INCIDENCE K. M. N. C.
OF TESTICULAR MICROLITHIASIS
HijBARTH, M.D. SUSANI, M.D. SZABO, M.D. KRATZIK, M.D.
From the Departments of Urology and Pathology, University of Vienna Medical School, Vienna, Austria ABSTRACT-In adults polytopic intratubular calcifications of the testes are rare. Known as testicular microlithiasis, they manifest themselves in a characteristic echo pattern on sonography with high-frequency transducers (5 to 10 MHz). This consists of multiple echogenic specks in an otherwise normal testicular parenchyma. In a retrospective analysis of 1,710 testicular sonograms of adults, bilateral intratesticular microliths were found in 11 cases (0.6%). In 5 of them, the microliths were associated with a testicular tumor. One patient with a tumor in the contralateral testis had undergone radiotherapy and another one presented with hypogonadism. Four patients with noncontributory histories presented with varicocele or epididymal cyst. Sonographic findings were confirmed histologically in 6 patients. Multiple intratubular calcifications were found in all of them. The pathogenesis of testicular microliths is still poorly understood. Their clinical relevance is unclear, but their incidence in adults appears to be higher than reported in the literature.
Testicular microlithiasis, i.e., the presence of polytopic intratubular calcifications, is a rare condition. Its pathogenesis is controversial, and its clinical relevance is unclear. Although only sporadically reported in adults, 1-5 testicular calcifications appear to be more common in children and tend to be associated with cryptorchidisms-l1 or Klinefelter syndrome.12J3 Their occurrence in otherwise normal prepuberal testes also has been reported.‘J?J4J5 Testicular microliths also have been found in association with similar calcifications of the lung and the central nervous system.4J0 While microcalcifications may be implicated in male infertility,3 a causal relationship has not been established because of the small number of cases reported. In a retrospective evaluation of 11 adults presenting with the typical pattern of microlithiasis on testicular sonography, we have tried to correlate these rare intratesticular abnormalities with clinical and associated pathologic findings (Fig. 1). Material and Methods In an analysis of 1,710 testicular sonograms evidence of microlithiasis was found in 11 pa-
464
tients (0.6%). Mean patient age was 27.1 years (range, 20 to 47 years). Sonography was done by sector scanning with a high-frequency transducer (7.5-10 MHz; Ultramark 4, Squibb Medical Systems). Mean follow-up time was 15.9
FIGURE 1.
and typical lithiasis.
UROLOGY
I
Transverse scan shows testicular tumor echopattern of peritumoral micro-
NOVEMBER
1992 / VOLUME 40, NUMBER 5
TABLE I. Clinical and pathologic findings on 11 patients with sonographically demonstrated testicular microlithiasis
FIGURE 2. Ultrasound image of testicular microlithiasis (10 MHz transducer). Bilateral appearance of multiple echogenic foci in otherwise normal testes.
months (range 2 to 49 months). At the time of diagnosis, all patients were screened for testicular tumor markers (AFP, NSE, /3-HCG), and they underwent retroperitoneal sonography as well as chest x-ray examinations. To rule out fertility problems spermatograms were obtained and serum hormones (T, LH, FSH, E2, and P) were determined. All patients were followed up by somography, which was scheduled as dictated by the tumor follow-up program in patients with testicular tumors and twice yearly in all other patients. Results In all patients sonograms showed a speckled pattern of multiple echogenic intratesticular bodies, which were bilateral throughout (Fig. 2). The clinical signs and symptoms associated with the micro-calcifications are shown in Table I. Histologic confirmation of the sonographic diagnosis based on light microscopy of tissue blocks (hematoxylin and eosin stain) was available in 6 patients. In 5 patients with testicular tumors the peritumoral testicular parenchyma showed areas of atrophy. Spermatogenesis was either absent or arrested at the spermatocyte stage. Some tubules were packed with concentric spherical calcifications with their bases in contact with the myoepithelium. In some segments, the atrophic tubules, which contained remmants of normal spermatogonia with interspersed atypical germinal cells, showed thickening of the wall due to myoepithelial cell proliferation. Leydig cell hyperplasia was present in 2 patients (Figs. 3-5).
UROLOGY
/ NOVEMBER1992
/ VOLUME40,NUMBER5
Pt. Age (Yrs.)
