eMedicine Specialties > Obstetrics and Gynecology > General Gynecology

Dysmenorrhea

Author: Karim Anton Calis, PharmD, MPH, FASHP, FCCP, Professor, Medical College of Virginia, Virginia Commonwealth University, Clinical Professor, University of Maryland; Clinical Investigator, Program in Developmental Endocrinology and Genetics, Eunice Kennedy Shriver National Institute of Child Health and Human Development, National Institutes of Health.
Coauthor(s): Vaishali Popat, MD, MPH, Clinical Investigator, Intramural Research Program on Reproductive and Adult Endocrinology, National Institutes of Child Health and Human Development, National Institutes of Health; Devra K Dang, PharmD, BCPS, CDE, Assistant Clinical Professor, University of Connecticut School of Pharmacy, Clinical Faculty, Burgdorf Health Center; Sophia N Kalantaridou, MD, Assistant Professor, Department of Obstetrics and Gynecology, University of Ioannina Medical School, Greece
Contributor Information and Disclosures

Updated: Jan 28, 2009

Introduction

Background

Dysmenorrhea is defined as difficult menstrual flow or painful menstruation. The term dysmenorrhea is derived from the Greek words dys, meaning difficult/painful/abnormal, meno, meaning month, and rrhea, meaning flow.

Dysmenorrhea is one of the most common gynecologic complaints in young women who present to clinicians.1 The optimal management of this symptom depends on an understanding of the underlying cause. Dysmenorrhea is classified as primary (spasmodic) or secondary (congestive).2

Primary dysmenorrhea is defined as menstrual pain not associated with macroscopic pelvic pathology (ie, absence of pelvic disease). It typically occurs in the first few years after menarche3 and affects up to 50% of postpubescent females.4

Secondary dysmenorrhea is defined as menstrual pain resulting from anatomic and/or macroscopic pelvic pathology,3,5 such as that seen in women with endometriosis or chronic pelvic inflammatory disease. This condition is most often observed in women aged 30-45 years.

The following risk factors have been associated with more severe episodes of dysmenorrhea:6

  1. Earlier age at menarche
  2. Long menstrual periods
  3. Heavy menstrual flow
  4. Smoking
  5. Positive family history

Obesity and alcohol consumption were found to be associated with dysmenorrhea in some (not all) studies.7,8,9 Physical activity and the duration of the menstrual cycle do not appear to be associated with increased menstrual pain.7

Pathophysiology

The etiology and pathophysiology of dysmenorrhea have not been fully elucidated. Nonetheless, the following may be involved.

Primary dysmenorrhea

Current evidence suggests that the pathogenesis of primary dysmenorrhea is due to prostaglandin F2alpha (PGF2alpha), a potent myometrial stimulant and vasoconstrictor, in the secretory endometrium.10 The response to prostaglandin inhibitors in patients with dysmenorrhea supports the assertion that dysmenorrhea is prostaglandin mediated. Substantial evidence attributes dysmenorrhea to prolonged uterine contractions and decreased blood flow to the myometrium.

Elevated prostaglandin levels were found in the endometrial fluid of women with dysmenorrhea and correlated well with the degree of pain.11 A 3-fold increase in endometrial prostaglandins occurs from the follicular phase to the luteal phase, with a further increase occurring during menstruation.12 The increase in prostaglandins in the endometrium following the fall in progesterone in the late luteal phase results in increased myometrial tone and excessive uterine contraction.5

Leukotrienes have been postulated to heighten the sensitivity of pain fibers in the uterus. Significant amounts of leukotrienes have been demonstrated in the endometrium of women with primary dysmenorrhea that does not respond to treatment with prostaglandin antagonists.8,13,14,15,16

The posterior pituitary hormone vasopressin may be involved in myometrial hypersensitivity, reduced uterine blood flow, and pain in primary dysmenorrhea.17,18 Vasopressin's role in the endometrium may be related to prostaglandin synthesis and release.

