- Email: [email protected]
Does peroperative gut-mucosa hypoperfusion cause postoperative nausea and vomiting?
*12/12 children born of HCV-RNA-negatne and 14/19 to HCV-RNA-positne mothers. tPatlents with HCV hepatitis; these patients were also anti-HCV positive. Table : HCV markers in mother-baby couples
All the newborn babies had antibodies
to HCV, tested by EIA at second-generation delivery, and, in most cases, showed the RIBA-2 presence of the same antibody pattern in the mother-baby couple (table). No child born of HCVRNA negative mothers had viraemia at birth or during follow-up. Three-quarters of babies born to HCV-RNApositive mothers were HCV-RNA negative at birth and during follow-up, and 3 were HCV-RNA positive at birth but HCV-RNA negative at 1 year. All these children in the two groups lost maternal anti-HCV during follow-up. 2 children were born to anti-HCV-positive, HCV-RNApositive mothers who did not have severe hepatic disease. The first was HCV-RNA positive at the birth and persistently during follow-up (every 3 months for 2 years): this infant had the same maternal antibody pattern until 6 months (c 33c, c 100); from 9 months, the child showed moderate liver damage (alanine aminotransferase [ALT] 65 IU/L) with a changed antibody pattern (c 22, c 33c, c 100 3, c 5-1-1). The second child was HCV-RNA positive at birth and at 3 months. He showed signs of liver disease (ALT 250 IU/L) at 6 months and 1 year (ALT 185 IU/L). Unfortunately, however, we have no record of his virological pattern at those times. These last 2 children acquired perinatal HCV infection and developed HCV disease. Our results show that mother-to-infant transmission of HCV is possible when the mother is not coinfected with HIV. The rate of vertical transmission from HCV-positive, HIV-negative mothers is about 6% (2/31) in our experience; if virological tests are done about 10% (2/19) of babies born to HCV-RNA-positive mothers acquire HCV infection. These results in Europeans accord with Ohto’s data for 1
HIV-negative Japanese patients.’ We thank Dr C Gotta, Dr G Giambartolomei, and Dr P Moscatelli from the department of neonatology for their collaboration.
*R
Giacchino, A Picciotto, L Tasso, A Timitilli, N Sinelli
’Department of Infectious Diseases, G Gaslmi Children’s Hospital, 16148 Genova, Italy; and Department of Gastroenterology, Hospital of San Martino, Genova
1 Ohto H, Terazawa S, Sasaki N, et al. Transmission of hepatitis C virus from mothers to infants. N Engl J Med 1994; 17: 744-50.
Intraoperative colonoscopy during laparoscopic bowel resection SiR-Kitamura and colleagues’ recommended preoperative colonoscopic injection of activated carbon particles to identify the colonic lesion during laparoscopic surgery. We have also used such a marking method to identify small gastric cancers and found it to result in a clear blackened spot on the serosal surface.2 In our first 7 experiences of laparoscopic colon resection, we tried preoperative injection of carbon particles into the submucosa as a marker for location of the lesion. However, only 4 showed a small blackened patch under laparoscopic view and in 1 case a subserosal haematoma was falsely identified as the lesion. We consider this preoperative marking method to be unstable and indistinct in colonic cases. The poor lymphatic
flow in the colonic wall and fat tissue covering the serosa might cause the weak staining by activated carbon particles. We have now done 26 laparoscopic colonic resections and used intraoperative colonoscopy in most of these cases. With the patient in the supine position with the legs abducted slightly, the colonoscope was inserted easily from the anus to the site of the lesion. The operator ligated the wall at the site of the light of the colonoscope. By this method all lesions were identified easily in a short time. As an additional benefit of intraoperative colonoscopy, the endoscopist could assist bowel mobilisation by moving andstretching the colon with the scope after identification of the lesion. Although the laparoscopic bowel operation was not an improvement on the standard procedure,3 this assistance might shorten the duration of surgery.
*Takayuki Asao, Yukio Nagamachi First Department of Surgery, Gunma University School of Medicine, Maebashi 371, Japan
1
2
3
Kitamura K, Takahashi T, Yamaguchi T, Yamane T, Hagiwara A, Oyama T. Identification, by activated carbon injection, of cancer lesion during laparoscopic surgery. Lancet 1994; 343: 789. Takahashi T, Sawai K, Hagiwara A, Takahashi S, Seiki K, Tokuda H. Type-oriented therapy for gastric cancer effective for lymph node metastasis using activated carbon particles adsorbing an anticancer agent. Semin Surg Oncol 1991; 7: 373-84. Wexner SD, Cohen SM, Johansen OB, Nogueras JJ, Jagelman DG. Laparoscopic colorectal surgery: a prospective assessment and current perspective. Br J Surg 1993; 80: 1602-05.
