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Figure c60/f001
Figure 60.1
The haem molecule and its key structural features. The alternation of single and double bonds around the tetrapyrrole ring indicates the aromaticity o...
Figure c60/f005
Figure 60.5
Typical subepidermal bulla in a bullous porphyria: (a) clinical appearance, and (b) histological appearance.
Figure c60/f009
Figure 60.9
Porphyria cutanea tarda: erosions, blisters, pigmentary changes and scarring.
Figure c60/f002
Figure 60.2
The pathway of haem biosynthesis showing the six key structural changes.
Figure c60/f006
Figure 60.6
High‐performance liquid chromatography (HPLC) analysis: the more carboxylate groups it possesses, the faster a porphyrin molecule passes through the c...
Figure c60/f010
Figure 60.10
Oedema during an acute painful attack in a child with erythropoietic protoporphyria.
Figure c60/f003
Figure 60.3
The pathway of haem biosynthesis showing the enzyme deficiency associated with each porphyria. Abbreviations of the disease names are defined in the t...
Figure c60/f007
Figure 60.7
Congenital erythropoietic porphyria: scarring of skin with resorption of terminal phalanges. (Courtesy of Dr A. du Vivier, King's College Hospital, L...
Figure c60/f011
Figure 60.11
Typical scars on the cheeks in erythropoietic protoporphyria.
Figure c60/f004
Figure 60.4
The pathogenesis of skin disease in porphyria.
Figure c60/f008
Figure 60.8
Porphyria cutanea tarda is caused by production of an inhibitor of uroporphyrinogen decarboxylase (UROD) in the liver, in the presence of iron. (Adap...
Figure c60/f012
Figure 60.12
Liver biopsy in protoporphyric liver disease showing nodules of cirrhosis and black staining by deposits of protoporphyrin.