All Posts Tagged With: "autoantibodies"

Dr. Gordon’s Comments:

5’MTHF issues are much more complex than is generally recognized, so normal test results can mean nothing. Whatever you knew until today is not enough to protect your patients and loved ones.

The attached NEJM article from July 9 adds considerable likelihood that when someone tells you that the patient’s nutritional status is just fine, they very likely may be dead wrong. The patient suffers seizures and mental disorders that fail to respond to anything because you had not read the attached, which found that the level of folic acid was fine everywhere except in the cerebral spinal fluid. Now they can explain what is going on and it amenable to proper folate treatment, as found in Beyond B-12 sublingual tablets available only from Longevity Plus.

Garry F. Gordon MD,DO,MD(H)
President, Gordon Research Institute
www.gordonresearch.com

Link: http://gordonresearch.com/articles_various/NEJMoa043160.pdf

Excerpt:

In infantile-onset cerebral folate deficiency, 5-methyltetrahydrofolate (5MTHF) levels in the cerebrospinal fluid are low, but folate levels in the serum and erythrocytes are normal. We examined serum specimens from 28 children with cerebral folate deficiency, 5 of their mothers, 28 age-matched control subjects, and 41 patients with an unrelated neurologic disorder. Serum from 25 of the 28 patients and 0 of 28 control subjects contained high-affinity blocking autoantibodies against membrane-bound folate receptors that are present on the choroid plexus.

Full article: http://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=20824620&retmode=ref&cmd=prlinks

Excerpt:

Transfusion-acquired babesiosis can be an asymptomatic or
self-limited febrile hemolytic illness in a healthy host. A
persistent, relapsing, and/or fulminant course with the
development of life-threatening complications may be seen in
immunocompromised or splenectomized patients. As in malaria,
erythrocyte parasitemia is often associated with nonimmune
hemolysis, and can be treated with erythrocytapheresis. Just as
warm autoantibodies have been reported in malaria infection, the
development of autoantibody-mediated immune hemolysis has been
reported in babesiosis. We treated a previously healthy male with
multiple injuries from a motor vehicle accident necessitating
massive transfusion. Late in the hospitalization, his blood smear
revealed Babesia microti, confirmed by PCR study and serology.
This was eventually traced to a unit of blood from an
asymptomatic blood donor that was transfused during his initial
trauma care.
Specific antibiotic therapy was begun, and severe hemolysis from
a high parasite burden required red blood cell exchange which led
to rapid abatement of the hemolysis. He had a positive DAT (IgG
with a pan-reactive eluate) but no serum autoantibody. This
persisted for 10 days following cessation of hemolysis, and
became negative while still on antibiotics while his parasite
burden became undetectable. Reports of autoimmunity associated
with community acquired babesiosis often have severe hemolysis
from their autoantibodies, but our case shows that autoantibodies
may also follow transfusion-acquired babesiosis. The nature of
the autoantigen is unknown. J. Clin. Apheresis, 2010. (c) 2010
Wiley-Liss, Inc.

Excerpt:

If you have multiple sclerosis (MS)––or you know someone who does––you probably remember how long it took to make the diagnosis.  You also may remember a lot of blood tests, a lumbar puncture, at least one magnetic resonance imaging (MRI) scan, as well as many visits and examinations by various doctors.  You may wonder why it still takes so long to make the diagnosis in this modern age of MRIs and other sophisticated tests.  We are going to try to explain why it can be so difficult for even the most expert MS neurologist to determine that someone has MS.  You have to live with the diagnosis and face the disease and the treatments.  You should understand and have confidence in the diagnosis.  Also, if your case of MS does not fit the typical pattern, you need to be aware of the other disorders that can mimic MS.  This is important because the treatments may be very different and, just as in most cases of MS, treatment begun early in the course of the disease is the best way to prevent or slow further neurologic damage.

MRI and new laboratory tests have definitely helped speed the diagnosis, but it still takes longer than anyone would wish, even in easy cases.  This is partly because of the variable nature of the disease in its many signs and symptoms. But it is also because a rather long list of other medical disorders can cause neurologic symptoms and signs that resemble MS. Furthermore, the “white spots” on brain MRI can be caused by a number of other conditions that also need to be ruled out.

The diagnosis of clinically definite MS requires that a person experience at least two neurologic symptoms of the type seen in MS, in two different areas of the central nervous system (CNS), at two different times (‘disseminated in space and time’).  Most typically, the symptoms are optic neuritis plus either an abnormal sensation or a problem with movement.  It can also be numbness in one part of the body and weakness or lack of coordination in another.  But in every case, there can be no other explanation for the symptoms, the changes seen on the MRI, and the abnormalities in the spinal fluid.  Many “mimics” need to be ruled out in order to make the diagnosis of MS.