lupus with a guillian barre like polyneuritis onset etc.
AnonymousOctober 17, 2009 at 7:57 am
I cross referenced lupus and aidp and got a few case studies with aidp being a rare complication of lupus. I showed my internist and he was floored and said I wouldnt even know where to begin to tell the difference. that is why I called mayo myself. so either lupus and cidp or guillian barre like polyneuritis as an onset for lupus.
oh wait this just in my neuro likes mixed connective tissue rather than lupus. I finally see a rheumy next week I think I will pull out all my hair before chemo gets a hold of it. at anyrate I am hanging on though I feel like everyday a new symptom comes out and it is all happening so suddenly. I feel like I am the only one who is going to pull this diagnosis off as far as self advocacy. the doctor ordered a cbc the other day and I added a few tests that needed to be done that no one has considered doing yet like b-12 and comprehensive ANA panel. I just check marked the boxes and then looked up the diagnostic code for mixed connective tssue and wrote it at the top. etc etc
you all heard me complain before august. for 7 years there was just neuropathy and a negtive ana. the doctor didnt even think the first ana was significant. in the past 2 years I did have one weird day here and there that could be interpreted as lupus in retrospect. then all of a sudden I took bactrim and I have felt like I am plummeting down a hill ever since. sorry it is 4:00 in the morning and I had to vent to get some sleep. stupid predisone.lol
AnonymousOctober 17, 2009 at 8:31 am
[Acute Guillain-Barré-like polyradiculoneuritis revealing acute systemic lupus erythematosus: two case studies and review of the literature]
[Article in French]
Aït Benhaddou E, Birouk N, El Alaoui-Faris M, Mzalek-Tazi Z, Aïdi S, Belaïdi H, Kably B, Ouazzani R, Chkili T.
Service de Neurologie, Hôpital des Spécialités, Rabat, Maroc.
The involvement of the peripheral nervous system in systemic lupus erythematosus (SLE) is rare and is dominated by distal symmetric axonal polyneuropathy and multiple mononeuropathy. It usually occurs in late course of the disease. Acute polyradiculoneuropathy of Guillain-Barré syndrome type is very rare and can frequently constitute the first symptom of systemic lupus. We report two cases of acute inflammatory demyelinating polyradiculoneuropathy (AIDP) complicated by respiratory failure due to systemic lupus. In the first case, the pure motor AIDP was the first manifestation of the SLE. The outcome under prednisone treatment was dramatically good with regression of clinical deficit and normalisation of nerve conduction within one month and 12 months of treatment respectively. In the second case the AIDP occurred only one week after diagnosis of SLE and corticotherapy. It was a demyelinating sensory-motor neuropathy. Clinical improvement was obtained after two cures of intravenous gammaglobulin (IVIg). The normalisation of nerve conduction was obtained within 8 months. AIDP is a very rare complication of SLE, but it should be searched as an aetiology of Guillain-Barré syndrome associated to systemic clinical symptoms or to blood inflammation. Corticotherapy could be sufficient, but in some cases the addition of IVIg or plasmapheresis might be necessary
Chronic inflammatory demyelinating polyneuropathy in patients with systemic lupus erythematosus: prognosis and outcome.
Vina ER, Fang AJ, Wallace DJ, Weisman MH.
Internal Medicine, Cedars-Sinai Medical Center, Los Angeles, CA 90048, USA.
OBJECTIVES: To identify clinical characteristics, laboratory features, approaches to management, and predictors of outcome of chronic inflammatory demyelinating polyneuropathy (CIDP) in patients with systemic lupus erythematosus (SLE). METHODS: An analysis of 6 adults with the concurrent diagnosis of CIDP and SLE seen at a SLE Clinic from 1994 to 2004 with a review of 13 patients with SLE and CIDP reported in the medical literature from 1950 through 2004. RESULTS: Among our 6 patients with SLE and CIDP, 3 (50%) achieved a substantial clinical response to intravenous immunoglobulin (IVIg) and the remainder had a minimal response. The improved patients were more likely to have received treatment earlier (within 1 year of CIDP onset) and to respond faster (<1 to 3 months) than minimally improved patients. They tended to have CIDP features of weakness of all extremities, hyporeflexia of the upper extremities, and slowed nerve conduction velocity of the motor median nerve. Compared with minimal responders, responders had more serious internal organ manifestations and multiple autoantibodies associated with SLE. Review of the literature identified 13 previously reported CIDP patients with SLE. Many had neurological involvement of all extremities, nerve biopsies showing demyelination, and serious SLE internal organ manifestations. Most were treated with steroids, but the 1 treated with IVIg had similar characteristics to our subset of patients who improved with IVIg. CONCLUSIONS: CIDP is an uncommon, but not rare, manifestation of SLE. Certain characteristics including early CIDP diagnosis, involvement of all 4 extremities, hyporeflexia of the upper extremities, and slowed motor nerve conduction velocity of the median nerve in addition to SLE involvement of critical internal organs and the presence of multiple antibodies associated with SLE all appear to predict a good response to IVIg.
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