- Email: [email protected]
RADIOSENSITIVITY OF IN-SITU CARCINOMA OF BREAST
675 in viscosity, 39±14% and 39±8% (mean±SD), respectively (results from three different preparations). Several studies have claimed therapeutic benefit from the use of SCMC (’Mucodyne’) in glue ear, although others have found no effect.5 Our results demonstrate that SCMC would have no effect on effusion viscosity whereas NAC would reduce it. The difference between SCMC and NAC is almost certainly due to the fact that SCMC has its sulphur blocked by a carboxymethyl group while NAC has the free -SH group necessary for the cleavage of S-S bridges. Two points need to be considered before extrapolating these results to the clinical situation-although NAC reduces the viscosity of the isolated effusion will enough reach the middle ear, and if the effusion is thinned excessively any mucocilliary clearance will be impaired.
drops (p= 0-0005)
Department of Physiological Sciences, University of Newcastle upon Tyne, Medical School, Newcastle upon
Tyne NE2 4HH
P. PEARSON E. FITZGERALD G. G. R. GREEN
J. J.
Royal National Throat, Nose and Ear Hospital, London WC1
J. P. BIRCHALL
ENT Department, Royal Victoria Infirmary, Newcastle upon Tyne
F. W. STAFFORD
1 Harrison
K, Watson TJ. Longterm follow up of chronic exudative otitis media (glue ear) Proc Roy Soc Med 1969; 62: 455-60. 2. Sadé J. Secretory otitis media and its sequelae. New York: Churchill Livingstone, 1979. 3. Meyer FA. Comparison of structural glycoproteins from mucus of different sources. Biochim Biophys Acta 1977; 493: 272-82. 4. Pearson JP, Robson MJ, Green GGR, Birchall JP. An investigation of the glycoprotein component of middle ear effusions in otitis media In: Vliegenthart JFG, et al, eds. Abstracts of the XIIth International Carbohydrate Symposium. Amsterdam. Holland Vonk, 1984: 341. 5. Hughes KB. Management of middle ear effusions in children. J Laryngol Otol 1984;
duodenal or gastric ulcer. The only abdominal abnormality was a tense and turgid liver with a rounded lower edge lying under the costal margin. The liver could be gently squeezed to its normal size but filled rapidly on releasing pressure. At this point the patient’s blood pressure became unrecordable. The hepatic findings and clinical deterioration prompted aspiration of the pericardium via the diaphragm. Straw-coloured fluid, under pressure, was obtained and a ’Supra Cath’, used for bladder drainage, was carefully inserted via the central tendon. 500 ml of fluid was immediately drained, followed by another 500 ml over the next 30 min and a further 300 ml drained slowly thereafter. His blood pressure rose immediately and his condition improved strikingly. The abdomen was closed, the intrapericardial catheter being left as a stab drain. His postoperative recovery was uneventful and he was discharged on the 10th postoperative day. No cause was subsequently found for the pericardial effusion and he has been well since this incident. Abdominal pain due to stretching of the liver capsule as a result of congestive cardiac failure is usually accompanied by hepatomegaly, a history of poorly controlled heart failure, distended neck veins, and oedema. Progressive cardiac and respiratory failure are the usual manifestations of pericardial effusion and tamponade. In this case, epigastric pain was the salient feature. It is not clear why such severe hepatic outflow obstruction should occur in isolation, but this may be the pattern when pericarditis develops with no underlying heart disease. Primary pericarditis, although rare, should enter the differential diagnosis of the acute abdomen. Surgical Department, District General Hospital, Eastbourne, East Sussex BN21 2UD 1 Dunn
GD, Hayes P, Breen KJ, Schenker S. The liver Am J Med Sci 1973; 265: 175-89.
A. N. GHANEM
J. M. POWLEY in
congestive heart failure,
a
review.
98: 677-84.