Clinical/Pathologic signs
25 45 20 20 47
Seminoma Seminoma Teratoma Seminoma/teratoma St. p. semicastration (seminoma) and irradiation Hypogonadismloligospermia Varicocele left Cyst in spermatic cord
36 20 38 25 44 20
Cyst in epididymis Cyst in epididymis Seminoma
FIGURE 3. Peritumoral testicular parenchyma with intratubular microlith (arrow). Considerably reduced spermatogenesis and Leydig cell hyperplasia (arrow) (hematoxylin and eosin, original magnification x 40).
FIGURE 4. Atrophic testicular tubule with hyaline border (arrow) and central calcification (hematoxylin and eosin, original magnification x 200).
465
FIGURE 5. Intratubular microlith, atrophic germinal epithelium, with predominant Sertoli cells and some spermatogonia (hematoxylin and eosin, original magnification x 200).
Testicular biopsy obtained in a patient undergoing surgery for an epididymal cyst showed similar tubular calcifications, but spermatogenesis was normal, and there were no signs of tubular atrophy. In the patients with testicular tumors, follow-up sonograms showed the calcifications in the contralateral testis to be unchanged throughout. Except in 1 patient with hypogonadism and oligospermia, the testicular volume was normal. The remaining 4 patients did not show any signs of infertility, i.e., both spermatograms and hormone levels were within the normal range. None of our 11 patients had a history of cryptorchidism or inflammatory urogenital disease. All patients were followed up by sonography at regular intervals. The testicular echo pattern did not change in any case. The speckled appearance typical of microlithiasis was present throughout. In none of the patients did testicular tumors develop. Comment While calcifications have often been reported in patients with testicular tumors, the occurrence of bilateral intratubular microliths (testicular microlithiasis) presenting a distinct and typical sonographic appearance is rare. In about 74 percent of caseP testicular tumors have been reported to be associated with calcifications. These tend to be localized in the periphery of the tumor and present as psammoma bodies, i.e., calcifications in the seminiferous tubules of the compressed and degenerated peritumoral testicular tissue, or as dystrophic calcifications in necrotic tumor tissue. Cartilage or bone fragments in teratomas also have been described.” In our 5 patients with testicular tumors sonography showed the microcalcifi466
cations to be scattered throughout both tumorbearing and contralateral testes. While a relationship with the neoplastic disease cannot be ruled out altogether, it would appear to be rather unlikely. Dystrophic calcifications also have been reported to occur in patients with compromised testicular blood flow and in those with inflammatory conditions associated with abscess formation and with tuberculous lesions. Nonmalignant testicular conditions were found to be associated with microcalcifications in no less than 16 percent of cases.le However, all of these calcifications tend to be unilateral and isolated, and they are distinct from those seen in testicular microlithiasis, which diffusely involves both testes. Similar calcifications have been found to occur after cytostatic chemotherapy or radiotherapy for testicular tumors in the contralatera1 testis.18 These were present in one of our patients undergoing external radiation of a testicular tumor. A causal relationship with radiotherapy, therefore, cannot be excluded. The relationship, if any, of testicular microlithiasis and infertility is still unclear. In the literature a case with oligospermia is described in a twenty-five-year-old man with only one functional testis and an atrophic nondescended testis contralaterally. It has been suggested that, in patients with below-normal tubular diameter, the concrement may obstruct the seminiferous tubules and thus interfere with fertility.‘O Calcifications were also described in another oligospermic patient with contralateral cryptorchidism, who was on a clomiphene citrate regimen and a testicular tumor developed six months later. l0 The occurrence of testicular tumors during hormone therapy has been reported in several studies.20-22 Whether or not microlithiasis is related to the neoplastic disease in these cases is still unclear. In our cases oligospermia in association with hypogonadism was seen only once. As the findings on spermatograms of the other 4 patients were normal, a causal role of microlithiasis in the development of infertility would appear to be unlikely. In a large-scale study of prematures, newborns, and infants, Hornstein and Hedinger” found intratesticular spherical hyaline tubular bodies to be present in 51.4 percent of cases. Usually single, these bodies consisted of proteins and mucupolysaccharides. Their pathogenesis is poorly understood. Liquefaction of tubular
