Cases reported "Dysmenorrhea"

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1/3. Effect of the levonorgestrel-releasing intrauterine system on uterine myomas in a renal transplant patient.

    The levonorgestrel-releasing intrauterine system (LNG-IUS) has been used in the treatment of both idiopathic menorrhagia and adenomyosis. An electronic search of the on-line medical literature revealed no reports of its use for menorrhagia secondary to uterine myomas. Presented here is the successful treatment of uterine myomas with menorrhagia in a woman with a renal transplant. There was a significant reduction in menorrhagia, dysmenorrhea, and uterine and myoma size with the use of the LNG-IUS. We believe that this system provides an alternative to conventional hysterectomy and gonadotrophin-releasing hormonal analog medical treatment for uterine myomas, with a possibly inhibitory effect on myoma growth.
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2/3. live birth after conservative surgery for severe adenomyosis following magnetic resonance imaging and gonadotropin-releasing hormone agonist therapy.

    This is a report of a live birth after conservative surgery for severe adenomyosis following diagnosis by MRI and therapy with GnRH-a. A 33-year-old gravida 1 para 1 woman with a 5-year history of secondary infertility received a gonadotropin-releasing hormone agonist (GnRH-a), leuprolide acetate, for 16 weeks to control symptoms of severe adenomyosis and to treat infertility. However, severe dysmenorrhea recurred after the discontinuation of therapy. Because an elevated serum level of CA-125 and MRI findings suggested that she was experiencing a relapse of adenomyosis, GnRH-a therapy was re-instituted. After 24 weeks of the second therapy, her uterus decreased to normal size and an MRI revealed a localized low-signal-intensity myometrial mass with well-defined borders. We easily resected the localized lesion of adenomyosis using the same technique used to treat uterine leiomyoma. The patient became pregnant after 12 weeks of additional danazol therapy. A healthy male infant was delivered at term by cesarean section.
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3/3. CTG trinucleotide repeat length and clinical expression in a family with myotonic dystrophy.

    Unstable expansion of the CTG repeats in the 3' untranslated region encoding a member of the protein kinase family in the q13.3 band on chromosome 19 is a mutation specific for myotonic dystrophy. To examine the correlation between clinical expression and CTG trinucleotide repeat length, we carried out Southern blot analysis in a family with myotonic dystrophy. In this pedigree, the expanded CTG repeats were transmitted maternally. The mother had three female children. The mother had about 200 CTG repeats, and the number of repeats for each child was about 800, 1500 and 1600 in birth order. The mother and the patient with 800 repeats were unaware of muscle weakness or myotonia. Symptoms were present from age 3 years in the patient with 1500 repeats and from birth in the one with 1600 repeats. Although the mother menstruated regularly, the patients with 800 and 1500 repeats both menstruated irregularly, and the one with 1600 repeats has never menstruated. The age of onset and severity of the disease were correlated with the size of the expanded repeats. Endocrinological studies revealed that the basal levels of the gonadotropins, PRL and E2 were within normal range, and a pituitary response to LHRH was observed. These data suggest that the amenorrhea and menstrual irregularities were caused by a suprahypophyseal dysfunction. When expanded CTG repeats are transmitted maternally, abnormal products resulting from the metabolic disturbance in the affected mother may harm the fetus in utero. A heterozygous fetus, who has more CTG repeats, may be unable to metabolize the pathologic products sufficiently and therefore may become more severely affected. This may explain the exclusive maternal transmission of congenital myotonic dystrophy.
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