Does
peroperative gut-mucosa hypoperfusion cause postoperative nausea and vomiting? SiR-Postoperative nausea and vomiting (PONV) are distressing and may have serious medical consequences to the patient and financial implications from delayed discharge from hospital. The causes of PONV are multifactorial’ but peroperative gut-mucosa hypoperfusion has not been recognised as one of them. The gastrointestinal tonometer allows relatively noninvasive assessment of gastrointestinal perfusion by of the carbon dioxide pressure of the lumen of the stomach and calculation of the intramucosal pH. An abnormal intramucosal pH developing over the course of major surgery has been associated with a poor outcome.2 In a prospective randomised trial2 peroperative plasma volume expansion reduced the incidence of abnormal intramucosal pH in patients having elective cardiac surgery and was associated with an improved outcome. Although not a planned study endpoint we also noted that patients who maintained a normal intramucosal pH had a lower incidence of persistent PONV (ie, >72 h postoperatively).2 We have also noted the poorly understood difference in incidence of PONV between nations as reported by Haigh and colleagues.3 Patients in the UK and the Netherlands have higher probabilities of experiencing PONV than those from Scandinavian countries (Denmark and Norway). Could differences in gastrointestinal perfusion, at least in part, account for some of the discrepancies observed and be reflection of fundamental differences in patient a management not accounted for in trials conducted to date? For example, Cook et al reported a reduced incidence and duration of postoperative nausea in patients who were fluidloaded before general anaesthesia to facilitate elective measurement
Furthermore, gynaecological surgery.4 laparoscopic radioligand-binding studies have shown that a high density of 5-HT3 receptors are found on vagal terminals that innervate the intestinal mucosa and on the same vagal afferent nerves located in the brainstem vomiting system. 1123
against PONV and chemotherapy-induced nausea and vomiting. It has been shown that cisplastin-induced damage to the mucosa of the gastrointestinal tract of ferrets was accompanied by a
5-HT, antagonists
are
effective
twofold increase in the content of 5-HT and its metabolite 5-hydroxyindoleacetic acid in the ileal mucosa.5 We therefore propose that gut mucosal hypoperfusion is a cause of PONV. Although there are numerous factors involved in the pathogenesis of PONV, peroperative gutmucosa hypoperfusion as a contributory factor may warrant
further investigation. T J Gan, *M G
Mythen
Department of Anesthesiology, Duke University Medical Center, Durham, NC 27710, USA
1
2
3
4
5
Lerman J. Surgical and patient factors involved in postoperative nausea and vomiting. Br J Anaesth 1992; 69 (7 suppl 1): 24S-32S. Mythen MG, Webb AR. Per-operative plasma volume expansion reduces the incidence of gut mucosal hypoperfusion during cardiac surgery. Arch Surg 1995; 130: 423-29. Haigh CG, Kaplan LA, Durham JM, Duyeyron JP, Harmer M, Kenny GN. Nausea and vomiting after gynaecological surgery: a metaanalysis of factors affecting their incidence. Br J Anaesth 1993; 71: 517-22. Cook R, Anderson S, Riseborough M, Blogg CE. Intravenous fluid load and recovery: a double-blind comparison in gynaecological patients who had day-case laparoscopy. Anaesthesia 1990; 45: 826-30. Stables R, Andrews PL, Bailey HE, et al. Antiemetic properties of the 5HT3-receptor antagonist, GR38032F. Cancer Treat Rev 1987; 14: 333-36.
