B12 insufficiency/MS

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Re: B12 insufficiency/MS

Postby lyndacarol » Thu Jun 19, 2014 12:29 pm

Here is another possible symptom to add to the list of B12 deficiency: chronic cough.

"Unexplained chronic cough and vitamin B12 deficiency": http://ajcn.nutrition.org/content/93/3/542.abstract
The American Journal of Clinical Nutrition

Abstract
Background: Chronic cough is characterized by sensory neuropathy. Vitamin B-12 (cobalamin) deficiency (Cbl-D) causes central and peripheral nervous system damage and has been implicated in sensory neuropathy and autonomic nervous system dysfunction.

Objective: We evaluated whether Cbl-D has a role in chronic, unexplained cough.

Design: Laryngeal threshold (histamine concentration that provokes a 25% decrease in the midinspiratory flow), bronchial threshold (histamine concentration that provokes a 20% decrease in the forced expiratory volume in 1 s), and cough threshold (histamine concentration that causes ≥5 coughs) in response to an inhaled histamine were assessed in 42 patients with chronic, unexplained cough [27 Cbl-D patients and 15 patients without Cbl-D (Cbl-N)] before and after intramuscular injections of cobalamin for 2 mo. Laryngeal, bronchial, and cough hyperresponsiveness was diagnosed when histamine concentration thresholds were ≤8 mg/mL. Seven Clb-D and 3 Cbl-N patients underwent an oropharyngeal biopsy before treatment.

Results: Cbl-D patients had a higher prevalence of laryngeal hyperresponsiveness than did Cbl-N patients (92.6% compared with 66.7%; P = 0.03), a thinner oropharyngeal epithelium [133.7 μm (95% CI: 95, 172 μm) compared with 230.8 μm (95% CI: 224, 237 μm); P = 0.002], a lower number of myelinated nerve fibers [2.25/mm2 (95% CI: 1.8, 2.7/mm2) compared with 3.44/mm2 (95% CI: 3, 3.8/mm2); P = 0.05], and a higher immunoreactive score for nerve growth factor (NGF) [6.7 (95% CI: 6, 7.3) compared with 2.8 (95% CI: 2.5, 3.1); P = 0.02]. After cobalamin supplementation, symptoms and laryngeal, bronchial, and cough thresholds were significantly improved in Cbl-D but not in Cbl-N patients.

Conclusions: This study suggests that Cbl-D may contribute to chronic cough by favoring sensory neuropathy as indicated by laryngeal hyperresponsiveness and increased NGF expression in pharyngeal biopsies of Cbl-D patients. Cbl-D should be considered among factors that sustain chronic cough, particularly when cough triggers cannot be identified.
Received August 5, 2010.
Accepted December 20, 2010.
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Re: B12 insufficiency/MS

Postby NHE » Wed Jun 25, 2014 10:33 pm

standingtall wrote:Yes, I have been tested. But before I give the data, let me tell my B12 story. About 3 months after my first MS attack with all symptoms subside and just prior to diagnosis of MS I tested low on B12. I do not have that exact data, but I think it was in the 20pg/ml range. This was in the fall of 2010. The doc prescribed B12 injections for a few weeks, but the B12 did not increase. I have no recollection or data on hand about mma or hcy at that time. Post B12 injections, the doctor suggested that I begin 1mg sublingual methylcobalamin which I did. Then in the course of addressing the B12 deficiency, I got the MS diagnosis and the B12 concern sort of went out the window for the doctors. You know, the old MS patient shuffle where every disfunction or symptom is pinned to the MS diagnosis.