A neuronal hypothesis has also been advocated for the pathogenesis of primary dysmenorrhea. Type C pain neurons are stimulated by the anaerobic metabolites generated by an ischemic endometrium.

Primary dysmenorrhea has also been attributed to behavioral and psychological factors. Although these factors have not been convincingly demonstrated to be causative, they should be considered if medical treatment fails.

Secondary dysmenorrhea

A number of factors may be involved in the pathogenesis of secondary dysmenorrhea. The following pelvic pathologies can lead to the condition:

  • Endometriosis
  • Pelvic inflammatory disease
  • Ovarian cysts and tumors
  • Cervical stenosis or occlusion
  • Adenomyosis
  • Fibroids
  • Uterine polyps
  • Intrauterine adhesions
  • Congenital malformations (eg, bicornate uterus, subseptate uterus)
  • Intrauterine contraceptive device
  • Transverse vaginal septum
  • Pelvic congestion syndrome
  • Allen-Masters syndrome

Almost any process that can affect the pelvic viscera can produce cyclic pelvic pain.19

Frequency

United States

Dysmenorrhea may affect more than half of menstruating women, and its reported prevalence has been highly variable. A survey of 113 patients in a family practice setting showed a prevalence of dysmenorrhea of 29-44%,20 but prevalence rates as high as 90% in women aged 18-45 years have been reported.1 The use of oral contraceptives (OCs) and nonsteroidal anti-inflammatory drugs (NSAIDs), both of which are effective in ameliorating symptoms of primary dysmenorrhea, may confound the prevalence.

Primary dysmenorrhea peaks in late adolescence and the early 20s.21 The incidence falls with increasing age and with increasing parity. The prevalence and severity of dysmenorrhea in parous women are reportedly significantly lower in many7,22,23 but not all1 studies. No significant difference with respect to prevalence and severity of dysmenorrhea was found between nulligravid women and those in whom pregnancy had been terminated by either spontaneous or induced abortion.7

In an epidemiologic study of an adolescent population (aged 12-17 y), Klein and Litt reported a prevalence of dysmenorrhea of 59.7%.24 Of patients reporting pain, 12% described it as severe; 37%, as moderate; and 49%, as mild. Dysmenorrhea caused 14% of patients to miss school frequently. Although black adolescents reported no increased incidence of dysmenorrhea, they were absent from school more frequently (23.6%) than whites (12.3%), even after adjusting for socioeconomic status.

International

The prevalence of dysmenorrhea worldwide is similar to that in the US, with rates ranging from 15.8-89.5%, with higher prevalence rates reported in adolescent populations.25,26,27,7,28,22,29,30

Mortality/Morbidity

Dysmenorrhea can disrupt personal life and is a significant public health problem associated with substantial economic loss related to work absences. Ten percent of women with the condition have severe pain that can be incapacitating. In the United States, the annual economic loss has been estimated at 600 million work hours and 2 billion dollars.31

Race

No data suggest that race affects the incidence of dysmenorrhea.

Sex

See Frequency.

Age

See Frequency.

