Secondary Porphyria: what you should know before starting a CAP

Secondary Porphyria: what you should know before starting a CAP

Cpn induced secondary porphyria

Treatment of Chlamydia infection may exacerbate pre-existing genetic porphyria or more likely cause a secondary acute porphyria by making the intracellular Chlamydia more active or by killing infected cells that already are loaded with high porphyrin levels. Some of what is mis-labeled as a “herx” reaction to treatment, is actually an acute porphyria reaction and not a reaction to bacterial endotoxin which is what a true herxheimer reaction is referring to.

What is Secondary Porphyria? 

 Porphyrias are diseases in which the heme pathway has malfunctioned. They can be genetic or be secondary secondary to another disease process. Part of what is so special about the thoroughness with which Dr. Charles Stratton and his colleagues have studied Chalmydial disease is their discovery that Cpn interferes with the heme pathway, and that many patients with chronic Cpn infections have secondary porphyria to start with, and that this is further exacerbated under treatment. When you understand more about porphyria, it can help you sort out "die-off" as well as chronic symptoms you have, which may be due to heme byproducts-- and how to treat for it.Heme is a Fe2+ complex. A number of critical cellular functions rely on it and the biosynthesis of heme occurs in all human cells. Toxic compounds called porphyrinogens are formed in one transitional phase of the heme biosynthesis pathway but under normal circumstances are quickly transformed into heme which is not toxic.The porphyrias are consequences of any impairment of the formation of porphyrinogens or in their transformation to heme. Chlamydiae interfere with this step. Porphyrins then accumulate in the cell itself, and then in the extracellular milieu. Within the mitochondrial matrix, the final steps in the biosynthesis of heme are halted. Depletion of host cell energy by the intracellular infection with Chlamydia species causes additional energy-related complications.Highly simplified, heme synthesis should look like this:

Heme precursors >> porphrinogens>> transformation to heme >> increased cellular transport including ATP production.

Instead, Cpn interferes with this normal process, and this happens:

Heme precursors >> porphrinogens >> interference with transformation to heme >> build up of unstable heme precursors and porphyrins inside and outside cells >> free radical damage and reduced ATP (energy) synthesis.

Symptoms of Porphyria- 

Porphyria may affect the nervous system or the skin.When porphyria affects the nervous system, it can cause:

  • chest pain
  • shortness of breath 
  • abdominal pain
  • nausea
  • muscle cramps
  • weakness
  • hallucinations
  • depression
  • anxiety
  • paranoia
  • seizures

When porphyria affects the skin it can cause:

  • blisters
  • itching
  • swelling
  • sensitivity to the sun (which also can be caused by some antibiotics)
  • purple-red-colored urine

Stratton's protocol suggests testing for porphyrins prior to treatment, and initiating nutritional and other interventions prior to starting treatment for Cpn to help prevent or limit secondary porphyria.

"Systemic/chronic chlamydial infections have been noted to have an associated secondary porphyria. Porphyrins, including water-soluble porphyrins (e.g., delta-aminolevulinic acid and porphyrobilinogen) and fat-soluble porphyrins (e.g., coproporphyrin III and protoporphyrin) may produce clinical episodes of porphyria. The presence of such porphyrins in an individual patient with chronic/systemic chlamydial infection can be confirmed pre- and during therapy by appropriate porphyrin tests such as obtaining 24-hour urine and 24-hour stool specimens for porphyrins." (from Stratton & Mitchell's THERAPY OF CHRONIC CHLAMYDIAL INFECTIONS INCLUDING THEIR ASSOCIATED PORPHYRIA AND VITAMIN B12 DEFICIENCY: SEVENTH VERSION

Two other suggestive indicators of porphyria which don't require the more challenging 24 hour collection of specimens is measuring B-12 deficiency both directly and also from blood elements which are affected by B12 such as serum methyl malonate levels and homocystine levels. However Dr. Stratton notes:

Homocystine levels are elevated with B12 and folate deficiency, but can be reduced by folate alone. On the other hand, serum methyl malonate levels are elevated in B12 deficiency and are not changed by folate. Therefore, serum methyl malonate levels are the best indicator of B12 deficiency. 

 Another indicator, according to Dr. Stratton, is high hemoglobin and high hematocrit.For those already in treatment, to have a rough idea if treatment is overloading them with porphyrigens Dr. Stratton has noted this "Poor Man's Test" of secondary porphyria:

"Poor Man's" Porphyrin Test According to Chuck Strattoni: If people notice dark urine after taking metronidazolei, have them put their urine in a clear glass container and place it outdoors in the sun for several hours. If the color gets darker (i.e., copper-purple color), then it is due to porphyrins. This is the "poor man's porphyrin test".