UROLOGY
/ NOVEMBER1992
/ VOLUME40,NUMBER5
References
cells,23 degeneration of spermatogonia,8 or abnormal Sertoli cell activityz4 have all been implicated. But these bodies appear to be condensations of undifferentiated secretory tubular cells” and even have been suggested to be normal for the fetal testes in some reports.7,s Structures similar to these hyaline bodies, but with a lamellar organization and with calcifications are much less commonly seen5*z5~zeand have been interpreted to reflect testicular malposition or ma1f0rmati0n.” The incidence of testicular microlithiasis in adults is unknown. Various mechanisms have been implicated in its pathogenesis. Microliths were thought to develop from degenerated spermatogonia in the tubular lumen14 and by secondary calcification of glycoproteins secreted in the tubules.6~g The concept of ectopic oocytes in dysgenetic testesI lacks credibility, because microcalcifications also occur in entirely normal testes. * Some authors found these calcifications to be present in dilated tubular segments. 27While they may be a sign of testicular immaturity, 28 this would not explain their occurrence in adults with normal testicular function and normal fertility. Cell degeneration of unknown origin with failure of Sertoli cell phagocytosis or tubular expulsion of the degenerated cells and secondary calcification2g also has been considered. As an association with pulmonary microlithiasis has been reported in some cases4 systemic disease has been suggested equally as a possible cause. The true pathogenesis of testicular microlithiasis remains to be unraveled. Its clinical implications in adults are unclear, because there is no evidence of a consistent association with infertility or neoplastic disease. Nevertheless, the detection of testicular calcifications should prompt a complete diagnostic workup to rule out associated malignancies, infertility, or systemic disease. The incidence of testicular microlithiasis appears to be much higher than originally assumed. In light of this, sonography plays a valuable role, because it permits its noninvasive detection and documentation. To evaluate its true incidence and its pathogenetic importance, further prospective trials with routine sonographic screening particularly of patients with fertility problems would appear to be desirable. Urologische
UROLOGY
: NOVEMBER
1. Doherty FJ, et al: Testicular microlithiasis: a unique sonographic appearance, J Ultrasound Med 6: 398 (1987). 2. Klinz C, and Hartmann M: Bilaterale multizentrische Hodenkonkremente bei Carney-Syndrom, Akt Uro122: 51 (1991). 3. Schantz A, and M&ten R: Testicular microlithiasis with sterility, Fertil Steril 27: 801 (1976). 4. Coetzee T: Pulmonary alveolar microlithiasis with involvement of the sympathetic nervous system and gonads, Thorax 25: 637 (1970). 5. Oiye T: iiber anscheinend noch nicht beschriebene Steinchen in den menschlichen Hoden, Beitr Path01 Anat 89: 479 (1928). 6. Bieger RC, Passarge E, and McAdams AJ: Testicular intratubular bodies, J Clin Endocrinol25: 1340 (1965). 7. Sniffen RC: The testis: I. The normal testis. Arch Path01 50: 259 (1950). 8. Sohval AR: Histopathology of cryptorchidism. A study based upon the comparative histology of retained and scrotal testes from birth to maturity, Am J Med 16: 346 (1954). 9. Weinberg AG, Currarino G, and Stone IC Jr: Testicular microlithiasis. Arch Path01 95: 312 (1973). 10. Nistal M, Paniagua R, and Diez-Pardo JA: Testicular microlithiasis in 2 children with bilateral cryptorchidism, J Urol 121: 535 (1979). 11. Hornstein B, and Hedinger CR: Spharische intratubulare Korperchen im prapuberalen Hoden und Nebenhoden, Virchows Arch Path01 Anat 339: 83 (1965). 12. Bunge RG, and Bradbury JT: Intratubular bodies of the human testis, J Uro185: 306 (1961). 13. Lanman JT, et al: Klinefelter’s syndrome in a ten-monthold mongolian idiot, report of a case with chromosome analysis, N Engl J Med 263: 887 (1960). 14. Blumensaat C: Uber einen neuen Befund im Knabenhoden, Virchows Arch Path01 Anat 273: 51 (1929). 