Clinical

History

  • History is critical in establishing the diagnosis of dysmenorrhea and should include an assessment of the onset, duration, type, and severity of pain. A thorough menstrual history is also essential and should include the age at menarche, cycle regularity, cycle length, last menstrual period, and duration and amount of menstrual flow.
  • Determine factors that exacerbate or ameliorate the symptoms and the degree of disruption to school, work, and social activities.
  • Consider gravidity and parity status, previous pelvic infections, dyspareunia, infertility, and pelvic surgeries, injuries, and procedures.
  • Also assess symptoms such as nausea, vomiting, bloating, diarrhea, and fatigue, which may be observed in patients with dysmenorrhea.
  • Consider sexual history, including the choice of contraceptive methods. If used, establish the effect of OCs on relieving or exacerbating the condition. Moreover, discuss the use of other agents that affect dysmenorrhea pain.
  • A family history may be helpful in differentiating endometriosis from primary dysmenorrhea.32 The history should include questions pertaining to sexual abuse because this is reportedly associated with dysmenorrhea and chronic pelvic pain.33
  • In summary, a complete history should include the following:
    • Age at menarche
    • Menstrual frequency, length of period, estimate of the menstrual flow, and presence or absence of intermenstrual bleeding
    • Associated symptoms
    • Severity of pain and its relationship to the menstrual cycle
    • Impact on physical and social activity
    • Progression of symptom severity
    • Sexual history
  • Primary dysmenorrhea should be distinguished from secondary dysmenorrhea on the basis of clinical features.
    • Primary dysmenorrhea almost invariably occurs in ovulatory cycles and usually appears within a year after menarche. In classic primary dysmenorrhea, the pain begins with the onset of menstruation (or just shortly before) and persists throughout the first 1-2 days. The pain is described as spasmodic and superimposed over a background of constant lower abdominal pain, which radiates to the back or anterior and/or medial thigh.
    • Associated general symptoms, such as malaise, fatigue (85%), nausea and vomiting (89%), diarrhea (60%), lower backache (60%), and headache (45%), may be present with primary dysmenorrhea. Dizziness, nervousness, and even collapse are also associated with dysmenorrhea.
    • The clinical features of primary dysmenorrhea include the following:
      • Onset shortly after menarche
      • Usual duration of 48-72 hours (often starting several hours before or just after the menstrual flow)
      • Cramping or laborlike pain
      • Often unremarkable pelvic examination findings (including rectal)
    • A different pattern of pain is observed with secondary dysmenorrhea that is not limited to the onset of menses; this is usually associated with abdominal bloating, pelvic heaviness, and back pain. Typically, the pain progressively increases during the luteal phase until it peaks around the onset of menstruation.
    • The following may indicate secondary dysmenorrhea19,34 :
      • Dysmenorrhea occurring during the first or second cycles after menarche, which may indicate congenital outflow obstruction
      • Dysmenorrhea beginning after the age of 25 years
      • Pelvic abnormality with physical examination: Consider endometriosis, pelvic inflammatory disease, pelvic adhesions, and adenomyosis.
      • Little or no response to therapy with NSAIDs, OCs, or both

Physical

  • A pelvic examination is indicated at the initial evaluation, which should be carefully performed in order to exclude uterine irregularities, cul-de-sac tenderness, or nodularity that may suggest endometriosis, pelvic inflammatory disease, or a pelvic mass.
  • Women with primary dysmenorrhea usually have normal findings on examination.
  • Pelvic pathology may be found during pelvic examination in women with secondary dysmenorrhea, although normal findings do not exclude the condition.
    • Women with endometriosis who present with secondary dysmenorrhea have physical findings approximately 40% of the time.35,36
    • Patients presenting with secondary dysmenorrhea may have unique and specific findings on physical examination that correspond to their particular pathologies.

Causes

  • Causes of secondary dysmenorrhea include the following:
    • Intrauterine contraceptive devices
    • Adenomyosis
    • Uterine myoma (fibroids)
    • Uterine polyps
    • Adhesions
    • Congenital malformation of the müllerian system
    • Cervical strictures or stenosis
    • Ovarian cysts
    • Pelvic congestion syndrome
    • Allen-Masters syndrome
    • Mittelschmerz (midcycle ovulation pain)
    • Psychogenic pain

More on Dysmenorrhea

Overview: Dysmenorrhea
Differential Diagnoses & Workup: Dysmenorrhea
Treatment & Medication: Dysmenorrhea
Follow-up: Dysmenorrhea
References
[ CLOSE WINDOW ]

References

  1. Jamieson DJ, Steege JF. The prevalence of dysmenorrhea, dyspareunia, pelvic pain, and irritable bowel syndrome in primary care practices. Obstet Gynecol. Jan 1996;87(1):55-8. [Medline].

  2. Dawood MY. Dysmenorrhea. J Reprod Med. Mar 1985;30(3):154-67. [Medline].

  3. Koltz MM. Dysmenorrhea, endometriosis and pelvic pain. In: Lemeke DP, Pattison J, Marshall LA, Cowley DS, eds. Primary Care of Women. Norwalk Conn. Appleton & Lange: 1992:420-32.

