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Surgical guidelines and are monitored conservatively do lose bone mass. This bone loss is reversed at the lumbar spine and hip after parathyroidectomy 22 ; . It this potential complication of PHPT that has caused concern and led to the recommendation by some that all patients with the disease should have parathyroid surgery 23 ; . However, if there were an agent that could effectively prevent bone loss in PHPT, then the case for monitoring patients who are not surgical candidates becomes much stronger. In this regard, alendronate would seem to be an attractive alternative. No similar data are available yet for risedronate, the other oral bisphosphonate in common use. The mechanism by which alendronate improves bone mass in PHPT would seem to be similar to its actions in postmenopausal women and men with osteoporosis. Alendronate demonstrated efficacy in improving BMD at the lumbar spine and hip. The radial site was not affected. The results of our study are consistent with previous observations using alendronate in PHPT 1316 ; . The first study, an.
This event will present the review and outcome of projects from the field and ongoing research, which has contributed to improved living conditions in informal settlements, including slums and squatter communities of disadvantaged citizens and marginalized groups. The crosscutting issues generated in all aspects of human settlements have motivated this presentation by representatives from youth, practitioners from the private sector, and seniors. This intergenerational overview will highlight how the provision of affordable housing and basic infrastructure leads to increased amenities, better health conditions and improved livelihoods for all members of the recipient communities. These efforts reflect the implementation prospects for the Habitat Agenda, Johannesburg Plan of Implementation and the Millennium Development Goals.
Swallowing pills is a slow, inefficient way to introduce medicine to the body. Many new drugs, from insulin to antianxiety medicines, are being packaged in spray form with inhalers similar to those of asthma medication. How it works: Liquid-based medicine goes into the lungs through an aerosol. Company to watch: Dov Pharmaceutical, Inc. a company in which my firm has invested ; , which is developing an inhalant for anxiety and panic attacks. The potential is substantial--with 19 million Americans aged 18 to 54 affected. In pill form, the drugs take too long to work on an event-specific basis, and they have side effects when taken continuously. Risk: Getting US FDA approval. Dov is in clinical trials. The approval time is unknown. If approved, it will take at least a year for the product to come to market. Information: Dov Pharmaceutical, Inc., 1-201-968-0980, dovpharm.
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ABSTRACT We used a recently developed ELISA format to test the hypothesis that inhibin B is the physiologically active form of inhibin in men. We measured and compared inhibin A, inhibin B, and pro-a-c-related immunoreactive peptides pro-a-C-RI ; in normal men before and after perturbations of their gonadotropin levels and baseline values in normal men and men with various disturbances of the hypothalamicpituitary-testicular axis including men with idiopathic hypogonadotropic hypogonadism, infertile men with elevated FSH, men with Klinefelter's syndrome, and orchidectomized men. Mean serum inhibin concentrations were significantly higher in normal men than untreated men with idiopathic hypogonadotropic hypogonadism, infertile men with elevated FSH, untreated men with Klinefelter's syndrome, and orchidectomized men 187 % 28 us. 45 i 11, 37 -C 6, 11 -t 3, and ~-10 pg mL, respectively; P 0.05 ; . Inhibin B levels were below the limit of detection in all of the orchidectomized men. Pro-c&-RI levels were detectable in all men studied including the orchidectomized men, and no significant differences in the proa-C-RI levels were noted between the normal men and men with various testicular diseases were noted except that orchidectomized men had significantly lower pro-a-C-RI levels than all other groups P 0.05 ; . Inhibin A was undetectable in all men tested in this study. Six normal men who were administered exogenous levonorgestrel and testosterone had significantly lower serum gonadotropin, inhibin B, and pro-a-C-RI levels during the treatment period than the control and recovery periods P 0.05 ; . Ten normal men who were administered human recombinant FSH had significantly higher peak serum FSH 21.85 2 3.23 IU L us. 3.01 2 0.51 IU L ; , inhibin B 311 2 88 pg us. 151% 23 pg mL ; and pro-a-C-RI 646 2 69 us. 402 ? 38 pg levels during the treatment period than the baseline values P 0.05 ; . We conclude that inhibin B is a unique testicular product that is not detectable in the sera of orchidectomized men, is responsive to FSH stimulation, and has a reciprocal relationship with serum FSH levels in men with various forms of testicular disease. Therefore, inhibin B is likely to be the physiologically important form of inhibin in men. J Clin Endocrinol Metab 81: 3341-3345, 1996.
