Has anyone else tried clemastine fumarate @ new relapse?

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Re: Has anyone else tried clemastine fumarate @ new relapse?

Postby jimmylegs » Fri Jan 05, 2018 5:12 pm

regular lab like lifelabs or dyna, with requisition from doc. in the states they have wicked cheap labs you can requisition for yourself online and take the form to whatever local lab you like. the company starting to roll out the canadian version in recent years is charging outrageous prices. same co. as provides a similar service in the uk. highway robbery, but at least we have provincial coverage for some things (if you can get the doc on board to order the tests you want)

in the past for results i would just ask the doc for a printout from her computer. she most always gave me a break bc starving student.
all my old results from various sources are in my hard copy files.
i have hard copies of my mris on disc from the hospital as well. i had to pay a few bucks for those, but once they realized i was not trying to scam them for free, they were quite happy to let me have a paid copy. the fee was something inconsequential like 10 bucks or something. CAD.

as for run of the mill doc requisitioned health card covered tests and results, most recently local (ontario) results have become available online. show health card at lab, get access code to the lab's site, pay a nominal access fee, log in, and check out all your stuff. i haven't gotten into the system yet for myself. on my list of things to do. have been occasionally logging in to others' online lab result info, from elsewhere in the world, for years.
odd sx? no dx? check w/ dietitian
DRI=MINIMUM eg bit.ly/1vgQclQ
99% don't meet these. meds/lifestyle can affect levels
status can be low in ms & other cond'ns
'but my results are normal'. typical panels don't test all
deficits occur in 'normal' range
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Re: Has anyone else tried clemastine fumarate @ new relapse?

Postby jimmylegs » Fri Jan 05, 2018 6:02 pm

Clinical Zinc Deficiency as Early Presentation of Wilson Disease (2015)
https://www.researchgate.net/publicatio ... on_Disease
Wilson disease is a rare autosomal recessive disorder of the copper metabolism caused by homozygous or compound heterozygous mutations in the ATP-ase Cu(2+) transporting polypeptide (ATP7B) gene. The copper accumulation in different organs leads to the suspicion of Wilson disease. We describe a child with clinical zinc deficiency as presenting symptom of Wilson disease, which was confirmed by 2 mutations within the ATP7B gene and an increased copper excretion.

Wilson's disease and other neurological copper disorders (2015)
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4336199/

"WD needs to be differentiated from other conditions that present clinically with hepatolenticular degeneration or share biochemical abnormalities with WD, such as reduced serum ceruloplasmin levels. Disordered copper metabolism is also implied in an increasing number of other neurological conditions, including a subtype of axonal neuropathy due to ATP7A mutations, and the common late-onset neurodegenerative disorders Alzheimer’s disease and Parkinson’s disease."

hmm, prion diseases. abnormal protein folding. zinc x structural role.

"Late onset with WD manifesting> 70 years of age is also well documented.28 Thus, the diagnosis of WD should never be excluded because a patient is “too old”. Conversely, WD with onset in early infancy has also been reported, the youngest age of onset being 9 months"

so heritable but crops up at any age.. sure, i guess. :? but are we talking more about epigenetics than genetics?

"Neurologists also need to consider the diagnosis of WD if asked to see a patient with “unexplained hepatic encephalopathy”. Conversely, the absence of clinical or biochemical evidence of liver disease does not exclude WD"

unexplained my butt. let me guess, the zinc level would be (low) 'normal' in these mysterious cases?

A systematic review and meta-analysis of the use of oral zinc in the treatment of hepatic encephalopathy (2013)
https://nutritionj.biomedcentral.com/ar ... 2891-12-74
"The present meta-analysis is limited by the small number and poor quality of trials included. Available trials studied heterogeneous outcomes and failed to measure critical outcomes such as quality of life. This hinders the ability to draw conclusions about the value of oral zinc supplementation in the treatment of hepatic encephalopathy."

they didn't all measure post treatment serum levels either, by the looks of things. better get busy, science!

back to wilson's.