 Because secondary porphyria is so common in Cpn infections, Dr. Stratton recommends treating for it almost as a matter of course prior to initiating a CAP's, and continuing treatment for it during the whole process of treatment. This involves:Excerpted from: THERAPY OF CHRONIC CHLAMYDIAL INFECTIONS INCLUDING THEIR ASSOCIATED PORPHYRIA AND VITAMIN B12 DEFICIENCY: SEVENTH VERSIONCharles W. Stratton, MD William M. Mitchell, MD PhD Vanderbilt University School of Medicine Nashville, Tennessee 37232IMPORTANT DISCLAIMER Currently there are protocols for appropriate clinical trials for the therapy of a number of different forms of systemic/chronic chlamydial infections being prepared at Vanderbilt. The preliminary suggestions for chlamydial therapy that are contained within this document have been gleaned from early therapy for compassionate reasons and may not represent the final therapy. The use of these suggestions is similarly for compassionate therapy of patients suspected of having a systemic/chronic chlamydial infection.Patient education begins with an explanation of the clinical significance of the test results and the potential for associated effects such as porphyria and vitamin B12 deficiency. Additional laboratory tests may be useful in defining the extent of the chlamydial infection and associated metabolic/vitamin disorders. Initial blood work can be obtained for the following tests: 1) CBC, 2) liver function tests, 3) uric acid, and 4) serum iron studies. Other useful tests include: red blood cell ALA dehydratase, red blood cell PBG deaminase, vitamin B-12 level, serum homocysteine level, and serum methymalonate level. A 24-hour urine and stool may be collected for porphyrins. Step 2: Next, the patient is placed on the antiporphyric regimen and vitamin B12 therapy. This is continued throughout the antimicrobial therapy and is an important component as it minimizes cellular damage and facilitates cellular repair. Step 3: Following initiation of the antiporphyric regimen, the first antimicrobial agent is started. I. THERAPEUTIC REGIMEN FOR SECONDARY PORPHYRIA Systemic/chronic chlamydial infections have been noted to have an associated secondary porphyria. Porphyrins, including water-soluble porphyrins (e.g., delta-aminolevulinic acid and porphyrobilinogen) and fat-soluble porphyrins (e.g., coproporphyrin III and protoporphyrin) may produce clinical episodes of porphyria. The presence of such porphyrins in an individual patient with chronic/systemic chlamydial infection can be confirmed pre- and during therapy by appropriate porphyrin tests such as obtaining 24-hour urine and 24-hour stool specimens for porphyrins. It is recommended that a therapeutic regimen addressing porphyria should be instituted along with the use of antimicrobial agents. This therapeutic regimen is aimed at controlling the chlamydial-associated secondary porphyria that may be present prior to antimicrobial therapy and/or may be triggered or increased during antimicrobial therapy of the chlamydial infection. This "porphyric reaction" to antimicrobial therapy should be recognized as such and differentiated from an expected cytokine-mediated immune response. Specific measures for the therapy of porphyria as derived from published medical literature on porphyria are employed and include:1. High Carbohydrate Diet Approximately 70% of the daily caloric intake should be in the form of complex carbohydrates such as those found in bread, potato, rice, and pasta. The remaining 30% of calories in protein and fat ideally should be in the form of white fish or chicken. 2. High Oral Fluid Intake Drink plenty of oral fluids in the form of water (e.g., bicarbonated water or "sports-drinks" [water with glucose and salts]). This helps flush water-soluble porphyrins. Moreover, dehydration concentrates porphyrins and makes patients more symptomatic. The color of the urine should always be almost clear rather than dark yellow. 3. Avoid Red Meats Red meats, including beef and dark turkey as well as tuna and salmon contain tryptophan and should be avoided as much as possible. 4. Avoid Milk Products Milk products contain lactose and lactoferrin, both of which should be avoided as much as possible. 5. Glucose, Sucrose and Fructose Glucose is an important source of cellular energy: cellular energy is reduced with chlamydial infections. Increasing the availability of glucose provides optimal conditions for the cells to produce energy. However, sucrose is not the best way to increase the glucose availability. Sucrose is a mixture of glucose and fructose. Fructose is the sugar contained in fruit. Because high levels of fructose act as a signal to the liver to store glycogen, an excess of fructose may temporarily reduce the availability of glucose at the cellular level. Fructose should be avoided as much as possible. Instead, "sports-drinks" containing glucose (as well as containing important cations/anions) can be used. Glucose tablets also can be used. 6. Avoid Alcohol. Alcohol is a well-known aggravator of porphyria and should be avoided as much as possible.Vitamins/Antioxidants/Supplements 7. B-Complex Vitamins Glucose is needed by host cells that are infected by chlamydiae. The availability of glucose to the host is assisted by taking B-complex vitamins. These include folic acid (400 mcg twice per day), vitamin B-1 (thiamin 10 mg twice per day), vitamin B-2 (riboflavin 10 mg twice per day), vitamin B-5 (pantothenate 100 mg twice per day), vitamin B-6 (pyridoxine 100 mg twice per day or pyridoxal-5 phosphate 25 mg twice per day), and vitamin B-12 (5000 mcg sublingual three to six per day). 8. Antioxidants Antioxidants and related agents should be taken twice per day. These should include vitamins C (1 gram twice per day) and E (400 units twice per day) as well as L-carnitine (500 mg twice per day), ubiquinone (coenzyme Q10; 30 mg twice per day), biotin (5 mg twice per day), and alpha-lipoic acid (400 mg twice per day). Bioflavinoids (also called proanthocyanidins of which pygnoginol and quercetin are two examples) are very effective antioxidants. Selenium (100 mcg twice per day) should be taken with the vitamin E. L-Glutamine (2 - 4 grams twice per day), querceten (400 - 500 mg twice per day), glucosamine (750 - 1000 mg two or three times per day) and chondroitin sulfate (250 - 500 mg twice per day) should also be included.Antiporphyrinic Drugs 9. Benzodiazapine Drugs The specific benzodiazapine drugs used depends, in part, on the symptoms. For example, if panic attacks are the problem, xanax (0.5 mg three or four times per day) can be used. If sleeping is a problem, restoril (30 mg at night) can be used. 10. Hydroxychloroquine Hydroxychloroquine (100 - 200 mg once or twice per day) is often used to treat porphyria. For patients with symptoms of porphyria, a single 100 mg dose of hydroxychloroquine may be tried. If this trial dose relieves the symptoms, hydroxychloroquine may be continued. The hydroxychloroquine dose must be adjusted for each patient. This is done by increased the dose slowly, starting with 100 mg every other day, then slowly increasing to a maximum dose of no more than 200 mg twice per day. Most patients do well on 100 mg once per day. Visual/eye exams should be done periodically as per manufacturerís recommendations (See PDR).Miscellaneous 11. Oral Activated Charcoal Activated charcoal absorbs fat-soluble porphyrins. Treatment with oral activated charcoal, which itself is nonabsorbable, binds these porphyrins in the gastrointestinal tract and hence prevents them from being reabsorbed in the small intestine. Start with 2 grams (eight 250 mg capsules) of activated charcoal taken three times per day on an empty stomach (i.e., 2 hours after and 2 hours before a meal). Gradually increase this to 4 grams taken three times per day. Much more activated charcoal can be safely taken; up to 20 grams six time a day for nine months has been taken without any adverse side effects. It is important that this charcoal be taken on a completely empty stomach without any food, vitamins, or medications taken within 2 hours before or 2 hours after charcoal ingestion as the charcoal may absorb the food, vitamins, or drugs as well as the porphyrins. Activated charcoal can be obtained from <puritanspride.com>.II. THERAPEUTIC REGIMEN FOR VITAMIN B12 DEFICIENCY Many patients with systemic/chronic chlamydial infection appear to have a subtle and unrecognized vitamin B12 deficiency at the cellular level. This functional B12 deficiency can be documented in an individual patient by obtaining both a vitamin B12 level (usually normal or low) and serum homocysteine and methylmalonate levels (one or both of these metabolites will be elevated). This vitamin B12 deficiency can corrected by high-dose vitamin B12 therapy as follows: 1. Vitamin B12 Therapy Prior to Chlamydial Therapy Adults normally have approximately 3,000 mcg of vitamin B12 in body stores, mostly in the liver. Initial vitamin B12 therapy before chlamydial therapy includes replacement therapy for any vitamin B12 deficit in these body stores. Therefore, over the first several days of antiporphyrin therapy, 6,000 mcg of parental (intramuscular or subcutaneous) vitamin B12 is given. For each of the next 3 weeks, 6,000 mcg of parental vitamin B12 is given once per week. 2. Vitamin B12 Therapy During Chlamydial Therapy Chlamydial antimicrobial therapy is associated with increased need for vitamin B12. Therefore, 6,000 mcg of parental vitamin B12 (3,000 mcg in each anterior thigh) is given once per week while the patient is receiving antimicrobial therapy for systemic/chronic chlamydial infection. This is in addition to the 5,000 mcg of sublingual vitamin B12 taken three times each day. 3. Vitamin B12 Therapy Post Chlamydial Therapy Following the completion of antimicrobial therapy of systemic/chronic chlamydial infection, the vitamin B12 and serum homocysteine/methylmalonate levels should be rechecked. If the methylmalonate level remains elevated, it suggests a continued vitamin B12 deficiency. Oral therapy with 5,000 mcg of sublingual cobalamin three times per day should be continued. After several months, 6,000 mcg of parental vitamin B12 may be given as a therapeutic trial. If the patientís energy is not increased by the parental dose, continued therapy with sublingual vitamin B12 is probably adequate. Periodic trials of parental vitamin B12 can be used to assess the sublingual therapy.For years, vitamin B12 languished as the vitamin that cures anemia. Hardly any research was done into what this vitamin could do for non-anemic people. It turns out that it may do a lot. New studies show that the right amount of B12 can protect against dementia, boost immune function, maintain nerves, regenerate cells and more. B12 is in the news because it lowers homocysteine and protects against atherosclerosis. It's also vital for maintaining methylation reactions that repair DNA and prevent cancer. One of the crucial areas for B12 is the brain. It's not surprising that people with B12 deficiency develop mental disorders. The vitamin is crucial for the synthesis or utilization of important neuro-factors including monoamines, melatonin and serotonin. In addition, B12 is absolutely critical for the function and maintenance of nerves themselves. B12 is needed for methylation reactions that maintain these cells, and enable them to function. B12 contributes to brain function by lowering homocysteine. Homocysteine is a toxic by-product of methionine metabolism that can damage neurons. Importantly, homocysteine interferes with the methylation reactions critical for brain function. Studies show that people with elevated homocysteine can't think.

Jim K Wed, 2006-02-08 11:18

How Cpn causes porphyria: pdfs of Stratton/Mitchell Articles

How Cpn causes porphyria: pdfs of Stratton/Mitchell Articles

 Two downloadable pdf files are included here for those who want more detail on Cpn and secondary porphyria. 1) This link will download an important and classic article by Dr.'s Stratton & Mitchell called

The Pathogenesis of Systemic Chlamydial Infections: Theoretical Considerations of Host Cell Energy Depletion and Its Metabolic Consequences

 Download   Alternate DownloadIt explains in detail the impact of Cpn cellular parasitism on ATP depletion and on heme synthesis and resulting porphyria.  2) This link will download an excerpt from Stratton & Mitchell's Patent #6,884,784 specifically on the cellular biology of Cpn and porphyria. A succinct and clear explanation for those of us who are biology geeks.

Excerpt from Stratton & Mitchell's Patent #6,884,784 on Cpn & Secondary Porphyria

