- Email: [email protected]
DUODENITIS
1437
(with normal CT scans in 2). illustrate increased and decreased tracer uptake in the left temporal lobe. These data suggest that 99mTc-HMPAO has similar imaging properties to 123I-labelled amphetamine derivatives. This new tracer seems to be the radiopharmaceutical of choice for brain imaging in epilepsy because it has more profitable gamma energy (no high-energy components) and is available on an everyday basis.
PERFORATED PEPTIC ULCER IN THE ELDERLY
SPECT revealed decreased uptake
Figs 1 and 2
Institute for Clinical and Nuclear Medicine,
Experimental
University of Bonn, D-5300 Bonn 1, West
Germany
H. J. BIERSACK K. REICHMANN C. WINKLER
Department of Neurology/Epileptology, H. STEFAN P. BÜLAU University of Bonn Amersham International plc, Amersham, Buckinghamshire 1. Biersack
K. KUHNEN H. PENIN
D. A. TYRRELL R. D. NEIRINCKX K. R. GRUNER
H, Penin H, Hartmann A, Reichmann K, Winkler C. Zerebrale Emissions-
Computertomographie (SPECT) mit123 J-markierten Amphetaminen.
Dtsch Med
Wschr 1984, 109: 1155-59. 2 Magistretti P, Uren R, Blume H, Schomer D, 3
4
Royal H. Delineation of epileptic focus by single photon emission tomography. Eur J Nucl Med 1982; 7: 484-85. O’Leary DH, Hill TC, Lee RGL, Clouse ME, Holman BL. The use of 123Iindoamphetamine and single-photon emission computed tomography to assess local cerebral blood flow. AJNR 1983, 4: 547-49. Sanabria E, Chauvel P, Askienazy S, et al. Single photon emission computed tomography (SPECT) using 123-I-isopropyl-iodo-amphetamine (IAMP) in partial epilepsy. In- Baldy-Moulinier M, et al, eds Cerebral blood flow, metabolism, and epilepsy. London/Paris John Libbey Eurotext, 1983: 82-87
SIR,-Dr Negre’s findings (Nov 16, p 1118) confirm ours. In the over an 18-year period (1965-82) the mean age of patients presenting with a perforated peptic ulcer increased from 54 -8 to 60 - 9 years. This change was due entirely to an increase in the age of men with perforated duodenal ulcers from 52 - 3 to 59 - 0 years. There was no significant change in the mean age of women with perforated duodenal or gastric ulcers or of men with perforated gastric ulcers. Lately, there has been a small decline in the incidence of perforated peptic ulcerl-3 and the increasing age at which perforation is occurring suggests a cohort phenomenon. This is supported both by Negre’s figures and by more detailed age-specific ulcer perforation rates.4 Ulcer perforation rates have fallen sharply in the young while in the older age groups they have increased. The progressive increase in mean age at which perforation occurs is tending to mask the reduction in age-specific mortality rates, so that Oxford region
most series continue to report a case fatality rate from this condition of more than 10%.1,2 Unlike Negre, we have found a continued reduction in the male:female ratio of patients with perforated peptic ulcer, due to a fall in the incidence of the condition in men and a concomitant rise in women. The male:female ratio of 1-9:1 in Oxford in 1977-821 is the lowest reported in Britain for 60 years.