It's nearly incomprehensible how you could be diagnosed with MS with a B12 level as low as 20 pg/mL. 8O

standingtall wrote:I continued to take the B12 supplements anyway, because I could tell a real difference in my energy level when I took them twice daily. When I missed the supplements a few times, I felt very tired and fatigued. Approximately, a year later I got another B12 check myself and the level continued to be on the low side at 82pg/ml. I then switched from the 1mg supplement to a 5mg supplement.
After making the B12 dosage change, I felt great. Best I had felt in probably 10 years. After about a year, I did another B12 recheck myself. This time the level was 3300pg/ml, I could not believe it. I dropped the dosage back to the 1mg amount, and after 3 month recheck it remained about the same. I stopped the supplementation altogether, except for a small amount I get in my multi and after 3 more months the level had dropped down to 1271. I can't afford to pay for too much blood work on my own, and the docs I had at the time wouldn't order it so I was doing this without Dr. supervision. I did not think to check mma or hcy at the time, duh? Recheck of B12 in 2013 was 1078pg/ml. During this time, when I reduced or stopped the B12 supplementation I noticed that my energy level was much reduced. This continues today.
Finally in April 2014, B12 was 781pg/ml. Homocysteine was 5.1umol and methylmalonic acid was 113nmol. I switched primary physicians this year and I think I finally found a good one, as he checked everything. Although he was not very intrigued by my B12 story.
Sorry for the long story, but I still believe I have B12 issues. I do not understand the mechanism that would cause such a deficiency in B12, preventing it from coming up with supplementation. Then only to be followed by an extended period of high B12, preventing it from coming down. Also, the physical benefits of supplementation were tangible and had to be more than coincidence. I will stop here, but feel at least for me that unraveling this mystery holds much of the key for everything I have been battling for the last four years. Maybe the B12 issue is a symptom of what else is going on with my body, but I just don't think so.


Thanks for sharing your experience with B12. How have your MS symptoms been since you were able to get the B12 levels up? Are you on any of the DMDs?
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Re: B12 insufficiency/MS

Postby NHE » Sat Jun 28, 2014 4:28 pm

Plasma vitamin B12 status and cerebral white-matter lesions.
J Neurol Neurosurg Psychiatry. 2009 Feb;80(2):149-57.

    BACKGROUND AND OBJECTIVE: Elevated homocysteine has been associated with a higher prevalence of cerebral white-matter lesions and infarcts, and worse cognitive performance. This raises the question whether factors involved in homocysteine metabolism, such as vitamin B(12), are also related to these outcomes. This study examined the association of several markers of vitamin B(12) status with cerebral white-matter lesions, infarcts and cognition.

    METHODS: The study evaluated the association of plasma concentrations of vitamin B(12), methylmalonic acid, holotranscobalamin and transcobalamin saturation with cerebral white-matter lesions and infarcts at baseline and cognition at baseline and during follow-up among 1019 non-demented elderly participants of the population-based Rotterdam Scan Study. Analyses were adjusted for several potential confounders, including homocysteine and folate concentration.

    RESULTS: Poorer vitamin B(12) status was significantly associated with greater severity of white-matter lesions, in particular periventricular white-matter lesions, in a concentration-related manner. Adjustment for common vascular risk factors (including blood pressure, smoking, diabetes and intima media thickness) did not alter the associations. Adjustment for homocysteine and folate modestly weakened the associations. No association was observed for any of the studied markers of vitamin B(12) status with presence of brain infarcts and baseline cognition or cognitive decline during follow-up.

    CONCLUSIONS: These results indicate that vitamin B(12) status in the normal range is associated with severity of white-matter lesions, especially periventricular lesions. Given the absence of an association with cerebral infarcts, it is hypothesised that this association is explained by effects on myelin integrity in the brain rather than through vascular mechanisms.
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Re: B12 insufficiency/MS

Postby NHE » Sun Jun 29, 2014 12:05 am

Decreased vitamin B12 and folate levels in cerebrospinal fluid and serum of multiple sclerosis patients after high-dose intravenous methylprednisolone.
J Neurol. 1993 May;240(5):305-8.

