118
Unusual
diagnosis of phaeochromocytoma
SiR,—Your May 19 editorial prompts us to report a patient under for the investigation of hypertension. During his admission to hospital this 54-year-old man underwent renal arteriography for a suspected renal artery stenosis. After the procedure, which our care
included femoral arterial puncture and injection of contrast medium, he became hot and perspired, and remarked to the female radiologist that it was the first time in years that a woman had made his glasses steam up. He had no further untoward side-effects over the next few hours, and his blood pressure remained stable. Review of the angiograms showed normal calibre renal arteries with no evidence of a stenosis. There was, however, a faint arterial "blush" in the left supra-renal area. Computed tomographic scanning demonstrated a 6 cm left adrenal mass with a necrotic centre. Urinary metanephrines and vanillylmandelic acid were both greatly raised at over 50 and over 200 unol/1 per 24 hours, respectively (normal 0-5 and 0-35), and an m-iodobenzylguanidine scan confirmed a solitary left phaeochromocytoma (figure). The tumour has since been safely resected and the patient remains well. I
She had a normal immunoglobulin profile with no paraprotein and a negative autoantibody screen; the direct Coombs test was negative, a whole body computed tomographic scan was normal, and she had no proteinuria. Bone-marrow examination showed diffuse infiltration by her leukaemia. She had no history of a connective tissue disorder and no family history of angioedema. She was treated with chlorambucil and prednisolone daily with little benefit to her oedema, rash, or blood picture-her white count rising to 230 x 109/1 (90% lymphocytes). At this time Cl esterase inhibitor was low (0-134 g/l; normal 026-072), as was C4 (under 0-06 g/1,0 11-0-39), and these values were subsequently confirmed twice. Chemotherapy (CHOP) was then instituted. In addition, fresh frozen plasma three units daily, stanozolol 10 mg daily, and tranexamic acid 1 g four times daily were given. The oedema and rash dramatically improved. One week after chemotherapy Cl esterase inhibitor was normal (0-392 g/1) and C4 (01 g/1) was only slightly reduced, in keeping with the clinical improvement. This patient demonstrates a previously undescribed association between acquired Clesterase inhibitor deficiency and a T-cell lymphoproliferative disorder. The angioedema was temporally related to disease progression, as indicated by a rise in the lymphocyte count and the appearance of skin infiltration. In the B-cell lymphoproliferative disorders a paraprotein was usually detected,Z and it was suggested that this was related to the associated deficiency. No such paraprotein was seen in our patient and we are tempted to implicate the leukaemic cells directly or indirectly via cytokines as the immunological trigger causing Cl activation and consequent Cl esterase inhibitor depletion. Our patient therefore demonstrates the importance of recognising this syndrome in anyone with a T-cell lymphoproliferadve disorder and unexplained oedema. R. J. GRACE Department of Haematology, St James’s University Hospital, Leeds LS9 7TF, UK
m-iodobenzylguanidine scan showing uptake in left suprarenal
region. We suspect that in this patient the occult phaeochromocytoma stimulated by the contrast injection, causing the patient to perspire heavily. This was clearly a case of serendipity which surprised the patient and the doctors, fortunately without the catastrophe so often seen with these tumours.
A. JACOB C. J. MAINWARING B. A. MCVERRY
1. Donaldson VH, Evans RR. A biochemical abnormality in hereditary angioneurotic edema: absence of serum inhibitor of C’ l esterase. Am J Med 1963; 35: 37-44. 2. Sheffer AL, Austen KF, Rosen FS, Fearon DT. Acquired deficiency of the inhibitor of the first component of complement: report of five additional cases with commentary on the syndrome. J Allergy Clin Immunol 1985; 75: 640-46.
was
K. L. DONOVAN D. J. FISHER
Cardiff Royal Infirmary, Cardiff CF2 1SZ, UK
Acquired C1
esterase inhibitor deficiency as manifestation of T-cell lymphoproliferative disorder
SiR,—Angioedema is caused by an increase in vascular permeability resulting in subcutaneous or mucosal swelling. A reduction in Cl
esterase
inhibitor has been shown
to cause
angioedema. Congenital and acquired deficiencies have been described. A review of acquired deficiency showed that 23 of 25 patients had an associated B cell abnormality-the other 2 being associated with myelofibrosis and adenocarcinoma of the rectum. We report a patient with acquired Cl esterase inhibitor deficiency associated witha T-cell lymphoprotiferative disorder. A 53-year-old woman presented at age 51 with lymphocytosis. She had no lymphadenopathy or hepatosplenomegaly. Morphologically, cytochemically, and immunologically the lymphocytosis was classified as a CD8 + /CD4 - T-cell prolymphocytic leukaemia. For 2 years she needed no treatment, during which time her white count rose from 23-3 x 109/1 (64% lymphocytes) to 35x 109/1 (90% lymphocytes). Generalised oedema then developed, especially affecting the face. This was associated with an erythematous infiltrative rash over the trunk and arms. Skin biopsy confirmed infiltration from aT-cell disorder.