15. Henke F, and Lubarsch 0: Harnorgane, Mannliche Geschlechtsorgane, Handbuch der speziellen pathologischen Anatomie und Histologie, Berlin, J. Springer, 1931, p 601. 16. Ikinger U, et al: Microcalcifications in testicular malienancv. Urolow 5: 525 (1982). -17. Wurster-‘K, and ‘Menges V: Mikroverkalkungen bei testikularen Keimzellgeschwiilsten, Virchows Arch [A] 374: 45 (1977). 18. Weber M, et al: Fokale Hodenparenchymveranderungen nach Polychemotherapie and Radiatio, Ultraschall Klin Prax 5: 200 (1990). 19. Salisz JA, and Goldman KA: Testicular calcifications and neoplasia in patient treated for subfertility, Steril Fertil 6: 557 (1990). 20. Nilsson A, and Nilsson S: Testicular germ cell tumors after clomiphene therapy for subfertility, J Urol 134: 560 (1985). 21. Reyes FI, and Faiman C: Development of a testicular tumor during cisclomiphene therapy, Can Med Assoc J 109: 502 (1973). 22. Neoptolemos JP, Locke TJ, and Fossard DP: Testicular tumor associated with hormonal treatment for oligospermia, Lancet 2: 754 (1981). 23. Crewe FAE, and Fell HB: The nature of certain ovum-like bodies found in the seminiferous tubules, Quart J mier Sci 66: 557 (1922). 24. Azzopardi JG, Mostofi FK, and Theiss EA: Lesions of testis in certain patients with widespread choriocarcinoma and related tumours, Am J Path01 38: 207 (1961). 25. Saller K: Das Vorkommen von Steinchen im menschlichen Hoden, Anat Anz 69: 239 (1930). 26. Altmann F: Uber Eunuchoidismus, Virchows Arch Path01 Anat 276: 445 (1930). 27. Huber R, Weber E, and Hedinger C: Struktur intratubularer Korperchen (sog. Ringtubuli) des kindlichen Hodens, Virchow Arch [A] 344: 40 (1968). 28. Priebe CJ, and Garret R: Testicular calcification in a 4year-old boy, Pediatrics 46: 785 (1970). 29. Vegni-Talluri M, et al: Testicular microliths: their origin and structure, J Urol 124: 105 (1980).
Universitatsklinik Wien Alserstrasse 4 A-1090 Vienna, Austria (DR. HOBARTH)
1992
/ VOLUME
40, NUMBER
5
467
OF TESTICULAR MICROLITHIASIS
HijBARTH, M.D. SUSANI, M.D. SZABO, M.D. KRATZIK, M.D.
From the Departments of Urology and Pathology, University of Vienna Medical School, Vienna, Austria ABSTRACT-In adults polytopic intratubular calcifications of the testes are rare. Known as testicular microlithiasis, they manifest themselves in a characteristic echo pattern on sonography with high-frequency transducers (5 to 10 MHz). This consists of multiple echogenic specks in an otherwise normal testicular parenchyma. In a retrospective analysis of 1,710 testicular sonograms of adults, bilateral intratesticular microliths were found in 11 cases (0.6%). In 5 of them, the microliths were associated with a testicular tumor. One patient with a tumor in the contralateral testis had undergone radiotherapy and another one presented with hypogonadism. Four patients with noncontributory histories presented with varicocele or epididymal cyst. Sonographic findings were confirmed histologically in 6 patients. Multiple intratubular calcifications were found in all of them. The pathogenesis of testicular microliths is still poorly understood. Their clinical relevance is unclear, but their incidence in adults appears to be higher than reported in the literature.
Testicular microlithiasis, i.e., the presence of polytopic intratubular calcifications, is a rare condition. Its pathogenesis is controversial, and its clinical relevance is unclear. Although only sporadically reported in adults, 1-5 testicular calcifications appear to be more common in children and tend to be associated with cryptorchidisms-l1 or Klinefelter syndrome.12J3 Their occurrence in otherwise normal prepuberal testes also has been reported.‘J?J4J5 Testicular microliths also have been found in association with similar calcifications of the lung and the central nervous system.4J0 While microcalcifications may be implicated in male infertility,3 a causal relationship has not been established because of the small number of cases reported. In a retrospective evaluation of 11 adults presenting with the typical pattern of microlithiasis on testicular sonography, we have tried to correlate these rare intratesticular abnormalities with clinical and associated pathologic findings (Fig. 1). Material and Methods In an analysis of 1,710 testicular sonograms evidence of microlithiasis was found in 11 pa-
464
tients (0.6%). Mean patient age was 27.1 years (range, 20 to 47 years). Sonography was done by sector scanning with a high-frequency transducer (7.5-10 MHz; Ultramark 4, Squibb Medical Systems). Mean follow-up time was 15.9
FIGURE 1.
and typical lithiasis.
