Several light sources, including sunlight, xenon lamps, fluorescent lamps, mercury lamps and carbon arc lamps, have been used to provoke skin changes for phototests in patients with porphyrias, or to induce experimental hemolysis of porphyrins for research. The metal halide lamp has a strong emission range between 400 nm and 450 nm, and a relatively low emission range in the ultraviolet region. For this reason, we explored the possibility that this lamp could be used to induce photohemolysis caused by hematoporphyrin (HP) and the radiation of light. Twenty to forty μg of HP‐HCl was added to 25 ml of a normal red blood cell suspension. The flask containing this red blood cell suspension was then irradiated using a metal halide lamp with 3.6 to 10.8 J/cm2 of light. All of the irradiated red blood cell suspension was hemolyzed, but the non‐irradiated control showed very little hemolysis. Compared to natural sunlight, the energy emitted by the metal halide lamp is small. Therefore, a longer exposure from the metal halide lamp is required to obtain an amount of energy equivalent to sunlight. This type of light source covers a wide area for irradiation. From these results, we can speculate that a metal halide lamp source is of value when used experimentally to produce the chronic skin changes of porphyria.

We performed a histopathological investigation of the bullous lesions in 3 cases of porphyria cutanea tarda. All cases showed subepidermal bullae by light microscopy. PAS positive materials were present on the roof of the bullae and partially present on their bases. Electronmicroscopically, the basal lamina was clearly recognized on the base. From these results, we suggest that the blister in porphyria cutanea tarda occurs initially within the junctional zone; this initial bulla may quickly change into a dermolytic bulla with additional stimulation.

To investigate the influence of polychlorinated biphenyls (PCB) on porphyrin metabolism, Wistar rats were orally administered KC‐400. The mean value of liver/body weight ratio in normal rats was 3.86%, with a range of 3.44% to 5.22%. Their mean blood protoporphyrin level was 23.3 μg/dl packed cell volume (p.c.v.), with a range of 11.8 to 64.4 μg/dl p.c.v., and their mean liver protoporphyrin level was 0.17 μg/gm wet weight, with a range of 0.03 to 0.40 μg/gm wet weight. A feed containing KC‐400 (140–160 ppm) was given for 2 to 20 weeks to 20 rats. The mean value of liver/body weight ratio was 5.00%, with a range of 3.80% to 6.16%. The mean erythrocyte protoporphyrin level was 47.4 μg/dl p.c.v., with a range of 19.7 to 83.2 μg/dl p.c.v., and the mean liver protoporphyrin level was 0.36 μg/gm wet weight, with a range of 0.04 to 0.67 μg/gm wet weight. The liver coproporphyrin level showed abnormalities in 2 of 20 rats fed the feed containing KC‐400, with values of 0.71 and 9.89 μg/gm wet weight, respectively. After administration of KC‐400 feed for 43 weeks, the mean value of blood coproporphyrin level rose to 32.1 μg/dl p.c.v., with a range of 11.4 to 54.6 μg/dl p.c.v. The mean erythrocyte protoporphyrin level was 74.3 μg/dl p.c.v., with a range of 49.5 to 102.1 μg/dl p.c.v. The mean liver coproporphyrin level was elevated to 5.15 μg/gm wet weight, with a range of 0.45 to 9.48 μg/gm wet weight, and the mean liver protoporphyrin level was 0.65 μg/gm wet weight, with a range of 0.43 to 9.88 μg/gm wet weight. Thus, there was an increase in both liver porphyrin and coproporphyrin following KC‐400 feeding. Liver cells in the rats with abnormal porphyrin levels exhibited a red fluorescence. From these results, we can deduce that KC‐400 may induce abnormalities in porphyrin metabolism, when it is fed orally for a long period of time. These abnormalities in porphyrin metabolism are limited to the liver only.

In order to determine the lowest concentration of griseofulvin (GF) needed to induce abnormal porphyrin metabolism, D‐D strain mice were fed with a feed containing GF in concentrations of 0.1%, 0.5%, and 1.0%. The liver and blood porphyrin levels were analyzed, and the red fluorescence of the liver and blood observed with a fluorescent microscope. In the 0.5% GF and 1.0% GF groups, a swelling of the liver was observed, and coproporphyrin and protoporphyrin levels in the liver and the blood increased markedly. However, the increase in protoporphyrin levels was more prominent than the increase of coproporphyrin levels. The increase in the liver protoporphyrin was more marked than that in the blood porphyrin. Comparisons of the 0.5% GF and 1.0% GF groups revealed that liver swelling was more prominent in the 1.0% GF group. A high degree of metabolic abnormality in blood protoporphyrin was found in 1.0% GF animals whose feeding period was rather short. In the 0.1% GF group, liver swelling was hardly noticeable, and there were no differences between the short feeding and long feeding groups. Although no abnormalities in blood porphyrins were noticed in comparison with the normal group, abnormally high levels of liver porphyrins were found in 3 out of the 34 treated mice. No differences from the normal group were noted in the remaining 31 animals. In the 0.5% GF and 1.0% GF groups, red fluorescence of the liver was seen in all cases, while in the 0.1% GF group, reticular red fluorescence was noted in only one animal. From these findings, it appears that a marked increase in porphyrin occurs at a concentration above 0.5% in D‐D strain mice, whereas, at the concentration of 0.1%, the majority of the treated mice remain within normal limits. Only a few showed any abnormality of porphyrin metabolism. We feel that, for this reason, it would be better to use a GF concentration of 0.1% for the lowest concentration experiments involving GF‐induced protoporphyria in D‐D strain mice and especially for investigations of the interaction of other chemicals with GF, and investigations of initial changes of porphyrin metabolism.

Recent reports have revealed the high prevalence of serological markers of viral hepatitis in porphyria cutanea tarda (PCT). We present two cases of PCT associated with hepatitis C and discuss the relationship between PCT and viral hepatitis. Case 1: A 50-year-old Japanese male noticed blisters, erosions, and fragility on sun-exposed areas of his skin in November of 1990. He had no history of excessive alcohol intake. He had been taking analgesics for eighteen years. Case 2: A 64-year-old Japanese male was referred in October of 1989 because of pigmentation on sun-exposed areas of his skin. He had been drinking alcohol excessively for 43 years. The hepatitis C virus (HCV) antibody was present in each case. Tests for the HCV antibody and hepatitis B serological markers were run in 5 other patients. HCV antibody was present in 3 of them. The two cases negative for the HCV antibody exhibited the hepatitis B antibody. We speculated that viral hepatitis infection may play an important role in precipitating PCT in cases with a history of a long term excessive intake of alcohol or chemicals.