Surgical Unit, Westminster Hospital,
R. M. WATKINS
London SW1P 2AP Nuffield Department of Surgery, John Radcliffe Hospital,
JACK COLLIN
Oxford
DUODENITIS
1. Watkins RM, Dennison AR, Collin J What has
SIR,-Your Nov 30 editorial on duodenitis while recognising that a relation between duodenitis and peptic ulcer is controversial, clearly favours this view. This opinion is based on several assumptions, some of which deserve comment. The statement that moderate and severe grades of duodenitis are rare should be read with caution. Erosive duodenitis alone (the most 2 severe grade in this condition) was observed in 5’ 8%1 and in 9 - 5 of cases in two large endoscopic series. In 68% and 46%, respectively, of patients with erosive duodenitis, this was found to be an autonomous disorder, unrelated to peptic ulcer. 1,2 Furthermore hyperchlorhydria may be uncommon in patients with chronic non-specific duodenitis.33 In erosive duodenitis gastric acid secretion can be either normal or higher than normal,’ the secretory profile thus resembling that of duodenal ulcer. However, unlike duodenal ulcer, "autonomous" erosive duodenitis seems to respond poorly to treatment with gastric acid inhibitors. Ranitidine promoted endoscopic disappearance of ulcer-unrelated duodenal erosions only in 39% of cases, whereas complete healing was obtained in 70% of cases of autonomous erosive duodenitis treated with pirenzepine (p<0 05).4 Pirenzepine is only a mild acid inhibitor exhibiting the unusual property to increase mucosal blood flow. The above findings seem to suggest that in autonomous erosive duodenitis gastric acidity, plays only a minor pathogenetic role and that other factors (eg, impairment of local microcirculation) are involved. The inclusion of all duodenitis in the duodenal ulcer diathesis must be questioned, while our knowledge on the subject is so limited. Two subtypes of erosive duodenitis should be recognisednamely, erosive duodenitis accompanying or following duodenal ulcer and autonomous erosive duodenitis, a distinct disorder differing from peptic ulcer in regard to pathogenesis and therapy. Medical Clinic III,
University of Milan, 20100 Milan, Italy
MARIO GUSLANDI
1. Cheli 2
3
R, Giacosa A, Bovero E Clinical significance of duodenal erosions. Endoscopy 1984, 16: 105-08 Guslandi M, Bel Soldato P. Gastroduodenal erosions an overview of clinical and pathogenetic problems and of some experiences with pirenzepine. In: Bettarello A, ed Pirenzepine. New aspects in research and therapy. Amsterdam: Excerpta Medica, 1985 101-10 Cheli R What is new about duodenitis? Scand J Gastroenterol 1979; 14 (suppl 54): 28-30
4. Guslandi M, Daniotti
S, Ballarin E, Basilico M, Tittobello A. Pirenzepine in erosive duodenitis A controlled clinical trial versus ranitidine. Scand J Gastroenterol 1985; 20: 751-55
happened to perforated peptic ulcer?
Br J Surg 1984, 71: 774-76 2. Dark 3.
4.
Coll JH, MacArthur K. Perforated peptic ulcer in South-West Scotland. Roy J Surg Edinb 1983, 28: 19-23. Hendry WS, Valerio D, Kyle JPerforated peptic ulcer in North-East Scotland. J Roy
Coll Surg Edinb 1984; 29: 69-72 Coggon D, Lambert P, Langman MJS. 20 years of hospital admission for peptic ulcer in England and Wales. Lancet 1981; i 1302-04.
KIDNEY LESIONS IN URAEMIC PATIENTS AND &bgr;2-MICROGLOBULIN DERIVED AMYLOID
SIR,-Amyloid deposition in bone, synovium, and other tissues recognised as a long-term complication of maintenance haemodialysis.,,2One suggestion is that the precursor protein was has been
the L-chain of
immunoglobulins. However, several laboratories,
ours, have been unable to substantiate this
hypothesis. P2-microglobulin (ft2-MG) has close structural homologies with the immunoglobulin L-chain and may be an amyloidogenic substrate. &bgr;rMG has been identified as the precursor of dialysis-related amyloid recovered from carpal tunnel or bone cysts.3Deposition of &bgr;rMG derived amyloid may be facilitated by high serum concentrations of 02-MGor (32-MG derived oligopeptides5 in dialysed patients. We have examined amyloid-like matrix stones, commonly found in patients on maintenance haemodialysis,to see if they consist of &bgr;rMG or its fragments. We found a close correlation between our aminoacid analyses of five matrix stones in dialysed patientsand the known aminoacid composition of P2-MG(see table). Furthermore, sodium dodecyl sulphate gel electrophoresis revealed a molecular weight of 7000 for a major component of matrix stones-ie, within the range of polydisperse (32-MG derived fragments found in amyloid of dialysis patients.3 The molecular weight of intact (32-MG is 11 000. Indirect immunofluorescence of including
matrix
stones
showed that
a
considerable
amount
of the
proteinaceous material reacted with antiserum to 02-MG (Behring)
but not so with antiserum from Dako. The demonstration that urinary matrix concretions are derived from &bgr;rMG has several interesting implications. We have demonstrated deposition of similar amyloid positive concretions in kidneys of patients with preterminal renal failure and have suggested that such nephronal obstruction contributes to progression of renal fai1ure.8 Nephronal obstruction by this material may be causally related, at least in part, to the genesis of
(with normal CT scans in 2). illustrate increased and decreased tracer uptake in the left temporal lobe. These data suggest that 99mTc-HMPAO has similar imaging properties to 123I-labelled amphetamine derivatives. This new tracer seems to be the radiopharmaceutical of choice for brain imaging in epilepsy because it has more profitable gamma energy (no high-energy components) and is available on an everyday basis.
