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» LymeNet Flash » Questions and Discussion » Medical Questions » Claritin cures Lyme!?&$! (Page 2)

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Author Topic: Claritin cures Lyme!?&$!
Lymetoo
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Do NOT stop taking magnesium!

--------------------
--Lymetutu--
Opinions, not medical advice!

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randibear
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I have to be really careful because of high b lood pressure. everything seems to raise it.

--------------------
do not look back when the only course is forward

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Marnie
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WOW !!! AND yes, Bb does indeed use/need

MANGANESE.

I wonder if there would be a synergy with this:

http://digitalcommons.pcom.edu/biomed/27/

http://toxsci.oxfordjournals.org/content/135/1/218.full

Researchers...brainstorming... the above link

oddly indicated...

Mn accumulates in the mitochondria and inhibits oxidative phosphorylation (= normally make about 36 ATP using glucose and oxygen - simplified). Now the only way the cell can remain viable is to rely on glycolysis (2 ATP) - or does it? Keep reading.

Does this (oxidative phosphorylation inhibited) then -> mitophagy = degradation of mitochondria by autophagy = self destruct...which might provide Bb with additional nutrients - the "yummies" (proteins) that make up the mitochondria = powerhouses serving as food for Bb

-> upregulation of new mitochondria being made via PQQ/mtDNA transfer from a donor cell...

repeating the same process over and over, i.e.,

Mitochondria take up Mn (*temporarily* robbing Bb of same), oxidative phosphorylation shuts off, but glycolysis stays on. Mitochondria die off and Bb "feeds" on the some of the "garbage" (including Mn), and replacement mitochondria "happen" via mtDNA shuttled to the infected cell to create more mitochondria.

"We report that tumor cells without mitochondrial DNA (mtDNA) show delayed tumor growth, and that tumor formation is associated with

***acquisition of mtDNA from host cells.***"

In other words Bb infected and/or cancerous cells (Bb can infect HeLa cancer cells) triggers mitochondrial DNA shuttling = horizontal transfer between cells.

This might explain it better (healthy cell "donates" mtDNA = mitochondrial DNA to unhealthy cell):

http://www.news-medical.net/news/20150329/Mitochondrial-DNA-movement-an-interview-with-Professor-Jiri-Neuzil-Griffith-University.aspx


Read about mitophagy as it relates to cancer here:

https://en.wikipedia.org/wiki/Mitophagy

Look at what is right below the mitophagy and cancer paragraph...

We've known that for a long time, right?

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ukcarry
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SacredHeart, it is borrelia's usage of manganese, not magnesium, that Claritin affects.
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foxinsox
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I have not read through all these replies so I don't know if this was already covered, but I researched thoroughly into Claritin after I read about it's so-called ability to kill Lyme (or rather, to starve it).

Claritin was tested on rodents in massive doses. The amount equal and necessary for humans to achieve the same result would be far past the level of an overdose.

I called and questioned my LLMD in LA, who has been treating Lyme for 30+ years, about the study to see what he knew about Claritin...He said the exact same thing.

The study was released prematurely and really should not have been interpreted in the way it was by the Lyme community. An average dose of claritin, or even a double or triple dose, would have absolutely no effect on Borrelia.

The amount of loratadine would be far too small to make a difference. It has also not been completely proven to have a true effect. If Claritin truly kills Bb, or in any way prevents it by blocking manganese, it does so in such huge amounts that it would overdose a person before it had any effect.

If anyone is feeling results from Claritin, it is a placebo effect.

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marcholland81
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@marnie

regarding resveratrol; it has extreme low bioavailability. There are some liposomal formulations on the market but no-one knows how effective they are.

Further I don't understand a thing from your story. Maybe you can explain in layman's terms what you are trying to say.

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Marnie
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My "take" on Claritin (I'm hopeful):

The following is very long (about 38 pages printed out), but if you want to work with me and try to figure out what is going on, please try to muddle thru this. I will translate terms you may not understand with some links as necessary.

It may be helpful if you cut, paste and drop this into a MS word file and print it out to read slowly, multiple times if necessary to grasp all of the information.