Prenatal diagnosis of cytochrome-deficient chronic granulomatous disease SIR,-We have established a method for the prenatal diagnosis of cytochrome bss8-deficient chronic granulomatous disease (CGD) and its carrier state. This type of CGD is the most common (about 70%) and most severe of all CGD. The method is based on the immunostaining of Hofbauer cells (villous macrophages) in villi of placentas with a monoclonal antibody raised against cytochrome bss8’ The samples are obtained by chorionic villi sampling (CVS) at the 7th to 8th week of gestation. Villi obtained by CVS (or at abortion) were fixed with 4% paraformaldehyde at 4°C for 2 h, and frozen sections were immunohistochemically stained with a monoclonal antibody 7D5 against cytochrome1 After immunoperoxidase/diaminobenzidine staining, the samples were counterstained with haematoxylin. In the villi obtained in the 7th or later weeks of gestation large cells lying between capillaries and trophoblastic shells were deeply stained with antibody (figure). These cells were identified as Hofbauer cells, on the basis of morphology and location and specific staining with OKM14, which binds to CD14 in monocytes and
macrophages. We examined the chorionic villi for female offspring from a carrier mother who had once delivered a boy with X-linked, cytochrome-b-deficient CGD. Phagocytic cells from a carrier ought to consist of cytochrome b positive and negative populations, resulting in decrease in 7D5 + cells. However, the density of 7D5 antigen-positive (cytochrome bss8-positive) cells in the villi was normal, which suggested that the baby was not a carrier. This was confirmed later by other means. Cells in her villi obtained at
119
products which have a rapid release profile in the vagina can cause unduly rapid labour, fetal bradycardia, frequent and powerful uterine contractions, and, occasionally, uterine hypertonus. This is why the controlled release product was developed. Our experience, however, has shown that although this claim is made about other rapid-release vaginal prostaglandin preparations, it is very infrequently seen in practice. Propess may be a slow-release preparation in vitro but in vivo the release pattern seems different. In vitro 08 mg/h PGEz is said to be released from the pessary, while in vivo "dose dumping" is
frequent. The diffusion ofPGEz from the pessary depends on the degree of polymerisation, which in turn depends on hydration and temperature in the vagina. More research into polymer crosslinkage and the dimensions of the pessary and its crystallinity might
Immunostaining for cytochrome b558 in sample villus obtained at the 10th week of gestation.
of chorionic
Hofbauer cells located between capillaries and trophoblastic shells are stained deeply.
double-stained with mouse monoclonal antiOKM14/phycoerythrin-conjugated goat anti-mouse IgG and rabbit anti-human cytochrome b558/FITC-conjugated goat antirabbit IgG. 98% of CD 14 + cells examined under a fluorescence microscope were labelled with the cytochrome antibody. 99% of phorbor ester-stimulated cord blood granulocytes were positive in the nitroblue tetrazolium test. MICHIO NAKAMURA Institute of Medical Science, SHINOBU IMAJOH-OHMI of University Tokyo,
delivery
SHIRO KANEGASAKI
Kanagawa Children’s Medical Centre,
HIROKO KUROZUMI
Yokohama
Hospital, Tokyo
Boshi-aukukai Aiiku Ortho
William
Harvey Hospital,
Ashford, Kent TN24 0LZ, UK
M. N. KHOUZAM R. S. LEDWARD
were
Tokyo 108, Japan
Toranomon
lead to the better control of the rate of release of PGE2. Inclusion ofa thread, to allow easy removal from the vagina when complications develop, would also be useful. The efficacy of this controlled release PGEz pessary is not in question; its safety requires further research.