    Twenty-one patients (15 women, 6 men) with definite multiple sclerosis (MS) were treated with 1000 mg intravenous methylprednisolone-succinate (MP) daily for 10 days. Before MP treatment there was a negative correlation (r = 0.59, P = 0.0084) between serum vitamin B12 and progression rate, defined as the ratio of the score on Kurtzke's Expanded Disability Status Scale and disease duration. A significant decrease was demonstrated in the cerebrospinal fluid (CSF) and serum levels of folate and in the CSF level of vitamin B12 after MP treatment. The decrease in serum B12 was not statistically significant. After MP treatment all median levels of vitamin B12 and folate were below the reference medians. We hypothesize that low or reduced vitamin B12/folate levels found in MS patients may be related to previous corticosteroid treatments. Otherwise a more causal relationship between low vitamin B12/folate and MS cannot be excluded. Further studies may be required to clarify the vitamin B12 and folate metabolism in patients with MS.
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Re: B12 insufficiency/MS

Postby NHE » Fri Jul 11, 2014 3:20 am

Total homocysteine is associated with white matter hyperintensity volume: the Northern Manhattan Study.
Stroke. 2005 Jun;36(6):1207-11.

    BACKGROUND: Total homocysteine (tHcy) has been implicated as a risk factor for stroke and dementia, but the mechanism is unclear. White matter hyperintensities may be a risk factor for both, but studies of the relationship between tHcy and quantitative measures of white matter hyperintensity volume (WMHV) are lacking, especially in minority populations.

    METHODS: A community-based sample of 259 subjects with baseline tHcy levels underwent pixel-based quantitative measurement of WMHV. We examined the relationship between tHcy and WMHV adjusting for age, sociodemographics, vascular risk factors, and B12 deficiency.

    RESULTS: Higher levels of tHcy were associated with WMHV adjusting for sociodemographics and vascular risk factors.

    CONCLUSIONS: These cross-sectional data provide evidence that tHcy is a risk factor for white matter damage.

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Re: B12 insufficiency/MS

Postby standingtall » Fri Jul 18, 2014 12:48 am

Lynda, my symptoms have been all over the place. Specifically since getting B12 up I felt good with few symptoms at all. The only thing symptom I had was spasticity. While on aubagio I discovered the unusually high b12, stopped the b12 and my symptoms have increased. There is so much going on it is hard to tell what helps and what is working against me!
My neuro switched me over to rebif, which is really working me over at the moment. One thought I can't get out of my head....what if the B12 was my issue and the aubagio impacted the liver which caused the unusually high b12? Then stopping the b12 brought about the resurgence of symptoms? Probably wishful thinking on my part, but I will find out soon as I have restarted the b12 supplement despite my last bloodwork showing it was still plenty high.
Thanks for the info NHE.
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Re: B12 insufficiency/MS

Postby THX1138 » Fri Jul 18, 2014 8:40 am

standingtall, when you say your B12 was high, what exactly do you mean. Do you have a number and unit measurement :?:
B12 is extremely safe and being "high" in it is no cause for concern that I have ever heard of.
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Re: B12 insufficiency/MS

Postby lyndacarol » Fri Jul 18, 2014 9:41 am

standingtall wrote:Lynda, my symptoms have been all over the place. Specifically since getting B12 up I felt good with few symptoms at all. The only thing symptom I had was spasticity. While on aubagio I discovered the unusually high b12, stopped the b12 and my symptoms have increased. There is so much going on it is hard to tell what helps and what is working against me!
My neuro switched me over to rebif, which is really working me over at the moment. One thought I can't get out of my head....what if the B12 was my issue and the aubagio impacted the liver which caused the unusually high b12? Then stopping the b12 brought about the resurgence of symptoms? Probably wishful thinking on my part, but I will find out soon as I have restarted the b12 supplement despite my last bloodwork showing it was still plenty high.
Thanks for the info NHE.

Standingtall, I echo THX1138 and wonder if you will share the number and unit measurement for your "high" B12 with us.

