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Premenstrual syndrome
Premenstrual
syndrome
SiR-In his Dec 2 commentary’ van Leusden has difficulty in explaining the results of drug treatment of affective symptoms related to menstruation. If in addition to considering the hormonal component in the aetiology, he would also consider the role of life’s vicissitudes in generating anxiety or change of mood, he would have less
difficulty. The
stimulus, in this
case hormonal from which point you start when it changes, depends is applied. If something has happened to make a woman anxious, though not sufficiently anxious to cause her to complain of anxiety, then the normal premenstrual rise that she may experience in the level of anxiety may push her anxiety above the threshold of tolerance and she will complain of symptoms. If the cause of anxiety can be
response
to
a
on
the
any additional premenstrual anxiety become life is more tranquil, there may tolerable. When may be no complaints of premenstrual symptoms. The reason why treatments aimed at reducing the effects of the biological changes of the menstrual cycle are either ineffective or have the variable results that van Leusden finds difficult to explain is that the amount of relief that they can afford may be small relative to the distress resulting from events in the patient’s life.
appropriately treated,
change in ACE activity between the groups (Wilcoxon’s signed-rank test). Within-subject variation in ACE activity was small (intraclass correlation coefficient 0-75). Plasma ACE was not significantly correlated with hormone concentrations. Our results do not confirm that there is a substantial reduction in plasma ACE activity when hormone replacement therapy is initiated as reported.2 The influence of progestogens and ACE genotype should be further considered. This work was supported by grants from Mutuelle Generate de 1’Education Nationale (MGEN) and Laboratoires Bezins-Iscovesco
*P Y
1
Leusden HAIM. Premenstrual syndrome no progesterone: premenstrual dysphoric disorder no serotonin deficiency. Lancet 1995; van
Scarabin, E Billaud, G Plu-Bureau, R Agher
INSERM U258 and Service de Cedex 14, France
1
2
3
4
Samuel I Cohen 8 Linnell Drive, London NW11 7LT, UK
(Paris,
France).
5
Pharmacologie, Hôpital Broussais, 75674 Paris
Stampfer MJ, Colditz GA. Estrogen replacement therapy and coronary heart disease: a quantitative assessment of the epidemiologic evidence. Prev Med 1991; 28: 47-63. Proudler AJ, Ahmed AI, Crook D, Fogelman I, Rymer JM, Stevenson JC. Hormone replacement therapy and serum angiotensinconverting-enzyme activity in postmenopausal women. Lancet 1995; 346: 89-90. Bonithon-Kopp C, Ducimetière P, Touboul PJ, et al. Plasma angiotensin-converting-enzyme activity and carotid wall thickening. Circulation 1994; 89: 952-54. Cambien F, Poirier O, Lecerf L, et al. Deletion insertion at the angiotensin-converting enzyme gene is a potent risk factor for myocardial infarction. Nature 1992; 359: 641-44. Cushman DW, Cheung MS. Spectrophotometric assay properties of the angiotensin converting enzyme of the rabbit lung. Biochem Pharmacol 1971; 20: 1637-38.
246: 1443-44.