Hospital, Tokyo
Diagnostic Systems KK Japan
KODO SATO
SUEKO KATO YOKO MIYAZAKI
1. Nakamura M, Murakami M, Kogo T, Tanaka Y, Minakami S. Monoclonal antibody 7D5 raised to cytochrome b558 of human neutrophils: immunocytochemical detection of the antigen m peripheral phagocytes of normal subjects, patients with chronic granulomatous disease and their carrier mothers. Blood 1987; 69: 1404.
Difficulties with controlled release
prostaglandin E2 pessaries SIR,-We describe here three cases of adverse reactions to the controlled release prostaglandin E2 pessary (’Propess’, Roussel). Case 1 (25, para 1 + 0). She was induced for pregnancy-related hypertension and had tetanic contractions 1 h after induction with propess. Severe vaginismus developed and it was impossible to remove the pessary. Recurrent late decelerations on the fetal monitor trace ensued and she progressed very rapidly to full dilatation. The second stage was short, but she had agonising continuous pain. The baby had an Apgar score of 6 at 1 min and 10 at 5 min. Case 2 (23, para 1 + 0). Induced with the PGE2 pessary because of post-maturity, she had very short first and second stages of labour, the whole labour lasting 1 h. Her first labour had lasted 14 h. Case 3 (27, para 0 + 0). Induced because of intrauterine growth retardation. The pessary was inserted at 2200 hours and subsequently she had recurrent bowel motions and attacks of nausea and vomiting. Complex fetal tachycardia developed, and thick meconium-stained liquor was noted. The pessary was removed but the fetal decelerations continued for a further 45 min without significant cervical dilatation. The baby had to be delivered by caesarean section and had an Apgar score of 8 at 1 min and 10 at 5 min.
These three cases out of the thirty in which we have used the controlled release PGE2 pessary have prompted us to stop using this product We learn from other hospitals of similar side-effects with the controlled release PGE2 pessary. The manufacturers state that
SIR,—In a randomised trial we have been comparing the safety and efficacy of the ’Propess’ hygroscopic polymer sustained-release prostaglandin Ez vaginal pessary (Roussel) with ’Prostin’ (3 mg dinoprostone) vaginal tablets (Upjohn) in ripening the cervix for induction of labour. A potential advantage of the new pessary is that it can be removed once the cervix has ripened, thus avoiding the risk of prostaglandin overdose and consequent uterine hyperstimulation. Also, it is claimed that a single pessary is usually sufficient, and induction rates are said to be comparable with those seen with existing soluble pessaries.1,2 We had to stop the trial after admission of only 36 patients (15 on propess) because of serious problems with this pessary. There was no significant difference between the two groups in terms of time from pessary/tablet insertion to onset of labour or time from insertion to delivery. The two groups were similar in age, parity, gestation, and obstetric history. However, the polymer from which the pessary is made is not soluble so that removal is essential. In 5 patients the pessary proved difficult to remove. In 3 women the pessary was easily located by digital examination but it was adherent to the vaginal wall. The hygroscopic polymer requires water absorption so that the matrix can release its active prostaglandin, and this can lead to adhesion. The prolonged vaginal examination required caused considerable discomfort, and in one case speculum examination in the lithotomy position was needed, the pessary being removed with an arterial clamp. In the other 2 patients, the pessary was never recovered, even after delivery; it is not radio-opaque so an X-ray is unhelpful. These two pessaries may have fallen out of the vagina unnoticed, but retention within the uterine cavity or within a repaired episiotomy are also possible. There is no information available about the long-term effects of such a retained foreign
body. Propess pessaries cost about c26 each while prostin pessaries cost £6. The claim that a single pessary is always sufficient to achieve cervical ripening was not substantiated, despite leaving the device in situ for 8 hours. A radio-opaque marker thread might seem the answer to problems with location and withdrawal but, once it is wet, the pessary is no longer strong enough to resist break-up during traction for removal (personal communication, Roussel Laboratories). Some form of disposable "cage" with a thread attached may be an alternative. In its present form this sustained-release pessary is fraught with difficulty. Department of Obstetrics and Gynaecology, Watford General Hospital, Watford WD1 8HB, UK
P. BEX P. C. GUNASEKERA J. H. PHIPPS
1. Embrey MP, Graham NB, McNeill ME. Induction of labour with a sustained-release prostaglandin E2 vaginal pessary. Br Med J 1980; 281: 901-02. 2. Embrey MP, MacKenzie IZ. Labour induction with a sustained release prostaglandin E2 polymer vaginal pessary. J Obstet Gynaecol 1985; 6: 38-41.