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From the Division of Molecular Cardiology, Research Institute of Angiocardiology C.W., S.K., H.K. ; and the Center for Research and Practice in Medical Education H.Y. ; , Faculty of Medicine, Kyushu University, Fukuoka, Japan. Supported in part by grants-in-aid for Scientific Research on Priority Areas Nos. 01641532, 02223107, and 02257297 ; and for General Scientific Research Nos. 0148025 and 02670399 ; from the Ministry of Education, Science and Culture, Japan, and grants from the "Research Program on Cell Calcium Signals in the Cardiovascular System, " from Uehara Memorial Foundation, from CIBA-GEIGY Foundation Japan ; for the Promotion of Science, from the Mitsukoshi Prize of Medicine 1990, and from Japan Research Foundation for Clinical Pharmacology. Address for correspondence: Hideo Kanaide, MD, Professor, Division of Molecular Cardiology, Research Institute of Angiocardiology, Faculty of Medicine, Kyushu University, 3-1-1, Maidashi, Higashi-ku, Fukuoka 812, Japan. Received April 9, 1991; accepted February 4, 1993 and levorphanol.
1. Suppressive not curative so requires ongoing surveillance. 2. Reduces or eliminates libido sexual desire ; while on treatment; diminished libido can persist after ADT is stopped 3. Treatment may have to be repeated at some point in the future 4. May reduce potency rates if subsequent nerve sparing surgery is performed 5. Dry orgasms while on treatment with slow recovery afterward 6. Loss of muscle strength, can be offset by strength-training exercises 7. Weight gain, which can be offset by dietary discipline.
Progestin Replacement Study ; trial is the first randomized, double-blind, placebo-controlled trial of daily use of oestrogen plus progestin medroxyprogesterone acetate ; on the combined rate of death from non-fatal myocardial infarction and CHD death among postmenopausal women with established coronary artery disease and advanced age average of 66.7 years ; . After a follow-up of 4.1 years, treatment with this combination did not reduce the overall rate of CHD events. The lack of an overall effect occurred despite a 11% net reduction of low-density lipoprotein concentrations and a 10% increase of high-density lipoprotein concentrations in the hormone group compared with the placebo. Therefore, the authors do not recommend starting this treatment for the purpose of secondary prevention of CHD, although it could be appropriate for women already receiving hormone treatment to continue Hulley et al., 1998 ; . Another important issue to address is whether preparations containing third-generation progestogens reduce the risk of myocardial infarction Thorogood, 1997 ; . The WHO Collaborative Study of Cardiovascular Disease and Steroid Hormone Contraception found the completely unexpected result that the risk of a thrombosis venous thromboembolism, stroke and myocardial infarction ; was related to the type of progestogen used in the oral contraceptives, with the thirdgeneration progestogens desogestrel and gestodene being associated with a relative risk more than twice as large as that associated with use of combined preparations containing levonorgestrel Meirik et al., 1995 ; . Interim data from the Transnational Study Lewis et al., 1996 ; show that there is no increase in risk associated with third-generation preparations, and the ratio of risk for third as opposed to second generation was 0.36. This estimation of the odds ratio for third-generation preparations is based on just six cases, and should be interpreted with extreme caution. A further analysis has been carried out on data from a computerized database of primary care records in the UK the GPRD database ; . The study included 600 000 women-years at risk among women aged under 45 years with no known risk factors for myocardial infarction and who had received at least one oral contraceptive prescription. Eleven women with the diagnosis of myocardial infarction or sudden death were identified, and a nested case control study was carried out to estimate relative risks of myocardial infarction by type of progestogen in the preparations. This analysis also suggests less risk with thirdgeneration pills, but with very small numbers of cases and wide confidence intervals Jick et al., 1996 and lexiva.
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AAKP re-released its 1997 National Kidney Foundation Dialysis Outcomes Quality Initiatives NKF- DOQI ; patient survey results. In 1997, AAKP surveyed approximately 3, 600 patients in an effort to provide patient opinions on the then introduced NKF-DOQI guidelines. The purpose of the survey was to understand the direct patient impact such recommendations as subcutaneous administration of Epogen, vascular access placement, administration of iron and increase in dialysis prescription had on patients' willingness to participate in such procedures. You can read the original survey results in Public Policy Briefing located at : aakp newsletters AAKP-Public-Policy-Briefing August-2007.
