27 Apr 2018
Author
basil
Title

Some more thoughts on porphyria and Cpn

Body

Because it has been such a prominent part of my own illness, I've done quite a bit of research on porphyria. Almost everything in the literature refers to primary genetic porphyria, though there are a few references to secondary (non-genetic) porphyria caused by various liver-destroying processes.Primary porphyria is a genetic disease in which there is a deficiency of one of eight different enzymes, each of which is required to effect one of the eight sequential steps required to synthesis the iron-containing protein heme.

Comments

Thank you, thank you, Jim and Dr. Stratton!

More good research leads and explanations of what's happening during treatment and how best to address it. 

I'll be curious to hear what you find on Sarsparilla, Daisy.  It's a big part of Steven Buhner's Herbal Lyme protocol.  Is it anti-porphyric or does it work on the HS60 or LPS toxins Jim mentions above I wonder?  I thought I had some improvement on it once but haven't done the research to find out why yet or whether it's safe to use it in conjuction with the CAP and recommended supplements.

Cheers,

Marysia 

CDC Lyme + 02/06; Cpn, HHV6, and EBV + 03/08. 2 yrs slow improvement on variations of CAP for Lyme. Currently slowly resuming treatment and changing to newly discovered (for me) Cpn protocol after a severe porphyria attack 09/07 on Diflucan.

 From the article referenced above by Hervé Puy and Jean-Charles Deybach (who seem to have jointly written a good deal of the medical textbooks on haem issues)

"Significant amounts of porphyrins are excreted in faeces (mostly all of the protoporphyrins and 70% of coporphyrins)... "

When they measured the basal rate of bile secretion of porphyrins in healthy humans ... reference

"Approximately 85% of hepatic protoporphyrin remains metabolically unaltered before being eliminated by bile secretion;"

To me, this really makes the case for why Questran works so well to stop this type of porphyria attack in its tracks.

This is an excerpt from American Society of Hematology Education program on porphyria.   Excellent descriptions of differing types of porphyria as well as clear charts and tables.

All of the information I have researched would seem to type my husband as either hereditary coproporphyria or variegate porphyria.  I am more inclined towards hereditary coproporphyria.

Neither of which - to my knowledge my husband had prior to this illness. 

Nothing about his porphyria attack was normal and readily described in the routine porphyria literature. 

Variegate prophyria (VP) attacks are characterized by photocutaneous lesions.  My husband had none . 

According to a clinical review by EMedicine "Whether psychiatric disturbances observed in patients with VP are truly attributable to the disease is contentious. Confusion, disorientation, agitation, mania, depression, and schizophrenialike behavior have all been reported. Psychiatric symptoms were noted in 80% of 18 Finnish patients during attacks, with 25% described as delirious and psychotic. The larger South African experience, however, suggests that neuropsychiatric disturbances should not be attributed to VP, especially in the absence of other signs and symptoms of an attack.

Most attacks of porphyria and especially hereditary co-porphyria report abdominal pain at an incidence rate of 85 to 95% of all cases.  My husband had none. 

My husband only matches one routinely categorized manifestation of porphyria - psychological changes.  His situation matches none of the other known and readily described manifestations of porphyria.

What to make of all of this?  Was his porphyria attack induced by Drug or Bug?        Rifampin, Bactrim, Diflucan, doxycycline induced or CPN induced ?

 

This link from Emedicine contains a fairly extensive list of drugs known to trigger porphyria.  A large number of posters here are taking many of these agents.

 Is it possible that my husband did have a pre-existing tendency for porphyria?  Yes. 

 Is it possible that Rifampin, Diflucan, sulfonamides and other liver taxing agents induced ?  Yes and especially if my husband was a porphyria accident waiting to happen.

Is it possible that Cpn has created a defect in his haem pathways that was further exacerbated by liver taxing agents known to create porphyria?  Yes.

To me, my husband's symptoms rapidly improved upon initiation of  Questran double dose BID therapy so I guess it doesn't matter although I am curious as a cat about this and would like to know.

I want to believe it was Bug not Drug but the little bit of scientist left in me wants to know conclusively.

How many people over time have been labeled as Porphyriacs because they took Rifampin or any of the other roughly 200 drugs that are known to trigger porphyria attacks and they were really CPN infected?

Thank goodness for this site because without the prodding towards porphyria the outcome would likely have been disasterous for my husband.

Thanks again to all who publically and privately helped us out!

Significant amounts of porphyrins are excreted in faeces (mostlyall of the protoporphyrin and 70% of coproporphyrin; Table 1).Significant amounts of porphyrins are excreted in faeces (mostlyall of the protoporphyrin and 70% of coproporphyrin; Table 1).Significant amounts of porphyrins are excreted in faeces (mostlyall of the protoporphyrin and 70% of coproporphyrin; Table 1).Significant amounts of porphyrins are excreted in faeces (mostlyall of the protoporphyrin and 70% of coproporphyrin; Table 1).

Daisy - Husband on CAP 5/07.   Roxy, Diflucan round three 4-4, Rifampin, Bactrim DS, Mepron 4-6, Prednisone, Novantrone, Doxy, Azithromycin, Flagyl, Mino

Daisy - Husband on CAP 5/07.  Husband died from Acute Myelogenous Leukemia Secondary to the Infusion of Novantrone.  Ie - the treatment with the conventional MS drugs killed him. Daisy on her own CAP 11/2012. 

Basil writes...

"NACi flu is an issue that is essentially unrelated to porphyria. It is a cytokinei-mediated allergic reaction to the proteins released when EBs are killed"

I hypothiszed about EB's being an allergen. Is this information saying just that?

If this is the case, wouldnt the eb's be considered a main reason why some people develop accumulation? Meaning due to allergy to the eb protien, the immune system fails to recognize the eb as a germ and  to kill it, and instead sees it as an allergen and thus mounts an allergic response. ( the same way some respond to molds/ fungus )

If this is the case, wouldnt it make sense to create a cpn eb allergy serum and proceed to desensitize people via injections the same way they do with molds?

 

 

     &nbs

Thanks for bringing this topic to the surface and contributing to it I need to read it in depth and want to keep track of any addtions. Louise

CFS/ME.

CPnPositive.BbPositive.

WheldonCAPbegan6/24/07. NowNAC,Doxy, Roxi, TiniPulse#4 Ended2/3/08. 

Cholestyramine at BedtimeforPhorphoria&liposacarideEndotoxinDie-OffExperiences.

  • CAP(TiniOnly): 06/07-02/09 for CFS
  • MethylationProtocolSupplements: Started08/08
  • Intermtnt CAP: 02/09-02/10
  • Full MethylProtocol & LDN 02/09
  • Off CAP: 02/10, cont LDN & MethlyProtocol support

Porphoria and CPn. This is a classic post from 2006 we are currenty into 2009.

I'm bringing it up again for several posters that are currently dealing with symptoms that could indicate it. 

  • CAP(TiniOnly): 06/07-02/09 for CFS
  • MethylationProtocolSupplements: Started08/08
  • Intermtnt CAP: 02/09-02/10
  • Full MethylProtocol & LDN 02/09
  • Off CAP: 02/10, cont LDN & MethlyProtocol support