HRT and ACE
activity in postmenopausal
women
SiR-Studies with large numbers of patients have shown that postmenopausal oestrogen may reduce the risk of coronary heart disease (CHD).’ It has been reported that hormone replacement therapy could have a cardioprotective effect by lowering the activity of serum angiotensin-convertingenzyme (ACE).2 Excessive plasma ACE activity may adversely affect arterial walls, and deletion polymorphism in the ACE gene may increase the risk of CHD.3.4 We have studied the effects of oral and percutaneous cyclic (25 d/mo) 17-J3 oestradiol (E2), combined with progesterone, on ACE activity in an open randomised trial. 43 healthy postmenopausal women (amenorrhoea >6 months and follicle-stimulating hormone >40 IU/L), aged 45-64 years, were randomly assigned to receive either oral E2 valerate (2 mg/d) or percutaneous E2 (1-5 mg/d), both combined with micronised progesterone (200 mg/d, 10 days per month), or no hormonal treatment. Plasma ACE activity was measured spectrophotometrically5 at baseline, and at 6 mo (table). Compliance with treatments (monitored by plasma E2 and follicle-stimulating hormone concentrations) was satisfactory. There was no significant difference in mean
Bacterial SiR-The
meningitis
patient
and the
described
painful eye
by MacConnell and
Ferro
(Nov
11, p 1269)’ with endophthalmitis and meningitis caused by
Streptococcus agalactiae, who presented with a painful eye, certainly unusual. Group B streptococcal meningitis is very uncommon in adults. We have recently reviewed 69 published cases, and 11I of our own, and although extrameningeal foci of infection are common, we have not found a single instance of meningitis secondary to or complicated by endophthalmitis. In fact metastatic group B streptococcal endophthalmitis, apart from being rare, is almost always secondary to endocarditis.2 Primary eye infections with secondary invasion of the subarachnoid space are exceedingly rare nowadays. metastatic infections, Secondary eye including were an almost invariable endophthalmitis, complication of the terminal stages of cerebrospinal meningitis in the preantibiotic era but are now also infrequent.2 In our environment the most common primary bacterial eye infection, sometimes heralding invasive disease, is meningococcal infection. Between 1984 and 1993 we saw 34 children with a primary meningococcal conjunctivitis (more commonly the right eye was affected) and 21 of these patients presented with intensive ocular pain. Ten developed disease with (seven systemic meningococcal three with meningococcaemia plus meningococcaemia, meningitis). All patients survived with appropriate therapy. The single most important factor associated with development of invasive meningococcal disease was the use of topical antimicrobial therapy to treat the conjunctivitis. Thus, a painful eye with purulent conjunctival exudate, together with signs of systemic infection, should raise the suspicion of meningococcal disease and prompt systemic antibiotic therapy as early as possible. was
3
122
syndrome
SiR-In his Dec 2 commentary’ van Leusden has difficulty in explaining the results of drug treatment of affective symptoms related to menstruation. If in addition to considering the hormonal component in the aetiology, he would also consider the role of life’s vicissitudes in generating anxiety or change of mood, he would have less
difficulty. The
stimulus, in this
case hormonal from which point you start when it changes, depends is applied. If something has happened to make a woman anxious, though not sufficiently anxious to cause her to complain of anxiety, then the normal premenstrual rise that she may experience in the level of anxiety may push her anxiety above the threshold of tolerance and she will complain of symptoms. If the cause of anxiety can be
response
to
a
on
the
any additional premenstrual anxiety become life is more tranquil, there may tolerable. When may be no complaints of premenstrual symptoms. The reason why treatments aimed at reducing the effects of the biological changes of the menstrual cycle are either ineffective or have the variable results that van Leusden finds difficult to explain is that the amount of relief that they can afford may be small relative to the distress resulting from events in the patient’s life.
appropriately treated,
change in ACE activity between the groups (Wilcoxon’s signed-rank test). Within-subject variation in ACE activity was small (intraclass correlation coefficient 0-75). Plasma ACE was not significantly correlated with hormone concentrations. Our results do not confirm that there is a substantial reduction in plasma ACE activity when hormone replacement therapy is initiated as reported.2 The influence of progestogens and ACE genotype should be further considered. This work was supported by grants from Mutuelle Generate de 1’Education Nationale (MGEN) and Laboratoires Bezins-Iscovesco
*P Y
1
Leusden HAIM. Premenstrual syndrome no progesterone: premenstrual dysphoric disorder no serotonin deficiency. Lancet 1995; van
Scarabin, E Billaud, G Plu-Bureau, R Agher
INSERM U258 and Service de Cedex 14, France
1
2
3
4
Samuel I Cohen 8 Linnell Drive, London NW11 7LT, UK
(Paris,
France).