Midland Therapeutic Review & Advisory Committee Licensed Indication: 'Contraception; idiopathic menorrhagia'.1 Background information Menorrhagia is defined as menstrual blood loss MBL ; of at least 80ml per cycle. 2, 3 In practice, estimating menstrual blood loss is difficult therefore ultimately the diagnosis of menorrhagia relies on the woman's assessment of blood loss. Haemoglobin Hb ; concentrations may be used as an objective measure of heavy menstrual loss because menorrhagia is a common cause of iron deficiency anaemia. 4 Menorrhagia can be associated with ovulatory or anovulatory ovarian cycles. Excessive menstrual loss within regular menstrual cycles is the most common clinical presentation. In these women, several abnormalities can occur in the endometrium, such as increased fibrinolytic activity, and increased production of prostaglandins.4 Each year one in twenty women 5% ; aged 30-49 years consult their GP with menorrhagia. 5 Once referred to a gynaecologist, surgical intervention is highly likely. One in five women in the UK will have a hysterectomy before the age of 60 years; in at least half of these cases, menorrhagia is the main presenting problem. Furthermore, in about half of all women who have a hysterectomy for menorrhagia, a normal uterus is removed. 5 Current treatment options Menorrhagia: Drugs that can reduce heavy MBL include tranexamic acid, non-steroidal antiinflammatory drugs, combined oral contraceptives, progestogens, and the levonorgestrel intrauterine system L-IUS ; . Surgery hysterectomy or endometrial resection ; is an alternative treatment, but as this usually results in infertility, it is not suitable for women who may wish to become pregnant at a later date. 3 Factors influencing treatment choice are: whether cycles are ovulatory or anovulatory; the need for contraception; patient preference; and contraindications to treatment. It is recommended that women are offered at least one course of drug treatment before referral for surgery.5 Contraception: There are three main methods of contraception other than sterilisation: hormonal preparations, intrauterine devices IUDs ; , and barrier methods. The hormonal method is most effective, but carries potential side effects in certain groups. Copper-releasing IUDs are also effective contraceptives, but may produce undesirable local and librium.
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Medications, especially gastrointestinal side effects with mexiletine, must be considered before use. The efficacy of topical capsaicin is less clear 22, 23 ; . Nonaddictive analgesics may be used to alleviate pain. Although subclinical autonomic neuropathic manifestations are common, symptomatic involvement is infrequent. The diagnosis of symptomatic autonomic neuropathy is based on exclusion of specific cardiovascular, gastrointestinal or genitourinary pathology, usually requiring assessment by a specialist in the affected system. Treatment of autonomic neuropathy is based mainly on expert opinion, but research in this field remains active 24.
Physicians recommend that levonorgestrel should not be used as an oral contraceptive if a woman is pregnant, or has a history of unexplained vaginal bleeding, allergy to the drug, blood clots, breast cancer, pelvic inflammatory disease, or active liver disease and licorice.
Gynecology&Andrology Climara ProTM U.S.: submitted for registration Patch containing a combination of estradiol and levonorgestrel for the treatment of climacteric complaints and osteoporosis prevention; only needs to be renewed once a week ClimarelleTM Phase III Patch with a particularly low estrogen dose for continuous estrogen therapy in the treatment of climacteric complaints and osteoporosis prevention
Fig. 5. A ; Total number of spontaneous epileptic seizures recorded with video-EEG in all epileptic animals during the 6-mo follow-up divided into 2-week epochs. Seizures that appeared during handling were excluded n 113 ; . The total number of seizures in the whole animal group increased up to 14 weeks. B ; Total number of partial seizures Score 0 2 ; and C ; total number of generalized seizures Score 3 5 ; during the 6-month follow-up period. Note that the progressive increase in seizure number during the first 14 weeks was because of an increase in the number of behaviorally partial seizures and linezolid.
Other studied parameters. It is worth noting that the studied population was strictly selected, including women without any apparent reproductive disorders that might bias the results, and that all of them underwent controlled ovarian stimulation according to the long agonist protocol. In conclusion, VEGF and leptin concentrations in FFs may serve as reliable predictive markers for ICSI.