Vitamin B12 is water soluble, which means that any excess amount your body does not need will be flushed out in urine. 80-90% of the B12 in our body is stored in the liver.

That "one thought [you] can't get out of [your] head" seems completely plausible to me: A B12 deficiency could be your issue. The Aubagio could have impacted your liver and caused it to dump its stores of B12. Your body was getting B12 through supplements and when you stopped, your symptoms returned (there was nothing stored in the liver to fall back on). Seems completely possible to me!!!

I will be very interested to hear what happens now that you have restarted B12 supplements (with a generous dose, I hope – remember, any excess will be flushed out of your body harmlessly). With B12, only "low" test results are important, in my opinion. There is no toxicity, no side effects, connected to a "high" level. In the book, Could It Be B12?, the authors recommend that the serum B12 level should be at least 1000 pg/mL in people who have neurological symptoms (and spasticity would be one of those). In Japan the standard level extends to 1300 pg/mL. I'm not sure it is possible for us to be too high. Some of us may simply require more. Remember: B12 is water soluble; excess is flushed out.

Please keep us posted on how things go.
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Re: B12 insufficiency/MS

Postby lyndacarol » Sun Aug 03, 2014 3:13 pm

Here is some good general information that I think belongs here:

http://www.b12deficiency.info/b12-testing/

B12 Testing

Please be aware that taking any B12 supplements at all prior to being tested could skew your results and this may cause you to remain undiagnosed. TRY NOT TO SELF TREAT before testing!

Folate and ferritin levels must be checked with B12, you may not be low in these but B12 deficient patients often are.

Diagnostic Tests - please note symptomatic children often show as within range on a serum B12 test. They may require ALL tests to establish a deficiency.
The most common test is serum B12 - The reference range can be set as low as <110 - 900 ng/l in some parts of the UK. This is a problem as the test often misses desperately deficient people. The fact is that it tests all B12 in the blood, active and inactive; it does not record what is happening at cellular level. The body cannot access inactive B12 and this can be as much as 80% of the level in serum. There are documented problems with the accuracy of this test; however, most health professionals are not aware of this, click here to read the NEQAS B12 alert. What we really need is for doctors to understand that it is important to treat the symptomatic patient and not just rely on test results.

Serum MMA - (methylmalonic acid) is available on the NHS and privately in the UK.

• Urinary MMA - This test is only available privately in the UK or can be ordered directly without referral from the US. Click here to learn more from Dr Eric Norman's website.

• Active B12 (HoloTc or Holotranscobalamin) - This private test can be carried out in the UK at St Thomas' with the consent of your GP or as a home test kit.

• Homocysteine - In the UK this test can be carried out privately or at your local hospital if requested by your doctor. Homocysteine is an amino acid produced by the chemical conversion of methionine. It can rise to a toxic level if levels of B12, B6, folate (B9), B2 and magnesium are low. It has been thoroughly documented that even moderately elevated homocysteine levels are a strong risk factor for cardiovascular disease, stroke, and neuro-degenerative diseases, including dementia and Alzheimer’s.

• MTHFR - methylenetetrahydrofolate reductase (gene mutation)

The following tests are used to determine the reason for a B12 deficiency, one of the causes of B12 deficiency is Autoimmune Pernicious Anaemia.
• Gastric Intrinsic Factor Antibodies.

• Gastric Parietal Cell Antibodies.

• If you are B12 deficient it is essential to have your folate (vitamin B9) and ferritin levels (iron storage) monitored in order to make sure you optimise your healing. Your doctor may not be aware of this!

Your MCV level (mean corpuscular volume) which is tested as part of full blood count will also be key in determining macrocytosis - (large red blood cells). Please note absence of high MCV does not exclude B12 deficiency. Click here for more information.
Adding B12, folate and ferritin tests to a 'full blood count' would help doctors to diagnose a B12 deficiency much earlier than at present.