Rapid progressive subacute sclerosing panencephalitis after perinatally acquired measles virus infection SiR-Subacute
sclerosing panencephalitis (SSPE) is a rare slowly progressive disease of the central nervous system in children and young adults caused by defective measles virus;1,2 it has been observed in many ethnic groups with an incidence of about 1 case per million children.3 First signs and symptoms of SSPE are usually recognised several years after initial contact with the virus with a mean age of onset of 7 to 8 years.3 One of the risk factors for SSPE so far recognised is measles virus infection below 1 year of age.4 We report a case of onset of SSPE in early infancy as a consequence of intrauterine measles virus infection acquired shortly before delivery. A male infant (born in the 38th week of pregnancy, birth weight 2810 g) was admitted to the department of paediatrics of the General Hospital St Polten at the age of 4 days because his mother had measles virus pneumonia requiring mechanical ventilation. A slight morbilliform exanthema was observed on the day of admission, reaching its peak of intensity on the 8th day_after birth. No measles virus specific antibodies in the infant’s serum were detectable at this stage with IgG and IgM antibody ELISA and a complement fixation test. On the day of discharge (13 days postpartum) the patient showed no clinical signs of abnormality. The boy was readmitted at the age of 4 months because of a history of daily generalised cerebral seizures. At this stage of the disease neuromotor retardation was obvious, as well as high-grade areas of abnormal signal intensity on
magnetic resonance imaging scans, indicating not only generalised cerebral atrophy but also an older area of infarction in the left parietotemporal region. Throughout the clinical course of disease increasing titres of measles-specific IgG in serum and cerebrospinal fluid (CSF) were recorded (see table). IgM antibodies, however, were not detectable in the samples collected. Local antibody production in CSF was detected despite an intact blood-brain barrier. In the 1124
Neg=negative. CFT=complement fixation test. Table: Serological findings
,
examinations the frequency of cerebral seizures increased and therapeutic control with antiepileptic drugs
follow-up
possible. Typical periodic discharges (Rodermacker complexes) appeared by the age of 11 months. The child died at the age of 16 months, the last part of his life being characterised by severe apnoeas and frequent respiratory
was not
infections. At necropsy the atrophic brain (weight 580 g) revealed SSPE with multiple cystic lesions in both hemispheres, diffuse damage and gliosis of the white matter and basal ganglia with moderate lymphomonocytic infiltrates, and immunohistochemical demonstration of measles virus antigen. The central nervous system lesions were similar to those in other rare atypical cases of SSPEwhile paired helical filament-tau immunohistochemistry and electron microscopy revealed early stages of neurofibrillary tangle formations in hippocampal neurons, usually described in older cases of SSPE.5 In contrast to all the previously reported cases in older children SSPE developed in this infant with perinatally acquired measles infection after an extremely short incubation period and was characterised by rapid progressive clinical deterioration. *K Zwiauer, Elisabeth Forstenpointner, Therese E Hauser, K A Jellinger
Popow-Kraupp,
*Department of Paediatrics, General Hospital St Polten, A-3100 St Pölten, Austria; Institute of Virology, University Medical School of Vienna, Vienna; Department of Paediatrics, University Medical School of Vienna; and Ludwig Boltzman Institute of Clinical Neurobiology, Vienna
1 2
3
4 5
Sidhu MS, Crowley J, Lowenthal A, et al. Defective measles virus in subacute sclerosing panencephalitis. Virology 1994; 202: 631-41. Ter Meulen V, Hall WW. Slow virus infections of the nervous system: virological and pathogenetic considerations. J Gen Virol 1981; 41: 1-25. Miller C, Farrington CP, Harbert K. The epidemiology of subacute sclerosing panencephalitis in England and Wales 1970-1989. Int J Epidemiol 1992; 21: 998-1006. Schubert P. Atypischer Fall einer subakuten sklerosierenden Leukoencephalitis (van Bogaert). Acta Neuropathol 1966; 6: 93-97. Wisniewski HM, Dymecky J, Wegiel J, et al. Neurofibrillary pathology in subacute sclerosing panencephalitis. Dementia 1991; 2: 133-41.
CORRECTIONS Preventing nosocomial transmission of tuberculosis-In this Commentary (Jan 28, p 204), the name of the second author, Marguerite Jackson, was inadvertently omitted.
Reversible lymphopenia in patient with Rocky Mountain spotted fever contracted in New York City-In this letter by G S Turett and colleagues (March 11, p 647), the name of the third author should have been Michael Crooks. In the third paragraph, the fifth sentence should have read "Soundview Park in the Bronx, where D variabilis ticks mfected with R rickettsii have been found,’ was the likely source of exposure for most".