PERFORATED PEPTIC ULCER IN THE ELDERLY
SPECT revealed decreased uptake
Figs 1 and 2
Institute for Clinical and Nuclear Medicine,
Experimental
University of Bonn, D-5300 Bonn 1, West
Germany
H. J. BIERSACK K. REICHMANN C. WINKLER
Department of Neurology/Epileptology, H. STEFAN P. BÜLAU University of Bonn Amersham International plc, Amersham, Buckinghamshire 1. Biersack
K. KUHNEN H. PENIN
D. A. TYRRELL R. D. NEIRINCKX K. R. GRUNER
H, Penin H, Hartmann A, Reichmann K, Winkler C. Zerebrale Emissions-
Computertomographie (SPECT) mit123 J-markierten Amphetaminen.
Dtsch Med
Wschr 1984, 109: 1155-59. 2 Magistretti P, Uren R, Blume H, Schomer D, 3
4
Royal H. Delineation of epileptic focus by single photon emission tomography. Eur J Nucl Med 1982; 7: 484-85. O’Leary DH, Hill TC, Lee RGL, Clouse ME, Holman BL. The use of 123Iindoamphetamine and single-photon emission computed tomography to assess local cerebral blood flow. AJNR 1983, 4: 547-49. Sanabria E, Chauvel P, Askienazy S, et al. Single photon emission computed tomography (SPECT) using 123-I-isopropyl-iodo-amphetamine (IAMP) in partial epilepsy. In- Baldy-Moulinier M, et al, eds Cerebral blood flow, metabolism, and epilepsy. London/Paris John Libbey Eurotext, 1983: 82-87
SIR,-Dr Negre’s findings (Nov 16, p 1118) confirm ours. In the over an 18-year period (1965-82) the mean age of patients presenting with a perforated peptic ulcer increased from 54 -8 to 60 - 9 years. This change was due entirely to an increase in the age of men with perforated duodenal ulcers from 52 - 3 to 59 - 0 years. There was no significant change in the mean age of women with perforated duodenal or gastric ulcers or of men with perforated gastric ulcers. Lately, there has been a small decline in the incidence of perforated peptic ulcerl-3 and the increasing age at which perforation is occurring suggests a cohort phenomenon. This is supported both by Negre’s figures and by more detailed age-specific ulcer perforation rates.4 Ulcer perforation rates have fallen sharply in the young while in the older age groups they have increased. The progressive increase in mean age at which perforation occurs is tending to mask the reduction in age-specific mortality rates, so that Oxford region
most series continue to report a case fatality rate from this condition of more than 10%.1,2 Unlike Negre, we have found a continued reduction in the male:female ratio of patients with perforated peptic ulcer, due to a fall in the incidence of the condition in men and a concomitant rise in women. The male:female ratio of 1-9:1 in Oxford in 1977-821 is the lowest reported in Britain for 60 years.
