The detection of heparin platelet factor 4 antibodies of >20% also strongly suggests the diagnosis of HIT. The major complications are bleeding and thrombosis. In the present report, all the blood analysis and the use of heparin strongly suggest the diagnostic of HIT. As described previously, the fall in the platelet count and the heparin platelet factor 4 antibodies were positive for HIT 5 days after the introduction of heparin. The patient had already been exposed to heparin at the beginning of the hospitalization. Early SAHA HDAC molecular weight cessation of heparin and initiation of Argatroban was the appropriate medical management

in our case. Other factors might have contributed to penile necrosis, such as low cardiac flow followed by cardiac failure and diabetic nephropathy. However, the severity of the penile necrosis and the chronology of the events are in favor of penile necrosis secondary to HIT. To our knowledge, it is only the second case of penile necrosis secondary to HIT described in the literature. The first case described was that of a 56-year-old man with lung cancer.5 He was admitted in the hospital for pulmonary thrombosis, for which a treatment of heparin and Warfarine was initiated. Similar to our case, the patient complained of symptoms of penile necrosis 4 days after the beginning of heparin therapy. The diagnosis of HIT was made after a drop in platelet

count of 69%. As illustrated by this case see more and our case, penile symptoms of HIT were present when thrombocytopenia

was confirmed. The patient underwent a partial penectomy and died of complications 3 weeks later. The pathology demonstrated hemorrhagic necrosis with thrombi. Factoring in all the previously mentioned, we believe that penile necrosis is an unusual complication of HIT. However, the pathology of penile necrosis because of HIT seems unclear. Despite thrombocytopenia, HIT is rarely described in association with bleeding.3 In fact, thrombosis is more frequent. In our case, pathology demonstrated extensive hemorrhagic necrosis of the penis without thrombus. However, an hypothesis is that the patient could have and developed venous thrombosis. The thrombus could have disappeared with the treatment of Argatroban and have caused hemorrhagic damages to the penis. There was no other explanation apart from the HIT to explain the extensive acute penile necrosis our patient has developed. This case demonstrates that the hypercoagulable state brought on by HIT is a cause of acute penile necrosis. Approximately 1%-5% of patients exposed to some form of heparin will develop a HIT.4 Prompt diagnosis of HIT should be encouraged to avoid complications such as penile necrosis. Moreover, HIT should be researched when a diagnosis of penile necrosis is made to avoid thrombosis of other organs and deterioration of penile acute ischemia. “
“Genital pain is a common urologic complaint.