5
Pharmacologie, Hôpital Broussais, 75674 Paris
Stampfer MJ, Colditz GA. Estrogen replacement therapy and coronary heart disease: a quantitative assessment of the epidemiologic evidence. Prev Med 1991; 28: 47-63. Proudler AJ, Ahmed AI, Crook D, Fogelman I, Rymer JM, Stevenson JC. Hormone replacement therapy and serum angiotensinconverting-enzyme activity in postmenopausal women. Lancet 1995; 346: 89-90. Bonithon-Kopp C, Ducimetière P, Touboul PJ, et al. Plasma angiotensin-converting-enzyme activity and carotid wall thickening. Circulation 1994; 89: 952-54. Cambien F, Poirier O, Lecerf L, et al. Deletion insertion at the angiotensin-converting enzyme gene is a potent risk factor for myocardial infarction. Nature 1992; 359: 641-44. Cushman DW, Cheung MS. Spectrophotometric assay properties of the angiotensin converting enzyme of the rabbit lung. Biochem Pharmacol 1971; 20: 1637-38.
246: 1443-44.
HRT and ACE
activity in postmenopausal
women
SiR-Studies with large numbers of patients have shown that postmenopausal oestrogen may reduce the risk of coronary heart disease (CHD).’ It has been reported that hormone replacement therapy could have a cardioprotective effect by lowering the activity of serum angiotensin-convertingenzyme (ACE).2 Excessive plasma ACE activity may adversely affect arterial walls, and deletion polymorphism in the ACE gene may increase the risk of CHD.3.4 We have studied the effects of oral and percutaneous cyclic (25 d/mo) 17-J3 oestradiol (E2), combined with progesterone, on ACE activity in an open randomised trial. 43 healthy postmenopausal women (amenorrhoea >6 months and follicle-stimulating hormone >40 IU/L), aged 45-64 years, were randomly assigned to receive either oral E2 valerate (2 mg/d) or percutaneous E2 (1-5 mg/d), both combined with micronised progesterone (200 mg/d, 10 days per month), or no hormonal treatment. Plasma ACE activity was measured spectrophotometrically5 at baseline, and at 6 mo (table). Compliance with treatments (monitored by plasma E2 and follicle-stimulating hormone concentrations) was satisfactory. There was no significant difference in mean
Bacterial SiR-The
meningitis
patient
and the
described
painful eye
by MacConnell and
Ferro
(Nov
11, p 1269)’ with endophthalmitis and meningitis caused by
Streptococcus agalactiae, who presented with a painful eye, certainly unusual. Group B streptococcal meningitis is very uncommon in adults. We have recently reviewed 69 published cases, and 11I of our own, and although extrameningeal foci of infection are common, we have not found a single instance of meningitis secondary to or complicated by endophthalmitis. In fact metastatic group B streptococcal endophthalmitis, apart from being rare, is almost always secondary to endocarditis.2 Primary eye infections with secondary invasion of the subarachnoid space are exceedingly rare nowadays. metastatic infections, Secondary eye including were an almost invariable endophthalmitis, complication of the terminal stages of cerebrospinal meningitis in the preantibiotic era but are now also infrequent.2 In our environment the most common primary bacterial eye infection, sometimes heralding invasive disease, is meningococcal infection. Between 1984 and 1993 we saw 34 children with a primary meningococcal conjunctivitis (more commonly the right eye was affected) and 21 of these patients presented with intensive ocular pain. Ten developed disease with (seven systemic meningococcal three with meningococcaemia plus meningococcaemia, meningitis). All patients survived with appropriate therapy. The single most important factor associated with development of invasive meningococcal disease was the use of topical antimicrobial therapy to treat the conjunctivitis. Thus, a painful eye with purulent conjunctival exudate, together with signs of systemic infection, should raise the suspicion of meningococcal disease and prompt systemic antibiotic therapy as early as possible. was
3
122