A1,
A2,
B,
C1,
C2,
D,
E,
F,
G-H,
I-K,
L,
M,
N,
O,
P1,
P2,
Q-R,
S,
T,
U-V,
W-Z
Panhematin Pharmacology, Pharmacokinetics, Studies, Metabolism - Hemin
Panhematin Pharmacology, Pharmacokinetics, Studies, Metabolism - Hemin
CLINICAL PHARMACOLOGY
Heme acts to limit the hepatic and/or marrow synthesis of porphyrin. This action
is likely due to the inhibition of [delta]- aminolevulinic acid synthetase,
the enzyme which limits the rate of the porphyrin/heme biosynthetic pathway.
The exact mechanism by which hematin produces symptomatic improvement in patients
with acute episodes of the hepatic porphyrias has not been elucidated. 1,9
Following intravenous administration of hematin in non-jaundiced human patients,
an increase in fecal urobilinogen can be observed which is roughly proportional
to the amount of hematin administered. This suggests an enterohepatic pathway
as at least one route of elimination. Bilirubin metabolites are also excreted
in the urine following hematin injections. 2
PANHEMATIN (hemin for injection) therapy for the acute porphyrias is not curative.
After discontinuation of PANHEMATIN treatment, symptoms generally return although
in some cases remission is prolonged. Some neurological symptoms have improved
weeks to months after therapy although little or no response was noted at the
time of treatment.
Other aspects of human pharmacokinetics have not been defined.
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