RADIOSENSITIVITY OF IN-SITU CARCINOMA OF BREAST
HEPATIC OUTFLOW OBSTRUCTION
hepatic outflow obstruction (Aug 10, reviews the chronic causes for this case shows how acute hepatic outflow mimic an abdominal emergency and lead to
SIR,-Your editorial
on
p 310) comprehensively condition. The following obstruction
can
potentially catastrophic errors in diagnosis. A previously fit man aged 46 was investigated in a Copenhagen hospital because of a 3-week history of increasingly severe epigastric pain. He was in good general condition, with epigastric tenderness but no rebound and no palpable organs. Serum amylase, urea, and electrolytes were normal. Abdominal X-rays were normal. Chest infiltration at the left pulmonary base. A barium meal revealed no leak. On gastroscopy gastritis and a 1 cm duodenal ulcer were found. Ranitidine and antacids were prescribed and he was referred to his general practitioner in the UK. His symptoms increased despite the treatment prescribed in Denmark and he was admitted as an emergency 24 hours after his return to Eastbourne, with a provisional diagnosis of perforated duodenal ulcer. He was distressed, cold, and clammy with a tinge of cyanosis and tachypnoea. His temperature was 37’2°C, pulse 100/min and blood pressure 110/70 mm Hg. He could not tolerate lying flat but the significance of this was not realised at the time. His jugular veins were not obviously congested. There was no oedema. He had rales and crepitations over the base of the left lung. Heart sounds were normal. The epigastrium was tender with guarding but no rebound tenderness. No liver or spleen enlargement was detected. There was no clinical evidence of ascites and bowel sounds were diminished. Urea, electrolytes, and amylase were normal but the white-cell count was 15 - 8 x 109 with a preponderance of neutrophils. X-rays revealed no gas under the diaphragm, a small pleural reaction at the left lung base, and a straight left cardiac border but a normal cardiothoracic ratio. Although the clinical picture was not wholly typical, the most likely diagnosis was still thought to be perforated duodenal ulcer. During laparotomy his blood pressure fell further. There was no pus or fluid in the peritoneal cavity and no serosal evidence of
X-ray revealed
SIR,-Dr Vorherr (Aug 3, p 282) infers the radiosensitivity of in-situ carcinoma of the breast from similarities between the longterm survival prospects of women treated by mastectomy and women treated by local excision plus radiotherapy for early stage breast cancer. He argues that there would be an excess mortality from breast cancer in the conservatively treated patients if residual multifocal areas of in-situ carcinoma were radioresistant. Apart from obvious difficulties in accepting the comparability of composite survival data derived from seventeen published reports, it is not clear that long-term survival is a reliable or sensitive measure of the radiosensitivity of multicentric foci of in-situ carcinoma remaining in the breast after local excision of an invasive tumour. First, we know little about the probability and time-course of progression of in-situ disease to invasive disease. Retrospective studies of selected patients with a history of surgery for benign breast disease and found, incidentally, to have incompletely excised in-situ carcinoma in the pathological specimen, report the development of invasive carcinoma with frequencies of 15-27% over a 5-10 year period.l-3 It is not known whether multifocal areas of in-situ carcinoma in women presenting with invasive disease are associated with comparable risks of progression to invasive disease, but it is possible that in-situ carcinoma does not necessarily progress within the life-span of a patient to a clinical carcinoma. Even if in-situ carcinoma carries a high lifetime risk of evolving into an invasive tumour, an excess mortality related to second ipsilateral primaries may be difficult to detect if the preclinical and clinical phases of the disease span one or two decades. Academic Radiotherapy Unit, Royal Marsden Hospital, Sutton, Surrey SM2 5PT
P. PRICE
J. R. YARNOLD
Westdahl PR, Margolin FR, Rose MR Duct carcinoma in situ. Cancer 1982, 50: 1309-14 2. Page DL, Dupont WD, Rogers LW, Landenberger M Intraductal carcinoma of the breast. follow-up after biopsy only Cancer 1982, 46: 751-58. 3 Rosen PP, Braun DW, Kinne DW. The clinical significance of pre-invasive breast carcinoma Cancer 1980, 46: 919-25 1.
Lagios MD,
drops (p= 0-0005)
Department of Physiological Sciences, University of Newcastle upon Tyne, Medical School, Newcastle upon
Tyne NE2 4HH
P. PEARSON E. FITZGERALD G. G. R. GREEN
J. J.
Royal National Throat, Nose and Ear Hospital, London WC1
J. P. BIRCHALL
ENT Department, Royal Victoria Infirmary, Newcastle upon Tyne
F. W. STAFFORD
1 Harrison
K, Watson TJ. Longterm follow up of chronic exudative otitis media (glue ear) Proc Roy Soc Med 1969; 62: 455-60. 2. Sadé J. Secretory otitis media and its sequelae. New York: Churchill Livingstone, 1979. 3. Meyer FA. Comparison of structural glycoproteins from mucus of different sources. Biochim Biophys Acta 1977; 493: 272-82. 4. Pearson JP, Robson MJ, Green GGR, Birchall JP. An investigation of the glycoprotein component of middle ear effusions in otitis media In: Vliegenthart JFG, et al, eds. Abstracts of the XIIth International Carbohydrate Symposium. Amsterdam. Holland Vonk, 1984: 341. 5. Hughes KB. Management of middle ear effusions in children. J Laryngol Otol 1984;
duodenal or gastric ulcer. The only abdominal abnormality was a tense and turgid liver with a rounded lower edge lying under the costal margin. The liver could be gently squeezed to its normal size but filled rapidly on releasing pressure. At this point the patient’s blood pressure became unrecordable. The hepatic findings and clinical deterioration prompted aspiration of the pericardium via the diaphragm. Straw-coloured fluid, under pressure, was obtained and a ’Supra Cath’, used for bladder drainage, was carefully inserted via the central tendon. 500 ml of fluid was immediately drained, followed by another 500 ml over the next 30 min and a further 300 ml drained slowly thereafter. His blood pressure rose immediately and his condition improved strikingly. The abdomen was closed, the intrapericardial catheter being left as a stab drain. His postoperative recovery was uneventful and he was discharged on the 10th postoperative day. No cause was subsequently found for the pericardial effusion and he has been well since this incident. Abdominal pain due to stretching of the liver capsule as a result of congestive cardiac failure is usually accompanied by hepatomegaly, a history of poorly controlled heart failure, distended neck veins, and oedema. Progressive cardiac and respiratory failure are the usual manifestations of pericardial effusion and tamponade. In this case, epigastric pain was the salient feature. It is not clear why such severe hepatic outflow obstruction should occur in isolation, but this may be the pattern when pericarditis develops with no underlying heart disease. Primary pericarditis, although rare, should enter the differential diagnosis of the acute abdomen. Surgical Department, District General Hospital, Eastbourne, East Sussex BN21 2UD 1 Dunn
GD, Hayes P, Breen KJ, Schenker S. The liver Am J Med Sci 1973; 265: 175-89.