Unusual
diagnosis of phaeochromocytoma
SiR,—Your May 19 editorial prompts us to report a patient under for the investigation of hypertension. During his admission to hospital this 54-year-old man underwent renal arteriography for a suspected renal artery stenosis. After the procedure, which our care
included femoral arterial puncture and injection of contrast medium, he became hot and perspired, and remarked to the female radiologist that it was the first time in years that a woman had made his glasses steam up. He had no further untoward side-effects over the next few hours, and his blood pressure remained stable. Review of the angiograms showed normal calibre renal arteries with no evidence of a stenosis. There was, however, a faint arterial "blush" in the left supra-renal area. Computed tomographic scanning demonstrated a 6 cm left adrenal mass with a necrotic centre. Urinary metanephrines and vanillylmandelic acid were both greatly raised at over 50 and over 200 unol/1 per 24 hours, respectively (normal 0-5 and 0-35), and an m-iodobenzylguanidine scan confirmed a solitary left phaeochromocytoma (figure). The tumour has since been safely resected and the patient remains well. I
She had a normal immunoglobulin profile with no paraprotein and a negative autoantibody screen; the direct Coombs test was negative, a whole body computed tomographic scan was normal, and she had no proteinuria. Bone-marrow examination showed diffuse infiltration by her leukaemia. She had no history of a connective tissue disorder and no family history of angioedema. She was treated with chlorambucil and prednisolone daily with little benefit to her oedema, rash, or blood picture-her white count rising to 230 x 109/1 (90% lymphocytes). At this time Cl esterase inhibitor was low (0-134 g/l; normal 026-072), as was C4 (under 0-06 g/1,0 11-0-39), and these values were subsequently confirmed twice. Chemotherapy (CHOP) was then instituted. In addition, fresh frozen plasma three units daily, stanozolol 10 mg daily, and tranexamic acid 1 g four times daily were given. The oedema and rash dramatically improved. One week after chemotherapy Cl esterase inhibitor was normal (0-392 g/1) and C4 (01 g/1) was only slightly reduced, in keeping with the clinical improvement. This patient demonstrates a previously undescribed association between acquired Clesterase inhibitor deficiency and a T-cell lymphoproliferative disorder. The angioedema was temporally related to disease progression, as indicated by a rise in the lymphocyte count and the appearance of skin infiltration. In the B-cell lymphoproliferative disorders a paraprotein was usually detected,Z and it was suggested that this was related to the associated deficiency. No such paraprotein was seen in our patient and we are tempted to implicate the leukaemic cells directly or indirectly via cytokines as the immunological trigger causing Cl activation and consequent Cl esterase inhibitor depletion. Our patient therefore demonstrates the importance of recognising this syndrome in anyone with a T-cell lymphoproliferadve disorder and unexplained oedema. R. J. GRACE Department of Haematology, St James’s University Hospital, Leeds LS9 7TF, UK
m-iodobenzylguanidine scan showing uptake in left suprarenal
region. We suspect that in this patient the occult phaeochromocytoma stimulated by the contrast injection, causing the patient to perspire heavily. This was clearly a case of serendipity which surprised the patient and the doctors, fortunately without the catastrophe so often seen with these tumours.
A. JACOB C. J. MAINWARING B. A. MCVERRY
1. Donaldson VH, Evans RR. A biochemical abnormality in hereditary angioneurotic edema: absence of serum inhibitor of C’ l esterase. Am J Med 1963; 35: 37-44. 2. Sheffer AL, Austen KF, Rosen FS, Fearon DT. Acquired deficiency of the inhibitor of the first component of complement: report of five additional cases with commentary on the syndrome. J Allergy Clin Immunol 1985; 75: 640-46.
was
K. L. DONOVAN D. J. FISHER
Cardiff Royal Infirmary, Cardiff CF2 1SZ, UK
Acquired C1
esterase inhibitor deficiency as manifestation of T-cell lymphoproliferative disorder
SiR,—Angioedema is caused by an increase in vascular permeability resulting in subcutaneous or mucosal swelling. A reduction in Cl
esterase
inhibitor has been shown
to cause
angioedema. Congenital and acquired deficiencies have been described. A review of acquired deficiency showed that 23 of 25 patients had an associated B cell abnormality-the other 2 being associated with myelofibrosis and adenocarcinoma of the rectum. We report a patient with acquired Cl esterase inhibitor deficiency associated witha T-cell lymphoprotiferative disorder. A 53-year-old woman presented at age 51 with lymphocytosis. She had no lymphadenopathy or hepatosplenomegaly. Morphologically, cytochemically, and immunologically the lymphocytosis was classified as a CD8 + /CD4 - T-cell prolymphocytic leukaemia. For 2 years she needed no treatment, during which time her white count rose from 23-3 x 109/1 (64% lymphocytes) to 35x 109/1 (90% lymphocytes). Generalised oedema then developed, especially affecting the face. This was associated with an erythematous infiltrative rash over the trunk and arms. Skin biopsy confirmed infiltration from aT-cell disorder.