UROLOGY
I
Transverse scan shows testicular tumor echopattern of peritumoral micro-
NOVEMBER
1992 / VOLUME 40, NUMBER 5
TABLE I. Clinical and pathologic findings on 11 patients with sonographically demonstrated testicular microlithiasis
FIGURE 2. Ultrasound image of testicular microlithiasis (10 MHz transducer). Bilateral appearance of multiple echogenic foci in otherwise normal testes.
months (range 2 to 49 months). At the time of diagnosis, all patients were screened for testicular tumor markers (AFP, NSE, /3-HCG), and they underwent retroperitoneal sonography as well as chest x-ray examinations. To rule out fertility problems spermatograms were obtained and serum hormones (T, LH, FSH, E2, and P) were determined. All patients were followed up by somography, which was scheduled as dictated by the tumor follow-up program in patients with testicular tumors and twice yearly in all other patients. Results In all patients sonograms showed a speckled pattern of multiple echogenic intratesticular bodies, which were bilateral throughout (Fig. 2). The clinical signs and symptoms associated with the micro-calcifications are shown in Table I. Histologic confirmation of the sonographic diagnosis based on light microscopy of tissue blocks (hematoxylin and eosin stain) was available in 6 patients. In 5 patients with testicular tumors the peritumoral testicular parenchyma showed areas of atrophy. Spermatogenesis was either absent or arrested at the spermatocyte stage. Some tubules were packed with concentric spherical calcifications with their bases in contact with the myoepithelium. In some segments, the atrophic tubules, which contained remmants of normal spermatogonia with interspersed atypical germinal cells, showed thickening of the wall due to myoepithelial cell proliferation. Leydig cell hyperplasia was present in 2 patients (Figs. 3-5).
UROLOGY
/ NOVEMBER1992
/ VOLUME40,NUMBER5
Pt. Age (Yrs.)
Clinical/Pathologic signs
25 45 20 20 47
Seminoma Seminoma Teratoma Seminoma/teratoma St. p. semicastration (seminoma) and irradiation Hypogonadismloligospermia Varicocele left Cyst in spermatic cord
36 20 38 25 44 20
Cyst in epididymis Cyst in epididymis Seminoma
FIGURE 3. Peritumoral testicular parenchyma with intratubular microlith (arrow). Considerably reduced spermatogenesis and Leydig cell hyperplasia (arrow) (hematoxylin and eosin, original magnification x 40).
FIGURE 4. Atrophic testicular tubule with hyaline border (arrow) and central calcification (hematoxylin and eosin, original magnification x 200).
465
FIGURE 5. Intratubular microlith, atrophic germinal epithelium, with predominant Sertoli cells and some spermatogonia (hematoxylin and eosin, original magnification x 200).
Testicular biopsy obtained in a patient undergoing surgery for an epididymal cyst showed similar tubular calcifications, but spermatogenesis was normal, and there were no signs of tubular atrophy. In the patients with testicular tumors, follow-up sonograms showed the calcifications in the contralateral testis to be unchanged throughout. Except in 1 patient with hypogonadism and oligospermia, the testicular volume was normal. The remaining 4 patients did not show any signs of infertility, i.e., both spermatograms and hormone levels were within the normal range. None of our 11 patients had a history of cryptorchidism or inflammatory urogenital disease. All patients were followed up by sonography at regular intervals. The testicular echo pattern did not change in any case. The speckled appearance typical of microlithiasis was present throughout. In none of the patients did testicular tumors develop. Comment While calcifications have often been reported in patients with testicular tumors, the occurrence of bilateral intratubular microliths (testicular microlithiasis) presenting a distinct and typical sonographic appearance is rare. In about 74 percent of caseP testicular tumors have been reported to be associated with calcifications. These tend to be localized in the periphery of the tumor and present as psammoma bodies, i.e., calcifications in the seminiferous tubules of the compressed and degenerated peritumoral testicular tissue, or as dystrophic calcifications in necrotic tumor tissue. Cartilage or bone fragments in teratomas also have been described.” In our 5 patients with testicular tumors sonography showed the microcalcifi466
