Autoimmune ovarian failure with elevated serum levels of luteinizing hormone and enlarged ovaries: case report

Article Abstract:

The absence of menstruation (amenorrhea) can be caused by an abnormal production of steroid hormones. A report is presented of a 30-year-old women who was unable to conceive for three years and did not menstruate for one year. The patient's reproductive history revealed a abnormal hydatiform mole pregnancy (an abnormal embryo composed of a grape-like mass without fetal activity) at 24 years of age, followed by a normal pregnancy three years later. A normal menstrual cycle resumed for two years, until the age of 29, when the patient developed hot flashes and amenorrhea. An examination of the ovaries using a laparoscope (a tube affixed with a magnifying lens inserted into the abdomen to visualize internal structures) revealed enlarged ovaries with many cysts. The original diagnosis of polycystic ovarian syndrome was abandoned when ovulation-inducing agents failed to induce egg follicle development; the diagnosis was changed to premature ovarian failure. The cause of premature ovarian failure is not well-understood, but may be related to a chromosomal abnormality, previous chemotherapy, or an autoimmune disease. In some patients, antibodies are produced against the body's own circulating follicle stimulating hormone (FSH) and luteinizing hormone (LH). However, in this patient, blood tests indicated an increase in LH with minimal increase in FSH. In patients with classical autoimmune ovarian failure, antibodies are directed to the cells that produced estrogen, and the low estrogen then causes an increase in FSH. The patient's ovaries were still able to suppress FSH, but not LH. Biopsies of the ovarian wall indicated an intact ovarian stroma with many developing egg follicles. However, since there was no increase in androgens and low estrogen levels, a diagnosis of polycystic ovarian syndrome was ruled out and autoimmune ovarian failure was indicated. (Consumer Summary produced by Reliance Medical Information, Inc.)

Case studies, Diseases, Autoimmune diseases, Ovaries, Ovarian cysts, Luteinizing hormone

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Oestrogen and androgen states in oligo-amenorrhoeic women with polycystic ovaries

Article Abstract:

Polycystic ovary disease, also called Stein-Leventhal syndrome, is an endocrine disorder characterized by lack of ovulation and cystic formations on the ovaries due to over-stimulation by pituitary luteinizing hormone (LH). This condition is associated with infertility, little or no menstruation (oligomenorrhea and amenorrhea, respectively), obesity, and excessive face and body hair growth (hirsutism). Previous studies have reported that women with polycystic ovaries (PCO) have higher than normal blood levels of LH and estrogen, and that menstrual bleeding can be induced in these women by treatment with a synthetic hormone called progestogen (progestogen challenge test). This article describes the clinical features of 65 women with abnormal menstrual cycles. Forty-four of the women had oligomenorrhea and 21 had amenorrhea. Forty of the 44 women with oligomenorrhea had PCO, while only 8 of the 21 women with amenorrhea had PCO. The women with PCO had higher mean blood levels of LH and androgens than those who did not have PCO. Ninety-two percent of the women with PCO had abnormally high levels of estrogen, and treatment with progestogens induced menstrual bleeding in all of these women. However, treatment with progestogens caused menstrual bleeding in only 18 percent of the women who did not have PCO. Thirty-five percent of the women with PCO had hirsutism, while none of the women who did not have PCO had hirsutism. The women with PCO who had hirsutism had higher blood levels of androgens than the women with PCO who did not have hirsutism, indicating that hirsutism is associated with a more severe form of PCO. (Consumer Summary produced by Reliance Medical Information, Inc.)

Reproductive organs, Genitalia, Estradiol, Stein-Leventhal syndrome, Polycystic ovary syndrome, Estrone

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Persistent fetal sinus bradycardia associated with maternal anti-Ro antibodies. Case report

Article Abstract:

A case is described of the pregnancy of a 29-year old woman with systemic lupus erythematosus, a chronic inflammatory disease of connective tissue. Thirty-two weeks into her third pregnancy, the lupus erythematosus worsened and fetal bradycardia (abnormal slowing of the fetal heart rate) was detected. The fetus appeared normal in development and activity, and showed no evidence of heart defects or failure. The woman was treated with the steroid drug prednisolone, which improved symptoms of the lupus. However, the patient developed severe cutaneous vasculitis (inflammation of the skin blood vessels) 37 weeks into the pregnancy. The infant was delivered without complications, but bradycardia persisted. Four months later, the infant was well with a heart rate of 90 beats per minute. Fetal bradycardia may be caused by hypoxia (abnormally low oxygen levels) or by heart block (the impairment of impulse conduction within the heart). Complete heart block may be caused by abnormal immune proteins called anti-Ro antibodies, which are associated with systemic lupus erythematosus. In this case, fetal activity and heart rate variation were normal, excluding the possibility of hypoxia. In addition, recordings of the heart rate pattern were not consistent with impaired impulse conduction in the heart. Other causes of fetal bradycardia were also excluded in this case. This case shows that not all fetal bradycardias associated with connective tissue disease of the mother are due to heart block or impaired impulse conduction. (Consumer Summary produced by Reliance Medical Information, Inc.)

Physiological aspects, Systemic lupus erythematosus, Bradycardia, Pregnancy, Complications of, Pregnancy complications, Fetal heart rate

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