Androgen status in healthy premenopausal women with loss of libido.

Androgen deficiency may contribute to female sexual dysfunction and loss of libido. The role of the active metabolite of testosterone, dihydrotestosterone (DHT), in these conditions is uncertain. The aim of this study was to determine the role of androgens and DHT in the etiology of loss of libido in healthy women. We studied 29 premenopausal women with reduced libido (subjects) and 12 healthy females (controls). They were aged 18 to 45 years and in a stable heterosexual relationship. At 9 a.m. we took venous blood in the follicular phase for serum estradiol, total testosterone, and DHT, dehydroepiandrosterone sulfate (DHEAS), and SHBG levels. Subjects were interviewed by a psychosexual counsellor. Using the modified Wilson's sexual fantasy questionnaire (Baumgartner, Scalora, & Huss, 2002) and sexual satisfaction by Golombok-Rust Inventory of Sexual Satisfaction (GRISS Rust & Golombok, 1985, 1986) we assessed sexual drive. The total testosterone and DHT levels (mean +/- SD) were respectively 0.97 +/- 0.38 mmol/L and 0.76 +/- 0.37 nmol/L in subjects and 0.97 +/- 0.41 mmol/L and 0.77 +/- 0.15 nmol/L in controls. The SHBG and DHEAS were respectively 65 +/- 42 mmol/L and 3.76 +/- 1.0 umol/L in subjects and 65 +/- 29 mmol/L and 3.67 +/- 2.6 in controls. The scores of the Wilson questionnaire and GRISS were respectively 21 +/- 14.1 and 5 +/- 2.1 in subjects and 35 +/- 14.8 & 2 +/- 1.2 in controls. Subjects were more likely than controls to have low income (48% versus 8%, p < 0.02), a minor illnesses (57% versus 17%, p < 0.02), a history of depression (57% versus 8%, p = 0.025) and to report sexual problems in their partners (24% versus 0%, p = 0.053). Loss of libido in otherwise healthy women may be related to relationship problem, depression, psychosocial factors, and sexual dysfunction in the partner but do not appear to be related to androgen status.

Low but detectable serum thyroid-stimulating hormone concentrations in ambulant subjects not receiving thyroxine.

BACKGROUND: In laboratories employing 'front-line' sensitive thyroid-stimulating hormone (TSH) measurement, it is generally accepted that a fully suppressed serum TSH concentration (third-generation assay) alongside normal serum concentrations of free thyroid hormones indicates subclinical hyperthyroidism. However, other explanations are often provided for low but detectable serum TSH concentrations, such as drug effects or non-thyroidal illness. METHODS: We investigated 25 consecutive ambulant individuals, identified over an 18-month period as having low but not fully suppressed TSH concentrations (third-generation assay; sensitivity 0.003 mIU/L) with additional free thyroxine (T(4)), free tri-iodothyronine (T(3)) and thyroid microsomal antibody estimations and thyroid isotope scanning (technetium). RESULTS: Concentrations of serum hormones (median, inter-quartile range) were: TSH, 0.23, 0.17-0.26 mIU/L (reference range 0.34-5.6 mIU/L); free T(4), 14.6, 10.6- 17.6 pmol/L (reference range 10-25 pmol/L); free T(3), 6.1, 5.7-6.6 pmol/L (reference range 4.5-7.5 pmol/L). Thyroid antibodies were negative in all but one individual. On isotope scanning, nine individuals had hot nodules and ten individuals had multinodular goitres (MNG). Of the six with normal scans, ultrasound scanning showed a definite MNG (n = 1) and early MNG (n = 2). CONCLUSIONS: A low but detectable serum TSH concentration, obtained using a third-generation assay, found in an ambulant individual, is frequently a pointer to underlying thyroid disease.

Cell salvage in obstetrics: an evaluation of the ability of cell salvage combined with leucocyte depletion filtration to remove amniotic fluid from operative blood loss at caesarean section.

