Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0028754 (obesity)
 124,988 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Daily plasma hormones, including luteinizing hormone (LH), follicle-stimulating hormone (FSH), estrone (E1), estradiol (E2), progesterone, androstenedione, and testosterone (T), were measured in 16 anovulatory patients for a span of 3 to 4 weeks. The clinical diagnoses in this group of patients included the following: anovulation-eumenorrhea (n = 5), anovulation-polymenorrhea (n = 1), anovulation-oligomenorrhea (n = 3), congenital adrenal hyperplasia (n = 1), polycystic ovarian disease (n = 4), severe hypothalamic amenorrhea (n = 1), and postpartum amenorrhea-galactorrhea (n = 1). Follicular activity was evident in polymenorrheic and oligomenorrheic patients, and menstruation occurred in these patients following estrogen withdrawal. No follicular maturation was noted in the group of patients with anovulation-eumenorrhea, and menstruation in these patients was considered breakthrough bleeding. Low FSH levels were observed in anovulatory patients with eumenorrhea, polymenorrhea, and oligomenorrhea. Significantly high LH values were noted in both classic and non-classic polycystic ovarian disease. Extremely low E1 and E2 levels were found in patients with severe hypothalamic amenorrhea and postpartum amenorrhea-galactorrhea. Slightly elevated progesterone levels were observed in polymenorrheic and oligomenorrheic patients prior to menstruation; this was frequently associated with an LH surge or elevation. Elevated T levels were consistently associated with hirsutism but not with obesity.
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PMID:Plasma hormone profile in anovulation. 57 58

This study included 125 women with specific complaints following tubal ligation. In most instances the ligations had been done 7 years previously, mostly for multiparity. 92% had been ligated by the abdominal route 88.8% had symptoms including menstrual irregularities, chronic pain, obesity, psychoses, intermittent acute retention of urine, ventral hernia, and 2 cases of sterilization failure. Average age at time of tubectomy had been 31 years; average parity, 3-4. There was a shift towards right in mean maturation index of cervical cells soon after sterilization. This shift then decreased for a year, then gradually rose, stabilizing at 12 years. Amenorrhea was present in 5 cases with high mean maturation levels. 17 cases of oligomenorrhea all showed ahigh estrogenic activtiy. Of 27 cases of menorrhagia endometrial biopsies were taken in 13. 12 showed the proliferative phase and 1 the secretory phase. These findings correlated with cytological findings, but cervical mucus in 3 cases did not coincide. Of the 27 cases 21 were anovular. In all the karyopyknotic index was high. 2 cases showed clinical evidence of inflammation. Of 10 cases of dysmenorrhea, 3 were ovulatory; inflammation was present in 3. In 12 cases of polymenorrhea 7 showed high estrogenic activities. In 1 a polyp had caused the irregular bleeding. The observed shifts of maturation index of cervical cells toward the right are considered indicative of hyperovarian activity. Results show that ovarian activity after sterilization by tubectomy was normal or increased. The increased activity was considered either psychological,neurovascular, or caused by inflammation. Of the 10 cases with inflammation, 9 were associated with menstrual disorders.
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PMID:Menstrual disorders after sterilization with special reference to ovarian activity. 1225 47

There is a close relationship between the amount of estogen and progesterone secreted by the ovary from puberty to menopause and the development of hyperplastic endometrium of all types and finally endometrial cancer. The endogenous endocrine pattern reflects progesterone deficiency (corpus luteum deficiency). Such deficiency can also develop when treatment with exogenous estrogen and progestogen is done and a deficiency of the progestogen in comparison to the used estrogen is induced in pre- and postmenopausal women. This risk is particular accentuated in the climacteric female when the endocrine milieu was unfavorable in the years before (menstrual cycle disorders, PCOS, obesity, no full-term pregnancy, no breast feeding, etc.). However, there are the additional factors, which modify the biological end result: "Progestogen deficiency". One main factor is the level of SHBG determined by the amount of free, biologically active estradiol. A low level of SHBG is for instance induced by high body weight. Therefore, the amount of overweight correlates with increased risk of endometrial hyperplasia and finally endometrial cancer. In addition, increasing body weight negatively affects proper ovarian function leading to corpus luteum deficiency and this in addition increases the risk of endometrial cancer. The classical risk increase for endometrial cancer is associated with oligomenorrhea or polymenorrhea combined with corpus luteum deficiency or anovulation. Therefore, women with PCOS are at increased risk for endometrial cancer in the pre- and postmenopausal years. Examples from the therapeutic point of view have been the risk increase found with biphasic estrogen high-dosed oral contraceptives with a long estrogen phase and a short progestogen phase. In climacteric females estrogen-only treatment results in a predictable increase in endometrial cancer risk. Therefore, it is mandatory to use estrogen/progestogen combinations. The lowest risk is achieved when a continuous estrogen/progestogen regimen is used. In addition, the lowest dose of estrogens for the individual woman should be chosen.
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PMID:Progestogen deficiency and endometrial cancer risk. 1923 Nov 17