Download Patent Excerpt

Jim K Sun, 2006-03-19 14:14

Secondary Porphyria in Cpn: Extracts from Stratton/Mitchell Patent

Secondary Porphyria in Cpn: Extracts from Stratton/Mitchell Patent

I thought this should be available to Cpnhelp users. This is extracted from the Mitchell/Stratton (Vanderbilt) patent:Secondary Porphyria In Cpn• Extracted and edited from: US Patent Issued on June 29, 2004• Chlamydia is a parasite of normal energy production in infected eukaryotic cells. The energy shortage also causes the host cell mitochondria to attempt to synthesize certain critical enzymes involved in energy production in order to increase energy production. The energy (ATP) shortage produced by Cpn infection results in incomplete heme production and resulting porphyrins.Because Chlamydia also prevents this synthesis from completing, these enzyme's precursors, called porphyrins, build up in cell and often escape into the intracellular [mileau] milieu. Porphyrins readily form free-radicals, that, in turn, damage cells. Thus, there is an obligate secondary porphyria that accompanies many chlamydial infections. • Impact of porphyrins on the body:Inadequate energy- Host cells have insufficient energy available for their normal functioning. • Neurotoxicity- Porphyrins are highly neurotoxic and produce oxidative damage to cells.• Tissue damage from oxidation- If these reactive oxygen species (porphyrins) are released into the extracellular space, as seen in acute porphyria, autooxidation of surrounding tissue may result. … Reactive oxygen species have been noted to disrupt membrane lipids, cytochrome P-450 (impairing metabolism of drugs and toxins) and DNA structure (increasing cancer risk).• Impairment of liver function- When hepatic cells are infected with Chlamydia species, the decreased energy in the host cell does not allow heme biosynthesis to go to completion and porphyrins in the liver/entero-hepatic circulation are increased. When hepatic cells are infected with Chlamydia species, the decreased energy in the host cell does not allow heme biosynthesis to go to completion and porphyrins in the liver/entero-hepatic circulation are increased. When the chlamydial infection involves hepatic cells, the use of any pharmacologic agents that are metabolized by cytochrome P-450 in the liver will increase the need for cytochrome P-450, which is a heme-based enzyme. Hence, the biosynthesis of heme in the liver becomes increased (resulting in worsening of the porphyria!). • Chronic oxidative stress- the accumulation of porphyrinogens/porphyrins in human tissues and body fluids produces a condition of chronic system overload of oxidative stress with long term effects particularly noted for neural, hepatic and renal tissue.. If reactive oxygen species are released into the extracellular space, as seen in acute porphyria, autooxidation of surrounding tissue may result. Long term effects particularly noted for neural, hepatic and renal tissue.• Glucose disruption—described under treatment below.• Accumulation in tissues and cells of porphyrins- The clinical result of the intracellular and extracellular accumulation of porphyrins, if extensive, is a tissue/organ specific porphyria which produces many of the classical manifestations of hereditary porphyria. • (symptoms of porphyria here)• Sub-clinical B-12 deficiency (i.e. not measurable by blood levels of B-12). The pathogenesis of chronic/systemic chlamydial infection is unique in that the intracellular infection by this parasite results in a number of … unrecognized concomitant … metabolic/autoimmune disorders including secondary porphyria with associated autoantibodies against the porphyrins. Cross reaction with Vitamin B12 can result in a subclinical autoimmune-mediated Vitamin B12 deficiency. These associated disorders often require diagnosis and preventive and/or specific adjunctive therapy.• As the chlamydial-infected host cells lyse, as happens in the normal life cycle of Chlamydia, the intracellular porphyrins are released and result in a secondary porphyria. It also has been noted that any host cell infected with Chlamydia species has an increased amount of intracellular porphyrins that are released when antimicrobial agents kill the microorganism.• …chlamydial-associated secondary/obligatory porphyria, symptoms of which can actually increase during antimicrobial therapy of the chlamydial infection. This porphyric reaction to antimicrobial therapy should be recognized as such and differentiated from the expected cytokine-mediated immune response precipitated by antigen dump during anti-chlamydial therapy.• • Diagnosis• The diagnosis of chlamydial-associated secondary porphyria may be difficult as the porphyria may be minimal and tissue-specific.• The measurement of 24 hour urine porphyrins is not sensitive enough in every case of chlamydial infection to detect the secondary porphyria caused by chlamydial infection.• There may not be an abnormal amount of porphyrinogen precursors and porphyrins in the blood, urine, or stool.• • D. Reducing Porphyrin Levels• Therapy for this secondary porphyria, which is adjunct to anti-chlamydial therapy, involves at least three strategies: a) Supplement the cellular energy supply to mitigate cell malfunction and the formation of porphyrins; b) reduce the levels of systemic porphyrins; and c) mitigate the harmful effects of the porphyrins.• Dietary and pharmaceutical methods can be used to reduce systemic porphyrin levels (both water-soluble and fat-soluble).• It is recommended that a patient suffering from porphyria avoid milk products. Milk products contain lactose and lactoferrin, and have been empirically shown to make symptoms of porphyria worse.• Patients should also avoid Red meats, including beef, dark turkey, tuna and salmon as they contain tryptophan which worsens porphyria (see below).• Glucose disruptiono Red meats, including beef, dark turkey, tuna and salmon, contain [tryprophan] tryptophan. Increased levels of tryptophan in the liver inhibit the activity of phosphoenol pyruvate carboxykinase with consequent disruption of gluconeogenesis. This accounts for the abnormal glucose tolerance seen in porphyria. o (Ed: in addition to which, Cpn induces its host cell to absorb more glucose from the blood stream so it can produce more ATP. In wide spread Cpn infection this can produce low blood sugar more rapidly than otherwise, such as when patients fast or skip meals).• Intake of glucose gives short term energy boost to depleted cells (increasing ATP and lessening porphyrin production), and in the case of infected liver cells (major producer of heme in the body) glucose shuts down further immediate heme production.• Plenty of oral fluids in the form of bicarbonated water or "sports drinks" (i.e., water with glucose and salts) should be incorporated into the regimen. This flushes water-soluble porphyrins from the patient's system. Drinking seltzer water is the easiest way to achieve this goal. The color of the urine should always be almost clear instead of yellow. It is noted that dehydration concentrates prophyrins and makes patients more symptomatic.• Activated charcoal can be daily administered in an amount sufficient to absorb fat-soluble porphyrins from the enterohepatic circulation. Treatment with activated oral is charcoal, which is nonabsorbable and binds porphyrins in the gastrointestinal tract and hence interrupts their enterohepatic circulation, has been associated with a decrease of plasma and skin porphyrin levels. Charcoal should be taken between meals and without any other oral drugs or the charcoal will absorb the food or drugs rather than the porphyrins. For those who have difficulty taking the charcoal due to other medications being taken during the day, the charcoal can be taken all at one time before bed. Taking between 2 and 20 grams, preferably at least 6 grams (24×250 mg capsules) of activated charcoal per day (Perlroth et al., Metabolism, 17:571-581 (1968)) is recommended. Much more charcoal can be safely taken; up to 20 grams six times a day for nine months has been taken without any side effects.• For severe porphyria, chelating and other agents may be administered, singularly or in combination, to reduce levels of porphyrins in the blood. Examples of chelating agents include but are not limited to Kemet (succimer; from about 10 mg/kg to about 30 mg/kg); ethylene diamine tetracetic acid (EDTA); BAL (dimercaprol; e.g., 5 mg/kg maximum tolerated dosage every four hours), edetate calcium disodium (e.g., from about 1000 mg/m2 to about 5000 mg/m2 per day; can be used in combination with BAL); deferoxamine mesylate (e.g., from about 500 mg to about 6000 mg per day); trientine hydrochloride (e.g., from about 500 mg to about 3 g per day); panhematin (e.g., from about 1 mg/kg to about 6 mg/kg per day), penacillamine. Quinine derivatives, such as but limited to hydroxychloroquine, chloroquine and quinacrine, should be administered to the patient daily at a dosage of from about 100 mg to about 400 mg per day, preferably about 200 mg once or twice per day with a maximum daily dose of 1 g. Hydrochloroquine is most preferred. The mechanism of action of hydroxychloroquine is thought to involve the formation of a water-soluble drug-porphyria complex which is removed from the liver and excreted in the urine (Tschudy et al., Metabolism, 13:396-406 (1964); Primstone et al., The New England Journal of Medicine, 316:390-393 (1987)).• E. Mitigating the Effects of Porphyrins• Antioxidants at high dosages (preferably taken twice per day) help to mitigate the effects of free radicals produced by porphyrins. Examples of suitable antioxidants include but are not limited to Vitamin C (e.g., 1 gram per dosage; 10 g daily maximum); Vitamin E (e.g., 400 units per dosage; 3000 daily maximum); L-Carnitine (e.g., 500 mg per dosage; 3 g daily maximum); coenzyme Q-10 (uniquinone (e.g., 30 mg per dosage; 200 mg daily maximum); biotin (e.g., 5 mg per dosage; 20 mg daily maximum); lipoic acid (e.g., 400 mg per dosage; 1 g daily maximum); selenium (e.g., 100 µg per dosage; 300 µg daily maximum); gultamine (e.g., from 2 to about 4 g per dosage); glucosamine (e.g., from about 750 to about 1000 mg per dosage); and chondroitin sulfate (e.g., from about 250 to about 500 mg per dosage).• The above-mentioned therapeutic diets can be combined with traditional or currently recognized drug therapies for porphyria. In one embodiment, benzodiazapine drugs, such as but not limited to valium, klonafin, flurazepam hydrochloride (e.g., Dalmanc™, Roche) and alprazolam (e.g., Xanax), can be administered. Preferably, sedatives, such as alprazolam (e.g., Xanax; 0.5 mg per dosage for 3 to 4 times daily), can be prescribed for panic attacks and flurazepam hydrochloride (e.g., Dalmane™, Roche or Restoril™ (e.g., 30 mg per dosage)) can be prescribed for sleeping. The rationale is based upon the presence of peripheral benzodiazepine receptors in high quantities in phagocytic cells known to produce high levels of radical oxygen species. A protective role against hydrogen peroxide has been demonstrated for peripheral benzodiazipine receptors. This suggests that these receptors may prevent mitochondria from radical damages and thereby regulate apoptosis in the hematopoietic system. Benzodiazepines have also been shown to interfere with the intracellular circulation of heme and porphyrinogens (Scholnick et al., Journal of Investigative Dermatology, 1973, 61:226-232). This is likely to decrease porphyrins and their adverse effects. The specific benzodiazipine will depend on the porphyrin-related symptoms.• The rationale for benzodiazepines) is based upon the presence of peripheral benzodiazepine receptors in high quantities in phagocytic cells known to produce high levels of radical oxygen species. A protective role against hydrogen peroxide has been demonstrated for peripheral benzodiazipine receptors. This suggests that these receptors may prevent mitochondria from radical damages and thereby regulate apoptosis in the hematopoietic system. Benzodiazepines have also been shown to interfere with the intracellular circulation of heme and porphyrinogens (Scholnick et al., Journal of Investigative Dermatology, 1973, 61:226-232). This is likely to decrease porphyrins and their adverse effects. The specific benzodiazipine will depend on the porphyrin-related symptoms.• Cimetidine can also be administered separately or in combination with benzodiazepine drugs. Cimetidine has been shown to effectively scavenge hydroxyl radicals although it is an ineffective scavenger for superoxide anion and hydrogen peroxide. Cimetidine appears to be able to bind and inactivate iron, which further emphasizes its antioxidant capacity. Cimetidine also is an effective scavenger for hypochlorous acid and monochloramine, which are cytotoxic oxidants arising from inflammatory cells, such as neutrophils. Cimetidine thus would be expected to be useful for the therapy of free-radical-mediated oxidative damage caused by chlamydial porphyria. Recent studies in Japan have found that cimetadine is effective for treating porphyria. The recommended amount of cimetadine is about 400 mg once or twice per day.

