(Purpose) Controversy exists on how to diagnose the vanishing testis and the degree of investigation required. In this series, we reviewed anatomical and histological findings in vanishing testes and investigated the effectiveness of diagnostic laparoscopy and imaging studies.
(Materials and Methods) Between 1974 and March 1999, 107 boys with nonpalpable testis underwent surgery. Of the total, 52 had spermatic vessels, vas deferens, and/or nubbin, and as a result the diagnosis of vanishing testis was made.
(Results) The affected side of vanishing testis was left 41, right 9 and bilateral 2.35 nubbins were found and the lengths of 24 nubbins were 5mm or less. Histological examinations were performed in 43 cases including 27 nubbins. From that total, 31 had vas deferens and 11 had epididymis. Only two nubbins had seminiferous tubules but they included no germ cells. The two nubbins were greater than 5mm long. Laparoscopic surgery was undertaken in 12 separate cases of the vanishing testis and as a result hypoplastic spermatic vessels were present in 7 of the 12 cases.
(Conclusion) The incidence of viable testicular tissue in vanishing testes was 4.7% in our series and it ranges from 0-16% in other series. We submit that one can diagnose the inguinal vanishing testis with preoperative imaging and laparoscopy, and that the nubbin seldom contains testicular tissue. Our results do not support the necessity to remove nubbins.

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(Background) Luteinizing hormone-releasing hormone (LHRH) agonists are popullary used drugs in the treatment of prostatic cancer. However, it has been reported that continuation of a low testosterone level following a longterm administration of these drugs reduces the bone mineral density and makes for osteoporosis, which is accountable for fracture. we measured the bone mineral density and bone metabolic markers in the cases who suffered fracture receiving LHRH agonists for prostatic cancer.
(Patients and Methods) Between 1994 and 1998, 196 patients (mean age 78.1 years) were treated with LHRH agonists for prostatic cancer. Of these patients, 13 (7%) who had bone fracture during treated with LHRH agonists were divided into fracture group, and 70 patients who had not bone fracture devided into non-fracture group. Fracture by traffic accident was excluded. The bone density in the third lumbar vertebra was measured using quantitative computed tomography (QCT). Osteocalcin, 1, 25-(OH)₂ vitamin D, urinary type 1 collagen cross-linked N-telopeptides (NTx), parathyroid hormone (PTH) and calcitonin were measured as bone metabolic markers.
(Results) The mean age of fractured cases was 78 years. The period from the start of treatment to fracture was 11 to 45 months (mean 27 months). No case of fracture at the site of metastasis of prostatic cancer was found. The bone density was significantly low in the fracture group compared with that of non-fracture group. Of the bone metabolic markers, NTx showed high values in the fracture group.
(Conclusion) There is a need to measure bone mineral density and bone metabolic markers periodically and to evaluate secondary osteoporosis in the patients receiving LHRH agonists for prostatic cancer.

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(Purpose) The determinations of oxalate in urine and plasma are important in the evaluation and treatment of patients with calcium oxalate nephrolithiasis. Although many analytical methods for determining oxalate have been developed, most of them need complicated sample preparation, and are expensive for routine examination. Especially for estimation of plasma oxalate, much more sensitive measurement is required because of the extremely low concentration. A simple and rapid assay for oxalate in urine and plasma by capillary electrophoresis has been described here, and utilized for assessment of renal oxalate clearance. In addition, simultanous determination of urinary oxalate and citrate was developed.
(Methods) A Waters Quanta 4000E system was used with a detection at 185nm. Separation was obtained on a fused silica capillary, 60cm long×75μm and 100μm (i. d.) for urine and plasma samples respectively. Urine samples were diluted with 60mM hydrochloric acid, and ultrafiltrates of plasma were acidified and diluted with 300mM boric acid and 50mM phosphoric acid.
(Results) The intraassay coefficient variation was 2.7-4.0% for urinary oxalate, and 1.3-3.9% for citrate. The mean recovery ratio of 0.2mM oxalate and 1.0mM citrate added to 10 samples were 99.0% (92.6-107.4%) and 98.4% (91.2-103.9%), respectively. In the determination of plasma oxalate, the minimum detectable limit was 0.9μM, the coefficient variation was 5.8-16.0%, and the recovery rate was 101.5% (87.8-125.6%). The plasma oxalate levels in 8 adult males were 2.39±1.46μM (Mean±SD). Renal oxalate clearances with one hour method were 72.9±20.0ml/min in 6 healthy controls and 83.2±27.8ml/min in 8 stone formers. Oxalate/creatinine clearance ratios in each groups were 0.70±0.16 and 1.11±0.34 respectively.
(Conclusion) The simultaneous determination of urinary oxalate and citrate was satisfactory. Capillary electrophoresis is suited for routine examination of urinary oxalate and citrate with the advantage on simplicity and economy. The assay of plasma oxalate by this method was also acceptably sensitive, specific under a low temperature and an acidifacation.

