PSEUDOMELANOSIS 481 



Libited by liematoporpbyrin and other porphyrins, and find evidence 

 suggesting a rehitionship between hematoporpliyria and "hydroa 

 aestiva," and other conditions in which the skin is abnormally sensi- 

 tive to light. 



After injection of 0.2 gm. hematoporphyi-in into his own veins, 

 Mej'^er-Betz '^'^^ found himself so sensitized to light that exposure to 

 the sun caused severe skin reactions during a period of weeks, and 

 exposure to the Finsen light produced severe ulceration ; but little 

 hematojiorphyrin escaped in the urine. Many other products of 

 blood destruction tested on animals were without sensitizing effects. 

 Meth^-lation of the p^'rrol groups only partially removes the activity 

 of hematoporphyrin. Porphyrin obtained from urine and feces by 

 Fischer also sensitized mice to light. Sufficient doses of hematopor- 

 phyrin may sensitize mice so that they become narcotized and die in a 

 few minutes after exposure to intense light, a true "light stroke." 



Pseudomelanosis. — When loosely bound iron is present in the tis- 

 sues, and in the same tissues sulphides are produced through bacterial 

 action, a discoloration with sulphide of iron will result, which is 

 'Called pseudomelanosis, because the pigment resembles true melanin 

 in its blackness. This is most frequently observed as a postmortem 

 phenomenon in and about the abdominal cavity, and in the ordinary 

 postmortem discoloration both the liberation of the iron from its firm 

 organic combination, and the production of hydrogen sulphide, are the 

 ■work of bacteria. Pseudomelanosis may also occur intra vitam, par- 

 ticularly in the margins of infected areas, and it may also be observed 

 in the intestines, liver and spleen, and about the peritoneum, in bodies 

 examined immediately after death, before any evident postmortem 

 decomposition has set in. This seems to depend upon the previous 

 intra vitam formation of hemosiderin, which is then combined by sul- 

 phur liberated from tissue proteins through bacterial action.''^ If 

 hj'drogen sulphide acts upon hemoglobin that has not been decom- 

 posed, a greenish compound of sulphur-mctheniogloTjin is formed 

 (Harnack^^), which is the cause of the greenish color seen in the 

 abdominal walls and along the vessels of cadavers. This union of 

 hemoglobin and hydrogen sulphide occurs only when oxygen is pres- 

 ent (oxyhemoglobin). The sulphur-hemoglobin compound is readily 

 decomposed by weak acids, even by CO., with the formation of 

 methemoglohin, which in turn readily becomes decomposed to form 

 hematin. 



During life sulphemoglohin may form, the sulphur presumably 



coming from ijitestinal putrefaction, and hence called "enterogenous 



cyanosis," which term also covers metliemoglohinemia produced by 



nitrites formed in the intestines.^" The latter condition is also pres- 



67a Dent. Arch. klin. Med., 191.3 (112). 476. 

 G8 Ernst, Virchow's Arch., 189S (152), 418. Literature. 

 69Zeit. physiol. Chem., 1899 (20), .558. 



70 West and CMarke. Lancet. Feb. 2, 1907: Davis, ihid., Oct. 26, 1912; Gibson 

 Quart. Jour. Med., 1907 (1), 29; Wallis, Hid., Oct., 1913. 

 31 



