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Leydig cell tumor of the ovary
718
Selected
“German,
Scpternbcr, IYtil \rn. J. C&c. & Gynec,
abstracts
E., Horowitz, II., VandeWiele, R., and Torack, R. M.: Leydig Cell Tumor of the Ovary: Case Report and Review, p. 91.
Daughaday, Holloszy, and Mark: Binding of Cortisol and Aldosterone by Corticosteroid-Binding Globulin and the Estrogen-Induced Binding System of Plasma, The
p. 53. binding of cortisol-4-C
14 and
aldosterone-
H3 by serum from pregnant or estrogen treated subjects is directly compared to the binding by serum from controlled subjects in a system of double equilibrium dialysis. Increased binding of cortisol-4-C 14 could be demonstrated by ‘&estrogen” plasma under conditions of minimal cortisol loading only at 370 C. and not at 4O C. This difference of binding behavior is evidence that the binding sites induced by estrogen arc qualitatively different from those on normal corticosteroid-binding globulin. The total concentration of cortisol-binding protein induced by estrogen may be two or three times greater than of corticosteroid-binding globulin. Under physiologic conditions of temperature, aldosterone-H3 is bound primarily by albumin, but, at 4O C., aldosterone-H3 is bound about equally by albumin and corticosteroid-binding globulin. At 4O C. the estrogen-induced finding system does not have appreciable affinity for aldosterone-H3.
J. Edward German
et al.: Leydig Cell Tumor
Hall
of the Ovary,
p. 91. The authors report a case of Leydig cell tumor of the ovary in a 60-year-old woman. The patient was originally admitted to the hospital for acute abdominal pain of 48 hours’ duration, and an exploratory operation was performed revealing diverticulitis with perforation and generalized peritonitis. A colostomy was performed and the postoperative course was uneventful. It was noted at that time the patient presented an extremely masculine appearance so she was transferred to the Medical Service for further evaluation. The patient had a receding hairline and an increase of facial and body hair. Her menstrual history was within normal limits and she had had a spontaneous menopause at age 53. She had been married 40 years without becoming
pregnant,
though
contraceptive
procedures
had
never been employed. Pertinent physical findings were those of a well-developed, elderly female with considerable hirsutism of the face, arms, legs, and trunk. There was a markedly receding hairline and spotty alopecia. The voice was female but there was some enlargement of the clitoris to about twice its normal size. The pelvis was filled with a hard, irregular mass which was located predominantly on the right side. It was impossible to differentiate uterus or adnexa from the mass. Extensive laboratory investigation was done including the various electrolytes and extensive study for possible androgen excretion in abnormal amounts. However, there was no indication of any excessive androgens, the 17-ketosteroids measuring only 0.5 mg. The vaginal smear was atrophic. The patient was ultimately reoperated on and a sigmoid resection with removal of the ovarian mass was performed. The ovarian tumor was reported as a firm, rubbery, nodular mass measuring 4.8 by 3.9 by 2.0 cm. It was gray-white and had the appearance of normal ovarian tissue. The microscopic examination revealed the tumor to consist of a large amount of pale eosinophilic homogenous stroma in which were varying sized islands of cells mostly arranged in small clusters. In places they tended to form cords and even rosettes. The nuclei of these cells were in general regular, and vesicular nucleoli were present. The cytoplasm of the cells was granular and deeply eosinophilic. This mass was interpreted to be a Leydig cell tumor of the ovary. This diagnosis was confirmed by the registry of ovarian tumors in Baltimore, Maryland. Unfortunately, the patient developed a severe wound infection with ascending renal involvement and died in a progressive renal failure. This case represents the fourteenth reported case of Leydig cell tumor of the ovary. It is of interest that, although this tumor undoubtedly was producing sufficient androgens to cause virilization, the androgenic material could not be demonstrated by the laboratory procedures used. This is not unusual in these cases since only 2 of 10 cases of the ones reported that had hormonal determinations had high androgen activity. The possible explanation for this discrepancy is discussed. J. Edward Hall
Selected
“German,
Scpternbcr, IYtil \rn. J. C&c. & Gynec,
abstracts
E., Horowitz, II., VandeWiele, R., and Torack, R. M.: Leydig Cell Tumor of the Ovary: Case Report and Review, p. 91.