A. N. GHANEM
J. M. POWLEY in
congestive heart failure,
a
review.
98: 677-84.
RADIOSENSITIVITY OF IN-SITU CARCINOMA OF BREAST
HEPATIC OUTFLOW OBSTRUCTION
hepatic outflow obstruction (Aug 10, reviews the chronic causes for this case shows how acute hepatic outflow mimic an abdominal emergency and lead to
SIR,-Your editorial
on
p 310) comprehensively condition. The following obstruction
can
potentially catastrophic errors in diagnosis. A previously fit man aged 46 was investigated in a Copenhagen hospital because of a 3-week history of increasingly severe epigastric pain. He was in good general condition, with epigastric tenderness but no rebound and no palpable organs. Serum amylase, urea, and electrolytes were normal. Abdominal X-rays were normal. Chest infiltration at the left pulmonary base. A barium meal revealed no leak. On gastroscopy gastritis and a 1 cm duodenal ulcer were found. Ranitidine and antacids were prescribed and he was referred to his general practitioner in the UK. His symptoms increased despite the treatment prescribed in Denmark and he was admitted as an emergency 24 hours after his return to Eastbourne, with a provisional diagnosis of perforated duodenal ulcer. He was distressed, cold, and clammy with a tinge of cyanosis and tachypnoea. His temperature was 37’2°C, pulse 100/min and blood pressure 110/70 mm Hg. He could not tolerate lying flat but the significance of this was not realised at the time. His jugular veins were not obviously congested. There was no oedema. He had rales and crepitations over the base of the left lung. Heart sounds were normal. The epigastrium was tender with guarding but no rebound tenderness. No liver or spleen enlargement was detected. There was no clinical evidence of ascites and bowel sounds were diminished. Urea, electrolytes, and amylase were normal but the white-cell count was 15 - 8 x 109 with a preponderance of neutrophils. X-rays revealed no gas under the diaphragm, a small pleural reaction at the left lung base, and a straight left cardiac border but a normal cardiothoracic ratio. Although the clinical picture was not wholly typical, the most likely diagnosis was still thought to be perforated duodenal ulcer. During laparotomy his blood pressure fell further. There was no pus or fluid in the peritoneal cavity and no serosal evidence of
X-ray revealed
SIR,-Dr Vorherr (Aug 3, p 282) infers the radiosensitivity of in-situ carcinoma of the breast from similarities between the longterm survival prospects of women treated by mastectomy and women treated by local excision plus radiotherapy for early stage breast cancer. He argues that there would be an excess mortality from breast cancer in the conservatively treated patients if residual multifocal areas of in-situ carcinoma were radioresistant. Apart from obvious difficulties in accepting the comparability of composite survival data derived from seventeen published reports, it is not clear that long-term survival is a reliable or sensitive measure of the radiosensitivity of multicentric foci of in-situ carcinoma remaining in the breast after local excision of an invasive tumour. First, we know little about the probability and time-course of progression of in-situ disease to invasive disease. Retrospective studies of selected patients with a history of surgery for benign breast disease and found, incidentally, to have incompletely excised in-situ carcinoma in the pathological specimen, report the development of invasive carcinoma with frequencies of 15-27% over a 5-10 year period.l-3 It is not known whether multifocal areas of in-situ carcinoma in women presenting with invasive disease are associated with comparable risks of progression to invasive disease, but it is possible that in-situ carcinoma does not necessarily progress within the life-span of a patient to a clinical carcinoma. Even if in-situ carcinoma carries a high lifetime risk of evolving into an invasive tumour, an excess mortality related to second ipsilateral primaries may be difficult to detect if the preclinical and clinical phases of the disease span one or two decades. Academic Radiotherapy Unit, Royal Marsden Hospital, Sutton, Surrey SM2 5PT
P. PRICE
J. R. YARNOLD
Westdahl PR, Margolin FR, Rose MR Duct carcinoma in situ. Cancer 1982, 50: 1309-14 2. Page DL, Dupont WD, Rogers LW, Landenberger M Intraductal carcinoma of the breast. follow-up after biopsy only Cancer 1982, 46: 751-58. 3 Rosen PP, Braun DW, Kinne DW. The clinical significance of pre-invasive breast carcinoma Cancer 1980, 46: 919-25 1.
Lagios MD,