Claritin is an inverse agonist ("helper") of the H1 receptor (one of 4 histamine receptors).

Inverse agonist means it locks onto the same receptor, but induces a pharmacological response
*opposite to that agonist.*

Okay, so what does an agonist do that Claritin works opposite of?

The H1 receptor agonist

2-(3-chlorophenyl)histamine

***activates Gi proteins in HL-60 cells***

Okay, so Claritin, working opposite, INACTIVATES Gi proteins in...HL-60 cells.

Okay, first,what the heck are HL-60 cells?

HL-60 cells are predominantly a neutrophilic promyelocyte (precursor). Neutrophilic is an adjective describing a neutrophil = an abundant type of granular white blood cell that is highly destructive of microorganisms.
Other compounds like 1,25-dihydroxyvitamin D3,

12-O-tetradecanoylphorbol-13-acetate (TPA) and GM-CSF

can induce HL-60 to differentiate to monocytic,

macrophage-like

and eosinophil phenotypes,
respectively.

Wiki.

Putting this another way:

Differentiation of HL-60

to neutrophil or monocyte-like cells

by Vitamin A (ATRA) and Vitamin D (1a,25(OH)2D3)

(Me...respectively.)

Complete differentiation should be apparent day 5

http://theolb.readthedocs.org/en/latest/cell-biology/hl-60-differentiation-to-neutrophilsmonocytes.html

So if Gi is inhibited in HL- 60 cells via Claritin metabolite, no new neutrophils and monocytes are created because the growth of them has been inhibited.

In other words,

***Claritin inhibits Gi in the precursor (HL - 60 cell line) which normally progresses to become to neutrophil and monocyte-like cells.***

Now...about inhibiting Gi in those (HL -60) cells, then what?

Gi-protein inhibitor...induces

senescence-associated beta-galactosidase positive cell formation through CREB phosphorylation.

Senescence = the irreversible growth arrest of cells

Beta galactosidase -> growth arrest?

Guess what...

Furthermore, when lacZ is expressed from the ospC promoter,

***β-galactosidase activity is detected only in B. burgdorferi clones that express ospC, ***

and it accurately monitors endogenous gene expression.

http://aem.asm.org/content/76/22/7407.full

OspC is the form Bb takes when it is leaving the tick's stomach. Two proteins "coat" that outer surface protein C. They are SALP15 and p8. Both of these proteins interfere with our immune system functioning (especially p8 which inhibits mannose binding lectin - the first necessary step in the defense system).

Bb downregulates OspA and upregulates OspC - temporarily. Then OspC goes down and OspA goes up.

When Lac Z is "called for"... up goes OspC.

The lac operon allows for the effective digestion of lactose ***when glucose is not available***.

The gene product of lacZ is β-galactosidase which cleaves lactose, a disaccharide, into glucose and galactose.

This dual control mechanism causes the sequential utilization of glucose and lactose in ***two distinct growth phases***, known as diauxie.

Wiki.

OspA for one growth phase, OspC for the other?!!!

Going back to OspA and OspC...

For our DOGS…

Nobivac (trademark) Lyme

The vaccine contains a traditional isolate

targeted at OspA and

a unique isolate proven to induce high levels of Borreliacideal antibodies to OspC1

http://www.merck-animal-health-usa.com/products/nobivac-lyme/overview.aspx

(Which maybe why the human vaccine based solely on OspA didn't work. Oops, needed to address OspC1 too.)

Let's go back for a moment to Gi - inhibited.

Those here who know me, know I was obsessed with finding out which protein/enzyme in the Western Fence Lizard is capable of destroying Bb within the ticks feeding on that lizard while it hunts for insects to eat at night.

For newbies...that lizard has a bright blue (cyan colored) belly and lounges around all day in the sun. At night it hunts for lots of various insects to eat. It has to be able to see in the dark...to capture as much light as possible to find its prey.

Hence, it has a LOT of eye rods which produce rhodopsin = visual purple. It is a pigment-containing sensory *protein* that converts light into an electrical signal.

(The WFL also has a prominent pineal gland, so my initial reaction was...melatonin.)