Jim K Thu, 2008-05-01 22:59

Porphyria......?

27 Apr 2018
Author
farandwide
Title

Porphyria......?

Body

I've read several posts on Porphyria, including the interview with Dr. Stratton (I think is who it was).  I'm still left wondering what I can do to combat porphyria as I definitely have it going on and it's something I want to deal with.As far as I know, the only thing that can be done is the following...

Comments

old posts, nevertheless ...very interesting info which I'm finding to be helpful

---------------------------------------------------------------------------------------------------------------Doing Thibault protocol (NAC/mino/roxi/tini/nattokinase)...but considering morphing to Stratton protocol

A very old post.   Interesting discussion.  Just know that the early folks will not likely answer any questions asked 7 years later.     Louise

  • 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

Marj- One way to track back to posts you have made (which might help you find the comments others made to you) is go to your 'my account' page and click on the tab that says "track." this will get a list of all the threads you have commented on. Same for finding threads posted by another member. Just click on their name anywhere on the site. That takes you to their member page and you can click track from there.

HELP Jim I am having problems finding things like previous comments sent to me. What was the book you said would help me? My husband is confused too and thinks the way to find info is to put a keyword into search. How exactly do I access answers to my questions, which is silly I know...I will  key in glucose into the search bar. I found loads of interesting stuff when I keyed in Yeast.....I fall asleep or am very lathergic after eating, I get up in the morning after a nights sleep and fall asleep after my breakfast! Where can I buy these glucose tablets? I tried go on the porphyria diet site, but failed. I will have another go.                                                                                                                                         Please don't despair of me, there is hope, I can now post a comment! Wow

  Manycatz, you can read all about what Norman is saying here, written by my own personal top-notch doctor: http://www.davidwheldon.co.uk/vit_D.html.......SarahImage removed.   An Itinerary in Light and Shadow...........Completed Stratton/Wheldon regime for aggressive secondary progressive MSi in June 2007, after four years, three of which intermittent.   Still slowly improving and no exacerbation since starting. EDSS was 7, now 2, less on a good day.Completed Stratton/Wheldon regime for aggressive secondary progressive MS in June 2007, after four years, three of which intermittent.   Still slowly improving and no exacerbation since starting. EDSS was 7, now 2, less on a good day.

Completed Stratton/Wheldon regime for aggressive secondary progressive MS in June 2007, after four years, three of which intermittent.   Still improving bit by bit and no relapses since finishing treatment.

"Top notch doctors" are not the people to believe about vitamin D. Doctors are busy people who seldom have time to do more than glance at the literature. The people to believe are top researchers specializing in the vitamin. I figure I've done quite enough listening to them and reading their articles, but if you have some good source of information which Vieth, say, missed in his review of the toxicology literature, which failed to find any believable reports of toxicity below 40,000 IU/day (and most reports at dose levels way above that), then by all means provide it.

While the body does stop making vitamin D after a certain daily sun exposure, it's a purely local effect that does not depend on systemic vitamin D stores. Instead, what happens is just that the ultraviolet light that creates vitamin D in the skin also destroys it, so after it builds up to a certain level, as much is being destroyed as being created. This doesn't have much to do with the body's stores, which are kept as 25-hydroxy-vitamin-D, mostly aren't in the skin, and have a half-life of about two months. This effect is what limits you to 10,000-25,000 IU/day from the skin (those numbers are from the above-linked paper); there is no additional regulatory mechanism beside it. So people who run around naked outdoors all day naturally acquire very high levels of vitamin D. Running around naked outdoors is of course abnormal behavior today; but it's the condition in which human biochemistry evolved. It's something we're designed to handle.

Norman

 

50k IU is loading dose for deficiency and that is once a week for a few weeks. I was just tested for and prescribed this. I also did a bunch of research myself.

daily dose for deficient folks is 2000iu

I did say 2000iu a day

And 2000 iu is considered the top anyone can take daily without overdoing it and being sick from it. Taking over 2k iu daily is risky at best unless you have proven to fall below 30 (although there is some argument it should be higher) on your vitamin d tests despite taking 2k iu a day.

This is currrent information from top notch doctors. Your body can not get rid of excess vit d, as it can with some other vitamins. This is NOT something you want to be dosing high with and not relying on blood tests to tell you where you are. Many people in Northern America are deficient.

Perhaps Norman you would understand why 2k is the limit if you did further research on it and looked at what happened to people when they get too much in their systems.

 For one your body naturally stops absorbing vit d from the sun when it is full. Your body can not naturally regulate what you are ingesting. 20k IU may be the maximum your body can take (I don't know the numbers here) but that doesn't mean that it will take that or anywhere near close to that everyday.  

 

CAP- zithro, flagyl, plaquenil - CPN +, fibromyalgia, endometriosis, b12 deficiency

CAP- zithro, flagyl, plaquenil - CPN +, fibromyalgia, endometriosis, b12 deficiency

Uh, no, 4000 IU isn't twice what's prescribed for deficient folks. Prescription pills of vitamin D are 50,000 IU. That's what doctors prescribe when they want to seriously move blood levels of the vitamin. The limit of 2000 IU/day (not 2000 milligrams; an IU is a twentieth of a microgram) is for everyday use by nondeficient people -- and how they ever convinced themselves that that is a good limit, when the body can make 20,000 IU/day from the sun, is a mystery.

Oh, by the way, the UV flashlight test I mentioned above didn't seem to work. (I didn't get any "intense red fluorescence" from urine when I was feeling porphyric -- there was some fluorescence, but it was yellow in color, and not that intense.)

It's noted elsewhere that we cpn'ers are generally D deficient, anyway. I think I saw somewhere here that the cpn burns it up faster??? I supplement with 7000 to 8000 units a day and I don't feel so great if I miss a day or two or three, which has happened a handful of times. I see no negatives with this level of D supplementation, but a decreased feeling of 'wellness' at lower or zero levels.

There has been so much new, updated information on D in that last year, what we all learned years ago is now greatly obsolete.

The difference between what we do and what we are capable of doing would suffice to solve most of the world’s problems.  Mohandas Gandhi

The difference between what we do and what we are capable of doing would suffice to solve most of the world’s problems. Mohandas Gandhi

"BTW, I've also noticed caffeine seems to increase porphyria symptoms greatly for me now that I've added Vit D3 (particularly on flagyli pulses), and I just read that apparently P450 CYP1A2 is involved in caffeine metabolism:"

 

I started both flagyl and vit d about the same time and ended up with what appears to be porphy problems. Perhaps there is some interaction also between Flagyl and Vitd beyond whats happening in the liver with the P-450.

 

"Unconvinced cynic - I think 'so what' when I read this thread, its fascinating hypothosis but is there any clinical evidence ?"

Thats what many of us think until it happens to us and the exacts bear out in the information gathered.

 

"Reducing protein would only lead to a more balanced diet if someone was eating too much in the first place, a blanket recommendation to cut down doesn't allow for individual requirements."

 

Actually North American type diets are well known to provide too much protien which in turn actually leaches calcium from bones and is a big part of our osteoporosis problem. The "normal" recommended amount is too high to begin with. The book Diet for a New American collects the evidence for this well.

 

"This makes me wonder if taking 4000 IU of D3 simply makes things worse. Is the increased porphyria due to Cpni dying? Or is it only making us feel worse?"

 

 4000iu is twice the recommended tops of whats prescribed for deficient folks. You can easily get too much vit d which causes its own set of problems. I wouldn't take more then 2000mg a day under a doc prescription for deficiency. And then only to get back to normal where I would then take small amounts if necessary to maintain.  

 

CAP- zithro, flagyl, plaquenil - CPN +, fibromyalgia, endometriosis, b12 deficiency

CAP- zithro, flagyl, plaquenil - CPN +, fibromyalgia, endometriosis, b12 deficiency

By the way, if anyone cares to try this out (I'm not particularly porphyric at the moment), ultraviolet flashlights can be had fairly cheaply. Mine is from here; and looking at it through a spectroscope, it seems to put out plenty of 400nm light.

oops

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. 

From Red's reference:

... Porphyrins emit intense red fluorescence when exposed to light at around 400 nm. Thus, spectrofluorometric methods provide very sensitive detection and quantification of porphyrins (Soret band).

This makes it sound like one could test for porphyria by pointing an ultraviolet flashlight into the toilet, and seeing if the contents fluoresced red. (A 'middle-class man's porphyria test'?)

I make Steve a multi-purpose pre-meal cocktail of water, lemon juice, stevia, cellulose powder, and olive oil.  The cellulose powder is a good source of insoluble fiber for upper GI healing and regularity.  The lemon juice is in it to absorb endotoxins.  The olive oil is in it to supplement his intake of "good" fat, hopefully to enhance the integrity of fatty membrane layers.  When I'm not available to do this for him, he just adds the cellulose to a drink of any kind.  I've noticed several times that he feels better when he has my drink as compared to his quickie version.  The "fat" content of this thread is perhaps another purpose for our multi-purpose cocktail.

Joyce~caregiver-advocate in Dallas for Steve J (SPMS) / Cpn indicated by reactions; Mpn, EBV, CMV positive; elevated heavy metals; gluten+casein sensitive / Wheldon CAP since Aug. '06 - doxycycline+azithromycin+flagyl pulses; antivirals; chelation; LDN.

Joyce~caregiver-advocate in Dallas for Steve J (SPMS).  CAP since August 06, Cpn, Mpn, B. burgdorferi, systemic candidiasis, EBV, CMV & other herpes family viral infections, elevated heavy metals, gluten+casein sensitivity. 