  4. Dawood MY. Nonsteroidal anti-inflammatory drugs and changing attitudes toward dysmenorrhea. Am J Med. May 20 1988;84(5A):23-9. [Medline].

  5. Dawood MY. Dysmenorrhea. Clin Obstet Gynecol. Mar 1990;33(1):168-78. [Medline].

  6. Harlow SD, Park M. A longitudinal study of risk factors for the occurrence, duration and severity of menstrual cramps in a cohort of college women. Br J Obstet Gynaecol. Nov 1996;103(11):1134-42. [Medline].

  7. Andersch B, Milsom I. An epidemiologic study of young women with dysmenorrhea. Am J Obstet Gynecol. Nov 15 1982;144(6):655-60. [Medline].

  8. Sundell G, Milsom I, Andersch B. Factors influencing the prevalence and severity of dysmenorrhoea in young women. Br J Obstet Gynaecol. Jul 1990;97(7):588-94. [Medline].

  9. Parazzini F, Tozzi L, Mezzopane R, Luchini L, Marchini M, Fedele L. Cigarette smoking, alcohol consumption, and risk of primary dysmenorrhea. Epidemiology. Jul 1994;5(4):469-72. [Medline].

  10. Willman EA, Collins WP, Clayton SG. Studies in the involvement of prostaglandins in uterine symptomatology and pathology. Br J Obstet Gynaecol. May 1976;83(5):337-41. [Medline].

  11. Eden JA. Dysmenorrhea and premenstrual syndrome. In: NF Hacker, JG Moore, eds. Essentials of Obstetrics and Gynecology. 3rd ed. Philadelphia: WB Saunders; 1998:386-92.

  12. Speroff L. Postmenopausal hormone therapy into the 21st century. Int J Gynaecol Obstet. Oct 1997;59 Suppl 1:S3-10. [Medline].

  13. Demers LM, Hahn DW, McGuire JL. Newer concepts in dysmenorrhea research: leukotrienes and calcium channel blockers. In: Dawood MY, McGuire JL, Demers LM, eds. Premenstrual Syndrome and Dysmenorrhea. London: Pitman; 1984:205-13.

  14. Chegini N, Rao CV. The presence of leukotriene C4- and prostacyclin-binding sites in nonpregnant human uterine tissue. J Clin Endocrinol Metab. Jan 1988;66(1):76-87. [Medline].

  15. Nigam S, Benedetto C, Zonca M, Leo-Rossberg I, Lubbert H, Hammerstein J. Increased concentrations of eicosanoids and platelet-activating factor in menstrual blood from women with primary dysmenorrhea. Eicosanoids. 1991;4(3):137-41. [Medline].

  16. Rees MC, DiMarzo V, Tippins JR, Morris HR, Turnbull AC. Leukotriene release by endometrium and myometrium throughout the menstrual cycle in dysmenorrhoea and menorrhagia. J Endocrinol. May 1987;113(2):291-5. [Medline].

  17. Akerlund M, Stromberg P, Forsling ML. Primary dysmenorrhoea and vasopressin. Br J Obstet Gynaecol. Jun 1979;86(6):484-7. [Medline].

  18. Akerlund M. Pathophysiology of dysmenorrhea. Acta Obstet Gynecol Scand Suppl. 1979;87:27-32. [Medline].

  19. Smith RP. Cyclic pelvic pain and dysmenorrhea. Obstet Gynecol Clin North Am. Dec 1993;20(4):753-64. [Medline].

  20. Sobczyk R, Braunstein ML, Solberg L, Schuman SH. A case control survey and dysmenorrhea in a family practice population: a proposed disability index. J Fam Pract. Aug 1978;7(2):285-90. [Medline].

  21. Fraser IS. Prostaglandins, prostaglandin inhibitors and their roles in gynaecological disorders. Baillieres Clin Obstet Gynaecol. Dec 1992;6(4):829-57. [Medline].

