What I can say about what's certain about Pyrrole Disorder is that it's a black box. My understanding from wading through articles on the subject is that oxidative stress goes in, HPL and illness come out and can loop back to cause further oxidative stress
That seems like a very fair description, one that I have no problem with.
I'm not saying the condition doesn't exist, there clearly has to be some reason for symptoms responding to B6 and zinc. It is the proposed mechanisms and the garbled explanations of the disorder that I object to. These also give the proponents a bad name and lead to comments about snake-oil salesmen (which some of the websites I looked at came close to).
For the sake of completeness I'll just add two more articles from the proponents which I tracked down via @Violetta's second reference above - here and here. These seem to be the most complete summaries that I have found with the best attempts at scientific references and without the garbling of most of the websites.
Essentially some very interesting observations were made quite some time ago, largely by clinicians. Certain clinical interventions were found to be effective and these have remained the mainstay of pyroluria. A few mechanistic studies were done early on but these have not been followed up.
Perhaps the thing I found most interesting was the statement at the beginning of part 2, that the biological origin of HPL is unknown. It does not appear to be a direct breakdown product of porphyrins, though it is often associated with elevated porphyrins and porphyrin intermediates.
One suggestion, and there was some experimental evidence to support this, is that HPL arises via the action of gut bacteria on an unusual porphyrin intermediate, isocoproporphyrin. So there could be a gut link and maybe a genetic link, since there is a hint that appearance of this unusual intermediate might have a genetic basis.
There was quite a bit of discussion about the role of oxidative stress in the disorder. This just reinforces for me the discussion in my previous post about functional B6 deficiency induced by oxidative stress.
As a complete outsider looking in on this story, it seems to me that the pyroluria proponent have maybe become their own worst enemies. They have a position to defend which they can't deviate from and thinking has become stuck in a groove. They see the primary defect as whatever leads to HPL accumulation. This in turn leads to B6 and zinc deficiencies since these are bound up by HPL. Treating with B6 and zinc reverses these problems and in some unknown way fixes the HPL accumulation also.
I could find no evidence whatsoever that HPL binds to B6 and zinc (not even in their own studies). If we set this notion aside, then we could start to think that B6 and/or zinc deficiencies might be causal rather than consequential, more like the porphyrias discussed above. This would also explain why B6 and zinc reduce HPL. This could be a very fruitful line of thinking with an enormous porphyria literature to call upon.