Red

Elinor & Michele,

Thanks so much for the added info.  I haven't linked my fat intake with porphyria symptoms yet, but I'll certainly pay more attention to it to see if it does help me too.

Today is my first day sans Vit D3 and am hoping for a swift recovery...   

On Combined Antibiotic Protocol for Cpn in Rosacea since 01/06

Treatment for Rosacea

  • CAP:  01/06-07/07
  • High-Dose Vit D3, NAC:  07/07-11/08
  • Intermtnt CAP, HDose Vit D3:  11/08-01/09
  • HDose Vit D3, Mg, Zn: 01/09-

Elinor, I have also noticed that if I eat cheese or other fatty stuff I have less porphyric symptoms.    Not very good for the waistline but is sure makes a difference to how I feel. Can't eat bread at all at the moment...

Michele (UK) GFA: Wheldon CAP1st May 2006 . 26th March 2007 continuous Flagyl at 400mg with 5 day pulses at 1200mg every three weeks. Spokesperson for Ella, RRMS Wheldon CAP 16th March 2006

Michèle (UK) GFA: Wheldon CAP 1st May 2006. Daily Doxy, Azi MWF, metro pulse.

 

If such a large proportion of porphyrins reach the digestive tract in bile would that explain why since upping my intake of protein I don't seem to be having such severe porphyria symptoms......more protein = more fat = more bile production to carry them out of the liver, or is that just too simple?  It could explain where I went wrong, in eating high carbs at the expense of protein and fat there just wasn't enough bile flow to keep the liver infestation down......works for me anyway. 

 

Elinor ..... from England  on CAP, doxy/roxi/tini  for ME/CFS/lyme borreliosis, positive Cpn and borrelia. Started Aug05, stopped Jan06, started again Sept 06.

Elinor ..... from England  on CAP, doxy/roxi/tini  for ME/CFS/lyme borreliosis, positive Cpn and borrelia. Started Aug05, stopped Jan06, started again Sept 06.

Red

Jim , Yes, and if I correctly understand the implications of Dr Stratton's comments on porphyrins spilling into circulation (above) and causing precursor blood cells (in the bone marrow) to make more heme, I'm assuming that this might even escalate things if the heme production is short-circuited in these cells as well as we expect it may be.

To me this really might explain how things can get out of hand so quickly, and why levels might fall fairly quickly too if you eliminate some offending level of the porphyrin production that causes this escalation.

At least I'm hoping this is the case.   Donga needs sleep!

On Combined Antibiotic Protocol for Cpn in Rosacea since 01/06

Treatment for Rosacea

  • CAP:  01/06-07/07
  • High-Dose Vit D3, NAC:  07/07-11/08
  • Intermtnt CAP, HDose Vit D3:  11/08-01/09
  • HDose Vit D3, Mg, Zn: 01/09-

Red- Your reference on porphyrin production and excretion is superb. It illuminates more about where heme is produced, and thus where Cpn infection can create porphyrins, and confirms the huge source of fat soluble excretion (85%) through the liver bile into the intestines. What surprised me is the amount of heme produced in the bone marrow (80%) vs liver (20%). Makes some sense for those of us with CFS and infected bone marrow cells and suppressed immune function that the porphyrins is not only produced in the liver. One can imagine that infection of femur marrow could be a major contributor to porphyria, and a slow to clear infection as well. 

CAP for Chlamydia pneumonia since 11/04. 25yrs CFS & FMS- Currently: 150mg INH, 200 Doxycycline, 500mg MWF Azithromycin, 500mg Tini daily (Continuous protocol)

Red

Hi Elinor,

Very interesting indeed.  Thanks.   I had not read it before nor anything else that suggests that oral absorbants like charcoal may worsen some types of porphyria.  

I can't remember if charcoal made my skin conditions worse, but it sure played heck on my IBS symptoms when I tried it early in treatment.   Because of this, I've had to stay away from it...

Thanks again...Very interesting... 

On Combined Antibiotic Protocol for Cpn in Rosacea since 01/06

Treatment for Rosacea

  • CAP:  01/06-07/07
  • High-Dose Vit D3, NAC:  07/07-11/08
  • Intermtnt CAP, HDose Vit D3:  11/08-01/09
  • HDose Vit D3, Mg, Zn: 01/09-

 

Red I just came across this and thought you might be interested......

http://tinyurl.com/34le2m           

Elinor

Elinor ..... from England  on CAP, doxy/roxi/tini  for ME/CFS/lyme borreliosis, positive Cpn and borrelia. Started Aug05, stopped Jan06, started again Sept 06.

Elinor ..... from England  on CAP, doxy/roxi/tini  for ME/CFS/lyme borreliosis, positive Cpn and borrelia. Started Aug05, stopped Jan06, started again Sept 06.

Red

BTW, eliminating caffeine seems to have helped me a little, but not completely. So I've decided to "cry uncle" (or scream "have mercy" really) and try eliminating Vit D3 for a little while to see if I can regain some of the ground (particularly energy levels) I  seem to have lost (and seem to continue to lose) while on it the last 6 months.

If eliminating Vit D3 does help, maybe I'll add it in a little more slowly next time or do a few months on and a few months off until I seem to tolerate it better...

On Combined Antibiotic Protocol for Cpn in Rosacea since 01/06

Treatment for Rosacea

  • CAP:  01/06-07/07
  • High-Dose Vit D3, NAC:  07/07-11/08
  • Intermtnt CAP, HDose Vit D3:  11/08-01/09
  • HDose Vit D3, Mg, Zn: 01/09-

As far as blaming porphyrins released by apoptosis for goading the liver into making more porphyrins, I'd have thought that apoptosis would release a whole menagerie of stuff which would need processing by the liver, and that one shouldn't necessarily blame the porphyrins in particular.

Basil: how are you distinguishing between the "antibiotic effect" of Vitamin D and its other effects? (I suppose that you're referring to an immunostimulatory effect, by "antibiotic", as I've not heard of Vitamin D having a direct lethal effect on bacteria.)

Red

Basil / Jim,

Along these lines, from Dr Stratton's patent:

"The diagnosis of chlamydial-associated secondary porphyria may be difficult as the porphyria may be minimal and tissue-specific. The measurement of 24 hour urine or stool porphyrins may not be sensitive enough in many cases of chlamydial infection to detect the secondary porphyria. Here, the diagnosis depends on the fact that if excess porphyrins are reaching the circulation, the precursor red blood cells will absorb these and make heme. Thus, the enzymes for heme biosynthesis in the differentiated red blood cell become elevated and remain elevated for the life of the red cell. This allows the diagnosis of episodic low-level secondary porphyria as is seen with chlamydial infections. Thus, elevated beme synthesis levels can be used to diagnose intracellular porphyria. See Example 7. "

http://www.patentstorm.us/patents/6884784-description.html

 

Could the excess porphyrins spilling out into circulation and causing precursor red blood cells (I'm assuming in the bone marrow) to make heme actually just help compound the problem with secondary porphyria (by the same method)? Also I read that the average life of a red blood cell is @ 120 days and that they are then scavenged by the liver again, (and I'm wondering , potentially just starting the cycle all over again?):

"Thus RBCs are terminally differentiated; that is, they can never divide. They live about 120 days and then are ingested by phagocytic cells in the liver and spleen. Most of the iron in their hemoglobin is reclaimed for reuse. The remainder of the heme portion of the molecule is degraded into bile pigments and excreted by the liver. Some 3 million RBCs die and are scavenged by the liver each second."

http://users.rcn.com/jkimball.ma.ultranet/BiologyPages/B/Blood.html

 

 

Hi Mark, fyi, from the same patent, Dr Stratton seems to be very concerned with elevated fat-soluble porphyrins:

"Activated charcoal can be daily administered in an amount sufficient to absorb fat-soluble porphyrins from the enterohepatic circulation. Treatment with activated oral charcoal, which is nonabsorbable and binds porphyrins in the gastrointestinal tract and hence interrupts their enterohepatic circulation, has been associated with a decrease of plasma and skin porphyrin levels"

And in fact in a little chat I had with him, he suggested that we Rosaceans likely may actually be suffering from a buildup of excess fat-soluble porphyrins in the skin, contributing greatly to our sun (and many types of light) sensitivities.

On Combined Antibiotic Protocol for Cpn in Rosacea since 01/06

Treatment for Rosacea

  • CAP:  01/06-07/07
  • High-Dose Vit D3, NAC:  07/07-11/08
  • Intermtnt CAP, HDose Vit D3:  11/08-01/09
  • HDose Vit D3, Mg, Zn: 01/09-

I had not tried cimetidine because my stomach doesn't digest. Food just sits there unchanged from when I chewed it for five or six hours. (I know this from my experience of Flagyl making me vomit.)

Will taking betaine work with cimetidine?

I think my sluggish stomach also stops charcoal from working as it should.I don't think it goes where it should when it should, but gets mixed up with food.

Combined Antibiotic Protocol for chlamydia pneumoniae in fibromyalgia, interstitial cystitis, sinus: minocycline, Zithromycin, Flagyl

minocycline, azithromycine, metronidazole 2007-2009, chelation for lead poisoning, muscle pain, insomnia, interstitial cystitis (almost well), sinus, dry eyes, stiff neck, veins, hypothyroid, TMJ, hip joints (no longer hurt)

This makes me wonder if taking 4000 IU of D3 simply makes things worse. Is the increased porphyria due to Cpn dying? Or is it only making us feel worse?

