1356 PERICARDIAL EFFUSIONS ASSOCIATED WITH
S.H.B.G. TITRE AND BREAST TUMOUR REGRESSION AFTER
MINOXIDIL
HORMONE THERAPY
SIR,-Dr Marques-Jn’io and Dr Uldall (Oct. 15, p. 816) out a potentially very important adverse effect of useful a minoxidil, antihypertensive drug. The following case may be pertinent since pericardial effusion developed in a patient with normal renal function. A 13-year-old male had crescentic glomerulonephritis which rapidly got worse despite steroids and immunosuppressive have pointed
resulting in end-stage renal failure in September, 1976. In July, 1976, because of hypertension refractory to other antihypertensive drugs, he had been put on minoxidil 7.5 mg twice daily. In November, 1976, coincident with a bout of shunt sepsis, he was noted to have a moderate pericardial effusion by echocardiogram. This was confirmed by chest X-ray. At this time his minoxidil dose was 10 mg three times a day and he was on regular haemodialysis. Antinuclear antibody was negative at this time. Although he had no clinical evidence of pericarditis or pericardial tamponade, he continued to have a pericardial effusion on chest X-ray and echocardiogram until the time of cadaveric transplant in May, 1977. In the first month post-transplant a pericardial friction rub developed without any evidence of pericardial tamponade. The rub persisted despite improvement of glomerular filtration-rate. Because his blood-pressure was easy to control without therapy, his antihypertensive regimen was discontinued on April 1, 1977. An echocardiogram 2 weeks later showed no pericardial effusion and chest X-ray showed normal heart size. At this time his blood-urea-nitrogen was 20 mg/dl and serum-creatinine 0-9 mg/dl. At the beginning of September, 1977, the patient became hypertensive requiring the reintroduction of minoxidil. agents,
At this time his renal function was normal, blood-urea23 mg/dl, creatinine 1.0 mg/dl; antinuclear antibody, C3, and C4 complement normal. Approximately a week later a massive pericardial effusion was noted. Pericardiocentesis revealed serosanguinous fluid with the characteristics of an exudate. Cultures were negative, and the patient was treated symptomatically. Because of continued accumulation of pericardial fluid and early signs of tamponade a pericardialwindow procedure was done on Sept. 23, 1977. Since that time the patient has done well and minoxidil has been discontinued. Persistent hypertension is being treated with other drugs because of the presumption that the pericardial effusion was in some way related to his minoxidil therapy. This important adverse effect of minoxidil must be clarified before this drug can come into widespread use; it seems it can develop in non-ursmic patients.
nitrogen
Department of Medicine, University of Oregon Health Sciences Center, Portland, Oregon 97201, U.S.A.
WILLIAM M. BENNETT
SEX-HORMONE-BINDING GLOBULIN PREDICTS RESPONSE OF BREAST CANCER TO HORMONE THERAPY
SiR,-We have investigated the relationship between oestrogen receptors in tumour tissue and plasma sex-hormonebinding globulin (S.H.B.G.) in breast cancer patients and found that S.H.B.G. might predict the response of the tumour to hormone therapy.’·2 Using a sensitive radioassay,3 s.H.B.G. was measured in 25 premenopausal and postmenopausal patients with primary breast cancer and 21 controls of whom 11 were mid-cycle and 10 postmenopausal normal females without a history of hormone therapy. There was an association between oestrogen receptors and S.H.B.G. in the postmenopausal patients.3 10 of 12 patients Murayama, Y., Utsunomiya, J., Asano, K. Jap J. Surg. 1976, 6, 119. 2. Murayama, Y., Asano, K. Jap. J. Cancer. Clin. 1977, 23, 1210. 3. Murayama, Y., Utsunomiya, J., Asano, K. J. clin. Endocr. Metab. (in the press). 1.
