Home / About Porphyria

What Is Porphyria?

Current research indicates that porphyria (poor-fear-e-uh) is a group of eight diseases that consists of an under active enzyme in seven of the porphyria's and an over active enzyme in one of the porphryia's, affecting the ability to make heme. Heme is a complex of iron with protoporphyrin IX that is essential for the function of all aerobic cells which is made in every cell of the body, but mainly in the bone marrow and the liver. Two classifications of porphyria are acute hepatic (liver) porphyria and erythropoietic (bone marrow) porphyria. Where heme synthesis is primarily affected in the body, in the bone marrow or liver, determines the symptoms that are experienced. When heme synthesis is affected in the bone marrow, the skin is primarily affected causing photosensitivity, which is an extreme sensitivity to ultraviolet (UV) rays from the sun and other light. 


In acute hepatic porphyria, the

The autosomal dominant porphyria's have a roughly 50% enzyme loss, and there is a greater deficiency of 75-95% in the autosomal recessive porphyria's. A person can have a compound porphyria, or double porphyria, or two porphyria's simultaneously.

These current classifications are incomplete as there is cross over in some types.

There are currently 8 known types of Porphyria (technically 9, one is a dual version of one type and is called HEP),  the cause is typically genetic, but also maybe environmental, physiologic, and genetic factors contribute to the cause of disease (- https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3512229/). It is important to note that both PCT and ALAD-P have chemically induced versions, as well as genetic versions. It is wise as a patient to request lead testing if ALAD-P is suspected, and medical professionals to carefully test a patient for lead poisoning if ALAD-P is suspected, in PCT it is important to avoid alcohol as a patient, and patients should avoid alcohol ingestion with any porphyria, but particularly PCT. Some patients with an acute porphyria find that they can moderately drink alcohol, and others have found they can drink certain types of alcohol, but abstaining from alcohol is probably best given the liver involvement in the acute porphyria's, and that a small percentage of attacks maybe life endangering.

In some cases, particularly those without proper diagnosis and treatment, the disease can potentially cause life-threatening complications.

It was thought before that patients only had acute "attacks" or crisis, it is now known that some patients have chronic signs and symptoms.


A new porphyria was discovered only a few years ago, and we expect there to be more porphyria's discovered in the next few years. 

(currently known)  (technically there is a 9th porphyria that is a double version of one porphyria), that affect the body's ability to make heme. 


The types of Porphyria are:


*ALAD ( aminolevuelenic acid dehydratase) Porphyria

*Acute Intermittent Porphyria

*Hereditary Coproporphyria

*Variegate Porphyria



Congential Erythropoeitic Porphyria (CEP)

Porphyria Cutanea Tarda (PCT)

Hepatoerythropoeitic porphyria (inheriting PCT from both parents)

Erythropoietic protoporphyria (EPP)

X-linked Protoporphyria (XLP)


Two of the acute Porphyria's, Hereditary Coproporphyria and Variegate Porphyria, and one type of Acute Intermittent Porphyria, called Chester Porphyria, may have skin issues,

30 % of HCP can have skin blistering, and a higher percentage of VP can have blistering, however, if sun exposure is limited, the skin issues may be very mild in some patients, and in some patients the skin issues can be quite severe. Skin blistering may occur with an acute attack, or can occur aside from an attack. Skin lesions may be caused by fluorescent lighting, as well as the sun.  

What Is the Medical History of a Patient with an Acute Hepatic Porphyria?

Attacks can occur anytime in a person's life, even in infancy and childhood, however females around the time of their menstrual cycle are at a very high risk of attacks due to hormonal fluctuations.

The patient may already have multiple diagnoses: POTS, gastroparesis, bipolar disorder, or a variety of psychiatric diagnosis.

The Patient may have seen multiple doctors: such as general practitioners, emergency physicians, gastroenterologists, psychiatrists, neurologists, cardiologists and had many tests.

Adverse reactions to a variety of medications are a common finding in patients with Acute Porphyria, and many medications can make an acute porphyria patient far sicker and must be stopped immediately.

Medications and street drugs are well documented as being triggers for attacks, Many seizure meds are unsafe (lamictal and lorazapam have been used fairly safely), barituates, sulfa meds, hormonal medications, ssri's, many antibiotics, and anti fungals, amphetamines, cocaine, lidocaine (use extreme caution with any "caine"), smoking, marijuana, alcohol, fasting, low carb diets such as paleo, keto, atkins, and very low calorie diets, alcohol, vaccines, caffeine, stress, painting with lead paint, and working with other paints, solvents. or chemicals, certain foods (the website porphyria tripod has an extensive list), hot or cold weather, and even flying in an air plane have all been documented to cause attacks.