When Dr. Lane boiled the lizard's blood, the protective factor was lost. He said it was likely a protein/enzyme since they are easily destroyed by heat. He never said WHICH protein/enzyme/other.

Our eye cones enable us to see colors. The rods help with night vision.

Now are you ready for this?

And finally, we show that the

***rhodopsin also forms stable complex with Gi.***

http://webcache.googleusercontent.com/search?q=cache:9f8q9tDsTV4J:http://journals.plos.org/plosone/article%3Fid%3D10.1371/journal.pone.0098714

A stable complex would prevent/inhibit Gi in HL- 60 cells from working, right?

Okay...so much for "I told you so."

About impacting the HL -60 cells and preventing them from growing into neutrophils and monocyte-like cells.

Don't we need neutrophils and monocyte-like cells?

Why does Bb trigger the recruitment of neutrophils (via the cytokines)-> arthritis?

"The infection generally responds well to antibiotic therapy;

however, if it is *left untreated*, infection can result in various pathologies, most commonly an inflammatory arthritis characterized by cellular infiltration into the joints,

predominated by neutrophils and macrophages."

But what if Bb has been destroyed, yet the inflammatory condition continues on - self perpetuating?

We know Mg levels DIVE at the outset of lyme and continue to spiral down...like there is no stopping it.

I need to digress a moment and tell you a true story.

A close friend was on Lipitor and Metformin for high BP and late onset diabetes. (His doctor did not tell him to take CoQ10 when on the statin.)

He developed a very serious condition called Rhabdomyolysis. That is the name of a condition where muscle cells are destroyed. It nearly killed him (kidney failure is one of the serious consequences).

Despite going OFF the Lipitor and Metformin, the muscle cell destruction continued. His creatinine levels were thru the roof.

After many days in the hospital, he became fed up and checked himself out. Needless to say, he contacted other doctors.

FINALLY he was put on high dose steroids. Slowly he began to recover and began physical therapy - first with an aide. He now exercises 2 hours a day (lives in a community with fitness equipment and a pool).

Of course, he lost about 60 pounds (was 280)and now his cholesterol and diabetes are totally under control - without meds. He is slowly titrating off the steroids under a doctor's care.

The point I am trying to make is that even when an infection/toxin (in his case, the drugs) is gone/withdrawn, sometimes the destruction continues.

It appears once inflammatory cytokines/ destruction kicks in, it is challenging to halt the process.

Inflammation is absolutely necessary for healing to take place. It helps signal the cells that are the "garbage collectors". But ongoing inflammation is bad, really bad.

I will acknowledge that in some cases, Bb may still be present (not just left-over pieces of it).

However, sometimes the tetracycline class of drugs may be less effective for some gene-types. What comes to mind is persons who have hereditary hemochromatosis - excess iron in vital organs such as the liver, heart and pancreas. All tetracyclines form insoluble complexes with calcium, magnesium, *iron* and aluminium, which markedly reduces absorption.

The following link discusses a patient given tetracycline for an infection who had hemochromatosis.

"Parasites hunt us for our iron; cancer cells thrive on our iron. Finding, controlling, and using iron is the game of life. For bacteria, fungi, and protozoa, human blood and tissue are an iron gold mine. Add too much iron to the human system and you may just be loading up the buffet table."

http://webcache.googleusercontent.com/search?q=cache:dgvBJDifh_sJ:http://www.today.com/id/17008658/ns/today-today_books/t/why-we-need-disease/#.VdSPJRDD9ZQ

Although Bb does not use iron to replicate, the excess iron likely would bind to "normal" doses of tetracycline and thus be less effective in clearing Bb and co-infections.

So the question is...can Claritin (metabolite of) destroy Bb (via interfering with Bb's Mn transport protein) that may be camped out in HeLa cells or macrophages (think of them as Pac Men - gobbling up the "garbage")or in endothelial cells (line the blood vessels) and/or in fibroblasts?

Or does it work by lowering the number of neutrophils and/or monocytes which, as bystanders, horizontally transfer to the infected cell some mtDNA (mitochondrial DNA)delaying the destruction of Bb's "home"?

In the case of Bb infected HeLa cells (immortal cancer cells that originated as a result of the virus HPV)- cancer drugs and therapy are going to be needed.