OV-ovariectomy; Oest=cestrogen; ADX=adrenalectomy; And=androgens with
CEStrogen-receptor-positive tumours, but none of 7 patients with oestrogen receptor-negative tumours had higher S.H.B.G. titres than normal in postmenopausal females. We then studied S.H.B.G. in 29 patients who had had radical mastectomy before they began hormone therapy. The tumour tissue’s response to therapy was assessed by the Programme on Clinical Oncology of the International Union against Cancer. Metastatic lesions in patients with higher s.H.B.G. titres than normal responded well to various types of hormone therapy, but those in patients with lower S.H.B.G. titres did not respond (see table). It thus appears that S.H.B.G. may be used to predict the response of breast cancer to hormone therapy.
Department of Surgery, School of Medicine, Tokyo Medical and Dental University, Tokyo, Japan
YO-ICHI MURAYAMA JOJI UTSUNOMIYA KEN-ICHI ASANO
PATIENTS AT RISK OF HYPOTHYROIDISM
SIR,-Dr Toft and Dr Irvine (Nov. 26, p. 1128) have not encountered the problem of temporary hypothyroidism after treatment of thyrotoxicosis with iodine-131. This surprised us because we have seen transient hypothyroidism complicating iodine-131therapy on several occasions. A 56-year-old woman, treated twice before with antithyroid drugs became thyrotoxic again in 1973. She was treated with 1311 in February, 1974. In May, 1974, still clinically and biochemically toxic, she received a second dose of 1311. In October, 1974, she still appeared clinically toxic; thyroid-function tests confirmed this impression, and a third dose of ’31I was administered. She was next seen on Jan. 15, 1975. She felt much better and had put on weight. Clinically she appeared euthyroid but thyroid-function tests revealed a serum thyroidstimulating hormone concentration of 34 mU/1 (normal 50 mU/1 in March, 1977, at which time her serum-T4 had fallen to 36 nmol/1. She was put on thyroxine and over the next 4 months lost 4.5kg in weight. A 52-year-old woman, clinically and biochemically thyrotoxic, received a therapeutic dose of 1311 in February, 1977. By the end of June her serum-T.s.H. was 6 mU;1, T3 1.2 nmol/1 and T4
S.H.B.G. TITRE AND BREAST TUMOUR REGRESSION AFTER
MINOXIDIL
HORMONE THERAPY
SIR,-Dr Marques-Jn’io and Dr Uldall (Oct. 15, p. 816) out a potentially very important adverse effect of useful a minoxidil, antihypertensive drug. The following case may be pertinent since pericardial effusion developed in a patient with normal renal function. A 13-year-old male had crescentic glomerulonephritis which rapidly got worse despite steroids and immunosuppressive have pointed
resulting in end-stage renal failure in September, 1976. In July, 1976, because of hypertension refractory to other antihypertensive drugs, he had been put on minoxidil 7.5 mg twice daily. In November, 1976, coincident with a bout of shunt sepsis, he was noted to have a moderate pericardial effusion by echocardiogram. This was confirmed by chest X-ray. At this time his minoxidil dose was 10 mg three times a day and he was on regular haemodialysis. Antinuclear antibody was negative at this time. Although he had no clinical evidence of pericarditis or pericardial tamponade, he continued to have a pericardial effusion on chest X-ray and echocardiogram until the time of cadaveric transplant in May, 1977. In the first month post-transplant a pericardial friction rub developed without any evidence of pericardial tamponade. The rub persisted despite improvement of glomerular filtration-rate. Because his blood-pressure was easy to control without therapy, his antihypertensive regimen was discontinued on April 1, 1977. An echocardiogram 2 weeks later showed no pericardial effusion and chest X-ray showed normal heart size. At this time his blood-urea-nitrogen was 20 mg/dl and serum-creatinine 0-9 mg/dl. At the beginning of September, 1977, the patient became hypertensive requiring the reintroduction of minoxidil. agents,
At this time his renal function was normal, blood-urea23 mg/dl, creatinine 1.0 mg/dl; antinuclear antibody, C3, and C4 complement normal. Approximately a week later a massive pericardial effusion was noted. Pericardiocentesis revealed serosanguinous fluid with the characteristics of an exudate. Cultures were negative, and the patient was treated symptomatically. Because of continued accumulation of pericardial fluid and early signs of tamponade a pericardialwindow procedure was done on Sept. 23, 1977. Since that time the patient has done well and minoxidil has been discontinued. Persistent hypertension is being treated with other drugs because of the presumption that the pericardial effusion was in some way related to his minoxidil therapy. This important adverse effect of minoxidil must be clarified before this drug can come into widespread use; it seems it can develop in non-ursmic patients.