Please check the Napos database http://www.drugs-porphyria.org/languages/UnitedKingdom/index2.php?l=gbr for any medication and always! be very cautious with any new medication as safe medications have also triggered attacks, please take the lowest dose or a fraction and wait several hours before taking any more/others.

Unfortunately many patients fighting for their life during an attack have been denied medical treatment, and sent to a psychologist, or admitted to a mental hospital, due to alack of understanding, and poor testing availability.

What Are the Signs and Symptoms of an Acute Hepatic Porphyria?

*Pain (extreme caution pain which is very extreme and can be in the abdomen, or head, neck, chest, back, legs, or arms, 7% don't have pain).




*Hypertension (can be labile or chronic)


*Constipation (this can be chronic) or diarrhea caution Ileus may occur


*Hyponatremia (be careful and screen for SIADH) 






*Muscle weakness (caution can be severe and cause respiratory insufficiency)


*Status Epilepticus extreme caution


*Skin issues may occur In HCP, VP, and a variant of AIP called Chester porphyria, the skin may have blistering (In VP these can be very large), peeling, millia, scarring of skin which can present as hypopigmentation or hyperpimentation, fragility, itching, sores, particularly on sun exposed areas such as the face, and backs of hands, but can occur anywhere, and may have sun sensitivity. 


*Mental symptoms (extreme anxiety, depression, hallucinations, disorientation, confusion, paranoia, argumentative, and severe encephalopathy can occur)


*Peripheral Neuropathy


*Seizures extreme caution most seizure medications are unsafe



(please see epilepsy.com not all seizures are the tonic clonic grand mal variety) 

*Cranial nerve palsies


*Insomnia or hypersomnia


*Temporary Vision loss




*Hyperventilation or Hypoventilation


*Paralysis (extreme caution)


*Respiratory insufficiency (extreme caution)


*Urine may be dark (cola colored, bright red, red wine colored, whiskey colored, or orange, or lime green when exposed for up to 72 hours to heat light and air) it also may not be dark, or not darken at all. 


*Elevated AST and or ALT


*Sweating or no sweating at all


*Dizziness (orthostatic hypertension is documented)


*Enlarged Adrenal glands https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5817294/

*PRES (https://www.ahajournals.org/doi/full/10.1161/HYPERTENSIONAHA.115.06271)

*Urinary retention

*Myclonic seizures (https://www.researchgate.net/publication/8007617_Familial_occurrence_of_myoclonic_epilepsy_syndrome_and_acute_intermittent_porphyria) 

*Elevated white blood cells

*Elevated Anti nuclear antibodies (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3190104/)

*Elevated prolactin (https://www.ncbi.nlm.nih.gov/pubmed/8049327)

*Elevated LDL 




* Hyperinsulism 


*Disturbances in glucose tolerance


Please note: not every patient will have elevated ALA/PBG in an attack. HCP, and VP, have been well documented to have negative testing in attacks for a variety of reasons, and conversely AIP may have positive urine testing outside of an attack. http://www.signavitae.com/2015/06/porphyrias-diagnostic-challenge-in-emergency-room/


How Is an Acute Porphyria Diagnosed?

A complete diagnostic evaluation for porphyria consists of 5 specialized tests for porphyria and genetic testing. Please see cautions below, there is a high rate of false negatives. 

1.) *Fractionated Fecal Porphyrins (test must be High Performance Liquid Chromatography)

2.) *Blood test of the Enzyme Porphobilnogen Deaminase and Aminolevuelenic acid Dehydratase 

3.) *Porphyrins Plasma fluorescence scan also called Porphyrins Fractionation

4 & 5.) *Urine Aminolevuelenic acid (ALA) and Porphobilnogen (PBG)  

6.) *Genetic testing (most mutations are family specific, a patient can have a negative DNA test and have porphyria, this happens in 1 of 5 patients, with just 1 type of porphyria test, according to one genetics lab, this is probably a much higher number, given there are 4 other tests, and only the urine test was used).  

Please note, it is important to rule out Lead poisoning, and to also carefully check the patient for Anemia's, and cancers, as both are seen to a higher degree in porphyria.

