1 tional status to heme biosynthesis and acute hepatic porphyria.

2 ntermittent porphyria, the most common acute hepatic porphyria.

3 d often fatal clinical symptoms of the acute hepatic porphyrias.

4  treatment of the acute attacks of the acute hepatic porphyrias.

5 ute heme-deficient states, such as the acute hepatic porphyrias.

6   We conclude that iron potentiates both the hepatic porphyria and toxicity of TCDD in susceptible mi

7 -nonresponsive) mice, iron overcame the weak hepatic porphyria and toxicity responses in BALB/c and S

8 etic testing to determine the specific acute hepatic porphyria, and a complete medical history and ph

9                                    The acute hepatic porphyrias are a group of four inherited disorde

10                                    The acute hepatic porphyrias are inherited disorders of heme biosy

11                                    Inducible hepatic porphyrias are inherited genetic disorders of en

12 ograms/kg) markedly potentiated not only the hepatic porphyria but also general hepatocellular damage

13 derstanding of the pathogenesis of the acute hepatic porphyrias, identification of the iron overload-

14  iron, previously implicated in TCDD-induced hepatic porphyria, in mice with alleles of Ahr that enco

15 ttent porphyria (AIP), the most common acute hepatic porphyria, is an autosomal dominant inborn error

16 the acute attacks in patients with the acute hepatic porphyrias, perform the chronic phlebotomies to

17 framework for monitoring patients with acute hepatic porphyrias to ensure optimal outcomes.

18 own to induce porphyrin accumulation causing hepatic porphyria, up-regulate ABCB6 expression in both