The unreliability of the serum B12 test
Read an extract on the unreliability of the serum B12 test from an NIHS (Irish National Institute of Health Sciences) Bulletin February 2013. Co authored by Margaret Harty PHN, RGN, RM and Dr Joseph Chandy.


AND please notice the #2 misdiagnosis (multiple sclerosis) on the following list: http://www.b12deficiency.info/misdiagnosis/
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Re: B12 insufficiency/MS

Postby lyndacarol » Tue Aug 05, 2014 2:42 pm

http://www.b12deficiency.info/assets/ni ... e-4-p9.pdf

"B12 Deficiency - The Need for a Protocol," an extract on the unreliability of the serum B12 test:

In Ireland, a diagnosis of vitamin B12 deficiency is typically contingent on the results of a total serum B12 test. However, emerging evidence indicates that the total serum B12 assay is inaccurate¹ and that total serum B12 is an insensitive and unspecific biomarker for B12 deficiency² suggesting that B12 deficiency may be considerably under diagnosed in Ireland.



CONCLUSIONS

There are no up-to-date national guidelines for the diagnosis and treatment of B12 deficiency, and no single test to definitively identify it. Consequently, the exact prevalence of B12 deficiency in the general population is not known. Interpretation of the threshold of total B12 for treating deficiency is controversial and this is probably the crucial issue. It is likely that general population screening using some diagnostic test will be cost effective sometime in the future. In the meantime, patients are likely to continue to manifest symptoms of B12 deficiency, in the absence of ‘abnormal’ serum total B12.
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Re: B12 insufficiency/MS

Postby NHE » Thu Aug 21, 2014 2:08 am

The Role of B Vitamins in Preventing and Treating Cognitive Impairment and Decline
Adv Nutr. 2012 Nov 1;3(6):801-12.

    Many epidemiologic studies have considered whether markers of B-vitamin status are associated with cognitive function and cognitive decline. This avenue of research was sparked by the homocysteine (Hcy) theory of cardiovascular disease, which was extended to Alzheimer's disease when a link between vascular dementia and Alzheimer's disease was discovered. Hcy could cause cognitive impairment via direct neurotoxicity. However, decreased remethylation of Hcy to methionine might also compromise cognitive function by means other than mere Hcy lowering. Folate and vitamin B-12 participate in Hcy remethylation and largely determine Hcy status. Consequently, much of the relevant research has focused on these 2 B vitamins. The many subtly different hypotheses that investigators have addressed by attempting to link several B-vitamin status indicators to diverse cognition-related outcomes have created a confusing body of conflicting studies that seems to defy summarization. Nevertheless, themes are discernible that aid interpretation, foster hypothesis generation, and inform future study design. For example, despite a shared metabolic pathway, Hcy, vitamin B-12, and folate are differently related to specific cognitive outcomes. Although consistency of findings across studies is often touted as essential to distinguishing causal from coincidental relationships, discrepancies among study findings can be even more informative.

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Re: B12 insufficiency/MS

Postby NHE » Sat Sep 20, 2014 1:17 am

Acceleration of brain amyloidosis in an Alzheimer's disease mouse model by a folate, vitamin B6 and B12-deficient diet.
Exp Gerontol. 2010 Mar;45(3):195-201