Please see the testing cautions below, Porphyria testing has high false negatives for a variety of reasons.

*These are not standard lab tests, we wince when people say "all my tests in the ER were normal", the truth is all routinely done tests were (close to) normal, these aren't routinely done tests. Our organization is in agreement with The Australian Porphyria experts to test each patients blood (enzyme), plasma, urine, and stool. The "stepwise approach" (recommended elsewhere) is incredibly dangerous as it forces patients to wait for an attack, and tests only urine initially, which will miss younger patients, many latent patients, and may miss (a high percentage of) HCP, and VP, in life threatening attacks, according to Australian Porphyria expert Dr. Janus, and Dr. Blake's research findings in his paper "Fecal Coporporphyrin Isomers in HCP", and in the drug trial for Panhematin the paper entitled "Porphyria" noted the VP patient had a false negative PBG test. 


A concerning number of HCP and VP patients are well documented in and out of attacks in research papers to never have a positive urine PBG test, it is simply incomplete and dangerous to do only urine testing, it is also illegal in the US, a non FDA approved test may not be used as a sole means of diagnosis under US Law.

We give cautions and tips below, porphyria is a metabolic disease and false negatives often occur.

*Test name:  Fecal porphyrins

(must be a High performance liquid chromatography test or about 30%will be missed)

Total fecal porphyrins the best test for Hereditary Coproporphyria.

Watch for:

Coproporphyrin (CIII+ CI) dominance, the Coproporphyrin should be no more than 16% of total porphyrins, and not more than equal to that of 24% of proptoporphyrin

*Abnormal CIII:CI ratio

*High porphyrins

*A patient may not have all characteristics.


*The sample must be light protected (container wrapped in foil, or black container) immediately, and frozen or refrigerated per labs requirements. 

*Please NOTE: Coproporphyrin dominance (CIII + CI) is an ABNORMAL finding (no matter what the lab says) and is only seen in one Acute Porphyria, Hereditary Coproporphyria, and is also not seen in "non porphyric" humans. A normal fecal porphyrins profile according to the paper "Compound Heterozygous HCP" by Doss is the coproporphyrin (CIII+CI) is 16% of total porphyrins and 24% of Protoporphyrin. Unfortunately US labs are not currently flagging some abnormal results, if you see that your results are abnormal, but not flagged, we can help you report the lab to the proper governing body, please reach out to us.

*In the paper Variegate Porphyria, Anderson found that Copro dominance is seen only in HCP, 

*Patients with HCP may not have high porphyrin excretions in fecal testing per Blake's paper "Fecal Coproporphyrin Isomers in Hereditary Coproporphyria" 40% of one family with HCP did not have high fecal porphyrin excretion.

*Children may have false negative below the age of 12. 

Fecal testing in Blake's paper could detect even rather young patients. Allen in his paper "HCP comparison of molecular and biochemical investigations in large family" found by age 10 a CIII:CI ratio was detectable. 

*Treatment success! Kuhnel in her Paper "HCP in Germany" found treating the patient with Normosang infusions of heme (The name for the non US version Panhematin) could reverse the abnormal fecal porphyrin profile in patients with HCP.


Enzyme Testing 

*Test name: The Porphobilinogen Deaminase whole blood enzyme test is tied with the PBG urine test as the best tests for AIP according to the research paper "196 patients with AIP" 

In the US there is currently only 2 of the 4 enzymes in the Acute Porphyria's that have testing: Aminolevuelenic Acid Dehydratase whole blood ALAD (for ALAD) and Porphobilnigen Deainase PBGD (for AIP). We are working to change this! You can donate to us we are working on bring Enzyme testing to the US for HCP and VP, France does them. Enzyme testing for acute porphyria consists of testing four enzymes. The enzymes that are tested are Aminolevuelenic acid dehydratase (ALAD) for aminolevulenic acid dehydratase deficiency porphyria (ADP), porphobilinogen deaminase (PBGD) for acute intermittent porphyria (AIP), coproporphyrinogen oxidase (CPOX) for hereditary coproporphyria (HCP), and protoporphyrinogen oxidase (PPOX) for variegate porphyria (VP). In those with acute porphyria, the enzyme are deficient by approximately half in a heterozygous carrier in AIP, HCP, and VP, to a almost a full loss of the enzyme function in ALAD and homozygous AIP HCP and VP. 


*False negatives in PBGD enzyme testing in AIP occur in up to 16% of patients with AIP.