But even with those powerful modalities, some protection from excessive inflammation will be wise.

Although some anti-inflammatory drugs alone have the ability to act as anti-cancer agents or simply to help decrease progression.

About the situation where viable Bb is camped out in macrophages. (Bb is not the only pathogen that can survive in macrophages - HIV, TB, etc. can too.)

First of all it is important to know how Bb is protecting itself from destruction.

One of the ways is due to Bb having a protein called SOD (superoxide dismutase)as well as a metal transporter protein called BmtA (for borrelia metal ( manganese) transporter A).

This is equivalent to SodA -> Mn-SOD which protects Bb's proteins from being "oxidized" /("fried").

This is another instance of Bb being a lot like us...WE make Mn-SOD in our cytosol (liquid portion inside the cells).

But if Bb is "stealing" our supply of Mn...we can't make enough for "self" and that puts our cytosol DNA at risk for ROS oxidative damage.

We have 2 kinds of DNA. In the cytosol, our DNA comes from mom and dad. In our mitochondria, powerhouses of the cells (many!), the DNA comes USUALLY from our mom only (I found one exception on the internet reported by geneticists. Exception to every rule...)

When persons talk about DNA damaged cancer cells multiplying out of control, they are talking about the cytosol DNA. In cancer, the mitochondria are working, albeit not great.

Hallmarks of cancer cells include their
resistance to apoptosis and their mitochondrial dysfunction, but not mitochondrial "death".

In fact, targeting the mitochondria (knocking them off) has anti-cancer potential i.e.,

Antibiotics that target mitochondria effectively *eradicate cancer stem cells*, across multiple tumor types: Treating cancer like an infectious disease...last sentence in summary:

Finally, recent clinical trials with doxycycline and azithromycin (intended to target cancer-associated infections, but not cancer cells) have already shown positive therapeutic effects in cancer patients, although their ability to eradicate cancer stem cells was not yet appreciated.

http://www.impactjournals.com/oncotarget/index.php?journal=oncotarget&op=view&page=article&path%5B%5D=3174

And the diabetic drug metformin shows promise too (though IMO, there are better choices - berberine HCL w/curcumin and black pepper extract to potentiate curcumin by Swanson).

Metformin for cancer:

http://webcache.googleusercontent.com/search?q=cache:421T1kRZKQgJ:http://www.lifeextension.com/magazine/2012/2/can-diabetes-drug-prevent-cancer-death/page-01

et al - many.

Back to Bb's ways to protect itself:

Bb has ways to spit out drugs (export) drugs that would otherwise do it in. It is called a trans-membrane export pump or Multidrug-resistance efflux pump. We do have some drugs to address that issue.

I suspect Bb triggers the macrophage release of cytokines to benefit its survival.


So we not only have to target Bb, but also Bb's "home" (the infected macrophage) and do as little "bystander" damage as possible.

This is important...

Monocytes' lifespan can switch dramatically, from prolonged survival during inflammation to apoptosis (cell death)

as inflammation resolves.

*Macrophages, in contrast, live up for months.*

(Monocytes can differentiate to become macrophages under certain circumstances.)

The question is...can Claritin inhibit Bb's Mn transporter protein when Bb is camped out in a macrophage?

It appears Claritin can inhibit the formation of neutrophils and monocytes (which can become macrophages), but what about viable Bb already infecting macrophages?

Do the infected macrophages secrete cytokines to recruit neutrophils and monocytes for Bb's benefit?

Do Bb(s)- replicating in the macrophage trigger macrophage autophagy/mitophagy or apoptosis (self "eat"/self destruction vs cell death) and then "escape" to adjacent cells it has "recruited"?

Autophagy (mitophagy = the *selective degradation of mitochondria* by autophagy) may co-occur with apoptosis (cell death). First the powerhouses, then the infected cell.

Autophagy (mitophagy) may partially participate in the execution of macrophage cell death by *enhancing apoptosis* (cell death).

When apoptosis (cell death) is blocked infected macrophages undergo increased autophagy.