nitrogen
Department of Medicine, University of Oregon Health Sciences Center, Portland, Oregon 97201, U.S.A.
WILLIAM M. BENNETT
SEX-HORMONE-BINDING GLOBULIN PREDICTS RESPONSE OF BREAST CANCER TO HORMONE THERAPY
SiR,-We have investigated the relationship between oestrogen receptors in tumour tissue and plasma sex-hormonebinding globulin (S.H.B.G.) in breast cancer patients and found that S.H.B.G. might predict the response of the tumour to hormone therapy.’·2 Using a sensitive radioassay,3 s.H.B.G. was measured in 25 premenopausal and postmenopausal patients with primary breast cancer and 21 controls of whom 11 were mid-cycle and 10 postmenopausal normal females without a history of hormone therapy. There was an association between oestrogen receptors and S.H.B.G. in the postmenopausal patients.3 10 of 12 patients Murayama, Y., Utsunomiya, J., Asano, K. Jap J. Surg. 1976, 6, 119. 2. Murayama, Y., Asano, K. Jap. J. Cancer. Clin. 1977, 23, 1210. 3. Murayama, Y., Utsunomiya, J., Asano, K. J. clin. Endocr. Metab. (in the press). 1.
OV-ovariectomy; Oest=cestrogen; ADX=adrenalectomy; And=androgens with
CEStrogen-receptor-positive tumours, but none of 7 patients with oestrogen receptor-negative tumours had higher S.H.B.G. titres than normal in postmenopausal females. We then studied S.H.B.G. in 29 patients who had had radical mastectomy before they began hormone therapy. The tumour tissue’s response to therapy was assessed by the Programme on Clinical Oncology of the International Union against Cancer. Metastatic lesions in patients with higher s.H.B.G. titres than normal responded well to various types of hormone therapy, but those in patients with lower S.H.B.G. titres did not respond (see table). It thus appears that S.H.B.G. may be used to predict the response of breast cancer to hormone therapy.
Department of Surgery, School of Medicine, Tokyo Medical and Dental University, Tokyo, Japan
YO-ICHI MURAYAMA JOJI UTSUNOMIYA KEN-ICHI ASANO
PATIENTS AT RISK OF HYPOTHYROIDISM
SIR,-Dr Toft and Dr Irvine (Nov. 26, p. 1128) have not encountered the problem of temporary hypothyroidism after treatment of thyrotoxicosis with iodine-131. This surprised us because we have seen transient hypothyroidism complicating iodine-131therapy on several occasions. A 56-year-old woman, treated twice before with antithyroid drugs became thyrotoxic again in 1973. She was treated with 1311 in February, 1974. In May, 1974, still clinically and biochemically toxic, she received a second dose of 1311. In October, 1974, she still appeared clinically toxic; thyroid-function tests confirmed this impression, and a third dose of ’31I was administered. She was next seen on Jan. 15, 1975. She felt much better and had put on weight. Clinically she appeared euthyroid but thyroid-function tests revealed a serum thyroidstimulating hormone concentration of 34 mU/1 (normal 50 mU/1 in March, 1977, at which time her serum-T4 had fallen to 36 nmol/1. She was put on thyroxine and over the next 4 months lost 4.5kg in weight. A 52-year-old woman, clinically and biochemically thyrotoxic, received a therapeutic dose of 1311 in February, 1977. By the end of June her serum-T.s.H. was 6 mU;1, T3 1.2 nmol/1 and T4