cations to be scattered throughout both tumorbearing and contralateral testes. While a relationship with the neoplastic disease cannot be ruled out altogether, it would appear to be rather unlikely. Dystrophic calcifications also have been reported to occur in patients with compromised testicular blood flow and in those with inflammatory conditions associated with abscess formation and with tuberculous lesions. Nonmalignant testicular conditions were found to be associated with microcalcifications in no less than 16 percent of cases.le However, all of these calcifications tend to be unilateral and isolated, and they are distinct from those seen in testicular microlithiasis, which diffusely involves both testes. Similar calcifications have been found to occur after cytostatic chemotherapy or radiotherapy for testicular tumors in the contralatera1 testis.18 These were present in one of our patients undergoing external radiation of a testicular tumor. A causal relationship with radiotherapy, therefore, cannot be excluded. The relationship, if any, of testicular microlithiasis and infertility is still unclear. In the literature a case with oligospermia is described in a twenty-five-year-old man with only one functional testis and an atrophic nondescended testis contralaterally. It has been suggested that, in patients with below-normal tubular diameter, the concrement may obstruct the seminiferous tubules and thus interfere with fertility.‘O Calcifications were also described in another oligospermic patient with contralateral cryptorchidism, who was on a clomiphene citrate regimen and a testicular tumor developed six months later. l0 The occurrence of testicular tumors during hormone therapy has been reported in several studies.20-22 Whether or not microlithiasis is related to the neoplastic disease in these cases is still unclear. In our cases oligospermia in association with hypogonadism was seen only once. As the findings on spermatograms of the other 4 patients were normal, a causal role of microlithiasis in the development of infertility would appear to be unlikely. In a large-scale study of prematures, newborns, and infants, Hornstein and Hedinger” found intratesticular spherical hyaline tubular bodies to be present in 51.4 percent of cases. Usually single, these bodies consisted of proteins and mucupolysaccharides. Their pathogenesis is poorly understood. Liquefaction of tubular
UROLOGY
/ NOVEMBER1992
/ VOLUME40,NUMBER5
References
cells,23 degeneration of spermatogonia,8 or abnormal Sertoli cell activityz4 have all been implicated. But these bodies appear to be condensations of undifferentiated secretory tubular cells” and even have been suggested to be normal for the fetal testes in some reports.7,s Structures similar to these hyaline bodies, but with a lamellar organization and with calcifications are much less commonly seen5*z5~zeand have been interpreted to reflect testicular malposition or ma1f0rmati0n.” The incidence of testicular microlithiasis in adults is unknown. Various mechanisms have been implicated in its pathogenesis. Microliths were thought to develop from degenerated spermatogonia in the tubular lumen14 and by secondary calcification of glycoproteins secreted in the tubules.6~g The concept of ectopic oocytes in dysgenetic testesI lacks credibility, because microcalcifications also occur in entirely normal testes. * Some authors found these calcifications to be present in dilated tubular segments. 27While they may be a sign of testicular immaturity, 28 this would not explain their occurrence in adults with normal testicular function and normal fertility. Cell degeneration of unknown origin with failure of Sertoli cell phagocytosis or tubular expulsion of the degenerated cells and secondary calcification2g also has been considered. As an association with pulmonary microlithiasis has been reported in some cases4 systemic disease has been suggested equally as a possible cause. The true pathogenesis of testicular microlithiasis remains to be unraveled. Its clinical implications in adults are unclear, because there is no evidence of a consistent association with infertility or neoplastic disease. Nevertheless, the detection of testicular calcifications should prompt a complete diagnostic workup to rule out associated malignancies, infertility, or systemic disease. The incidence of testicular microlithiasis appears to be much higher than originally assumed. In light of this, sonography plays a valuable role, because it permits its noninvasive detection and documentation. To evaluate its true incidence and its pathogenetic importance, further prospective trials with routine sonographic screening particularly of patients with fertility problems would appear to be desirable. Urologische