Daughaday, Holloszy, and Mark: Binding of Cortisol and Aldosterone by Corticosteroid-Binding Globulin and the Estrogen-Induced Binding System of Plasma, The
p. 53. binding of cortisol-4-C
14 and
aldosterone-
H3 by serum from pregnant or estrogen treated subjects is directly compared to the binding by serum from controlled subjects in a system of double equilibrium dialysis. Increased binding of cortisol-4-C 14 could be demonstrated by ‘&estrogen” plasma under conditions of minimal cortisol loading only at 370 C. and not at 4O C. This difference of binding behavior is evidence that the binding sites induced by estrogen arc qualitatively different from those on normal corticosteroid-binding globulin. The total concentration of cortisol-binding protein induced by estrogen may be two or three times greater than of corticosteroid-binding globulin. Under physiologic conditions of temperature, aldosterone-H3 is bound primarily by albumin, but, at 4O C., aldosterone-H3 is bound about equally by albumin and corticosteroid-binding globulin. At 4O C. the estrogen-induced finding system does not have appreciable affinity for aldosterone-H3.
J. Edward German
et al.: Leydig Cell Tumor
Hall
of the Ovary,
p. 91. The authors report a case of Leydig cell tumor of the ovary in a 60-year-old woman. The patient was originally admitted to the hospital for acute abdominal pain of 48 hours’ duration, and an exploratory operation was performed revealing diverticulitis with perforation and generalized peritonitis. A colostomy was performed and the postoperative course was uneventful. It was noted at that time the patient presented an extremely masculine appearance so she was transferred to the Medical Service for further evaluation. The patient had a receding hairline and an increase of facial and body hair. Her menstrual history was within normal limits and she had had a spontaneous menopause at age 53. She had been married 40 years without becoming
pregnant,
though
contraceptive
procedures
had
never been employed. Pertinent physical findings were those of a well-developed, elderly female with considerable hirsutism of the face, arms, legs, and trunk. There was a markedly receding hairline and spotty alopecia. The voice was female but there was some enlargement of the clitoris to about twice its normal size. The pelvis was filled with a hard, irregular mass which was located predominantly on the right side. It was impossible to differentiate uterus or adnexa from the mass. Extensive laboratory investigation was done including the various electrolytes and extensive study for possible androgen excretion in abnormal amounts. However, there was no indication of any excessive androgens, the 17-ketosteroids measuring only 0.5 mg. The vaginal smear was atrophic. The patient was ultimately reoperated on and a sigmoid resection with removal of the ovarian mass was performed. The ovarian tumor was reported as a firm, rubbery, nodular mass measuring 4.8 by 3.9 by 2.0 cm. It was gray-white and had the appearance of normal ovarian tissue. The microscopic examination revealed the tumor to consist of a large amount of pale eosinophilic homogenous stroma in which were varying sized islands of cells mostly arranged in small clusters. In places they tended to form cords and even rosettes. The nuclei of these cells were in general regular, and vesicular nucleoli were present. The cytoplasm of the cells was granular and deeply eosinophilic. This mass was interpreted to be a Leydig cell tumor of the ovary. This diagnosis was confirmed by the registry of ovarian tumors in Baltimore, Maryland. Unfortunately, the patient developed a severe wound infection with ascending renal involvement and died in a progressive renal failure. This case represents the fourteenth reported case of Leydig cell tumor of the ovary. It is of interest that, although this tumor undoubtedly was producing sufficient androgens to cause virilization, the androgenic material could not be demonstrated by the laboratory procedures used. This is not unusual in these cases since only 2 of 10 cases of the ones reported that had hormonal determinations had high androgen activity. The possible explanation for this discrepancy is discussed. J. Edward Hall