Combined Antibiotic Protocol for chlamydia pneumoniae in fibromyalgia, interstitial cystitis, sinus: minocycline, Zithromycin, Flagyl

minocycline, azithromycine, metronidazole 2007-2009, chelation for lead poisoning, muscle pain, insomnia, interstitial cystitis (almost well), sinus, dry eyes, stiff neck, veins, hypothyroid, TMJ, hip joints (no longer hurt)

Clinical evidence of just one person here......since cutting down on carbs and increasing protein (and therefore fat) I have not had ANY of the problems I had been experiencing with porphyria, is there  any evidence that dietary fat helps in processing porphyrins?  It's all relative though isn't it and maybe I wasn't eating enough before......one man's meat and all that........

Reducing protein would only lead to a more balanced diet if someone was eating too much in the first place, a blanket recommendation to cut down doesn't allow for individual requirements.

This guide to diet from the Canada Porphyria Foundation stresses that carb loading may only be needed during an acute attack and for the rest of the time an adequate intake of protein and fat is needed to balance the carb intake.

 http://www.cpf-inc.ca/dietandcarbs.htm

Elinor ..... from England  on CAP, doxy/roxi/tini  for ME/CFS/lyme borreliosis, positive Cpn and borrelia. Started Aug05, stopped Jan06, started again Sept 06.

Elinor ..... from England  on CAP, doxy/roxi/tini  for ME/CFS/lyme borreliosis, positive Cpn and borrelia. Started Aug05, stopped Jan06, started again Sept 06.

Be as cynical as you like Mark, that in the end is what leads to knowledge. Constant questioning and reviewing information and thinking is what moves things on.

The information that I am gathering for the handbook is meant for a discussion chapter and will not include instructions about diet and supplements. This is best left in the place that it already occupies and as we know from all of our experiences, different people need different regimens.

I think it is important for discussions such as the one above should be kept in a place where people can refer and add to them easily, rather than lost in the mire of threads where it is much more difficult to find.

Michele (UK) GFA: Wheldon CAP1st May 2006 . 26th March 2007 continuous Flagyl at 400mg with 5 day pulses at 1200mg every three weeks. Spokesperson for Ella, RRMS Wheldon CAP 16th March 2006

Michèle (UK) GFA: Wheldon CAP 1st May 2006. Daily Doxy, Azi MWF, metro pulse.

Some more thoughts on porphyria and Cpn

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

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

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

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

 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. 

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.

Before its final faecal excretion, a significant proportion of protoporphyrin is reabsorbed in the intestine and may circulate through the enterohepatic system

 Jim - Thanks for posting this! 

 I had actually come to the conclusion that this was the case for my husband after digging in and  reviewing bile formation and the GI tract.  This reference confirms it!

Using Questran has reduced the confusion my husband experiences relative to a Natural Elimination Event by 80 to 90 %.  Dramatic !

Removing porphyrins (and whatever else) from the bile is having a profoundly positive result on our quality of life. 

Now researching the Sasparilla.

 

 

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. 

Daisy,  Please add burbur to your list too.

Joyce~caregiver-advocate in Dallas for Steve J (SPMS).  CAP since August 06, Cpn, Mpn, B. burgdorferi, systemic candidiasis, EBV, CMV & other herpes family viral infections, elevated heavy metals, gluten+casein sensitivity. 

Joyce~caregiver-advocate in Dallas for Steve J (SPMS).  CAP since August 06, Cpn, Mpn, B. burgdorferi, systemic candidiasis, EBV, CMV & other herpes family viral infections, elevated heavy metals, gluten+casein sensitivity. 

Joyce, why do you mention burbur?  Is it the herb Burbur?  I know that some people use this for helping to deal with Lyme die-off.

Mark 

 

UK Carer of bedridden Severe ME/CFS Feb06. CPN dx. Apr07. Samento 15 drops per day July07.  2400mg NAC 200mg Doxy Jan 08.

UK Carer of bedridden Severe CFS Feb06. Tick bites Summer04.  CPN dx.Apr07. Borrelia dx Sept08. Samento 15 drps daily July07.  200mg Doxy Jan08.  300mg Roxy Apr08 Stopped abx Nov/Dec08. Building up on Supps again.

Still just learning about herbs - sarsparilla and burbur and a few others are believed to help with endotoxin and HSP issues (both with lyme and CPN).  

Loads of antedotal reports on the internet but I am looking for something with at least a little scientific research - even in rats :)

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. 

Mark,  I tripped over sasparilla and burbur while searching for substances to mop up Lyme neurotoxins.  So far, my search results have been as Daisy describes---alot of discussion and no meat.

Joyce~caregiver-advocate in Dallas for Steve J (SPMS).  CAP since August 06, Cpn, Mpn, B. burgdorferi, systemic candidiasis, EBV, CMV & other herpes family viral infections, elevated heavy metals, gluten+casein sensitivity. 

Joyce~caregiver-advocate in Dallas for Steve J (SPMS).  CAP since August 06, Cpn, Mpn, B. burgdorferi, systemic candidiasis, EBV, CMV & other herpes family viral infections, elevated heavy metals, gluten+casein sensitivity. 

Heme, porphryns and Questran- oh my!

I'll relay what Dr. Stratton said to me per above. He speculated, based on his understanding of the heme synthasis processes (see references below):

"Fat soluble porphyrins reach the liver and are made water soluble and excreted in the bile. In addition, the cytochromes including cytochrome P450 are heme based. Therefore, there is a lot of heme synthesis going on in the liver. I suspect that the persons who have a reaction to questran probably have liver involvement by Cpn. Those that don’t have a reaction don’t have much liver involvement. The reaction may well be due to reduced cholesterol. The reaction may not be “die off”, but may be increased heat shock proteins because the Cpn is going into persistent phase due to “starvation” conditions. "

Let me mention that he has been suspecting that a lot of "die-off" reaction can be attributed not to LPS endotoxin as much as to HSP60 which is generated by Cpn as a part of cellular life form transformation process.  HS60 is highly inflammatory in nature, moreso than LPS endotoxin. 

More than you ever wanted to know about Heme production in relation to porphyrins:

http://themedicalbiochemistrypage.org/heme-porphyrin.html

Also from a reference (I don't have a link) on porphyria by  Hervé Puy and Jean-Charles Deybach (emphasis added by me):

"Excretion of porphyrins and of
porphyrin precursors Porphyrins and porphyrin precursors are excreted in urine
and/or bile (Table 1). In relation to the total rate of haem
synthesis, excretion of porphyrins is very small;
in other words,
few porphyrins (and porphyrin precursors, ALA, PBG) ‘escape’
during haem formation and therefore are not transformed into
bilirubin. Each day, bone marrow and liver synthesize about
375 mg of haem. In humans, the mean level of ALA excreted
in urine is ~ 3 mg/day; this means that less than 0.5% of ALA
synthesized each day has not been used for haem synthesis [8]... However, urine contains only 30–35% of the total coproporphyrin; the remainder is found in bile...

Before its final faecal excretion, a significant
proportion of protoporphyrin is reabsorbed in the intestine and
may circulate through the enterohepatic system
[13]. However,
it is not yet known how much intestinal microorganisms or food
contribute to the total fecal porphyrin excretion"

Note that different porphyrin cogeners are referred to in the text, so you don't confuse them, as it is taken out of it's context.  

 

CAP for Cpn 11/04. Dx: 25yrs CFS & FMS. Protocol: 200mg Doxy, 250mg MWF Azith, Tini 1000mg/day pulses; Vit D1000 units, Iodoral 50mg, T4 & T3

Basil's explanation is excellent, and it made me question my porphyria assumptions and ask the same questions as Norman.

Jim, I was curious whether Dr. Stratton had weighed in yet on Norman's questions (repeated below)? Is this something that will have to wait until the Cpn Lab reopens perhaps?

I'm curious about the necessity of major liver infection as a cause of major porphyria episodes. My liver values always look perfect on labs, although, unless I'm on the wrong track with porphyria and need to keep looking for another explanation, I seem to have real problems with symptoms of porphyria. Perhaps standard liver tests aren't enough to go on?

Thanks!

Marysia

 

So what sort of numbers are

Submitted by Norman Yarvin on Mon, 2006-11-20 08:59.

So what sort of numbers are we talking about? Is heme production outside the liver a tenth of that in the liver, a hundredth, or a thousandth (omitting red blood cell heme production from both numbers in the ratio)? If either of the former, you still have a situation where an accumulation of porphyrins over weeks or months, outside the liver, can be competitive, if released suddenly, with an amount produced by the liver in response to immediate demands. Even if not enough to cause systemic porphyria, they might be enough to cause a local porphyria, before they dissipate.

(Now that I think of it, I also don't see why you're ruling out Cpni infection of the red blood cell production process, which might be another source of porphyrins other than the liver.)

 

 

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.

Let me mediate this a bit-- I think this has to do with one's perspective. As a clinical pharmacist Mark's orientation is to state what is known about a drug or condition clearly, and not go too much beyond that in speculation. Basil is orienting from stating what is know about the condition and then speculating as to the meaning of findings and links between them.

As we have such a variety of people finding these pages, it behooves us to clearly mark "this is known" from "Speculations:..."

I don't think "assertions" is clear enough language to mark this, where "Speculations based on these findings might be..." with more clearly ecquivocal language. Then rousing discussion can ensue about possible speculative outcomes. 

