Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0004153 (atherosclerosis)
 77,401 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A possible relation between parenteral Depo-Provera and the subsequent development of medullary infarction in a heavy smoker is reported. The patient, a 40-year old Chinese woman had smoked 30 cigarettes daily for many years. She received injections of 150 mg Depo-Provera in April and July 1979. 2 days after the 2nd injection she was admitted to the hospital for vomiting and vertigo of 2 days duration. Clinical examination showed a 12th nerve palsy with the tongue deviated to the right but no other neurological abnormalities. She was treated symptomatically with intravenous fluids and stemetil and improved. On the 5th day her vertigo and vomiting progressed and she developed more lower brain stem signs. The same day she had a grand mal fit and went into a coma. She died on the 7th hospital day. A partial autopsy limited to the skull revealed minimal atherosclerosis of the vertebral artery but no thrombosis or occlusion. Cut sections after perfusion revealed an area of softening associated with some hemorrhage involving the whole length of the right half of the medulla oblongata dorsal to the olivary nucleus. Histological examination revealed an infarct undergoing liquefaction necrosis. The possibility of a causative relationship is suggested by the development of tinnitis about 12 hours after injection of Depo-Provera.
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PMID:Medullary infarction--was it depo-provera? 645 93

Seventy postmenopausal women took part in the study. Subjects received either continuous oral 17 beta-estradiol 2 mg/day combined with norethisterone acetate 1 mg/day (E2/NETA, Kliogest) or transdermal treatment consisting of 28 day cycles with patches delivering 17 beta-estradiol 50 micrograms/day (Estraderm) combined with cyclic medroxyprogesterone acetate 10 mg/day (E2/MPA, Provera), on days 17-28. At baseline the serum lipid and lipoprotein concentrations, composition and concentrations of high density lipoprotein (HDL) subclasses, lipoprotein (Lp)(AI) and Lp(A-I:A-II) levels were comparable in the two groups. In the E2/NETA group, after 12 months hormone replacement therapy (HRT), the HDL2 cholesterol concentration decreased by 17% (P < 0.01) and the HDL3 cholesterol remained unchanged. The concentrations of HDL2b, HDL2a and HDL3a were reduced by 30, 26 and 15%, respectively, P < 0.001, and the cholesterol:triglyceride ratio decreased significantly in all HDL subclasses. Apolipoprotein (apo) A-I concentration decreased by 5% (P < 0.05), but apo A-II, Lp(A-I) and Lp(A-I:A-II) concentrations remained unchanged. In the E2/MPA group the HDL2 and HDL3 cholesterol levels were both reduced by 6% (P < 0.05) and the HDL3a, HDL3b and HDL3c concentrations decreased by 14, 12 and 17% during the E2/MPA phase compared with baseline (P < 0.01). No major changes in the composition of HDL subclasses occurred in the E2 MPA group during treatment. The apo A-I and Lp(A-I) levels were not changed, but apo A-II and Lp(A-I:A-II) concentrations decreased by 8 and 5%, P < 0.001 and P < 0.05, respectively. At 12 months the postheparin plasma hepatic lipase (HL) activity decreased only in the E2/NETA group (by 12%, P < 0.05). The cholesteryl ester transfer protein (CETP) activity was not affected by either HRT regimen. The results of our study show that the 2 HRT regimens have multiple effects on HDL particles and HRT induced changes in HDL are not associated with changes in activities of lipolytic enzymes or CETP.
Atherosclerosis 1997 Mar 21
PMID:Responses of HDL subclasses, Lp(A-I) and Lp(A-I:A-II) levels and lipolytic enzyme activities to continuous oral estrogen-progestin and transdermal estrogen with cyclic progestin regimens in postmenopausal women. 910 68

Since the last in a series of childbirth education classes discusses contraception, educators must know about various family planning methods. Oral contraceptives (OCs) comprise combined OCs, phasic OCs, and minipills. Combined OCs inhibit secretion of gonadotropin-releasing hormone, which in turn keeps the follicle-stimulating hormone from inducing the ovarian follicle to grow and keeps luteinizing hormones from activating ovulation. They also thicken cervical mucus. Minipills also thicken cervical mucus and render the endometrium unreceptive to fertilized egg implantation. They do not always inhibit ovulation, however. OCs can induce side effects, such as nausea, hypertension, increased risk of atherosclerosis, and fatigue. The IUD prevents pregnancy either by inhibiting implantation of a fertilized egg or by an inflammatory reaction of the endometrium resulting in a release of macrophages which may destroy sperm. The no-longer-produced Dalkon Shield IUD increased the risk of pelvic inflammatory disease and damaged the reputation of other IUDs. Rare IUD complications are uterine perforation, salpingitis, tubal scarring, pelvic inflammatory disease, and infertility. Diaphragms, cervical film, and condoms serve as barriers between the egg and sperm. The main problem with barrier methods is the increased risk of developing toxic shock syndrome. Spermicide increase the effectiveness of diaphragms, cervical caps, and condoms. Vasectomy keeps sperm from arriving at storage sites. Shortterm side effects are swelling, discomfort, and occasional rejoining of the cut ends of the vas. Research hints at a link between vasectomy and prostate cancer. Some complications of tubal ligation are urinary tract infections, accidental electrical burns, and pelvic infections. Natural family planning methods include withdrawal, the rhythm method, and the sypto-thermal method. Controversial injectable contraceptives are Depo-Provera (medroxyprogesterone acetate) and Noristerate (norethisterone enanthate).
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PMID:Birth control update for childbirth educators. 1234 29