June 1990, Vol. 29, No. 5
Cameo
Acquired Varicose Veins of the Penis FRANCESCO DRAGO, M.D., AND ALFREDO REBORA, M.D.
From the Department of Dermatology, University of Genoa, Genoa, Italy.
A
40-year-old man presented with several bluish nodules on his penis of 1 year's duration. They were not preceded by any trauma and alarmed the patient by the obvious deformity and the pain that gradually began both spontaneously and under pressure. The nodules disappeared when he developed an erection, but this proved troublesome. On examination, there were more than 20 0.5-1 cm wide bluish nodules located along the course of the superficial veins of the penile shaft (Fig. 1). They were tender and easily depressed. They reappeared immediately after pressure was released. The patient was in good general condition. No other vascular abnormalities were apparent. In particular, there were no varicose veins on his legs nor any personal or family history of venous thrombosis. Routine laboratory findings were normal. Histopathology revealed only a dilation of vessels (Fig. 2). Direct immunofluorescence did not detect any immunoglobulin or complement deposit in the vessel walls. Sonography and computed tomographic scan failed to reveal any abdominal, pelvic, or testicular change or any compression on the large vessels. Doppler fluximeter examination of iliac veins, lower cava, penis vessels, and spermatic arteries were normal and excluded any arteriovenous shunt. Consent for sclerotherapy was not granted.
ease of the deep veins and generally have a benign course. Varicosities that occur secondary to the obstruction of the deep venous system have a much more severe prognosis. In primary varicosities, the etiology remains obscure, although hormonal factors in women, increased abdominal pressure, and in rare cases, arterio-
Comment Although the differential diagnosis of multiple glomangiomas could have been made because of the nodules of our patient, their histopathology and behavior during erection ruled it out and confirmed the diagnosis of phlebectasias. Varicose veins may be primary or secondary. Primary varicose veins occur in the absence of any dis-
Address correspondence to: Alfredo Rebora, M.D., Department of Dermatology, University of Genoa, Genoa, Italy.
FiG. 1. Bluish nodules along the superficial veins of the shaft.
352
VARICOSE VEINS OF THE PENIS
No. 5
venous shunts have been claimed to aggravate the condition. Also inheritance may play a role and a congenital absence of valves has been supposed. In fact, an abnormal weakening of the valve commissures has been found.^ The interesting factor in this case the unusual location of the varicosity. Only in two instances, one congenitaP and one acquired,"* was the penis reported to be affected by varicosities, and in both of these the glans penis and not the shaft was involved. In our patient the glans was normal, while varicosities fol-
Drago and Rebora
353
lowed the course of the venous branches of the shaft. Their occurrence in adult life, their absence at birth, and the normality of laboratory findings account for the title of primary acquired varicose veins of the penis. Penile venous system can be divided into a superficial and a deep system that intercommunicate. The first system receives blood from the skin and the penis envelope, while the second, which is provided with valves, is fed by the cavernous tissues.'' Although prolonged sitting of our patient while he was at work may have contributed to induce hypertension in the abdominal venous trunks, a congenital hypoplasia of the deep vessel walls or the absence of valves should be considered for explaining the overloading of the superficial plexus that results in varicosity. In any case, there is no obvious reason for the condition, and we hope other reports will help to elucidate its cause. References
FIG. 2.
Histopathology reveals a simple dilation of the vein.
1. Edwards )E, Edwards EA. The saphenous valves in varicose veins Am Heart J. 1940;19:338-351. 2. Kouskouskis CE. Stump the experts—case report-resolution: venous lakes. J Dermatol Surg Oncol. 1983;9:110-165. 3. Balato N, Montanaro M, Lembo G. Acquired phlebectasia of the glans penis. J Am Acad Dermatol. 1985;13:824-826. 4. Testut L, Latarjet A. "Anatomia Umana" 5° Ed. UTET, Torino, 1969;6:313-315.
Tumor Necrosis Factor
ln response to invasive stimuli (microbial pathogens and their products or neoplasms), macrophages secrete, besides other cytokines, cachectin (tumor necrosis factor—TNF) a multipotent lymphokine with important immune and metabolic properties. TNF was originally described as a mediator of lipopolysaccharide-induced hemorrhagic necrosis of tumors but recent studies have shown that TNF is the same molecule as cachectin and has a wide spectrum of biologic properties in addition to the inhibition of tumor cell growth. These properties include the inhibition of lipoprotein lipase activity and the suppression of adipocyte gene expression, activities that lead to the wasting (cachexia) that accompanies chronic invasive disease states. Cachectin has also been shown to play a major role in the pathogenesis of Gram-negative (endotoxin-induced) shock and is responsible for most of the deleterious effects of endotoxinemia (hypotension, metabolic acidosis disseminated intravascular coagulation and their consequences) which may lead to death. In addition, cachectin has emerged as a general mediator of the acute phase response (e.g. it induces the production of interferons and interleukin-1 by macrophages) and, besides their direct antimicrobial or antineoplastic effects, a variety of recent observations suggest that this macrophage-hormone may have a significant role in the pathogenesis of inflammation and may play an important part in diverse human disease processes. In this review the authors discuss the biological properties and actions of cachectin, its role in the pathogenesis of inflammation, cachexia, tumor necrosis and endotoxic shock and its probable use as an antineoplastic or antiinflammatory agent.—Pardahs G. Gachectin or tumor necrosis factor. Latriki 1989;55:143-150 (Greek). Submitted by Yehudi M. Felman, M.D., Brooklyn, N.Y.
