraindicated

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So what was the etiology of our patient’s initial AN presentation? Microvascular hit in a specific anatomical region? hypothalamus Specific autoantibody effect? Anti-NR2 (anti-dsDNA) antineuronal Abs APLAS Cytokine effect? IL-1, IL-6

Slide 17 :

Hypothesis T cells, B cells, monocytes extravasate through BBB at hypothalamus. These cells are stimulated by neuronal antigens. Elevated IL6 in CSF facilitates differentiation of B cells, which produce antineuronal antibodies. These antibodies act directly on neurons in the hypothalamus producing anorexia without a radiographically demonstrable lesion.

Slide 18 :

Acknowledgments Sterling West, MD Nancy Lane, MD

Slide 19 :

References Bambery B., et. al. Anorexia nervosa in a patient with systemic lupus erythematosus. Rheumatology International (1987) 7:177-179. Sloan D., et. al. Anorexia nervosa complicating systemic lupus erythematosus (SLE). Ir Med J. 1998 May-Jun;91(3):97. West S., Systemic Lupus Erythematosus and the Nervous System. In Dubois’ Lupus Erythematosus (6th ed), Wallace DJ and Hahn BH (eds). Lippincott, Williams and Wilkins, Philadelphia, 2006, pp. 707-736.

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She developed classic anorexia nervosa, which eventually responded to conventional multi-modal ther more She developed classic anorexia nervosa, which eventually responded to conventional multi-modal therapy including individual and family psychotherapy, ... less

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