Combined Antibiotic Protocol for Chlamydia pneumonia in Chronic Fatigue Syndrome & Fibromyalgia- Currently: 150mg INH, Doxycycline/Zithromycin, 300mg Rifampin, Tinidazole pulses. Northern Ohio, USA

Leap too far - Basil you presented lots of useful and interesting data and then say:
"I'm going to assert that essentially ALL clinical porphyria phenomena seen in Cpn infection are a function of Cpn infection of the liver specifically."  I would want to see liver biopsy data before making such a leap.  The problem is that some website readers will take your thoughts as proven rather than  interesting conjecture.  Personally I did not see any bronze colour when I did a 'poor persons porphyria test' in sunlight during the summer........................Mark.

Mark Walker - Oxford, England.
RRMS since 91, Dx 97. CFS from Jan03.  DW Patient-Feb06, started emp CAP(DW) in Mar06, with Copaxone. Pharma Consultant (worked til Jan 03).

Mark Walker - Oxford, England.RRMS Nov 91, Dx 97. CFS Jan03. Copaxone + continuous CAP (NAC, Dox, Rox) Feb06 to May 07. Met pulses from Jun06. Intermittent Abx from June 07 onwards.

Mark, when I write, I've tried to distinguish between what I believe are "facts" found in the published medical literature, and my own person suppositions, which is why I use such words as "assert" when I make those suppositions, assuming that most readers here are educated enough to know what "assert" means. For those who might miss the distinction, I'm glad you've emphasized that point.

One reason that I make such assertions, is that I would like to pique the interest of the medical research community to either confirm that I am right or explain why I am wrong based on their superior knowledege of the subject, or if the issues I raise are open questions, to ultimately be stimulated to perform the research to prove or disprove those assertions if they believe the issues I raise are important ones. I would think that liver biopsies coupled with PCR detection techniques would indeed be very very useful. Even used on cadavers such a technique might shed some light on the epidemiology of intracellular liver infection.

basil. 

If cats are outlawed, only outlaws will have cats.

Liver Tests & MS - I have read the Tremlett et al paper (Neurology 2006,67:1291-1293). The summary says that for drug free MS patients liver tests may not be within normal ranges and the detailed paper gives full data.  For me a clinical action is that with MS patients a baseline liver assessment (ALT/AST) is taken.  This is needed before starting drugs which could impact liver function. Otherwise abnormal results later could mean that drugs are stopped or impacts on the liver are questioned when in fact drugs are not the problem.  If there is no limit for the number of liver function tests available then if would be useful to test MSers: before starting any drugs; after taking NAC but before adding abxs; after 3 months of abxs.  Never going to happen in the NHS (UK) but could give interesting results ........Mark.

Mark Walker - Oxford, England.
RRMS since 91, Dx 97. CFS from Jan03.  DW Patient-Feb06, started emp CAP(DW) in Mar06, with Copaxone. Pharma Consultant (worked til Jan 03).

Mark Walker - Oxford, England.RRMS Nov 91, Dx 97. CFS Jan03. Copaxone + continuous CAP (NAC, Dox, Rox) Feb06 to May 07. Met pulses from Jun06. Intermittent Abx from June 07 onwards.

Maybe this is off topic, maybe not. One of the oddest things about CFS is Cheney's observation (quoted in Osler's Web) that about 1/3 of his CFS patients had to have their gall bladders removed within 6 months of the onset of CFS.

When I started with CFS, my gall bladder immediately (within a week or two) began to cause me pain. I hesitantly asked three nurses, the surgeon, and my family doctor if the fatigue was related (hesitantly, because it made no sense to me.) They all assured me the two couldn't be related. The g.b. was removed 2 months later. Finding: one tiny stone. Just one. However, the surgeon also said, "SOMETHING was going on with that gall bladder, the wall was so thick."

I think it bolsters the notion of a C.Pn-liver connection in CFS. I also realize it's hardly a smoking gun proof.

Ron 

On CAP for CFS starting 01/06 (NE Ohio, USA)

Currently: doxy & zith -- continous; metronidazole -- 4days on, 7 days off.

RonOn CAP for CFS starting 01/06 (NE Ohio, USA)Began rifampin trial 1/14/09Currently: on intermittent

Why porphyins are really, really bad! 

Norman- these are great questions to run past Dr. Stratton. I'll accumulate them for my next contact with him. Re-reading the pages in the Patent you refer to on porphyria and it's treatment, it's clear that they had a whole bunch of lab measures available at that time for measuring porphyric load that are simply unavailable currently (until the lab goes up again). So, they might have looked at some of these questions of total porphyric load versus local porphyric reactions. It looks to me from the Patent discussion that the liver is considered one of the bigger sources, but other sources are referred to, such as the red blood cells you mention.

Overall, re-reading these materials hammers home the critical importance of porphyria treatment during Cpn treatment, regardless of where the source of the load is coming from:

  • Porphyrins produce a lot of serious and bad symptoms.
  • Porphyrins are neurotoxic and actually damage neurons (independent of the damage Cpn causes).
  • Porphyrins are hugely oxidizing (read-- the opposite of antioxidizing, what we are encouraged to take all those antioxidants for). Their oxidant effect is damaging to our tissues and organs. Porphyrins kill our body organs and cells.
  • Porphyrins help generate B-12 antigens in our body which binds up B-12, leaving us in a B-12 deprived condition even if we appear to have adequate blood levels of it.

There's probably more, but these are the ones I can pull up right now. 

Combined Antibiotic Protocol for Chlamydia pneumonia in Chronic Fatigue Syndrome & Fibromyalgia- Currently: 150mg INH, Doxycycline/Zithromycin, 300mg Rifampin, Tinidazole pulses. Northern Ohio, USA

So what sort of numbers are we talking about?  Is heme production outside the liver a tenth of that in the liver, a hundredth, or a thousandth (omitting red blood cell heme production from both numbers in the ratio)?  If either of the former, you still have a situation where an accumulation of porphyrins over weeks or months, outside the liver, can be competitive, if released suddenly, with an amount produced by the liver in response to immediate demands.  Even if not enough to cause systemic porphyria, they might be enough to cause a local porphyria, before they dissipate.

(Now that I think of it, I also don't see why you're ruling out Cpn infection of the red blood cell production process, which might be another source of porphyrins other than the liver.)

 

Eureka!  Thanks to Cpn Handbook and  Basil's wonderfully clear explanations I am finally getting my head around  secondary porphyria and beginning to realise how it could be a very important part of my illness.

You have given me much food for thought and a whole new area of treatment to explore. No doubt, by the time I've assimilated it all and formulated my questions this forum will have moved on to the 'next big thing' and  you'll be able to look back and see me trailing along behind you all desperately trying to fight my way out of the big grey foggy cloud round my brain.  I can't believe how many clues my doctors have missed.

Thank you for sharing it all

'Evolved individuals do not accumulate.

The more they do for others, the more they gain;

The more they give to others, the more they possess.'  (Tao Te Ching)

 

Elinor from England, UK..... on Wheldon protocol for ME/lyme borreliosis , positive for borrelia and Cpn.  Started  Aug 05, stopped Jan06, started again Sept 06.

Elinor ..... from England  on CAP, doxy/roxi/tini  for ME/CFS/lyme borreliosis, positive Cpn and borrelia. Started Aug05, stopped Jan06, started again Sept 06.

D W

Raven, thanks for the link.

D W - Myalgia and hypertension (typically 155/95.) Began (2003) taking doxycycline and macrolide and later adding pulsed metronidazole. Improved; normotensive

 

D W - [Myalgia and hypertension (typically 155/95.) Began (2003) taking doxycycline and macrolide and later adding metronidazole. No medication now. Morning BP typically 110/75]

Interesting discussion, Norman and Basil. I had not recalled such detail on porphyria in the patent materials, so it's good to be reminded of it. I'll have to go dig it up and read the whole damned thing again, as now I'm wondering what else I missed in my brain fog.

David- I wondered that about Chlorella also, as it would be nice to have something other than charcoal or Questran to bind porphyrins in the gut, especially since these also bind medications. As far as I know, there are no warnings with Chlorella that it should not be taken with other vitamins or medications because it would bind them. I know that Chlorella is said to bind heavy metals like mercury and lead, and is used for this purpose in various treatments. This would suggest that it's binding capacity isn't lipid based. We need a chemist to look at the molecules in Chlorella and tell us what it might do for porphyrins.

Combined Antibiotic Protocol for Chlamydia pneumonia in Chronic Fatigue Syndrome & Fibromyalgia- Currently: 150mg INH, Doxycycline/Zithromycin, 300mg Rifampin, Tinidazole pulses. Northern Ohio, USA

I still don't see anything that prevents porphyrins from building up in tissue outside the liver, then being released in quantities great enough to cause problems.