  22. Osuga Y, Hayashi K, Kobayashi Y, Toyokawa S, Momoeda M, Koga K, et al. Dysmenorrhea in Japanese women. Int J Gynaecol Obstet. Jan 2005;88(1):82-3. [Medline].

  23. Latthe P, Mignini L, Gray R, Hills R, Khan K. Factors predisposing women to chronic pelvic pain: systematic review. BMJ. Apr 1 2006;332(7544):749-55. [Medline].

  24. Klein JR, Litt IF. Epidemiology of adolescent dysmenorrhea. Pediatrics. Nov 1981;68(5):661-4. [Medline].

  25. Ohde S, Tokuda Y, Takahashi O, Yanai H, Hinohara S, Fukui T. Dysmenorrhea among Japanese women. Int J Gynaecol Obstet. Jan 2008;100(1):13-7. [Medline].

  26. Sharma P, Malhotra C, Taneja DK, Saha R. Problems related to menstruation amongst adolescent girls. Indian J Pediatr. Feb 2008;75(2):125-9. [Medline].

  27. Lee LK, Chen PC, Lee KK, Kaur J. Menstruation among adolescent girls in Malaysia: a cross-sectional school survey. Singapore Med J. Oct 2006;47(10):869-74. [Medline].

  28. El-Gilany AH, Badawi K, El-Fedawy S. Epidemiology of dysmenorrhoea among adolescent students in Mansoura, Egypt. East Mediterr Health J. Jan-Mar 2005;11(1-2):155-63. [Medline].

  29. Cakir M, Mungan I, Karakas T, Girisken I, Okten A. Menstrual pattern and common menstrual disorders among university students in Turkey. Pediatr Int. Dec 2007;49(6):938-42. [Medline].

  30. Burnett MA, Antao V, Black A, Feldman K, Grenville A, Lea R, et al. Prevalence of primary dysmenorrhea in Canada. J Obstet Gynaecol Can. Aug 2005;27(8):765-70. [Medline].

  31. Dawood MY. Ibuprofen and dysmenorrhea. Am J Med. Jul 13 1984;77(1A):87-94. [Medline].

  32. Simpson JL, Elias S, Malinak LR, Buttram VC Jr. Heritable aspects of endometriosis. I. Genetic studies. Am J Obstet Gynecol. Jun 1 1980;137(3):327-31. [Medline].

  33. Jamieson DJ, Steege JF. The association of sexual abuse with pelvic pain complaints in a primary care population. Am J Obstet Gynecol. Dec 1997;177(6):1408-12. [Medline].

  34. Smith RP. Gynecology in Primary Care. Baltimore. Williams & Wilkins; 1997:389-404.

  35. Propst AM, Storti K, Barbieri RL. Lateral cervical displacement is associated with endometriosis. Fertil Steril. Sep 1998;70(3):568-70. [Medline].

  36. Barbieri RL, Propst AM. Physical examination findings in women with endometriosis: uterosacral ligament abnormalities, lateral cervical displacement and cervical stenosis. J Gynecol Tech. 1999;135:102.

  37. Gürgan T, Urman B, Aksu T, Develioglu O, Zeyneloglu H, Kisnisçi HA. Laparoscopic CO2 laser uterine nerve ablation for treatment of drug resistant primary dysmenorrhea. Fertil Steril. Aug 1992;58(2):422-4. [Medline].

  38. Chen FP, Chang SD, Chu KK, Soong YK. Comparison of laparoscopic presacral neurectomy and laparoscopic uterine nerve ablation for primary dysmenorrhea. J Reprod Med. Jul 1996;41(7):463-6. [Medline].

  39. [Best Evidence] Latthe PM, Proctor ML, Farquhar CM, Johnson N, Khan KS. Surgical interruption of pelvic nerve pathways in dysmenorrhea: a systematic review of effectiveness. Acta Obstet Gynecol Scand. 2007;86(1):4-15. [Medline].