Hepatic glucose output unless transport capacity were also increased. Glucose transport in hepatocytes is mediated mainly by the GLUT2 glucose transport protein, one of a family of glucose transporters, which is expressed in liver, pancreatic P-cells, and intestinal and renal epithelium 5, 6 ; . [A small subset of hepatocytes perivenular ; additionally expresses GLUT'I 7 ; .] Consistent with its role as the principal mediator of glucose uptake and export across the hepatocyte plasma membrane, GLUT2 has a high K, for glucose 8, 9 ; and is expressed on the sinusoidal membrane 10 ; . Several laboratories have reported that hepatic GLUT2 messenger RNA mRNA ; and protein are elevated in experimental insulindeficient diabetes 1 l-14 ; , a state of greatly enhanced gIuconeogenesisand hepatic glucose output. Conversely, hyperinsulinemia rapidly suppresses GLUT2 mRNA levels, albeit transiently 15 ; . These observations provide direct evidence that hepatic GLUT2 gene expression, rather than being constitutive and not subject to regulation, is in fact regulated, at least in insulin deficiency, in a manner that would provide increased glucose transport capacity in parallel with increasedgluconeogenesis.Whether hepatic GLUT2 expression is regulated in states of altered hepatic glucose production other than diabetes and insulin exposure is not known. In hyperthyroid man 16-19 ; as well as in experimental thyrotoxicosis in animals 20, 21 ; , glucose turnover and hepatic glucose production are increased, meeting a need created by increased metabolic rate and peripheral glucose utilization and reflecting increased gluconeogenesis 22 ; . Experimental as well as spontaneous hyperthyroidism in humans causes increased basal glucose production and im and liothyronine.
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P. Michael Conn, recipient of the 2005 Sidney H. Ingbar Distinguished Service Award, has provided remarkable service to the field of endocrinology as an editor, patient advocate, and in leadership roles. While President of The Society, he promoted the development of the Hormone Foundation : hormone. org ; , constituted and served on its first board and, as interim CEO, developed its logo, mission statement, and oversaw development of its first brochure and first public event. Also during his presidency, he worked with his congressional representative, herself the mother of a diabetic, to promote use of federal dollars for blood sugar testing, a program that was ultimately included in the Clinton budget as a result of the widespread congressional support. His and levonorgestrel.
Agt ophth-prep ophth-antiinf, 190253 ; . LEVOMETHADYL N: SI: H-TTMED ; , med: 29095 ; . LEVOMETHADYL ACETATE N: H-TTMED ; , med: med-cl cnsagt analg narc-analg, 190254 ; . LEVOMETHADYL ACETATE HCL N: SI: H-TTMED ; , med: 29097 ; . LEVONORGESTREL N: H-TTMED ; , med: med-cl ch-cl-hrm sexhrm progest, 190255 ; . LEVOPHED N: SI: H-TTMED ; , med: 29099 ; . LEVOPHED BITARTRATE N: H-TTMED ; , med: med-cl cv-agt vasopr, 184607 ; . LEVOPROME N: H-TTMED ; , med: med-cl cns-agt analg misc-analg, 184608 ; . LEVOPROPOXYPHENE NAPSYLATE N: SI: H-TTMED ; , med: 29102 ; . LEVORA N: H-TTMED ; , med: med-cl ch-cl-hrm sex-hrm oral-contracept, med-cl ch-cl-hrm sex-hrm estrog, med-cl ch-cl-hrm sex-hrm progest, 184609 ; . LEVORA 0.15 30-21 N: SI: H-TTMED ; , med: 29104 ; . LEVORPHANOL N: H-TTMED ; , med: med-cl cns-agt analg narc-analg, 190256 ; . LEVORPHANOL TARTRATE N: H-TTMED ; , med: med-cl cnsagt analg narc-analg, 184610 ; . LEVOTABS N: H-TTMED ; , med: med-cl ch-cl-hrm thy-drg, 184611 ; . LEVOTHROID N: H-TTMED ; , med: med-cl ch-cl-hrm thy-drg, 184612 ; . LEVOTHYROXIN N: SI: H-TTMED ; , med: med-cl ch-cl-hrm thy-drg, 140402 ; . LEVOTHYROXINE N: H-TTMED ; , med: med-cl ch-cl-hrm thy-drg, 190257 ; . LEVOTHYROXINE 100 MCG PO QD N: SI: H-TTMED ; , med: med-cl chcl-hrm thy-drg, 1001604 ; . LEVOTHYROXINE SODIUM N: H-TTMED ; , med: med-cl ch-cl-hrm thydrg, 184613 ; . LEVOXINE N: SI: H-TTMED ; , med: 29111 ; . LEVOXYL N: H-TTMED ; , med: med-cl ch-cl-hrm thy-drg, 184614 ; . LEVSIN N: H-TTMED ; , med: med-cl gi-agt antichol-antispas, 184615 ; . LEVSIN SL N: H-TTMED ; , med: med-cl gi-agt antichol-antispas, 184616 ; . LEVSIN WITH PHENOBARBITAL N: H-TTMED ; , med: med-cl psyagt anx-sed-hyp barb, med-cl gi-agt antichol-antispas, med-cl cnsagt anticonv barb-anticonv, 184617 ; . LEVSINEX N: SI: H-TTMED ; , med: 29116 ; . LEVSINEX SR N: H-TTMED ; , med: med-cl gi-agt antichol-antispas, 184618 ; . July 15, 2005 and lomefloxacin.