Another possibility is that the infected macrophage which is marked for death (and in which the mitochondria are being destroyed via mitophagy),

transfers mtDNA from adjacent cells it has recruited -> "new" mitochondria from the "donated" mtDNA (mitochondrial DNA)

in order to prolong the life of the (cytosol DNA damaged) macrophage thus making it equivalent to a HeLa, immortal, cell.

If so, then all the more reason to stop the recruitment of the neutrophils and monocytes...Bb won't have a "bystander cell" from which to transfer mtDNA.

One last thing - about iron.

While Bb does not use iron to replicate (MANY pathogens do), it does look to use it for quorum sensing and ...

Recent studies have shown that

***sodA expression is regulated by

three iron-dependent

regulatory proteins,***

***Fur (ferric uptake regulation),***

Fnr (fumarate nitrate regulation) and

SoxR (superoxide regulon),

and by the ArcA/ArcB (aerobic respiration control) system.

http://www.ncbi.nlm.nih.gov/pubmed/7917419?dopt=Abstract


Remember, I linked:

One of the ways is due to Bb having a protein called SOD (superoxide dismutase)

as well as a metal transporter protein called BmtA (for borrelia metal ( manganese) transporter A).

This is equivalent to Sod + transporter,A = Sod - A (Mn transporter) ->

Mn-SOD which protects Bb's proteins from being "oxidized" /("fried").

Repeating...iron dependent proteins regulate SodA expression. By "stealing" our Mn so our cells make less Mn-SOD, the iron dependent regulatory proteins will kick in.

Borrelia burgdorferi contains a gene that codes for a (me...iron dependent) Fur homologue. The function of this Fur protein is unknown; however, spirochetes grown at 23 (73.4 F) or 35°C (95 F) expressed fur as determined by reverse transcriptase PCR.

Fur may function in B. burgdorferi as a repressor and regulate oxidative stress genes.

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC516618/

Cold lowers oxygen demand and Bb hangs out in cold-blooded ticks where it replicates (OspA?) and in warm-blooded animals. Remember, Bb is not a strict anaerobe – it needs some, but not much oxygen, but prefers less. It can be microaerophilic = requiring oxygen for growth but at lower concentration than is present in the atmosphere.

http://webcache.googleusercontent.com/search?q=cache:xEWJHLTp5G8J:http://www.antimicrobe.org/new/b84.asp
To the best of my ability. It was an all-nighter.

If I have made errors, feel free to correct them with links please.


Of course, you absolutely should discuss Claritin with your doctor and it wouldn't hurt to also talk to your pharmacist to be sure there will not be drug interactions and skim thru the list of possible side effects (which is as long as most drugs advertised on TV).

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marcholland81
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@Marnie

Thanks for that. I will have to read it several times and come back to you.

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WPinVA
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I'm actually on Clarinex, not claritin - anyone know if that was included in the study?

I wish I had the brainpower to tackle Marnie's post!

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Marnie
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Bottom line is this:

IF our antibody to Bb's OpsB (outer surface protein B)= IgG1K worked, it doesn't...histamine release would be inhibited!

IgG1K antibody blocks histamine release:

http://webcache.googleusercontent.com/search?q=cache:nA2T7z0qDd4J:http://www.dendritics.net/research-fields

Bb comes along with a tick histamine release factor...up goes histamine...to counter...a LOT of Mg was dumped. Is that histamine release factor (a protein) the 1st "toxin"?

Unfortunately it takes several days to make antibodies and it takes Mg and Ca to make them, but low and behold, Mg has gone *way down*. My guess....the liver cells take a huge hit from the get-go.

Mg is an anti-histamine, anti-inflammatory and inhibits HMG CoA reductase (works like a statin drug to lower cholesterol and Bb follows the "cholesterol pathway" to make its lipoproteins).

Valiant attempt by self to protect.

Be careful with Claritin...see my post about caution if underlying cardiac condition.

I don't see a problem with increasing Mg intake (spaced out doses to = RDA at least) and taking Claritin.

Thoughts?

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Robin123
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Marnie, so you're saying Bb stimulates a histamine response in us? I react easily with hives to surfaces and need to rinse my skin with water after so doing. This could be due to upregulated histamine?
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Marnie
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Likely your intracellular Mg level is very low.