  40. Barnard ND, Scialli AR, Hurlock D, Bertron P. Diet and sex-hormone binding globulin, dysmenorrhea, and premenstrual symptoms. Obstet Gynecol. Feb 2000;95(2):245-50. [Medline].

  41. Harel Z, Biro FM, Kottenhahn RK, Rosenthal SL. Supplementation with omega-3 polyunsaturated fatty acids in the management of dysmenorrhea in adolescents. Am J Obstet Gynecol. Apr 1996;174(4):1335-8. [Medline].

  42. Akin M, Price W, Rodriguez G Jr, Erasala G, Hurley G, Smith RP. Continuous, low-level, topical heat wrap therapy as compared to acetaminophen for primary dysmenorrhea. J Reprod Med. Sep 2004;49(9):739-45. [Medline].

  43. Akin MD, Weingand KW, Hengehold DA, Goodale MB, Hinkle RT, Smith RP. Continuous low-level topical heat in the treatment of dysmenorrhea. Obstet Gynecol. Mar 2001;97(3):343-9. [Medline].

  44. Milsom I, Andersch B, Sundell G. The effect of flurbiprofen and naproxen sodium on intra-uterine pressure and menstrual pain in patients with primary dysmenorrhea. Acta Obstet Gynecol Scand. 1988;67(8):711-6. [Medline].

  45. Chan WY, Fuchs F, Powell AM. Effects of naproxen sodium on menstrual prostaglandins and primary dysmenorrhea. Obstet Gynecol. Mar 1983;61(3):285-91. [Medline].

  46. Dawood MY, Khan-Dawood FS. Clinical efficacy and differential inhibition of menstrual fluid prostaglandin F2alpha in a randomized, double-blind, crossover treatment with placebo, acetaminophen, and ibuprofen in primary dysmenorrhea. Am J Obstet Gynecol. Jan 2007;196(1):35.e1-5. [Medline].

  47. Zhang WY, Li Wan Po A. Efficacy of minor analgesics in primary dysmenorrhoea: a systematic review. Br J Obstet Gynaecol. Jul 1998;105(7):780-9. [Medline].

  48. Rosenwaks Z, Jones GS, Henzl MR, Dubin NH, Ghodgaonkar RB, Hoffman S. Naproxen sodium, aspirin, and placebo in primary dysmenorrhea. Reduction of pain and blood levels of prostaglandin F2-alpha metabolite. Am J Obstet Gynecol. Jul 1 1981;140(5):592-8. [Medline].

  49. Daniels SE, Torri S, Desjardins PJ. Valdecoxib for treatment of primary dysmenorrhea. A randomized, double-blind comparison with placebo and naproxen. J Gen Intern Med. Jan 2005;20(1):62-7. [Medline].

  50. Morrison BW, Daniels SE, Kotey P, Cantu N, Seidenberg B. Rofecoxib, a specific cyclooxygenase-2 inhibitor, in primary dysmenorrhea: a randomized controlled trial. Obstet Gynecol. Oct 1999;94(4):504-8. [Medline].

  51. Sillem M, Schneidereit R, Heithecker R, Mueck AO. Use of an oral contraceptive containing drospirenone in an extended regimen. Eur J Contracept Reprod Health Care. Sep 2003;8(3):162-9. [Medline].

  52. Vercellini P, Frontino G, De Giorgi O, Pietropaolo G, Pasin R, Crosignani PG. Continuous use of an oral contraceptive for endometriosis-associated recurrent dysmenorrhea that does not respond to a cyclic pill regimen. Fertil Steril. Sep 2003;80(3):560-3. [Medline].