Cameo
Acquired Varicose Veins of the Penis FRANCESCO DRAGO, M.D., AND ALFREDO REBORA, M.D.
From the Department of Dermatology, University of Genoa, Genoa, Italy.
A
40-year-old man presented with several bluish nodules on his penis of 1 year's duration. They were not preceded by any trauma and alarmed the patient by the obvious deformity and the pain that gradually began both spontaneously and under pressure. The nodules disappeared when he developed an erection, but this proved troublesome. On examination, there were more than 20 0.5-1 cm wide bluish nodules located along the course of the superficial veins of the penile shaft (Fig. 1). They were tender and easily depressed. They reappeared immediately after pressure was released. The patient was in good general condition. No other vascular abnormalities were apparent. In particular, there were no varicose veins on his legs nor any personal or family history of venous thrombosis. Routine laboratory findings were normal. Histopathology revealed only a dilation of vessels (Fig. 2). Direct immunofluorescence did not detect any immunoglobulin or complement deposit in the vessel walls. Sonography and computed tomographic scan failed to reveal any abdominal, pelvic, or testicular change or any compression on the large vessels. Doppler fluximeter examination of iliac veins, lower cava, penis vessels, and spermatic arteries were normal and excluded any arteriovenous shunt. Consent for sclerotherapy was not granted.
ease of the deep veins and generally have a benign course. Varicosities that occur secondary to the obstruction of the deep venous system have a much more severe prognosis. In primary varicosities, the etiology remains obscure, although hormonal factors in women, increased abdominal pressure, and in rare cases, arterio-
Comment Although the differential diagnosis of multiple glomangiomas could have been made because of the nodules of our patient, their histopathology and behavior during erection ruled it out and confirmed the diagnosis of phlebectasias. Varicose veins may be primary or secondary. Primary varicose veins occur in the absence of any dis-
Address correspondence to: Alfredo Rebora, M.D., Department of Dermatology, University of Genoa, Genoa, Italy.
FiG. 1. Bluish nodules along the superficial veins of the shaft.
352
VARICOSE VEINS OF THE PENIS
No. 5
venous shunts have been claimed to aggravate the condition. Also inheritance may play a role and a congenital absence of valves has been supposed. In fact, an abnormal weakening of the valve commissures has been found.^ The interesting factor in this case the unusual location of the varicosity. Only in two instances, one congenitaP and one acquired,"* was the penis reported to be affected by varicosities, and in both of these the glans penis and not the shaft was involved. In our patient the glans was normal, while varicosities fol-
Drago and Rebora
353
lowed the course of the venous branches of the shaft. Their occurrence in adult life, their absence at birth, and the normality of laboratory findings account for the title of primary acquired varicose veins of the penis. Penile venous system can be divided into a superficial and a deep system that intercommunicate. The first system receives blood from the skin and the penis envelope, while the second, which is provided with valves, is fed by the cavernous tissues.'' Although prolonged sitting of our patient while he was at work may have contributed to induce hypertension in the abdominal venous trunks, a congenital hypoplasia of the deep vessel walls or the absence of valves should be considered for explaining the overloading of the superficial plexus that results in varicosity. In any case, there is no obvious reason for the condition, and we hope other reports will help to elucidate its cause. References
FIG. 2.
Histopathology reveals a simple dilation of the vein.
1. Edwards )E, Edwards EA. The saphenous valves in varicose veins Am Heart J. 1940;19:338-351. 2. Kouskouskis CE. Stump the experts—case report-resolution: venous lakes. J Dermatol Surg Oncol. 1983;9:110-165. 3. Balato N, Montanaro M, Lembo G. Acquired phlebectasia of the glans penis. J Am Acad Dermatol. 1985;13:824-826. 4. Testut L, Latarjet A. "Anatomia Umana" 5° Ed. UTET, Torino, 1969;6:313-315.
Tumor Necrosis Factor
ln response to invasive stimuli (microbial pathogens and their products or neoplasms), macrophages secrete, besides other cytokines, cachectin (tumor necrosis factor—TNF) a multipotent lymphokine with important immune and metabolic properties. TNF was originally described as a mediator of lipopolysaccharide-induced hemorrhagic necrosis of tumors but recent studies have shown that TNF is the same molecule as cachectin and has a wide spectrum of biologic properties in addition to the inhibition of tumor cell growth. These properties include the inhibition of lipoprotein lipase activity and the suppression of adipocyte gene expression, activities that lead to the wasting (cachexia) that accompanies chronic invasive disease states. Cachectin has also been shown to play a major role in the pathogenesis of Gram-negative (endotoxin-induced) shock and is responsible for most of the deleterious effects of endotoxinemia (hypotension, metabolic acidosis disseminated intravascular coagulation and their consequences) which may lead to death. In addition, cachectin has emerged as a general mediator of the acute phase response (e.g. it induces the production of interferons and interleukin-1 by macrophages) and, besides their direct antimicrobial or antineoplastic effects, a variety of recent observations suggest that this macrophage-hormone may have a significant role in the pathogenesis of inflammation and may play an important part in diverse human disease processes. In this review the authors discuss the biological properties and actions of cachectin, its role in the pathogenesis of inflammation, cachexia, tumor necrosis and endotoxic shock and its probable use as an antineoplastic or antiinflammatory agent.—Pardahs G. Gachectin or tumor necrosis factor. Latriki 1989;55:143-150 (Greek). Submitted by Yehudi M. Felman, M.D., Brooklyn, N.Y.