Hypertensive effect of antenatal thyrotropin-releasing hormone in pre-eclampsia-In this letter by M J Peek and colleagues (March 25, p 793), the labels for the normotensive and pre-eclamptic women on the
figure were the wrong way round. The upper line should be pre-eclamptic women and the lower line normotensive women.
labelled
All the newborn babies had antibodies
to HCV, tested by EIA at second-generation delivery, and, in most cases, showed the RIBA-2 presence of the same antibody pattern in the mother-baby couple (table). No child born of HCVRNA negative mothers had viraemia at birth or during follow-up. Three-quarters of babies born to HCV-RNApositive mothers were HCV-RNA negative at birth and during follow-up, and 3 were HCV-RNA positive at birth but HCV-RNA negative at 1 year. All these children in the two groups lost maternal anti-HCV during follow-up. 2 children were born to anti-HCV-positive, HCV-RNApositive mothers who did not have severe hepatic disease. The first was HCV-RNA positive at the birth and persistently during follow-up (every 3 months for 2 years): this infant had the same maternal antibody pattern until 6 months (c 33c, c 100); from 9 months, the child showed moderate liver damage (alanine aminotransferase [ALT] 65 IU/L) with a changed antibody pattern (c 22, c 33c, c 100 3, c 5-1-1). The second child was HCV-RNA positive at birth and at 3 months. He showed signs of liver disease (ALT 250 IU/L) at 6 months and 1 year (ALT 185 IU/L). Unfortunately, however, we have no record of his virological pattern at those times. These last 2 children acquired perinatal HCV infection and developed HCV disease. Our results show that mother-to-infant transmission of HCV is possible when the mother is not coinfected with HIV. The rate of vertical transmission from HCV-positive, HIV-negative mothers is about 6% (2/31) in our experience; if virological tests are done about 10% (2/19) of babies born to HCV-RNA-positive mothers acquire HCV infection. These results in Europeans accord with Ohto’s data for 1
HIV-negative Japanese patients.’ We thank Dr C Gotta, Dr G Giambartolomei, and Dr P Moscatelli from the department of neonatology for their collaboration.
*R
Giacchino, A Picciotto, L Tasso, A Timitilli, N Sinelli
’Department of Infectious Diseases, G Gaslmi Children’s Hospital, 16148 Genova, Italy; and Department of Gastroenterology, Hospital of San Martino, Genova
1 Ohto H, Terazawa S, Sasaki N, et al. Transmission of hepatitis C virus from mothers to infants. N Engl J Med 1994; 17: 744-50.
Intraoperative colonoscopy during laparoscopic bowel resection SiR-Kitamura and colleagues’ recommended preoperative colonoscopic injection of activated carbon particles to identify the colonic lesion during laparoscopic surgery. We have also used such a marking method to identify small gastric cancers and found it to result in a clear blackened spot on the serosal surface.2 In our first 7 experiences of laparoscopic colon resection, we tried preoperative injection of carbon particles into the submucosa as a marker for location of the lesion. However, only 4 showed a small blackened patch under laparoscopic view and in 1 case a subserosal haematoma was falsely identified as the lesion. We consider this preoperative marking method to be unstable and indistinct in colonic cases. The poor lymphatic
flow in the colonic wall and fat tissue covering the serosa might cause the weak staining by activated carbon particles. We have now done 26 laparoscopic colonic resections and used intraoperative colonoscopy in most of these cases. With the patient in the supine position with the legs abducted slightly, the colonoscope was inserted easily from the anus to the site of the lesion. The operator ligated the wall at the site of the light of the colonoscope. By this method all lesions were identified easily in a short time. As an additional benefit of intraoperative colonoscopy, the endoscopist could assist bowel mobilisation by moving andstretching the colon with the scope after identification of the lesion. Although the laparoscopic bowel operation was not an improvement on the standard procedure,3 this assistance might shorten the duration of surgery.
*Takayuki Asao, Yukio Nagamachi First Department of Surgery, Gunma University School of Medicine, Maebashi 371, Japan
1
2
3
Kitamura K, Takahashi T, Yamaguchi T, Yamane T, Hagiwara A, Oyama T. Identification, by activated carbon injection, of cancer lesion during laparoscopic surgery. Lancet 1994; 343: 789. Takahashi T, Sawai K, Hagiwara A, Takahashi S, Seiki K, Tokuda H. Type-oriented therapy for gastric cancer effective for lymph node metastasis using activated carbon particles adsorbing an anticancer agent. Semin Surg Oncol 1991; 7: 373-84. Wexner SD, Cohen SM, Johansen OB, Nogueras JJ, Jagelman DG. Laparoscopic colorectal surgery: a prospective assessment and current perspective. Br J Surg 1993; 80: 1602-05.