    Epidemiological and clinical studies indicate that elevated circulating level of homocysteine (Hcy) is a risk factor for developing Alzheimer's disease (AD). Dietary deficiency of folate, vitamin B6 and B12 results in a significant increase of Hcy levels, a condition also known as hyperhomocysteinemia (HHcy). In the present study we tested the hypothesis that a diet deficient for these three important factors when administered to a mouse model of AD, i.e. Tg2576, will result in HHcy and in an acceleration of their amylodotic phenotype. Compared with Tg2576 mice on regular chow, the ones receiving the diet deficient for folate, B6 and B12 developed HHcy. This condition was associated with a significant increase in Abeta levels in the cortex and hippocampus, and an elevation of Abeta deposits in the same regions. No significant changes were observed for steady-state levels of total APP, BACE-1, ADAM-10, PS1 and nicastrin in the brains of mice with HHcy. No differences were observed for the main Abeta catabolic pathways, i.e. IDE and neprilysin proteins, or the Abeta chaperone apolipoprotein E. Our findings demonstrate that a dietary condition which leads to HHcy may also result in increased Abeta levels and deposition in a transgenic mouse model of AD-like amylodosis. They further support the concept that dietary factors can contribute to the development of AD neuropathology.

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Re: B12 insufficiency/MS

Postby NHE » Sat Sep 20, 2014 1:22 am

Preventing Alzheimer's disease-related gray matter atrophy by B-vitamin treatment.
Proc Natl Acad Sci U S A. 2013 Jun 4;110(23):9523-8.

    Is it possible to prevent atrophy of key brain regions related to cognitive decline and Alzheimer's disease (AD)? One approach is to modify nongenetic risk factors, for instance by lowering elevated plasma homocysteine using B vitamins. In an initial, randomized controlled study on elderly subjects with increased dementia risk (mild cognitive impairment according to 2004 Petersen criteria), we showed that high-dose B-vitamin treatment (folic acid 0.8 mg, vitamin B6 20 mg, vitamin B12 0.5 mg) slowed shrinkage of the whole brain volume over 2 y. Here, we go further by demonstrating that B-vitamin treatment reduces, by as much as seven fold, the cerebral atrophy in those gray matter (GM) regions specifically vulnerable to the AD process, including the medial temporal lobe. In the placebo group, higher homocysteine levels at baseline are associated with faster GM atrophy, but this deleterious effect is largely prevented by B-vitamin treatment. We additionally show that the beneficial effect of B vitamins is confined to participants with high homocysteine (above the median, 11 µmol/L) and that, in these participants, a causal Bayesian network analysis indicates the following chain of events: B vitamins lower homocysteine, which directly leads to a decrease in GM atrophy, thereby slowing cognitive decline. Our results show that B-vitamin supplementation can slow the atrophy of specific brain regions that are a key component of the AD process and that are associated with cognitive decline. Further B-vitamin supplementation trials focusing on elderly subjets with high homocysteine levels are warranted to see if progression to dementia can be prevented.

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Re: B12 insufficiency/MS

Postby lyndacarol » Fri Sep 26, 2014 2:37 pm

Pernicious anemia is a B12 deficiency, specifically caused by lack of Intrinsic Factor – just one of the 14 or 15 proteins required for B12 absorption (Intrinsic Factor is produced in the stomach.). PA is considered an autoimmune disease.

Those interested in history and in B12 deficiency might wish to see this short (7 min.) silent film produced in the 1920s by William P. Murphy and colleague Minot who discovered liver (a rich source of B12) successfully treated PA. It is the B12 deficiency that causes the physical symptoms. When the deficiency is corrected, physical abilities DO return… in time with therapy. I found this encouraging.

http://www.bloodjournal.org/content/blo ... Video1.mov

"Pernicious Anemia – Diagnosis, Treatment, and Results"
Produced by William P. Murphy, M.D., and Miss Isabel Howard, Medical Clinic, Peter Bent Brigham Hospital

Important Signs and Symptoms
Weakness and lemon-yellow pallor
Sore tongue – often the first symptom
Numbness and tingling of the extremities and disturbed sense of balance
Occasionally, a loss of muscular co-ordination

The Blood
Normal blood…… view of blood cells

Anemia
The blood picture during relapse – macrocytosis and tailed forms

The Physiology of Blood Formation (A schematic presentation)
A tentative interpretation of the role of the digestive tract, liver, and bone marrow in the production of red blood cells
The normal mechanism of blood production
When this mechanism fails, pernicious anemia results…
… but liver supplies the necessary substances

Treatment during Relapse (A comparison of methods)
I. Whole liver (The original method)
By this method, the patient must take daily 300 gms (over 1/2 lb.) of liver…
… which in a month amounts to 8400 g (18 lbs.)
It may be taken at meal time

II. Liver Extract Perorally
By this method, the patient must take daily the extract derived from 500 g of liver…
… or in a month, that derived from 14,000 gms (30 lbs.)