Indeed, I think I've seen Stratton claim that there can be local porphyrias as well as general ones.  For instance, in an MS patient, one might get porphyria in the brain (and thus anxiety) without there being enough porphyrins outside the brain to produce, say, abdominal pain.  I even believe I've experienced that: on some occasions I've had both mild abdominal pain and mild anxiety, but on others stronger anxiety without abdominal pain.  The latter was shortly after taking Flagyl; presumably the released porphyrins hadn't had time to enter the general circulation.  At any rate, that's what I attributed it to at the time.  Let me see if I can dig up the Stratton reference... okay, US patent 6,884,784, page 33:

"The clinical result of the intracellular and extracellular accumulation of porphyrins, if extensive, is a tissue/organ specific porphyria which produces many of the classical manifestations of hereditary porphyria. As the chlamydial-infected host cells lyse, as happens in the normal life cycle of Chlamydia, the intracellular porphyrins are released and result in a secondary porphyria. Moreover, when the chlamydial infection involves hepatic cells, the use of any pharmacologic agents that are metabolized by cytochrome P-450 in the liver will increase the need for cytochrome P-450, which is a heme-based enzyme. Hence, the biosynthesis of heme in the liver becomes increased.  When hepatic cells are infected with Chlamydia species, the decreased energy in the host cell does not allow heme biosynthesis to go to completion and porphyrins in the liver/entero-hepatic circulation are increased. It also has been noted that any host cell infected with Chlamydia species has an increased amount of intracellular porphyrins that are released when antimicrobial agents kill the microorganism."

The patent also states (p.34):

"The diagnosis of chlamydial-associated secondary porphyria may be
difficult as the porphyria may be minimal and tissue-specific."

Liver function tests are already recommended for those following the protocol, for the reason you state.  (Or, more directly, because a number of the antibiotics used have been known to damage the liver on occasion, as has niacin in large doses; but that is likely to be because they kill Cpn infecting the liver.)

In other recent posts, I've pointed out that in all forms of porphyria, porphyrins are  extremely potent systemic neurotoxins, and that they produce extremely broad as well as extensive localized effects once released into the blood stream, regardless of where they originate.

Excepting erythroid cells, porphyrins are not manufactured in appreciable quantities in most cells outside of the liver because heme is not manufacutured in appreciable quantities in most tissues outside of the liver. Unless a cell makes heme in appreciable quantities, then it is not going to be making prophyrins in appreciable quantities.  Period.

One does not get porphyria in the brain or the gut, in the sense that the brain or the gut are sites for significant porphyrin production. It is well documented and accepted medicine that porphyrins arise primarily from the liver. However, both the brain and the gut are substantially affected by the neurotoxic properties of porphyrins once they are released into the blood stream, as are numerous other parts of the body.

 Many, many diseases of specific organs have wide-ranging systemic effects in locations far from the dysfunctional organ, including thyoid dysfunction,  adrenal dysfunction,  pancreatic dysfunction, etc.

 I'm not making this stuff up. I've merely been attempting to distill extensive research regarding porphyria into concise explanations relevant to Cpn infection.

 

basil. 

If cats are outlawed, only outlaws will have cats.

Interesting question about Chlorella, David. i was looking at one of Dr. Powell's handouts on Inflammatory Pathway Inhibitors and here's what it says about chlorella:

"decreases IL-6, INF-gamma, 5-LOX, MMP-9, PTP and TNF-alpha. Blocks NFkB .....increases Natural Killer cell activity...."

On this list the top performers that blocked the most inflammatory mediators were Curcumin, Luteolin and Niacinamide.

As for Chlorella being a detoxifying agent, there is a lot of alternative health info out there about that. One article I found:

http://findarticles.com/p/articles/mi_m0ISW/is_265-266/ai_n15622561

Raven

 

Feeling 98% well-going for 100. Very low test for Cpn. CAP since 8-05 for Cpn/Mycoplasma P.,Lyme, Bartonella, Mold exposure,NAC,BHRT, MethyB12 FIR Sauna. 1-18-11 begin new treatment plan with naturopath

Basil, I don't see how it follows that Cpn-induced porphyria is mostly from the liver.  Even with less heme being synthesized outside the liver than inside it, one still might have a buildup of porphyrins in some other tissue, due to Cpn infection, with the liver for whatever reason remaining uninfected.  Then, either when the Cpn is killed by antibiotics, or there is mass cell die-off for other reasons (perhaps as in an MS relapse), those porphyrins would be released, and might overload the system even though normally that population of cells doesn't contribute much to the porphyrin body burden.

This could, in a fashion, be tested: if it is liver cells whose dieoff produces the porphyria, then one would expect to see elevations of liver enzymes being correlated with elevations of porphyrins.

 Most of the body's heme is made during the process of red blood cell manufacture (85%), and almost all of the rest of the body's heme is made by the liver. Since accumulation of porphyrins results only from the dysfunctional  manufacture of heme, it follows that almost all porphyrin production due to dysfunctional circumstances must be a consequence of red blood cell production or liver function. If we discount erthyroid cell Cpn infection, then it follows that almost all prophyrins seen in a Cpn infection must therefore come from the liver, i.e, a liver infected with Cpn.

 Liver enzymes are rarely elevated in primary genetic porphyria as primary genetic porphyria rarely causes frank liver destruction. In my original post, I outlined three different types of Cpn porphyria phenomena. Only in Type 3 Cpn porphyria, namely rapid release of porphyins due to liver cell apoptosis of infected Cpn cells resulting from CAP (or other reasons as you point out) would one expect to see liver enzymes elevated due to liver cell destruction. In fact, a liver enzyme test might be a good way to assess whether CAP was proceeding too agressively in the case of an infected liver.

 

basil. 

 

 

Primary genetic porphyria rarely causes frank liver damage, and therefore elevated liver enzymes are rarely seen in primary genetic porphyria.

If cats are outlawed, only outlaws will have cats.

Thanks basil,  My only point in mentioning the NAC flu was as a demonstration of Cpn infection.  I would like to say Steve tested positive for it, but I can't.  For some mysterious reason, he was tested for C. psittaci instead of Cpn.  I also wish I knew if his urine was dark and/or foamy back in those days, but I wasn't around for most of those years.

NAC flu is very different for each individual.  Steve's was barely noticeable until he doubled the dosage at the same time he added selenium and vitamin E to his regime.  That precipitated joint aches and a worsening of his MS symptoms.  For me, it was a strong and long respiratory reaction.  You might have had a reaction and didn't realize it at the time.

Joyce~caregiver-advocate in Dallas for Steve J (SPMS) / Mpn, EBV, CMV, elevated heavy metals; strong indications of Cpn, gluten+casein sensitive / Wheldon CAP since Aug. '06 - 200mg doxycyline/day + 250mg azithromycin every other day; antivirals; chelation; LDN.

Joyce~caregiver-advocate in Dallas for Steve J (SPMS).  CAP since August 06, Cpn, Mpn, B. burgdorferi, systemic candidiasis, EBV, CMV & other herpes family viral infections, elevated heavy metals, gluten+casein sensitivity. 

D W

This is a really useful thread; thanks, Basil, for posting it, and thanks, Jim, for pointing out that the abnormal porphyrins appear to be cell-bound, but are released when apoptosis occurs. This makes good sense to me; in my own case I feel most porphyriac (and have tea-coloured urine) during periods of soft-tissue alteration and subsequent improvement. Apoptosis of unhealthy cells which contain toxins and perhaps bacterial remnants would account for this paradox. One of the pathologies of porphyria is a widespread pro-oxidant effect; one would suggest that antioxidants and agents capable of reversing glutathione depletion would help forestall pathological outcomes. Here is an apposite case-report of a 50 year old man, an exterior worker, who presented with skin blistering; he was found to have porphyria cutanea tarda with underlying Hepatitis C. He was also a heavy drinker. (link) The author gives a good resume of the disease and comments: 'Experimental treatments include 1)high dose Vitamin E, which was orignially shown in the late 1970s to prevent iron induced liver damage in rats; 2)N-acetyl-cysteine, for which there are a few case reports of benefit in patients with HIV (This agent is thought to work by prevention of skin damage from radical species by increasing intracellular glutathione); 3)Pyridoxine, which has been used in other porphyrias with light sensitive eruptions.' It's interesting that all three are recommended supplements for treating chronic C pneumoniae infection. Again, looking at my own experience, I find that, even though I have porphyriac symptoms, my skin is really healthy; all summer I cycled to work in a T shirt and shorts (changing when I got there) and was mildly sunburned but nothing unpleasant. (I covered up when taking doxycycline.) Secondary porphyria is, I am sure, very much underdiagnosed, and is unconsidered: but I am sure it's very common.

Now a question: does chlorella bind to porphyrins in the gut? I have a feeling that it should, but cannot find references.

 

D W - [Myalgia and hypertension (typically 155/95.) Began (2003) taking doxycycline and macrolide and later adding pulsed metronidazole. Improved; normotensive.]

 

D W - [Myalgia and hypertension (typically 155/95.) Began (2003) taking doxycycline and macrolide and later adding metronidazole. No medication now. Morning BP typically 110/75]

Neurovisceral Features of Acute Porphyria Attacks

Neurovisceral Features of Acute Porphyria Attacks Jim K Sat, 2007-12-22 10:11

Chanced upon this link available above, to excerpts to a text on the Diseases of the Liver and Bile Ducts.  I have used this text while pondering my own set of circumstances, it is quite technical in nature, not an easy read.  I was surprised to find so much of it open for examination on the internet.  Thanks Jim for providing this link.  

  • 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

Jim, You might peruse the files located under the images tab/at the top of the page and see what else might be found that could use an additional easy to find location.   I found a lot of graphic type files located here;  http://www.cpnhelp.org/image/tid/80  by first visiting this page;  http://www.cpnhelp.org/image and clicking on the Chlamydia Pneumoniae Pictures file this is added for for anyone elses who might like to browse around. 

  • 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

Bumped into this post again.  Been a while since it surfaced so here it is again.   Louise

  • 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

Book excerpt from: HERE