31. Wang SL, Wu SC, Xin XM, Chen JH, Gao J. Three years experience with levonorgestrelreleasing intrauterine device and Norplant-2 implants: a randomized comparative study. Adv Contracept 1992; 8: 10514. Faundes A, Alvarez F, Diaz JA. Latin American experience with levonorgestrel IUD. Ann Med 1993; 25: 14953. Heikkila M, Luukkainen T. Duration of breast-feeding and development of children after insertion of a levonorgestrel-releasing intrauterine contraceptive device. Contraception 1982; 25: 27992. Heikkila M, Haukkamaa M, Luukkainen T. Levonorgestrel in milk and plasma of breast-feeding women with a levonorgestrelreleasing IUD. Contraception 1982; 25: 419. Andersson K, Batar I, Rybo G. Return to fertility after removal of a levonorgestrel-releasing intrauterine device and Nova-T. Contraception 1992; 46: 57584. Luukkainen T, Allonen H, Haukkamaa M. Effective contraception with the levonorgestrel-releasing intrauterine device: 12month report of a European multicenter study. Contraception 1987; 36: 16979. Franks AL, Beral V, Cates W Jr, Hogue CJ. Contraception and ectopic pregnancy risk. J Obstet Gynecol 1990; 163: 11203. Peterson HB, Xia Z, Hughes JM, Wilcox LS, Tylor LR, Trussell J. The risk of pregnancy after tubal sterilization: findings from the US Collaborative Review of Sterilization CREST ; . J Obstet Gynecol 1996; 174: 116170. Treiman K, Liskin L, Kols A, Rinehart W. IUDs an update. Population Reports, series B no 6, 1995; 22: Philip T, Guillebaud J, Budd D. Late failure of vasectomy after two documented analyses showing azoospermic semen. Br Med J 1984; 289: 779. Westrom L. Genital tract infection in women. Long-term consequences of pelvic inflammatory disease. Hare MJ ed ; . Churchill Livingstone, Edinburgh, 1988; 35067. 42. Buchan H, Vessey M. Epidemiology and trends in hospital discharges for pelvic inflammatory disease in England 19751985. Br J Obstet Gynaecol 1989; 96: 121923. Westrom L. Effect of acute pelvic inflammatory disease on fertility. J Obstet Gynecol 1975; 121: 70713. Westrom L, Bengtsson LP, Mardh PA. The risk of pelvic inflammatory disease in women using intrauterine contraceptive devices as compared to non users. Lancet 1976; 2: 221 Buchen H, Villard-Mackintosh L, Vessey M, Yeates D, McPherson K. Epidemiology of pelvic inflammatory disease in parous women with special reference to intrauterine device use. Br J Obstet Gynaecol 1990; 97: 7808. Farley TMM, Rosenberg M, Rowe PJ, Chien J-H, Meirik O. Intrauterine devices and pelvic inflammatory disease: an international perspective. Lancet 1992; 339: 7858. Toivonen J, Luukkainen T, Allonen H. Protective effect of intrauterine release of levonorgestrel on pelvic infection: three years'comparative experience of levonorgestrel- and copper-releasing intrauterine devices [see comments]. Obstet Gynecol 1991; 77: 2614. Lee NC, Rubin GL, Ory HW, Burkman RT. Type of intrauterine device and the risk of pelvic inflammatory disease. Obstet Gynecol 1983; 62: 16. Mishell DS. The intrauterine device: a bacteriologic study of the endometrial cavity. J Obstet Gynecol 1966; 96: 11926. Rivera R. Is there an effect of the IUD string in the development of pelvic inflammatory disease in IUD users? In: Bardin CW, Mishell DR Jr eds ; . Proceedings from the Fourth International Conference on IUDs. Butterworth-Heinemann, 1994; 1718. 