*A low PBGD or ALAD but not diagnostically low enough for either disease could indicate another porphyria is present, it was found that Variegate Porphyria patients may also have low PBGD, our org has an HCP patients records who also had below normal PBGD, so please do through porphyria testing which is all available if a low enzyme is seen.

*Maybe a false negative if the patient is symptomatic and best done outside of an attack

*Must be refrigerated

Other illnesses may cause a low PBGD such as sideropenia, and the following illnesses may affect PBGD levels: anemia (this is often seen in Porphyria), uremia, malignicies, and hemodialysis. During an attack the level of PBGD can rise to reference levels creating a false negative. 

*Aminolevuelenic Acid dehydratase Enzyme Whole Blood 

A test for ALAD porphyria.

must be refrigerated and best done outside of an attack. 

Cautions: about 1-2% of the population have below normal ALAD enzyme, please do a through work up on these patients, and take any signs and symptoms consistent with an attack seriously. 

Test name: Plasma Porphyrins

Cautions: the sample must be light protected during collection, storage, and transport, and refrigerated. Plasma Fractionated porphyrins is the best test for VP when the patient is symptomatic.


*Sample must be kept light protected at collection, storage, and shipping. Maybe negative outside of an attack or if impropeprly handled



Urine Aminolevulinic acid (ALA), urine Porphobilinogen (PBG), urine total porphyrins, urine fractionated porphyrins,

*ALA / PBG Urine first pee of the day, or 24 hr. test,

Aminolevuelinic acid is the best test for ALAD-P, and is also used in conjunction with PBG testing for AIP,


*Must be done during symptoms,

*Must be light protected, and refrigerated. Improper lab handling or patient handling may also cause false negatives.

*May not ever be elevated in HCP, or if elevated may fall quickly, and VP may also have false negatives during an attack, or maybe elevated in VP in an attack, but fall quickly. Frequent false negatives occur in HCP whether the patient is in or outside of an attack, The Australian porphyria specialist state Ala/ Pbg may also be a negative during an in HCP both inside and outside of an attack, regardless of regardless of age. Levels quickly drop after an attack. 

*Patients with AIP may have a positive PBG test outside of an attack, in this case establish a baseline with testing outside of an attack, normal intraindividual increases in AIP range from 1.6-4 times. (196 patients with AIP)


*There can be a false negatives due to glucose infusion, or carbohydrate consumption, as well as lab mishandling. From the paper "Porphyria" 

*Treatment with Panhematin will cause false negatives as well as the Givorsiran drug. 

*Younger patients may have false negatives. The French Porphyria Center states patients 15 years and under in AIP may have false negatives, and The University Cape Town in S. Africa states testing done under age 22 in VP maybe a false negative.

*Signae Vitae's paper "Porphyria Diagnostic challenge in the ER" states the PBG test is prone to both false negatives and positives. 

*In the Spring of 2018 a Porphyria patient dropped a bombshell on the "Porphyria Sucks" face book support group publicly stating that a "porphyrin retainment" mutation was found in her DNA. Unfortunately when we reached out to the lab to obtain the RS # the lab cited HIPPA, and does not share their findings with the Human Genome Mutation Database, so we cannot independently verify what the mutation is, however it seems that about 17-30% of the patients in the paper "Fecal Isomers in HCP" had retention of porphyrins.


Other Biochemical testing


Serum porphobilinogen (PBG) is another way to test PBG in a patient, this is used in patients with renal failure.

Genetic Testing

Genetic testing is relatively new and not 100% reliable. Most porphyria mutations are "family specific" if your families mutation has not been found, you may have porphyria, but have a negative genetics test. A negative genetics test does not clear you of porphyria, one genetics counselor explained in their labs experience 20% of patients with a positive urine pbg test, had a negative genetics test, and 13% of the patients with out any positive biochemical testing, had a known pathogenic porphyria mutation. A negative genetics test- because they are not FDA approved, may not be used to deny treatment, or strip a diagnosis, it just means if you have porphyria that your variant has not been discovered yet.

The DNA tests that are available are: next-generation sequencing, sanger sequencing, and microarray-based comparative genomic hybridization.