Prenatal diagnosis of cytochrome-deficient chronic granulomatous disease SIR,-We have established a method for the prenatal diagnosis of cytochrome bss8-deficient chronic granulomatous disease (CGD) and its carrier state. This type of CGD is the most common (about 70%) and most severe of all CGD. The method is based on the immunostaining of Hofbauer cells (villous macrophages) in villi of placentas with a monoclonal antibody raised against cytochrome bss8’ The samples are obtained by chorionic villi sampling (CVS) at the 7th to 8th week of gestation. Villi obtained by CVS (or at abortion) were fixed with 4% paraformaldehyde at 4°C for 2 h, and frozen sections were immunohistochemically stained with a monoclonal antibody 7D5 against cytochrome1 After immunoperoxidase/diaminobenzidine staining, the samples were counterstained with haematoxylin. In the villi obtained in the 7th or later weeks of gestation large cells lying between capillaries and trophoblastic shells were deeply stained with antibody (figure). These cells were identified as Hofbauer cells, on the basis of morphology and location and specific staining with OKM14, which binds to CD14 in monocytes and
macrophages. We examined the chorionic villi for female offspring from a carrier mother who had once delivered a boy with X-linked, cytochrome-b-deficient CGD. Phagocytic cells from a carrier ought to consist of cytochrome b positive and negative populations, resulting in decrease in 7D5 + cells. However, the density of 7D5 antigen-positive (cytochrome bss8-positive) cells in the villi was normal, which suggested that the baby was not a carrier. This was confirmed later by other means. Cells in her villi obtained at
119
products which have a rapid release profile in the vagina can cause unduly rapid labour, fetal bradycardia, frequent and powerful uterine contractions, and, occasionally, uterine hypertonus. This is why the controlled release product was developed. Our experience, however, has shown that although this claim is made about other rapid-release vaginal prostaglandin preparations, it is very infrequently seen in practice. Propess may be a slow-release preparation in vitro but in vivo the release pattern seems different. In vitro 08 mg/h PGEz is said to be released from the pessary, while in vivo "dose dumping" is
frequent. The diffusion ofPGEz from the pessary depends on the degree of polymerisation, which in turn depends on hydration and temperature in the vagina. More research into polymer crosslinkage and the dimensions of the pessary and its crystallinity might
Immunostaining for cytochrome b558 in sample villus obtained at the 10th week of gestation.
of chorionic
Hofbauer cells located between capillaries and trophoblastic shells are stained deeply.
double-stained with mouse monoclonal antiOKM14/phycoerythrin-conjugated goat anti-mouse IgG and rabbit anti-human cytochrome b558/FITC-conjugated goat antirabbit IgG. 98% of CD 14 + cells examined under a fluorescence microscope were labelled with the cytochrome antibody. 99% of phorbor ester-stimulated cord blood granulocytes were positive in the nitroblue tetrazolium test. MICHIO NAKAMURA Institute of Medical Science, SHINOBU IMAJOH-OHMI of University Tokyo,
delivery
SHIRO KANEGASAKI
Kanagawa Children’s Medical Centre,
HIROKO KUROZUMI
Yokohama
Hospital, Tokyo
Boshi-aukukai Aiiku Ortho
William
Harvey Hospital,
Ashford, Kent TN24 0LZ, UK
M. N. KHOUZAM R. S. LEDWARD
were
Tokyo 108, Japan
Toranomon
lead to the better control of the rate of release of PGE2. Inclusion ofa thread, to allow easy removal from the vagina when complications develop, would also be useful. The efficacy of this controlled release PGEz pessary is not in question; its safety requires further research.
