Aged 47, she self-referred to the menopause clinic with a 12-month history of severe vasomotor symptoms. Her cycle was irregular and associated with premenstrual migraine. A cervical smear and pelvic examination six months earlier were reported as normal. She was started on a transdermal cyclical preparation and, after three months, reported improvement of her hot flushes but with mood swings in the progestogen phase and some intermenstrual spotting. She remained on transdermal oestrogen and the progestogen was changed. Six months later she was discharged with good symptom control, no migraines and regular withdrawal bleeds. She came back to clinic 10 months later with a return of her premenstrual migraines and was commenced on a low dose continuous combined preparation on a “named patient” basis, as continuous progestogen is often associated with a reduction in migraines.1 She remained well on this preparation for six months, with good symptom control and complete amenorrhoea, but then reported spotting and breakthrough bleeding. She was referred for transvaginal ultrasound but there were problems at the local hospital and this could not be done. The bleeding completely stopped during this time and she has had a further three months of amenorrhoea. Bleeding recommenced three months later and she was examined and a cervical smear taken (three years after the previous one). She had a bulky uterus with some contact bleeding from the cervix and was referred for hysteroscopy and cervical biopsy. Meanwhile the smear result was reported as “severe dyskaryosis” and a referral was made for colposcopy. Her hysteroscopy showed an atrophic endometrium but the colposcopy and biopsy showed a large area of CINIII with micro-invasion; she was listed for major surgery. This case illustrates the importance of exploring all avenues. Irregular bleeding in hormone replacement therapy is very common and is usually associated with the endometrium. In this case a routine cervical smear proved to be the critical investigation. Case history with written consent from the patient.
To stimulate the dorsolateral frontal cortex, 12 healthy, adult, human females played contract bridge for 1.5 h between initial and final blood sample collections. Flow cytometric analyses of samples, performed in triplicate, showed a significant increase in CD4-positive T lymphocytes. The dorsolateral frontal cortical thickness is significantly and bilaterally reduced in immune-incompetent female, nude mice. Thymic transplants reverse the deficient cortical thickness and CD4-positive cell numbers.