A note about DNA Sequencing Analysis:

It is important to note that labs that do not offer deletion and insertion testing will not

find mutations with large deletions or insertions. At this time it is not clear how often

deletion and insertion mutations occur. One source says that approximately fifteen

percent of genetic mutations for hereditary coproporphyria are deletions or insertions, 

whereas another source says that approximately five percent of genetic mutations for

acute intermittent porphyria are deletions or insertions. Heidi Rehm PhD, of Harvard

stated that genetics testing may only catch 20% of gene carriers.

All genetic testing in the US requires a Doctors signature. We encourage all the

request your underlying DNA mutations, under HIPPA regulations you are legally

entitled to receive those within 30-60 days of written request to the laboratory. Please


contact the lab directly to ensure the testing has not changed. 

 The genes are: ALAD, ALAS2, C15orf41, CPOX, FECH, HFE, HMBS, PPOX, SLC19A2, UROD, UROS.

If you feel you have had a problem with a lab, please file a Clinical Laboratory Improvement Amendments (CLIA) complaint to the Center for Disease Control in your state. Reasons to file a CLIA complaint are negligence, if your HIPPA rights were violated either by a lab disclosing your private information with out authorization or refusing to give you your underlying data please file a HIPPA complaint. And finally if a Dr. or medical professional interfered,compromised, or acted unsafely with your care please file a medical board complaint in your state. If you were stripped of your diagnosis based on a negative genetics test you may alsp file a FDA device complaint.

There are a limited number of laboratories in America that test for porphyria, so you or your doctor will have to send the samples to a laboratory or multiple laboratories that test for porphyria across the country. We want to make it very clear no one test is 100% accurate, and certain porphyria tests have false negative rates of close to 40%. Porphyria is an inborn error of metabolism and as such testing has to be compared to clinical history. As Acute Porphyria is a life threatening disease we encourage a full battery of testing which may have to be repeated until you the patient are satisfied. The current average time to an Acute Porphyria diagnosis is 15 years in the U.S.,our organization would like to shorten that to days.

The Porphyria's are diagnosed by several different laboratory tests, unfortunately at this time the US is missing several porphyria tests (our goal is to change that), so it is very important to do all available tests, as some tests are better for certain types, and other tests are better when not in an "attack".

How Is Porphyria Treated?

Hepatic Porphyria is treated with Panhematin and glucose. If Panhematin is ineffective for a patient, a liver transplant could be done. There are also medications for symptom treatments as well.

Panhematin® (hemin for injection)

Active Ingredient: Hemin 313 mg

Inactive Ingredients: Sodium Carbonate 215 mg, Sorbitol 300 mg

About Panhematin®

Panhematin® is a biologic that is made of red blood cells processed from human blood. Panhematin® is intended to limit the rate of heme biosynthesis by inhibiting the enzyme aminolevulinic acid synthase.  Panhematin® prevents porphyria symptoms from progressing, it does not repair damage and is not curative, after discontinuation of Panhematin® symptoms return if the patient is in a porphyria attack. Clinical benefit from Panhematin depends on prompt administration. Attacks of porphyria may progress to a point where irreversible neuronal damage has occurred. Panhematin therapy is intended to prevent an attack from reaching the critical stage of neuronal degeneration. Panhematin is not effective in repairing neuronal damage. 


The risk factors associated with the use of Panhematin® are allergic reactions, iron poisoning, and viruses including Creutzfeldt-Jakob disease. Panhematin® has been reported to cause allergic reactions in some individuals. Allergic reactions to Panhematin® are usually due to the inactive ingredients in Panhematin® such as sorbitol or sodium carbonate (cite source). An allergic reaction to Panhematin® can present as rash, hives, itching, difficulty breathing, tightness in the chest, and swelling of the mouth, face, lips, or tongue. Recommended dosage guidelines should be strictly followed as reversible renal shutdown has occurred with administration of excessive doses. Panhematin® is made from human plasma (part of the blood) which may contain viruses and other infectious agents. Donated plasma is tested and treated to reduce the risk of it containing infectious agents, but there is still a small possibility it could transmit disease. Increased levels of iron and serum ferritin have been reported in post-marketing experience; therefore, physicians should monitor iron and serum ferritin in patients receiving multiple administrations of Panhematin.​ Because vein inflammation has been reported after administering PANHEMATIN through small arm veins, a large arm vein or a central line should be used ( please switch off arms to allow the veins to rest. The risk that such products will transmit an infectious agent has been reduced by screening blood donors for prior exposure to certain viruses, by testing for the presence of certain current virus infections, and by inactivating certain viruses. Despite these measures, such products can still potentially transmit disease. There is also the possibility that unknown infectious agents may be present in such products. Because this product is made from human blood, it may carry a risk of transmitting infectious agents, e.g., viruses, and theoretically, the Creutzfeldt-Jakob disease (CJD) agent. 