There is a tick histamine release factor which maybe the 1st "toxin" we encounter.

As you were typing, so was I. Read my comments above.

Histamine...too much... counter with epi pen or upregulate epinephrine = adrenaline but...

"Epinephrine-induced hyperglycemia"...

ONGOING.

A thought...

Our defense cells have a H1 receptor on them...histamine IMPORT?

But our defense cells apparently also EXPORT histamine.

Histamine export triggers adrenaline (= epinephrine) -> hyperglycemia.

If we block the import, don't we then block the export (nothing to export) to trigger adrenaline and cause hyperglycemia?

When Bb is in dormant cyst form, is the need for histamine triggering hyperglycemia is less, thus it is exported triggering adrenaline triggering hyperglycemia and cyst form now has "nutrients" (glucose)?

If we block histamine import, do we force Bb into the dormant cyst form?

At which time diflucan + berberine HCL combo might work.

Brainstorming.

[ 08-24-2015, 06:35 PM: Message edited by: Marnie ]

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LymeWife
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Hi everyone! I just registered. My wife had a very rough night last night and I am very worried.

She has yet to recieve an actual Lyme diagnosis, but all signs point to it. A little over a year ago she had 2 tick bites in Pennsylvania. We now live in Colorado and it is much less common out here. In the time since her bites she has been through many specialists, possible diagnoses of everything from MS to Cushing's disease to RA, but no positive tests. Following a dose of corticosteroids her symptoms blew up and have gotten so much worse. Her pain is severe and body wide, pain pills can't even touch the pain. We are taking treatment into our own hands since doctors haven't been helpful. Still have not seen LLMD. We ordered antibiotics, doxy and tinidazole after a lot of research. That was yesterday so we are waiting for their arrival.

In the meantime, we read about Claritin possibly helping fight Lyme, so she has been taking it for several weeks. Since then she has been having some additional, scary symptoms. I am wondering if Claritin can cause herxing because thats what this seems like. Last night she had these intense body spasms and twitches that were extremely painful. She said they felt like shocks. She became very rigid and kind of contorted and yelled out in pain. This happened on and off for about 20 minutes. This was the worst episode yet, but this has happened several times in the past week or two.

Anyone know what is going on? Does this sound like a herx reaction? Something else? What can we do, besides doctors (she is doctored out for the time being after most recent bad experience)? Should she keep taking the Claritin?

Thank you everyone!

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Lymetoo
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Welcome, LymeWife!! I'm very sorry you had to find us here .. but glad you did!!

Please make a separate NEW post so you will receive more help and input. Not everyone will open this thread and you may miss out on a lot of tips and suggestions.

I have to leave the house right now, but pray that others will step up to help you.

Lyme info:

http://flash.lymenet.org/ubb/ultimatebb.php/topic/1/88555

-
HOW TO POST A NEW TOPIC:

Look right above the words "directory" and "search" .. in small print. Right above that are the words POST NEW TOPIC.

Click on that and away you go!!

It is in the upper right hand portion of the page.

--------------------
--Lymetutu--
Opinions, not medical advice!

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Keebler
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-
LymeWife I know you've seen the replies over in your new thread (and for those who wish to reply, here's that link:

http://flash.lymenet.org/scripts/ultimatebb.cgi?ubb=get_topic;f=1;t=132561;p=0#000000

LymeWife - Claritin - herx?


Wanted to be sure to put this here, too, so others may see it:

Claritin is Loratadine - and Loratadine is listed here as connected to seizures.

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3325011/

Histamine H1 antagonists and clinical characteristics of febrile seizures

Int J Gen Med. 2012; 5: 277–281. Mohammed A Zolaly

Excerpt:

. . . Seizures or convulsions have been reported in the literature with some first-generation antihistamines (chlorpheniramine, diphenhydramine, pheniramine, and pyribenzamine)

as well as with some of the newer-generation antihistamines (astemizole, cetirizine, fexofenadine, loratadine, and terfenadine). 7–9 . . .
-

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LymeWife
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Wow. Thank you, Keebler!
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