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Porphyria (1 of 2)


Porphyria is considered a rare disease in the general population. However, I believe it is an underrated issue and a largely unknown mechanism that could be behind many of the debilitating symptoms for some of those who are dealing with Lyme & coinfections and other chronic illnesses.

Since Porphyria is considered rare, there are not many doctors well versed in treating it, and possibly even fewer holistic practitioners. There is also a lack of research on Porphyria, again, since it is considered to be rare in the general population.

When I began researching Porphyria, I was a bit frustrated with the lack of consice explanations that tie together the basics of porphyria, types of porphria, symptoms, and testing. So, I spent several months researching and creating a couple of posts that I hope can be that go-to resource for others researching this biochemical process. I also hope to raise further awareness, especially for those in the Lyme community, as figuring out that I was dealing with Porphyria has been a sizeable piece to my puzzle. My goal is to continue updating and adding to this information as I learn more.

What is Porphyria?

Porphyria is a breakdown in the process of heme synthesis or creation. Heme synthesis is a complex, multi-step process that relies on eight enzymes. This process occurs in the mitochondria, with the major tissue sites for these processes residing in the bone marrow and the liver.

When one of these enzymes (which is each encoded by a gene) is not working at full capacity, the heme synthesis process is compromised. Intermediate compounds created in previous steps of the heme process are not able to be converted or bound properly. Then, these compounds circulate throughout the blood and rest of the body. These intermediate byproducts can act like toxins in the body, and this is when chaos ensues and symptoms of porphyria begin.

The body has a feedback loop for heme, and during porphyria, when the heme creation process is not being completed, it senses that the heme was not successfully created and signals are sent to ramp up heme production. However, with the heme process being "busted" somewhere within the process, this further accelerates the creation of the toxic byproducts, and the vicious cycle continues.

Due to the multi-step complexity of the heme process, testing for, diagnosing, and treating Porphyria is a challenge (this is an understatement). Porphyria is quite complex, and the patient picture can vary from person to person.

Porphyria Enzymes / Genes

The eight enzymes within the heme synthesis process are:

ALAS2

ALAD

HMBS

UROS

UROD

CPOX

PPOX

FECH

Each gene provides instructions for the enzyme at that step in the heme process. Those with porphyria have an enzyme or gene which is not working at full capacity, which results in the process becoming stalled at that step. The compounds created in previous steps cannot be moved unto the next step in the heme process, and the heme molecule cannot be completed. These compounds that were created in previous steps (called porphyrins) are then left to circulate within the body.

The type of porphyria a person presents with depends on which of these genes or enzymes is not working properly.

The Heme Process

Using the substrates Glycine and Succinyl CoA, the ALAS2 gene provides instructions for making a compound called ALA synthase (or Delta-Aminolevulinic Acid synthase). This is the first step of the heme process.

The ALAD gene then provides instructions for taking the formed ALA compound to then create a compound called PBG (porphobilinogen).

The HMBS gene (sometimes called PBGD) instructs how to take PBG and create HMB (hydroxymethylbilane synthase).

The UROS gene then instructs taking HMB to then create uroporpyrinogen III.

The UROD gene then encodes instructions for creating coproporphyrinogen III from the uroporpyrinogen III compound created in the previous step.

The CPOX gene provides instructions for taking coproporphyrinogen III and forming protoporphyrinogen IX.

PPOX then instructs how to create protoporphyin IX from protoporphyrinogen IX.

In the final step of the heme process, FECH (Ferrochelatase) encodes the insertion of ferrous iron (Fe) into protoporphyrin IX to form heme.

Symptoms of Porphyria

Symptoms of Porphyria differ based on where the breakdown occurs and the type of porphyria, and they can also vary from person to person.

Some porphyrias present with neurological symptoms (as the intermediate compounds that circulate can act as neurotoxins). Some present with skin (cutaneous) symptoms, and some types present with both neurological and cutaneous symptoms.

Also, some symptoms can be acute and come on during a "porphyria attack," and some symptoms can be chronic and ongoing. Again, it depends on where the breakdown occurs, which determines the type of porphyria.

Neurological symptoms can include severe abdominal pain, nausea or vomiting, peripheral neuropathy, anxiety or panic, tachycardia, insomnia, seizures, and even hallucinations or psychosis.

ALA, a compound discussed earlier that forms in the first step of the heme process and which can become elevated in many porphyrias, competes with GABA receptors. This causes the panic and other high norepinephrine / low GABA symptoms.

Cutaneous symptoms can include skin sensitivity, blistering, lesions, dermatitis, pigmentation change, and skin damage.

Some may also see that their urine changes to a dark color upon exposure to sun or light (because porphyrins are sensitive to light).

Acute attacks usually have symptoms that build for several days and can last anywhere from days to months.

Types of Porphyria

Because there are many steps within the heme process, with an enzyme / gene at each step, there are, therefore, several types of porphyria, each depending on where the breakdown in the process occurs.

There are two general types of Porphyria: Hepatic Porphyrias (of which there are the subsets Acute or Chronic) and Cutaneous Erythropoetic Porphyrias.

There are eight total subtypes of Porphyria, outlined below.

A breakdown at ALAS2 can cause XLP, or X-Linked Protoporphyria. This is a type of Cutaneous Erythropoietic Porphyria.

A deficiency at ALAD can cause ADP / ALAD-P, or ALAD Deficiency Porphyria. This is a type of Acute Hepatic Porphyria.

A breakdown at HMBS can cause AIP, Acute Intermittent Porphyria. This is a type of Acute Hepatic Porphyria.

A deficiency of UROS can cause CEP, Congenital Erythropoietic Porphyria. This is a type of Cutaneous Erythropoietic Porphyria.