Side Effects

Panhematin® can cause urinating less than usual or not at all, swelling, weight gain, feeling short of breath, fever, easy bruising or bleeding, or swelling, pain, or irritation around the IV needle.

Dosage and Administration

Panhematin® is given at a dose of 1-4 milligrams per kilogram of body weight once daily for 3 to 14 days, based on clinical signs. In more severe cases, Panhematin® is given at the previous dose twice daily. Panhematin® should not exceed 6 milligrams per kilogram of body weight per 24-hour period. Panhematin® is administered intravenously into a large peripheral vein, a central venous catheter, also known as a central line, a central venous line, or a central venous access catheter, or a port. If using an arm vein IV please switch arms daily to allow the vein to recover. Warming the arms with blankets or a heating pad before is also a good way to help the IV administration.

Dextrose Injection

Dextrose comes in a variety of options: 5% with saline, Dextrose 10% with


saline,and 5% Dextrose with saline or Dextrose 50% with saline. It is very important


that the infusion be done slowly and that the patients electrolytes are monitored, as

hyponatramia is seen fairly often in attacks, and Secretion of anti diuretic hormone

is also seen.  Dextrose is intended to limit the rate of heme biosynthesis possibly by

inhibiting the enzyme aminolevulinic acid synthase. It is very important to


understand only dextrose is only to be used in mild attacks.

The patient can also try to consume a high carbohydrate diet that consists of 300-


500 grams of carbohydrates daily, however many patients report the IV infusion


helps them more. It is suggested that when patients cannot consume


carbohydrates due to nausea or vomiting, glucose should be administered


intravenously. Some physicians have prepared a standing order for patients who


are prone to attacks to help facilitate intravenous glucose in the emergency room.


Often this prevents further hospitalization, however ideally Patients in attacks are


admitted and monitored in the ICU, attacks are serious and the mortality rate is 5-


20% if the attack is undiagnosed and untreated.


The infusion should be done slowly and continuously over 24 hours and the patient should have their electrolytes carefully monitored, watching for hypontraemia, SIADH, and for hyper or hypo glycemia.

Possible Side Effects


*Infection at the site of injection

*Blood clot or inflammation at the site of injection




Dosage and Administration

Two litres of normal saline with 5,10, or 20% glucose given in divided doses of 500 ml over 24 hours through a central venous catheter. 

Lupron Depot® (leuprolide acetate for depot suspension)

Active Ingredient: Leuprolide acetate 3.75 mg

Inactive Ingredients: D-mannitol 56.6 mg, DL-lactic and glycolic acids copolymer 33.1 mg, Carboxymethylcellulose Sodium 5 mg, Polysorbate 80 1mg, Purified gelatin 0.65 mg

About Lupron Depot®

Lupron Depot® is a gonadotropin-releasing hormone agonist, also known as GnRH agonist or GnRH-A. The body normally makes GnRH in the pituitary gland located in the brain and it is this hormone that stimulates the ovary to develop eggs and produce estrogen, leading to the normal menstrual cycle. If you give GnRH agonists, this floods the system and confuses the delicately controlled balance, leading to a complete block of egg development, estrogen production and menstrual cycle. It effectively makes you 'menopausal' for the time that you use the treatment. The success rate varied from 60-80%.  

Precautions: please carefully read the paper " An update to clinical management with AIP" it has a great write up on using GnRH in women with acute porphyria.

Side Effects

Lupron Depot® can cause menopausal symptoms such as hot flashes also known as flushing, increased sweating, night sweats, tiredness, headache, upset stomach, breast changes, acne, joint and muscle aches, thinning of the bones, trouble sleeping, reduced sexual interest, vaginal discomfort and dryness, swelling of the ankles and feet, dizziness. Burning, pain, and bruising at the injection site may occur.

Liver Transplant

Has been used successfully in a limited number of patients. The liver transplant must be done when the patient is strong enough to with stand the surgery and recovery.

What Are the Differential Diagnoses to Porphyria?

  • Diabetic Ketoacidosis

  • ​Neurofibromatosis

  • Dubin-Johnson Syndrome

  • Familial Mediterranean Fever

  • Huntington's Disease