"Thus, zinc impedes further copper accumulation but has lower de-coppering potential and thus less potential to mobilize copper from tissues already overloaded."
good to know.

other possibilities, most of which i have never before heard

Other copper transport disorders and related diseases

Menkes disease and variants
MEDNIK syndrome
Huppke-Brendl syndrome
Manganese storage disorder
Aceruloplasminemia

Copper and other neurodegenerative disorders
Copper and CP have been implicated in the pathogenesis of both Alzheimer’s disease (AD) and Parkinson’s disease (PD).

also possibly relevant

Inherited disorders of transition metal metabolism: an update (2017)
https://link.springer.com/article/10.10 ... 017-0030-x
"Recently, a role of trace metals in host defence (“nutritional immunity”) has been recognized. The host can deprive the pathogen of a trace metal or poison it with a toxic concentration. Disorders leading to low concentrations of a trace metal can often be treated by supplementing that metal; disorders leading to excessively high concentrations can often be treated with chelating agents such as penicillamine and disodium calcium edetate. This update will address: i) the manganese/zinc transporters (because two new treatable disorders were described in 2016 – SLC39A8 deficiency and SLC39A14 deficiency); ii) copper transporter disorders because we need to improve the treatment of patients with neurological symptoms due to Wilson’s disease; and iii) iron homeostasis because recent progress in research into the metabolism of iron and its regulation helps us better understand several inborn errors affecting these pathways."

kinda fascinating, the epigenetic stuff

Wilson Disease: Epigenetic effects of choline supplementation on phenotype and clinical course in a mouse model (2016)
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5221658/
"...transcriptional changes in oxidative phosphorylation and methionine metabolism genes in WD that originate during fetal life are, in part, prevented by prenatal maternal choline supplementation, a finding with potential relevance to preventive treatments of WD."

Wilson disease: At the crossroads between genetics and epigenetics—A review of the evidence (2017)
https://www.sciencedirect.com/science/a ... 8417000290
"Notably, environmental exposure affects the regulation of gene expression and mitochondrial function. We present the “multi-hit” hypothesis of WD progression, which posits that the initial hit is an environmental factor that affects fetal gene expression and epigenetic mechanisms and subsequent “hits” are environmental exposures that occur in the offspring after birth. These environmental hits and subsequent changes in epigenetic regulation may impact copper accumulation and ultimately WD phenotype. Lifestyle changes, including diet, increased physical activity, stress reduction, and toxin avoidance, might influence the presentation and course of WD, and therefore may serve as potential adjunctive or replacement therapies."

yes. yes indeed.
odd sx? no dx? check w/ dietitian
DRI=MINIMUM eg bit.ly/1vgQclQ
99% don't meet these. meds/lifestyle can affect levels
status can be low in ms & other cond'ns
'but my results are normal'. typical panels don't test all
deficits occur in 'normal' range
User avatar
jimmylegs
Volunteer Moderator
 
Posts: 11118
Joined: Sat Mar 11, 2006 4:00 pm

Re: Has anyone else tried clemastine fumarate @ new relapse?

Postby jimmylegs » Sun Jan 07, 2018 3:16 pm

just ran across this in another setting.. perils of leaving serum zinc at 90 μg/dl

Serum Zinc Status and Helicobacter Pylori Infection in Gastric Disease Patients
http://www.koreascience.or.kr/article/A ... 13n10_5043
"Our study showed that Helicobacter pylori infection has no change in gastritis, peptic ulcer and gastric cancer group, on the contrast, serum levels of Zn were significantly reduced in gastritis, peptic ulcer and gastric cancer group, compared with healthy controls, and the [lower] the Zn levels are, the more increased risk of gastric cancer. Helicobacter pylori infection is a cause of gastritis, peptic ulcers and even gastric cancer, while serum zinc level is an indicator of protection of gastric membranes against damage."

Table 2. Serum Zinc Value in Patients and Control Group
Control............18.7±3.9 wow, even higher than the 18-18.5 (120) ballpark i usually aim for!
Gastritis...........16.8±3.8
Peptic ulcer.......14.0±2.8
Gastric cancer...13.7±2.7 μmol/L = 13.7 / 0.153 = 90 μg/dl
odd sx? no dx? check w/ dietitian
DRI=MINIMUM eg bit.ly/1vgQclQ
99% don't meet these. meds/lifestyle can affect levels
status can be low in ms & other cond'ns
'but my results are normal'. typical panels don't test all
deficits occur in 'normal' range
User avatar
jimmylegs
Volunteer Moderator
 
Posts: 11118
Joined: Sat Mar 11, 2006 4:00 pm

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