51. Sinei SKA, Schulz KF, Lamptey PR. Preventing IUCD-related pelvic infection: the efficacy of prophylactic doxycycline at insertion. Br J Obstet Gynaecol 1990; 97: 4129. Walsh T, Grimes D, Frezieres R, Nelson A, Bernstein L, Coulson A, Bernstein G. Randomised controlled trial of prophylactic antibiotics before insertion of intrauterine devices. Lancet 1998; 351: 10058. Fedele L, Bianchi E, Raffaelli R, Portuese A, Dorta M. Treat- ment of adenomyosis associated menorrhagia with a levonorgestrel-releasing intrauterine device. Fertil Steril 1997; 68: 4269. Fong Y-F, Sing K. Medical treatment of a grossly enlarged adenomyotic uterus with the levonorgestrel-releasing intrauterine System. Contraception 1999; 60: 1735. Singer A, Ikomi A. Successful treatment of uterine fibroids using an intrauterine progesterone device. XIV FIGO Congress, Montreal, Canada. 1994. Abstract ; 56. Guidence LC, Irwin JC, Dsupin BAEA. Insulin-like growth factor IGF ; . IGF binding protein IGFBP ; and IGF receptor gene expression and IGFBP synthesis in human uterine leiomyomata. Hum Reprod 1993; 8: 17961806. Pekonen F, Nyman T, Lahteenmaki P, Haukkamaa M, Rutanen EM. Intrauterine progestin induces continous insulin like growth factor-binding protein-I production in the human endometrium. J Clin Endocrinol Metabol 1992; 75: 6604. McCausland AM, McCausland VM. Depth of endometrial penetration in adenomyosis helps determine outcome of rollerball ablation. J Obstet Gynecol 1996; 174: 1786 Takebayashi T, Fujino Y, Umesaki N, Ogita S. Danazol suspension injected into uterine cervix of patients with adenomyosis and myoma. Gynecol Obstet Invest 1995; 39: 20711. Nelson JR, Corson SL. Long-term management of adenomyosis with a gonadotropin-releasing hormone agonist: a case report. Fertil Steril 1993; 59: 4413. Critchley HOD, Wang H, Kelly RW, Gebbie AE, Glasier AF. Progestinreceptor isoforms and prostaglandin dehydrogenase in the endometrium of women using a levonorgestrel-releasing intrauterine system. Hum Reprod 1998; 13: 12107. Nilsson C, Haukkamaa M, Vierola H, Luukkainen T. Tissue concentrations of levonorgestrel in women using a levonorgestrel-releasing IUS. Clin Endocrinol 1982; 17: 52936. Cameron IT, Leask R, Kelly RW, Baird DT. The effects of danazol, mefenamic acid, norethisterone and a progesterone-impregnated coil on endometrial prostaglandin concentrations in women with menorrhagia. Prostaglandins 1987; 34: 99110. Hallberg L, Nilsson I. Determination of menstrual blood loss. Scand J Lab Invest 1964; 16: 2448. Hallberg L, Hgdahl AM, Nilsson L, Rybo G. Menstrual blood loss, a population study. Acta Obstet Gynecol Scand 1966; 45: 320 Cole SK, Billewicz WZ, Thomson AM. Sources of variation in menstrual blood loss. J Obstet Gynaecol Br Commonwlth 1971; 78: 9339. Kadir RA, Economides DL, Sabin CA. Frequency of inherited bleeding disorders in women with menorrhagia. Lancet 1998; 351: 4859. Scott HM, Scott WG. Hysterectomy for non-malignant conditions: cost to New Zealand society. NZ Med J 1995; 108: 4236. Coulter A, Bradlow J, Agass M, MartinBates C, Tulloch A. Outcomes of referrals to gynaecology outpatient clinics for menstrual problems: an audit of general practice. Br J Obstet Gynaecol 1991; 98: 78996. Vessey MP, Villard-Mackintosh L, McPherson K, Coulter A, Yeates D. The epidemiology of hysterectomy: findings in a large cohort study. Br J Obstet Gynaecol 1992; 99: 4027. Scottish Hysteroscopic audit Group: A scottish audit of hysteroscopic surgery for menorrhagia: complications and follow up. Br J Obstet Gynaecol 1995; 102: 24954. Dwyer N, Hutton J, Stirrat GM. Randomised controlled trial comparing endometrial resection with abdominal hysterectomy for the surgical treatment of menorrhagia. Br J Obstet Gynaecol 1993; 100: 237 Pinion S, Parkin DE, Abramovich DR. Randomised trial of hysterectomy, endometrial laser ablation and transcervical endome.
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