Surgical Unit, Westminster Hospital,
R. M. WATKINS
London SW1P 2AP Nuffield Department of Surgery, John Radcliffe Hospital,
JACK COLLIN
Oxford
DUODENITIS
1. Watkins RM, Dennison AR, Collin J What has
SIR,-Your Nov 30 editorial on duodenitis while recognising that a relation between duodenitis and peptic ulcer is controversial, clearly favours this view. This opinion is based on several assumptions, some of which deserve comment. The statement that moderate and severe grades of duodenitis are rare should be read with caution. Erosive duodenitis alone (the most 2 severe grade in this condition) was observed in 5’ 8%1 and in 9 - 5 of cases in two large endoscopic series. In 68% and 46%, respectively, of patients with erosive duodenitis, this was found to be an autonomous disorder, unrelated to peptic ulcer. 1,2 Furthermore hyperchlorhydria may be uncommon in patients with chronic non-specific duodenitis.33 In erosive duodenitis gastric acid secretion can be either normal or higher than normal,’ the secretory profile thus resembling that of duodenal ulcer. However, unlike duodenal ulcer, "autonomous" erosive duodenitis seems to respond poorly to treatment with gastric acid inhibitors. Ranitidine promoted endoscopic disappearance of ulcer-unrelated duodenal erosions only in 39% of cases, whereas complete healing was obtained in 70% of cases of autonomous erosive duodenitis treated with pirenzepine (p<0 05).4 Pirenzepine is only a mild acid inhibitor exhibiting the unusual property to increase mucosal blood flow. The above findings seem to suggest that in autonomous erosive duodenitis gastric acidity, plays only a minor pathogenetic role and that other factors (eg, impairment of local microcirculation) are involved. The inclusion of all duodenitis in the duodenal ulcer diathesis must be questioned, while our knowledge on the subject is so limited. Two subtypes of erosive duodenitis should be recognisednamely, erosive duodenitis accompanying or following duodenal ulcer and autonomous erosive duodenitis, a distinct disorder differing from peptic ulcer in regard to pathogenesis and therapy. Medical Clinic III,
University of Milan, 20100 Milan, Italy
MARIO GUSLANDI
1. Cheli 2
3
R, Giacosa A, Bovero E Clinical significance of duodenal erosions. Endoscopy 1984, 16: 105-08 Guslandi M, Bel Soldato P. Gastroduodenal erosions an overview of clinical and pathogenetic problems and of some experiences with pirenzepine. In: Bettarello A, ed Pirenzepine. New aspects in research and therapy. Amsterdam: Excerpta Medica, 1985 101-10 Cheli R What is new about duodenitis? Scand J Gastroenterol 1979; 14 (suppl 54): 28-30
4. Guslandi M, Daniotti
S, Ballarin E, Basilico M, Tittobello A. Pirenzepine in erosive duodenitis A controlled clinical trial versus ranitidine. Scand J Gastroenterol 1985; 20: 751-55
happened to perforated peptic ulcer?
Br J Surg 1984, 71: 774-76 2. Dark 3.
4.
Coll JH, MacArthur K. Perforated peptic ulcer in South-West Scotland. Roy J Surg Edinb 1983, 28: 19-23. Hendry WS, Valerio D, Kyle JPerforated peptic ulcer in North-East Scotland. J Roy
Coll Surg Edinb 1984; 29: 69-72 Coggon D, Lambert P, Langman MJS. 20 years of hospital admission for peptic ulcer in England and Wales. Lancet 1981; i 1302-04.
KIDNEY LESIONS IN URAEMIC PATIENTS AND &bgr;2-MICROGLOBULIN DERIVED AMYLOID
SIR,-Amyloid deposition in bone, synovium, and other tissues recognised as a long-term complication of maintenance haemodialysis.,,2One suggestion is that the precursor protein was has been
the L-chain of
immunoglobulins. However, several laboratories,
ours, have been unable to substantiate this
hypothesis. P2-microglobulin (ft2-MG) has close structural homologies with the immunoglobulin L-chain and may be an amyloidogenic substrate. &bgr;rMG has been identified as the precursor of dialysis-related amyloid recovered from carpal tunnel or bone cysts.3Deposition of &bgr;rMG derived amyloid may be facilitated by high serum concentrations of 02-MGor (32-MG derived oligopeptides5 in dialysed patients. We have examined amyloid-like matrix stones, commonly found in patients on maintenance haemodialysis,to see if they consist of &bgr;rMG or its fragments. We found a close correlation between our aminoacid analyses of five matrix stones in dialysed patientsand the known aminoacid composition of P2-MG(see table). Furthermore, sodium dodecyl sulphate gel electrophoresis revealed a molecular weight of 7000 for a major component of matrix stones-ie, within the range of polydisperse (32-MG derived fragments found in amyloid of dialysis patients.3 The molecular weight of intact (32-MG is 11 000. Indirect immunofluorescence of including
matrix
stones
showed that
a
considerable
amount
of the
proteinaceous material reacted with antiserum to 02-MG (Behring)
but not so with antiserum from Dako. The demonstration that urinary matrix concretions are derived from &bgr;rMG has several interesting implications. We have demonstrated deposition of similar amyloid positive concretions in kidneys of patients with preterminal renal failure and have suggested that such nephronal obstruction contributes to progression of renal fai1ure.8 Nephronal obstruction by this material may be causally related, at least in part, to the genesis of