Hospital, Tokyo
Diagnostic Systems KK Japan
KODO SATO
SUEKO KATO YOKO MIYAZAKI
1. Nakamura M, Murakami M, Kogo T, Tanaka Y, Minakami S. Monoclonal antibody 7D5 raised to cytochrome b558 of human neutrophils: immunocytochemical detection of the antigen m peripheral phagocytes of normal subjects, patients with chronic granulomatous disease and their carrier mothers. Blood 1987; 69: 1404.
Difficulties with controlled release
prostaglandin E2 pessaries SIR,-We describe here three cases of adverse reactions to the controlled release prostaglandin E2 pessary (’Propess’, Roussel). Case 1 (25, para 1 + 0). She was induced for pregnancy-related hypertension and had tetanic contractions 1 h after induction with propess. Severe vaginismus developed and it was impossible to remove the pessary. Recurrent late decelerations on the fetal monitor trace ensued and she progressed very rapidly to full dilatation. The second stage was short, but she had agonising continuous pain. The baby had an Apgar score of 6 at 1 min and 10 at 5 min. Case 2 (23, para 1 + 0). Induced with the PGE2 pessary because of post-maturity, she had very short first and second stages of labour, the whole labour lasting 1 h. Her first labour had lasted 14 h. Case 3 (27, para 0 + 0). Induced because of intrauterine growth retardation. The pessary was inserted at 2200 hours and subsequently she had recurrent bowel motions and attacks of nausea and vomiting. Complex fetal tachycardia developed, and thick meconium-stained liquor was noted. The pessary was removed but the fetal decelerations continued for a further 45 min without significant cervical dilatation. The baby had to be delivered by caesarean section and had an Apgar score of 8 at 1 min and 10 at 5 min.
These three cases out of the thirty in which we have used the controlled release PGE2 pessary have prompted us to stop using this product We learn from other hospitals of similar side-effects with the controlled release PGE2 pessary. The manufacturers state that
SIR,—In a randomised trial we have been comparing the safety and efficacy of the ’Propess’ hygroscopic polymer sustained-release prostaglandin Ez vaginal pessary (Roussel) with ’Prostin’ (3 mg dinoprostone) vaginal tablets (Upjohn) in ripening the cervix for induction of labour. A potential advantage of the new pessary is that it can be removed once the cervix has ripened, thus avoiding the risk of prostaglandin overdose and consequent uterine hyperstimulation. Also, it is claimed that a single pessary is usually sufficient, and induction rates are said to be comparable with those seen with existing soluble pessaries.1,2 We had to stop the trial after admission of only 36 patients (15 on propess) because of serious problems with this pessary. There was no significant difference between the two groups in terms of time from pessary/tablet insertion to onset of labour or time from insertion to delivery. The two groups were similar in age, parity, gestation, and obstetric history. However, the polymer from which the pessary is made is not soluble so that removal is essential. In 5 patients the pessary proved difficult to remove. In 3 women the pessary was easily located by digital examination but it was adherent to the vaginal wall. The hygroscopic polymer requires water absorption so that the matrix can release its active prostaglandin, and this can lead to adhesion. The prolonged vaginal examination required caused considerable discomfort, and in one case speculum examination in the lithotomy position was needed, the pessary being removed with an arterial clamp. In the other 2 patients, the pessary was never recovered, even after delivery; it is not radio-opaque so an X-ray is unhelpful. These two pessaries may have fallen out of the vagina unnoticed, but retention within the uterine cavity or within a repaired episiotomy are also possible. There is no information available about the long-term effects of such a retained foreign
body. Propess pessaries cost about c26 each while prostin pessaries cost £6. The claim that a single pessary is always sufficient to achieve cervical ripening was not substantiated, despite leaving the device in situ for 8 hours. A radio-opaque marker thread might seem the answer to problems with location and withdrawal but, once it is wet, the pessary is no longer strong enough to resist break-up during traction for removal (personal communication, Roussel Laboratories). Some form of disposable "cage" with a thread attached may be an alternative. In its present form this sustained-release pessary is fraught with difficulty. Department of Obstetrics and Gynaecology, Watford General Hospital, Watford WD1 8HB, UK
P. BEX P. C. GUNASEKERA J. H. PHIPPS
1. Embrey MP, Graham NB, McNeill ME. Induction of labour with a sustained-release prostaglandin E2 vaginal pessary. Br Med J 1980; 281: 901-02. 2. Embrey MP, MacKenzie IZ. Labour induction with a sustained release prostaglandin E2 polymer vaginal pessary. J Obstet Gynaecol 1985; 6: 38-41.
