The<unk> s are generally considered genetic in nature. Genetics Subtypes of<unk> s depend on which enzyme is deficient.<unk>  type Deficient enzyme Type of<unk>  Inheritance Symptoms Prevalence Aminolevulinate dehydratase deficiency<unk>  (ALADP) 5-aminolevulinate dehydratase (ALAD) Hepatic Autosomal recessive Abdominal pain, neuropathy Extremely rare; fewer than 10 cases ever reported. Acute intermittent<unk>  (AIP) Hydroxymethylbilane synthase (HMBS) formerly porphobilinogen deaminase (PBGD) Hepatic Autosomal dominant Periodic abdominal pain, peripheral neuropathy, psychiatric disorders, tachycardia 1 in 10,000–20,000 Congenital erythropoietic<unk>  (CEP) uroporphyrinogen synthase (UROS) Erythropoietic Autosomal recessive Severe photosensitivity with erythema, swelling and blistering. Hemolytic anemia, splenomegaly 1 in 1,000,000 or less.<unk>  cutanea tarda (PCT) uroporphyrinogen decarboxylase (UROD) Hepatic Approximately 80% sporadic, 20% Autosomal dominant Photosensitivity with vesicles and bullae 1 in 10,000 Hereditary coproporphyria (HCP) coproporphyrinogen oxidase (CPOX) Hepatic Autosomal dominant Photosensitivity, neurologic symptoms, colic 1 in 500,000 Harderoporphyria coproporphyrinogen oxidase (CPOX) Erythropoietic Autosomal recessive Jaundice, anemia, enlarged liver and spleen, often neonatal. Photosensitivity later. Extremely rare; fewer than 10 cases ever reported. Variegate<unk>  (VP) protoporphyrinogen oxidase (PPOX) Hepatic Autosomal dominant Photosensitivity, neurologic symptoms, developmental delay 1 in 300 in South Africa1 in 75,000 in Finland Erythropoietic protoporphyria (EPP) ferrochelatase (FECH) Erythropoietic Autosomal recessive Photosensitivity with skin lesions. Gallstones, mild liver dysfunction 1 in 75,000–200,000 X-linked dominant protoporphyria is a rare form of erythropoietic protoporphyria caused by a gain-of-function mutation in ALAS2 characterized by severe photosensitivity. In the autosomal recessive types, if a person inherits a single gene they may become a carrier. Generally they do not have symptoms, but may pass the gene onto offspring. Triggers Acute<unk>  can be triggered by a number of drugs, most of which are believed to trigger it by interacting with enzymes in the liver which are made with heme. Such drugs include: * Sulfonamides, including sulfadiazine, sulfasalazine and trimethoprim/sulfamethoxazole. * Sulfonylureas like glibenclamide, gliclazide and glimepiride, although glipizide is thought to be safe. * Barbiturates including thiopental, phenobarbital, primidone, etc. * Systemic treatment with antifungals including fluconazole, griseofulvin, ketoconazole and voriconazole. (Topical use of these agents is thought to be safe due to minimal systemic absorption.) * Certain antibiotics like rifapentine, rifampicin, rifabutine, isoniazid, nitrofurantoin and, possibly, metronidazole. * Ergot derivatives including dihydroergotamine, ergometrine, ergotamine, methysergide, etc. * Certain antiretroviral medications (e.g. indinavir, nevirapine, ritonavir, saquinavir, etc.) * Progestogens * Some anticonvulsants including: carbamazepine, ethosuximide, phenytoin, topiramate, valproate. * Some painkillers like dextropropoxyphene, ketorolac, metamizole, pentazocine * Some cancer treatments like bexarotene, busulfan, chlorambucil, estramustine, etoposide, flutamide, idarubicin, ifosfamide, irinotecan, ixabepilone, letrozole, lomustine, megestrol, mitomycin, mitoxantrone, paclitaxel, procarbazine, tamoxifen, topotecan * Some antidepressants like imipramine, phenelzine, trazodone * Some antipsychotics like risperidone, ziprasidone * Some retinoids used for skin conditions like acitretin and isotretinoin * Miscellaneous others including: cocaine, methyldopa, fenfluramine, disulfiram, orphenadrine, pentoxifylline, and sodium aurothiomalate.
Porphyria
Alcoholic liver disease
Chalicosis
Lead poisoning
Hepatic porphyria
Pellagra
Albinism
Harderoporphyria