Does
peroperative gut-mucosa hypoperfusion cause postoperative nausea and vomiting? SiR-Postoperative nausea and vomiting (PONV) are distressing and may have serious medical consequences to the patient and financial implications from delayed discharge from hospital. The causes of PONV are multifactorial’ but peroperative gut-mucosa hypoperfusion has not been recognised as one of them. The gastrointestinal tonometer allows relatively noninvasive assessment of gastrointestinal perfusion by of the carbon dioxide pressure of the lumen of the stomach and calculation of the intramucosal pH. An abnormal intramucosal pH developing over the course of major surgery has been associated with a poor outcome.2 In a prospective randomised trial2 peroperative plasma volume expansion reduced the incidence of abnormal intramucosal pH in patients having elective cardiac surgery and was associated with an improved outcome. Although not a planned study endpoint we also noted that patients who maintained a normal intramucosal pH had a lower incidence of persistent PONV (ie, >72 h postoperatively).2 We have also noted the poorly understood difference in incidence of PONV between nations as reported by Haigh and colleagues.3 Patients in the UK and the Netherlands have higher probabilities of experiencing PONV than those from Scandinavian countries (Denmark and Norway). Could differences in gastrointestinal perfusion, at least in part, account for some of the discrepancies observed and be reflection of fundamental differences in patient a management not accounted for in trials conducted to date? For example, Cook et al reported a reduced incidence and duration of postoperative nausea in patients who were fluidloaded before general anaesthesia to facilitate elective measurement
Furthermore, gynaecological surgery.4 laparoscopic radioligand-binding studies have shown that a high density of 5-HT3 receptors are found on vagal terminals that innervate the intestinal mucosa and on the same vagal afferent nerves located in the brainstem vomiting system. 1123
against PONV and chemotherapy-induced nausea and vomiting. It has been shown that cisplastin-induced damage to the mucosa of the gastrointestinal tract of ferrets was accompanied by a
5-HT, antagonists
are
effective
twofold increase in the content of 5-HT and its metabolite 5-hydroxyindoleacetic acid in the ileal mucosa.5 We therefore propose that gut mucosal hypoperfusion is a cause of PONV. Although there are numerous factors involved in the pathogenesis of PONV, peroperative gutmucosa hypoperfusion as a contributory factor may warrant
further investigation. T J Gan, *M G
Mythen
Department of Anesthesiology, Duke University Medical Center, Durham, NC 27710, USA
1
2
3
4
5
Lerman J. Surgical and patient factors involved in postoperative nausea and vomiting. Br J Anaesth 1992; 69 (7 suppl 1): 24S-32S. Mythen MG, Webb AR. Per-operative plasma volume expansion reduces the incidence of gut mucosal hypoperfusion during cardiac surgery. Arch Surg 1995; 130: 423-29. Haigh CG, Kaplan LA, Durham JM, Duyeyron JP, Harmer M, Kenny GN. Nausea and vomiting after gynaecological surgery: a metaanalysis of factors affecting their incidence. Br J Anaesth 1993; 71: 517-22. Cook R, Anderson S, Riseborough M, Blogg CE. Intravenous fluid load and recovery: a double-blind comparison in gynaecological patients who had day-case laparoscopy. Anaesthesia 1990; 45: 826-30. Stables R, Andrews PL, Bailey HE, et al. Antiemetic properties of the 5HT3-receptor antagonist, GR38032F. Cancer Treat Rev 1987; 14: 333-36.