UROLOGY
: NOVEMBER
1. Doherty FJ, et al: Testicular microlithiasis: a unique sonographic appearance, J Ultrasound Med 6: 398 (1987). 2. Klinz C, and Hartmann M: Bilaterale multizentrische Hodenkonkremente bei Carney-Syndrom, Akt Uro122: 51 (1991). 3. Schantz A, and M&ten R: Testicular microlithiasis with sterility, Fertil Steril 27: 801 (1976). 4. Coetzee T: Pulmonary alveolar microlithiasis with involvement of the sympathetic nervous system and gonads, Thorax 25: 637 (1970). 5. Oiye T: iiber anscheinend noch nicht beschriebene Steinchen in den menschlichen Hoden, Beitr Path01 Anat 89: 479 (1928). 6. Bieger RC, Passarge E, and McAdams AJ: Testicular intratubular bodies, J Clin Endocrinol25: 1340 (1965). 7. Sniffen RC: The testis: I. The normal testis. Arch Path01 50: 259 (1950). 8. Sohval AR: Histopathology of cryptorchidism. A study based upon the comparative histology of retained and scrotal testes from birth to maturity, Am J Med 16: 346 (1954). 9. Weinberg AG, Currarino G, and Stone IC Jr: Testicular microlithiasis. Arch Path01 95: 312 (1973). 10. Nistal M, Paniagua R, and Diez-Pardo JA: Testicular microlithiasis in 2 children with bilateral cryptorchidism, J Urol 121: 535 (1979). 11. Hornstein B, and Hedinger CR: Spharische intratubulare Korperchen im prapuberalen Hoden und Nebenhoden, Virchows Arch Path01 Anat 339: 83 (1965). 12. Bunge RG, and Bradbury JT: Intratubular bodies of the human testis, J Uro185: 306 (1961). 13. Lanman JT, et al: Klinefelter’s syndrome in a ten-monthold mongolian idiot, report of a case with chromosome analysis, N Engl J Med 263: 887 (1960). 14. Blumensaat C: Uber einen neuen Befund im Knabenhoden, Virchows Arch Path01 Anat 273: 51 (1929). 15. Henke F, and Lubarsch 0: Harnorgane, Mannliche Geschlechtsorgane, Handbuch der speziellen pathologischen Anatomie und Histologie, Berlin, J. Springer, 1931, p 601. 16. Ikinger U, et al: Microcalcifications in testicular malienancv. Urolow 5: 525 (1982). -17. Wurster-‘K, and ‘Menges V: Mikroverkalkungen bei testikularen Keimzellgeschwiilsten, Virchows Arch [A] 374: 45 (1977). 18. Weber M, et al: Fokale Hodenparenchymveranderungen nach Polychemotherapie and Radiatio, Ultraschall Klin Prax 5: 200 (1990). 19. Salisz JA, and Goldman KA: Testicular calcifications and neoplasia in patient treated for subfertility, Steril Fertil 6: 557 (1990). 20. Nilsson A, and Nilsson S: Testicular germ cell tumors after clomiphene therapy for subfertility, J Urol 134: 560 (1985). 21. Reyes FI, and Faiman C: Development of a testicular tumor during cisclomiphene therapy, Can Med Assoc J 109: 502 (1973). 22. Neoptolemos JP, Locke TJ, and Fossard DP: Testicular tumor associated with hormonal treatment for oligospermia, Lancet 2: 754 (1981). 23. Crewe FAE, and Fell HB: The nature of certain ovum-like bodies found in the seminiferous tubules, Quart J mier Sci 66: 557 (1922). 24. Azzopardi JG, Mostofi FK, and Theiss EA: Lesions of testis in certain patients with widespread choriocarcinoma and related tumours, Am J Path01 38: 207 (1961). 25. Saller K: Das Vorkommen von Steinchen im menschlichen Hoden, Anat Anz 69: 239 (1930). 26. Altmann F: Uber Eunuchoidismus, Virchows Arch Path01 Anat 276: 445 (1930). 27. Huber R, Weber E, and Hedinger C: Struktur intratubularer Korperchen (sog. Ringtubuli) des kindlichen Hodens, Virchow Arch [A] 344: 40 (1968). 28. Priebe CJ, and Garret R: Testicular calcification in a 4year-old boy, Pediatrics 46: 785 (1970). 29. Vegni-Talluri M, et al: Testicular microliths: their origin and structure, J Urol 124: 105 (1980).
Universitatsklinik Wien Alserstrasse 4 A-1090 Vienna, Austria (DR. HOBARTH)
1992
/ VOLUME
40, NUMBER
5
467
