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No joke: new hope for painful “four-hour erection”

Oct. 26, 2009
Courtesy FASEB
and World Science staff

Erec­tions last­ing four hours or more may seem like a rich source of jests, but to men suf­fer­ing this pain­ful con­di­tion—calle pri­ap­ism—they’re no laugh­ing mat­ter.

How­ev­er, new re­search of­fers hope that vic­tims at least won’t end up un­able to have sex.

Sci­en­tists from the Un­ited States and Chi­na have found in mouse stud­ies that a com­pound called aden­o­sine de­am­i­nase pre­vents pri­ap­ism from lead­ing to pe­nile fi­bro­sis, a con­di­tion as­so­ci­at­ed with build­up of scar tis­sue and even­tu­al im­po­tence. 

Pri­ap­ism it­self is, in turn, a com­plica­t­ion of sick­le cell dis­ease. 

The new find­ings are pub­lished on­line in the FASEB (Federa­t­ion of Amer­i­can So­ci­eties for Ex­pe­ri­men­tal Bi­ol­o­gy) Jour­nal.

“Cop­ing with pri­ap­ism is hard enough, but know­ing that it can ul­ti­mately lead to fi­bro­sis with­in the pe­nis adds in­sult to in­jury,” said Ger­ald Weiss­mann, editor-in-chief of the Jour­nal. “Hope­fully this dis­cov­ery can yield new drugs that re­lieve the ex­cit­a­to­ry sig­nals sent by aden­o­sine so that these men to get some re­lief.” 

Aden­o­sine de­am­i­nase—an en­zyme which breaks down aden­o­sine, a nat­u­ral cellular-sig­nal­ing molecule—is al­ready used in hu­mans as a treat­ment for a rare im­mune dis­or­der.

For the new stu­dy, re­search­ers used two pri­a­pism an­i­mal mod­els to de­ter­mine the role of in­creased aden­o­sine in pe­nile fi­bro­sis. One mod­el was that of aden­o­sine de­am­i­nase-deficient mice and the oth­er was mice en­gi­neered to have sick­le cell dis­ease. Both sets of mu­tant mice were treated with aden­o­sine de­am­i­nase. 

Af­ter eight weeks, the in­ves­ti­ga­tors found the en­zyme low­ered aden­o­sine lev­els in the pe­nises of both groups of ro­dents, pre­vent­ing or cor­rect­ing pe­nile fi­bro­sis.

“We have re­vealed that in­creased aden­o­sine sig­nal­ing con­tri­butes to… the pro­gres­sion of pri­ap­ism to pe­nile fi­bro­sis,” said Yang Xia, a sci­ent­ist in­volved in the study from the Un­ivers­ity of Texas-Houston Med­i­cal School. “This find­ing led to a nov­el ther­a­peu­tic pos­si­bil­ity to treat and pre­vent this dan­ger­ous com­plica­t­ion.”


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Erections lasting four hours or more may seem like a rich source of jests, but to men suffering this painful condition—called priapism—they’re no laughing matter. However, new research offers hope that victims at least won’t end up unable to have sex. Scientists from the United States and China have found in mouse studies that a compound called adenosine deaminase prevents priapism from leading to penile fibrosis, a condition associated with buildup of scar tissue and eventual impotence. Priapism itself is, in turn, a complication of sickle cell disease. The new findings are published online in the FASEB (Federation of American Societies for Experimental Biology) Journal. “Coping with priapism is hard enough, but knowing that it can ultimately lead to fibrosis within the penis adds insult to injury,” said Gerald Weissmann, editor-in-chief of the Journal. “Hopefully this discovery can yield new drugs that relieve the excitatory signals sent by adenosine so that these men to get some relief.” Adenosine deaminase—an enzyme which breaks down adenosine, a natural cellular-signaling molecule—is already used in humans as a treatment for a rare immune disorder. For the new study, researchers used two priapism animal models to determine the role of increased adenosine in penile fibrosis. One model was that of adenosine deaminase-deficient mice and the other was mice engineered to have sickle cell disease. Both sets of mutant mice were treated with adenosine deaminase to lower adenosine levels. After eight weeks, the investigators found that this enzyme significantly lowered adenosine levels in the penises of both groups of rodents, preventing or correcting penile fibrosis. “We have revealed that increased adenosine signaling contributes to… the progression of priapism to penile fibrosis,” said Yang Xia, a scientist involved in the study from the University of Texas-Houston Medical School. “This finding led to a novel therapeutic possibility to treat and prevent this dangerous complication.”