Rapid progressive subacute sclerosing panencephalitis after perinatally acquired measles virus infection SiR-Subacute
sclerosing panencephalitis (SSPE) is a rare slowly progressive disease of the central nervous system in children and young adults caused by defective measles virus;1,2 it has been observed in many ethnic groups with an incidence of about 1 case per million children.3 First signs and symptoms of SSPE are usually recognised several years after initial contact with the virus with a mean age of onset of 7 to 8 years.3 One of the risk factors for SSPE so far recognised is measles virus infection below 1 year of age.4 We report a case of onset of SSPE in early infancy as a consequence of intrauterine measles virus infection acquired shortly before delivery. A male infant (born in the 38th week of pregnancy, birth weight 2810 g) was admitted to the department of paediatrics of the General Hospital St Polten at the age of 4 days because his mother had measles virus pneumonia requiring mechanical ventilation. A slight morbilliform exanthema was observed on the day of admission, reaching its peak of intensity on the 8th day_after birth. No measles virus specific antibodies in the infant’s serum were detectable at this stage with IgG and IgM antibody ELISA and a complement fixation test. On the day of discharge (13 days postpartum) the patient showed no clinical signs of abnormality. The boy was readmitted at the age of 4 months because of a history of daily generalised cerebral seizures. At this stage of the disease neuromotor retardation was obvious, as well as high-grade areas of abnormal signal intensity on
magnetic resonance imaging scans, indicating not only generalised cerebral atrophy but also an older area of infarction in the left parietotemporal region. Throughout the clinical course of disease increasing titres of measles-specific IgG in serum and cerebrospinal fluid (CSF) were recorded (see table). IgM antibodies, however, were not detectable in the samples collected. Local antibody production in CSF was detected despite an intact blood-brain barrier. In the 1124
Neg=negative. CFT=complement fixation test. Table: Serological findings
,
examinations the frequency of cerebral seizures increased and therapeutic control with antiepileptic drugs
follow-up
possible. Typical periodic discharges (Rodermacker complexes) appeared by the age of 11 months. The child died at the age of 16 months, the last part of his life being characterised by severe apnoeas and frequent respiratory
was not
infections. At necropsy the atrophic brain (weight 580 g) revealed SSPE with multiple cystic lesions in both hemispheres, diffuse damage and gliosis of the white matter and basal ganglia with moderate lymphomonocytic infiltrates, and immunohistochemical demonstration of measles virus antigen. The central nervous system lesions were similar to those in other rare atypical cases of SSPEwhile paired helical filament-tau immunohistochemistry and electron microscopy revealed early stages of neurofibrillary tangle formations in hippocampal neurons, usually described in older cases of SSPE.5 In contrast to all the previously reported cases in older children SSPE developed in this infant with perinatally acquired measles infection after an extremely short incubation period and was characterised by rapid progressive clinical deterioration. *K Zwiauer, Elisabeth Forstenpointner, Therese E Hauser, K A Jellinger
Popow-Kraupp,
*Department of Paediatrics, General Hospital St Polten, A-3100 St Pölten, Austria; Institute of Virology, University Medical School of Vienna, Vienna; Department of Paediatrics, University Medical School of Vienna; and Ludwig Boltzman Institute of Clinical Neurobiology, Vienna
1 2
3
4 5
Sidhu MS, Crowley J, Lowenthal A, et al. Defective measles virus in subacute sclerosing panencephalitis. Virology 1994; 202: 631-41. Ter Meulen V, Hall WW. Slow virus infections of the nervous system: virological and pathogenetic considerations. J Gen Virol 1981; 41: 1-25. Miller C, Farrington CP, Harbert K. The epidemiology of subacute sclerosing panencephalitis in England and Wales 1970-1989. Int J Epidemiol 1992; 21: 998-1006. Schubert P. Atypischer Fall einer subakuten sklerosierenden Leukoencephalitis (van Bogaert). Acta Neuropathol 1966; 6: 93-97. Wisniewski HM, Dymecky J, Wegiel J, et al. Neurofibrillary pathology in subacute sclerosing panencephalitis. Dementia 1991; 2: 133-41.
CORRECTIONS Preventing nosocomial transmission of tuberculosis-In this Commentary (Jan 28, p 204), the name of the second author, Marguerite Jackson, was inadvertently omitted.
Reversible lymphopenia in patient with Rocky Mountain spotted fever contracted in New York City-In this letter by G S Turett and colleagues (March 11, p 647), the name of the third author should have been Michael Crooks. In the third paragraph, the fifth sentence should have read "Soundview Park in the Bronx, where D variabilis ticks mfected with R rickettsii have been found,’ was the likely source of exposure for most".
Hypertensive effect of antenatal thyrotropin-releasing hormone in pre-eclampsia-In this letter by M J Peek and colleagues (March 25, p 793), the labels for the normotensive and pre-eclamptic women on the
figure were the wrong way round. The upper line should be pre-eclamptic women and the lower line normotensive women.
labelled