[ CLOSE WINDOW ]

Further Reading

[ CLOSE WINDOW ]

Keywords

primary dysmenorrhea, secondary dysmenorrhea, painful menstruation, painful menses, spasmodic dysmenorrhea, congestive dysmenorrhea, endometriosis, pelvic inflammatory disease, PID, ovarian cysts, ovarian tumors, cervical stenosis, cervical occlusion, adenomyosis, fibroids, uterine polyps, intrauterine adhesions, congenital malformations, bicornuate uterus, subseptate uterus, intrauterine contraceptive devices, IUCDs, intrauterine devices, IUDs, transverse vaginal septum, pelvic congestion syndrome, Allen-Masters syndrome

[ CLOSE WINDOW ]

Contributor Information and Disclosures

Author

Karim Anton Calis, PharmD, MPH, FASHP, FCCP, Professor, Medical College of Virginia, Virginia Commonwealth University, Clinical Professor, University of Maryland; Clinical Investigator, Program in Developmental Endocrinology and Genetics, Eunice Kennedy Shriver National Institute of Child Health and Human Development, National Institutes of Health.
Karim Anton Calis, PharmD, MPH, FASHP, FCCP is a member of the following medical societies: American College of Clinical Pharmacy, American Society of Health-System Pharmacists, and Endocrine Society
Disclosure: Nothing to disclose.

Coauthor(s)

Vaishali Popat, MD, MPH, Clinical Investigator, Intramural Research Program on Reproductive and Adult Endocrinology, National Institutes of Child Health and Human Development, National Institutes of Health
Vaishali Popat, MD, MPH is a member of the following medical societies: American College of Physicians and Endocrine Society
Disclosure: Nothing to disclose.

Devra K Dang, PharmD, BCPS, CDE, Assistant Clinical Professor, University of Connecticut School of Pharmacy, Clinical Faculty, Burgdorf Health Center
Disclosure: Nothing to disclose.

Sophia N Kalantaridou, MD, Assistant Professor, Department of Obstetrics and Gynecology, University of Ioannina Medical School, Greece
Disclosure: Nothing to disclose.

Medical Editor

Anthony Charles Sciscione, DO, Director, Division of Maternal-Fetal Medicine, Professor, Department of Obstetrics and Gynecology, Drexel University College of Medicine
Anthony Charles Sciscione, DO is a member of the following medical societies: American College of Obstetricians and Gynecologists and American Medical Association
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: eMedicine Salary Employment

Managing Editor

A David Barnes, MD, PhD, MPH, FACOG, Consulting Staff, Department of Obstetrics and Gynecology, Mammoth Hospital (Mammoth Lakes, California), Pioneer Valley Hospital (Salt Lake City, Utah), Warren General Hospital (Warren, Pennsylvania), and Mountain West Hospital (Tooele, Utah)
A David Barnes, MD, PhD, MPH, FACOG is a member of the following medical societies: American College of Forensic Examiners, American College of Obstetricians and Gynecologists, American Medical Association, Association of Military Surgeons of the US, and Utah Medical Association
Disclosure: Nothing to disclose.

CME Editor

Frederick B Gaupp, MD, Consulting Staff, Department of Family Practice, Hancock Medical Center
Frederick B Gaupp, MD is a member of the following medical societies: American Academy of Family Physicians
Disclosure: Nothing to disclose.

Chief Editor

Michel E Rivlin, MD, Professor, Coordinator of Quality Assurance/Quality Improvement, Department of Obstetrics and Gynecology, University of Mississippi School of Medicine
Michel E Rivlin, MD is a member of the following medical societies: American College of Obstetricians and Gynecologists, American Medical Association, Mississippi State Medical Association, and Royal College of Surgeons of Edinburgh
Disclosure: Nothing to disclose.

 
 
HONcode

We subscribe to the
HONcode principles of the
Health On the Net Foundation

All material on this website is protected by copyright, Copyright© 1994- by Medscape.
This website also contains material copyrighted by 3rd parties.

DISCLAIMER: The content of this Website is not influenced by sponsors. The site is designed primarily for use by qualified physicians and other medical professionals. The information contained herein should NOT be used as a substitute for the advice of an appropriately qualified and licensed physician or other health care provider. The information provided here is for educational and informational purposes only. In no way should it be considered as offering medical advice. Please check with a physician if you suspect you are ill.