III. Liver Extract Intramuscularly
The following dosage for intramuscular injections applies to the extract prepared by the Lederle Laboratories, Inc.
This extract has now been further concentrated so that each 1cc vial contains 15 USP units of active substance
By this method, the patient may be given 2 vials of extract during the first day…
… but during the first month, only 4 vials
A comparison of the amounts of material needed for a month's treatment by these three methods:

How to Give the Injection
The initial dose of 2 vials may be given as a single injection or in two doses, preferably within the first 12 hours.
Inject in the gluteal region with a 21 gauge, 1 1/2 inch needle (The dark line follows the crest of the ilium)
Retract the plunger – if blood appears, withdraw the needle and reinsert
The intramuscular method is used with a minimum of inconvenience to the patient, and produces the most rapid recovery

Pernicious Anemia Part Two
The Effects of Muscular Treatment
Improvement of the Blood
Following the initial injection of 2 vials (30 USP units – Lederle), a reticulocyte increase appears by the second day, the peak, by the fourth or fifth
On the second day, reticulocytes (young red blood cells) are definitely increasing
The fifth day – reticulocyte "peak"
The reticulocytes now decrease as the red blood cells increase
The third 1 cc vial – 15 USP units – is injected on the 11th day
During the first two weeks, the red blood cells increased at the rate of 140,000 per day or a total of 2,000,000
The fourth 1 cc vial is injected on the twenty-first day
During four weeks, they increase at the rate of 115,000 per day or a total of 3,200,000

The blood at 4 weeks
Improvement is more rapid with the intramuscular than with the peroral methods
Iron (perorally) increases the diminished supply of hemoglobin

Improvement of the Neuro-muscular Disturbances
The patients, under the supervision of a trained physiotherapist, are taught exercises to retrain paralyzed muscles…
… and to improve balance
After three months treatment – a striking improvement
As a result of two years inadequate treatment, there has been increasing locomotive difficulty
Little improvement is apparent even after three months of intensive treatment
But with persistent, intensive treatment, improvement is now definite

Maintenance Treatment
Treatment must establish and maintain a normal blood with a red blood cell count of 5,000,000 or more
But adequate maintenance dosage varies with the needs of each patient
Treatment Must Be Continued Indefinitely
A comparison of the average dosage and the cost of treatment adequate for maintenance
Routine injection in the office or home is easily performed. 1 vial – 15 USP units – every 3 to 4 weeks is often adequate.

Recovery and Reemployment
Only with an early diagnosis, with prompt and vigorous treatment, and with an adequate maintenance dosage, can the patient be returned to and maintained in a state of economic efficiency

Pernicious anemia and diabetes mellitus
At 78, after 12 years of liver treatment – still hale and hearty

After 11 years of liver treatment – still employed as a housekeeper

Three years ago – unable to stand or walk alone. The response to intramuscular treatment has been striking and progressive

Three years ago – 1 million red blood cells. Two months after initial injections, 5 million cells and back on his job

Pernicious Anemia… The End
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Re: B12 insufficiency/MS

Postby lyndacarol » Fri Sep 26, 2014 3:40 pm

This sounds like an important paper "Vitamin B-12 deficiency" by A. Hunt, D. Harrington, and S. Robinson:

http://www.bmj.com/content/349/bmj.g5226

Especially: "If the clinical features suggest deficiency then it is important to treat patients to avoid neurological impairment even if there may be discordance between the results and clinical features."
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