A breakdown at UROD can cause PCT, Porphyria Cutanea Tarda, or HEP, Hepatoerythropoietic Porphyria. Mutations in the HFE gene, which regulates iron, have also been associated with PCT. PCT and HEP are types of Chronic Hepatic Porphyrias.

A deficiency at CPOX can cause HCP, Hereditary coproporphyria. This is a type of Acute Hepatic Porphyria.

A breakdown at PPOX can cause VP, Variegate Porphyria. This is a type of Acute Hepatic Porphyria.

Finally, a breakdown at FECH can cause EPP, or Erythropoietic Protoporphyria. This is a type of Cutaneous Erythropoietic Porphyria.

Porphyria Presentations

The following porphyrias present with only neurological symptoms: ADP, AIP.

The following porphyrias present with only cutaneous symptoms: XLP, CEP, HEP, PCT, EPP.

The following present with both neurological and cutaneous symptoms: HCP, VP.

Testing for Porphyria

Like everything else with porphyria, testing is also complex.

First-line testing is often urinary porphyrins (the first test listed below). Next-line would include testing for urinary ALA and PBG compounds (tests two and three below). If porphyria is highly suspected, I would consider running all three simultaneously.

From there, one can test stool porphyrins, serum porphyrins, and complete genetic testing to try to detemine if porphyria is at play. You can see below which levels are elevated in each type of porphyria.

You can discuss with your Doctor to see if they will agree to order these tests. I also asked Ulta Labs to add these tests to their menu (I asked Walkinlab, as well, but they declined to add them). Ulta was very responsive and helpful in my dealings with them on this request. Note that you have to first create an account with Ulta in order to search for these tests:

Lab Names / Test #'s via Quest Labs (can be ordered via Ulta):

36592 - Porphyrins, Fractionated, Quantitative, Random Urine

6301 - Delta Aminolevulinic Acid (ALA)

6329 - Porphobilinogen (PBG)

Testing for Ulta Labs is done at Quest. Note that LabCorp can also run these tests, but a Doctor will need to order on your behalf and the test numbers listed will be different for LabCorp.

As porphyrins degrade quickly when exposed to light, the sample should preferably be given while at the lab, and the lab tech should give you a dark colored urine cup with a lid. If they do not, you may need to educate them on the fragility of porphyrins to both light and heat, and ask for a dark cup and lid. The sample should be kept cool as well. Also note that porphyrins have a better chance of coming back high when the sample is given during an attack or symptomatic period.

I don't yet know of how one can independtly order the stool or serum porphyrin testing. However, if one has positive urinary tests, this data, along with symptoms, may be enough to convince a Doctor to order additional testing. Those with skin symptoms may not have high urinary markers, so they should consult with a Doctor and try to have the additional testing done as a first-line.

Genetic Testing:

The American Porphyria Foundation is currently offering no-cost genetic testing (via a company called Invitae) for the 4 acute hepatic porphyrias for those that meet criteria. However, you do still need a Doctor to sign off on this testing request. You can contact the APF directly at: https://www.porphyriafoundation.org/about-the-apf/about-apf/

23andme tests for several of the eight (nine, including HFE) genes involved in porphyria. Those results can be uploaded to an analytic site such as Livewello (my favorite template for this is titled "Porphyria: ALAD, ALAS2, CPOX, FECH, HFE, HMBS, PPOX, UROD, UROS"). However, there are disagreements on the use of 23andme data with porphyria, since 23andme is intended to be "for research purposes only, and not diagnostic purposes." In my opinion, this method of DNA testing still seems to provide relevant info, especially in conjunction with symptoms and positive urinary, stool, or serum testing. I did have 3 genes/steps that showed homozygous +/+, or possible weakness on my Livewello report.

Also note that a negative DNA test via the APF / Invitae may not mean someone does NOT have Porphyria, as they only test for 4 gene SNP's, and there are many more involved in the heme process.

Markers in each Type of Porphyria

XLP - No increased urinary markers. High protoporphyin in stool and plasma. High zinc, and sometimes free, protoporphyrin erythrocytes.

ADP / ALAD-P - High ALA, coproporphyin III in urine. High zinc protoporphyrin erythrocytes.

AIP - High uroporphyrin, and ALA in urine. Some say high PBG and porphobilinogen in urine. Uroporphyrin sometimes elevated in stool, plasma, and erythrocytes.

CEP - High uroroporphyin I and coproporhyrin I in urine. High coproporphyrin I in stool. High uroporphyrin and coproporphyrin in plama. High uroporphyrin I and coproporphyrin I in erythrocytes.

HEP - High uroporphyrin III and heptacarboxylporphyrin in urine. High isocoproporhyrin, heptacarboxylporphyrin, and coproporphyrin I in stool. High uroporphyrin and heptacarboxylporphyrin in plasma. High zinc protoporphyrin IX in erythrocytes.

PCT - High uroporphyrin, heptacarboxylporphyrin in urine. High isocoproporphyrin, heptacarboxylporphyrin in stool. Sometimes high uroporphyrin, heptacarboxylporpyhrin erythrocytes.

HCP - High coproporphyrin III, ALA, and PBG in urine. High coproporphyrin III in stool. Coproporphyrin is sometimes high in plasma.

VP - High coproporphyrin III, ALA, and PBG in urine. High protoporphyrin IX, coproporphyrin III in stool. High coproporphyrin and sometimes high protoporphyrin in plasma.

EPP - No increased urinary markers. High protoporphyrin in stool, plasma, and erythrocytes.

Next up: Porphyria (2 of 2) - Enzymatic Cofactors in Porphyria, Triggers and Possible Support, and My Experience with Porphyia -- https://www.uncagedhealth.com/single-post/2019/10/07/Porphyria-2-of-2

Additional Sources:

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