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(Objectives) The incidence of flutamide-induced liver toxicity was studied in 30 consecutive patients with prostate cancer who were treated with total androgen blockage (TAB) therapy (luteinizing hormone releasing hormone [LHRH] analogue and flutamide) in our hospital during the last 3 years and in 20 consecutive patients with prostate cancer who were treated by partial androgen blockage (PAB) therapy (LHRH analogue alone).
(Methods) Liver function test, including measurement of serum levels of aspartate aminotransferase (AST) alanine aminotransferase (ALT), total cholesterol, total bilirubin, γ-glutamyl transpeptidase (γ-GTP), and cholinesterase were performed at regular interval.
(Results) the incidence of liver toxicity in patients receiving TAB (10 cases of 25 patients) was significantly higher than in patients receiving PAB (2 of 18 patients). Two patients in whom severe liver toxicity developed after receiving TAB were hospitalized. However, after flutamide was discontinued all patients with liver damage recovered with normalization of AST and ALT levels. Levels of total cholesterol and γ-GTP did not differ significantly in either patient group. In two patients receiving TAB total bilirubin levels showed slight, transient elevations after maximum elevations of AST and ALT. In 80% of patients receiving TAB serum levels of cholinesterase were significantly higher than those in patients receiving PAB.
(Conclusion) These data suggest that the risk of flutamide-induced liver toxicity is significant in patients receiving TAB. However, this damage can be normalized after flutamide has been discontinued. Serum levels of cholinesterase also increase significantly in patients receiving TAB. This previously unreported phenomenon suggests an unknown effect of flutamide on liver function in patients with prostate cancer.

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A case of Collet-Sicard Syndrome caused by skull base metastasis of prostate carcinoma is reported. A fifty-five years old man presenting multiple lymph node and bone metastases of prostate carcinoma was treated with LH-RH agonist and Flutamide, which induced transient decrease in serum PSA levels and size of lymph node metastases. After 8 months of the treatment, the patient started complaining headache, dysphagia and dysarthria. Brain CT and MRI demonstrated a soft tissue mass replacing left pyramidal bone and occipital bone around left jugular foramen. The tumor was diagnosed as skull base metastasis of the prostate carcinoma and was treated with 50Gy of radiation. The symptom improved after the radiation but died of the disease in 4 months. The autopsy revealed the skull base metastasis of the prostate carcinoma and the tumor was proved to be poorly differentiated adenocarcinoma, which was positively stained by anti-PSA antibody.
The case showed cranial nerve palsy of IX to XII, which is usually called Collet-Sicard syndrome. This is the third case report of Collet-Sicard syndrome caused by the skull base metastasis of prostate carcinoma, and it is the first case in Japan.

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We report two cases of unilteral adrenal hyperplasia with contralateral renal cell carcinoma. First case was a 66-year-old man with right renal mass who came to our hospital for study. Although no major symptoms were complained, blood pressure was consistently above normal. Hypokalemia, low plasma renin activity and high plasma aldosterone level were detected. CT revealed that he had a right renal mass and a left adrenal tumor. Preoperative diagnosis was right renal tumor and primary aldosteronism due to left adrenal adenoma. Second case was a 59-year-old man with right renal mass who also came to our hospital for study. He also had a left adrenal tumor, however his blood pressure was normal and serum hormonal analysis showed normal adrenal cortical function. Preoperative diagnosis was right renal tumor and non-functional left adrenal adenoma. Two patients were performed right radical nephrectomy with contralateral adrenarectomy. Pathological diagnosis were right renal cell carcinoma and left adnenocortical hyperplasia. One Patient clinically showed primary aldosteronism and the other had no clinical symptoms. These patients were rare cases with unilateral adrenal hyperplasia.

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