During 27 elective caesarean sections, operative blood loss was collected and processed using the Haemonetics Cell Saver 5 and filtered by Pall RC 100 leucocyte depletion filtration. The efficiency of removal of amniotic fluid, and the degree. of contamination with fetal red cells were assessed in the resulting 'cleaned' blood. Cell saver processing effectively removed alpha-fetoprotein from the red cells of 14 patients whose amniotic fluid was removed by separate suction and from nine of the 13 patients whose amniotic fluid was aspirated into the cell saver along with operative blood loss. Cell saver processing and leucocyte depletion filtration completely removed trophoblastic tissue and white cells, but fetal squames were still clearly present in 10, and possibly in 14 samples after processing and fully removed in only two specimens. Amorphous debris was present in all samples after processing. The maximum mass of fetal red cells contaminating any patient's total salvaged blood was 19 ml (range 2-19 ml). Had this been re-transfused into a rhesus-incompatible mother it would have required 2500 i.u. (500 microg) anti-D immunoglobulin to prevent rhesus-immunization of the mother. Contamination of processed caesarean section blood with fetal red cells and fetal squames is defined and its clinical implications discussed, with an overview of the development and current status of cell salvage. Autotransfusion by cell salvage with leucocyte depletion filtration should be considered in life-threatening obstetric haemorrhage and offered to Jehovah's Witnesses.

Effect of hemodialysis membrane type on parathyroid hormone removal.

We studied the effect of polyacrylonitrile (PAN), polysulfone (PS) and cuprophane (CP) membranes on the removal of intact and middle molecule (MM) parathyroid hormone (PTH) during hemodialysis in 4 patients using a dialysis calcium of 1.0 mmol/l. Blood was taken from the arterial (predialyzer membrane) and venous (postdialyzer membrane) limbs of the dialysis circuits at the start, midpoint and end of dialysis. Intact PTH and MM PTH levels were significantly reduced by passage through dialyzers with PAN and PS membranes; the patients' plasma ionized calcium (predialyzer membrane) fell during the course of dialysis regardless of membrane type used. This was despite a rise in plasma ionized calcium during passage through the dialyzers containing PAN and CP membranes.

Prostate specific antigen--a screening test for prostatic cancer?

A series of 287 patients referred by their family doctors with symptoms of bladder outflow obstruction were asked to attend the hospital for "pre-clinic" screening for carcinoma of prostate (CaP). Blood samples were collected from 211 patients and analysed for serum prostate specific antigen (PSA) and prostatic acid phosphatase (PAP). Thirty-six patients had a serum PSA greater than 10 micrograms/l and 7 had PAP levels greater than 5 iu/l. In no instance was the PAP elevated without an associated increase in PSA concentration. Patients with raised markers underwent further investigations which included prostatic biopsy and/or resection; 17 patients were proved to have carcinoma of the prostate, 9 of whom had distant metastases. The specificity of PSA for detecting prostate cancer in this study was 90% with a sensitivity of 89.5%, in contrast to values for PAP of 100% and 36.8%. The routine use of PAP as a marker for prostatic cancer should be abandoned. The use of PSA as a screening test in a group of patients with prostatism appears justified, but with a positive predictive value of only 47%, its use in a mass unselected screening programme is not recommended.

Immunoglobulin classes of human serum antibodies in vaginal candidiasis.

The titre and immunoglobulin class of antibodies against Candida albicans in serum from 60 non-pregnant women was determined. IgG titres up to 1 : 32, IgA titres up to 1 : 8, and IgM titres up to 1 : 4 were detected in 30 women with vaginal candidiasis. Similar titres were found in 20 women harbouring yeasts in the mouth or rectum, and in 10 women who were not harbouring yeasts in the vagina, mouth or rectum. Serum fractionation confirmed that antibodies to C. albicans are found in the three immunoglobulin classes and that those antibodies reside in highest titre in the IgG class. No secretory IgA antibodies against C. albicans were detected in the serum of these women.

The absence of an inhibitory effect of metyrapone (2-methyl-1,2-di (3-pyridyl) propan-1-one) on hepatic microsomal hydroxylation in scurvy.

Microsomes from livers of scorbutic guinea-pigs showed a reduced rate of acetanilide hydroxylation. The response of "scorbutic" liver microsomes to the inhibitor Metyrapone (2-methyl-1,2 di (3-pyridyl) propan-1-one) was different from that of liver microsomes from non-scorbutic guinea-pigs.