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SERUM-GASTRIN AFTER PORTAL-SYSTEMIC SHUNTING
1300 breaks its side of the bargain. The N.H.S. doctor is therefore left with a spurious doctor-patient relationship. He knows what the treatment should be, but unfortunately cannot deliver the goods. Unlike their counterparts in private practice neither doctor nor patient can back out of this false relation-
ship easily. The difficulties are further exaggerated when whole new added by bald central announcements which have no regard for the local difficulties that such promises create (e.g., free contraception). The Government, therefore, now expects us to accept second best for the patient and lower our standards. In this situation, where the Government has distorted (by unkept promises) the doctor-patient relationship, the doctor has become an instrument of the Government. If we wish to reverse this trend and protect the patient, I can see no alternative but to follow in the steps of the junior doctors and fight the Government in the only way it understands. Just as the politicians like to take a global view, so also should the doctors. "The patient first" must include patients "past, present, and future". By allowing the Government to encourage us to lower standards and our colleagues to emigrate we do all patients a disservice.
seems that the D, cell is not the PP cell. We have conclude that the D, cell has once again been deprived of its peptide hormone.
Thus, it
to
Departments of Histology and Pharmacology, University of Lund, 223 62 Lund, Sweden
FRANK SUNDLER ROLF HÅKANSON
areas are
Royal South Hants Hospital, Southampton SO9 4PE
A. D. B. CHANT
SERUM-GASTRIN AFTER PORTAL-SYSTEMIC SHUNTING tic
SIR,-Patients with cirrhosis have an increased risk of pepulcer,’ but whether this risk is further increased by portal-
of sersystemic shunt procedures is uncertain.1 Measurement um-gastrin34and gastric acid secretion3’6in patients6 with cirrhosis and changes in acid secretion after shunting’ have given conflicting results. We have measured serum-gastrin in five patients 3-19 years after a portal-systemic shunt operation, in five cirrhotic patients without surgical shunts, and in a control group of ten healthy subjects. Venous blood-samples were taken after an overnight fast and at 5, 10, 20, and 30 min after drinking 130
ml of water into which two cubes of ’Oxo’ meat extract had been dissolved. Serum-gastrin was measured by radioimmunoassay. The patients with surgical shunts included four with cirrhosis (cases 1-4, table) and one (case 5) with extrahepatic porSTIMULATED SERUM-GASTRIN CONCENTRATION IN PATIENTS WITH AND WITHOUT PORTAL-SYSTEMIC SHUNTS AND IN CONTROLS
D1 CELL IN SEARCH OF A HORMONE SIR,—The Dl cell is characterised by its content of small (about 150 nm) granules, which but for their size, resemble those of the D cell. 1The Dl cell has been found by several workers in the gastric and duodenal mucosa, and its presence in the pancreas has also been established.’ Its function is a mystery, although it displays the typical features of polypeptide-hormone-secreting cells. It seemed that the D, cell in the gut had found its hormone when Pearse et al. localised gastric inhibitory peptide to this cell type. However, two years later gastric inhibitory peptide escaped from the D, cell and took refuge in the newly recognised K cell.4 Lately the Dl cells (now those in the pancreas) have had another peptide-hormone candidate thrust upon them, again by Pearse’s team;5 this time it is the pancreatic polypeptide (PP).6 However, there are some hard facts that should be considered before the Dl cell settles down quietly with its newfound hormone: (1) In certain species (notably cat and dog) the PP cell is identical with the F (or X) cell,2 having ultrastructural properties quite different from those of the D, cell (which is present in the pancreas of these species also). (2) Using the consecutive semithin/ultrathin section technique for defining the ultrastructure of immunoreactive cells we have shown that PP cells and D, cells are distinct from each other in species other than cat and dog.2 (3) In several species, PP cells are absent from gastric and duodenal mucosa whereas Dl cells have been found.12 (4) Bordi et al.1 have described a pancreatic tumour which contained cells having granules with the characteristics of D, cell granules. These tumour cells do not contain PP-immunoreactive material (unpublished). -
1.
Solcia, E., Capella, C., Vassallo, G., Buffa,
R. Int. Rev.
Cytol. 1975, 42,
223. 2. 3. 4. 5. 6. 7.
Larsson, L.-I., Sundler, F., Håkanson, R. Diabetologia, 1976, 12, 211. Polak, J. M., Bloom, S. R., Kuzio, M., Brown, J. C., Pearse, A. G. E. Gut, 1973, 14, 284. Buffa, R., Polak, J. M., Pearse, A. G. E., Solcia, E., Grimelius, L., Capella, C. Histochemistry, 1975, 43, 249. Heitz, Ph., Polak, J. M., Bloom, S. R., Adrian, T. E., Pearse, A. G. E. Virchows Arch. B Cell Path. 1976, 21, 259. Lin, T. M., Chance, R. E. Gastroenterology, 1974, 67, 737. Bordi, C., Bussolati, G., Ballerio, G., Togni, R. Cancer, Philadelphia, 1975, 35, 436.
(MEAN
±
S.D.)
tal-vein occlusion. The stimulated serum-gastrin concentrations were raised in the three patients with portacaval anastomosis (P.C.A.) but not in the two with splenorenal anastomosis (s.R.A.). The mean serum-gastrin for the five cirrhotic patients without surgical shunts was not significantly different from control values (table) but raised fasting and 5 and 10 min values were found in the two patients who had ascites. Lam3 found raised serum-gastrin levels in cirrhosis, but these were not further increased in five patients after splenorenal anastomosis. He suggested that the hypergastrinæmia reflected gastric hypoacidity, which in turn was produced by high levels of an acid-inhibiting hormone which the liver failed to metabolise. Our results suggest that hypergastrinsemia is more likely to follow portacaval than splenorenal anastomosis, and, if this were confirmed, it would point to the small intestine as the source of such a hormone. We thank Dr A.
for
Paton, Mr M.
Dudley Road Hospital, Birmingham B18 7QH East Birmingham Hospital, Birmingham B9 5ST 1. 2.
D.
Middleton, and Dr D. J. Parry
permission to study patients under their care. GEOFFREY NICHOLSON C. SAMPSON C. E. WOODHOUSE
Swisker, W. P., Baker, L. A., Bennett, H. D. Am. J. dig. Dis. 1955, 22, 291. Phillips, M. M., Ramsby, G. R., Conn, H. O. Gastroenterology, 1975, 68,
121. 3. Lam, S. K. Gut, 1976, 17, 700. 4. Pointer, H. Digestion, 1975, 13, 372. 5. Tabaqchali, S., Dawson, A. M. Gut, 1964, 5, 417. 6. Wilkinson, F. O. W., Riddell, A. G. Br. J. Surg. 1965,
52, 530.
ship easily. The difficulties are further exaggerated when whole new added by bald central announcements which have no regard for the local difficulties that such promises create (e.g., free contraception). The Government, therefore, now expects us to accept second best for the patient and lower our standards. In this situation, where the Government has distorted (by unkept promises) the doctor-patient relationship, the doctor has become an instrument of the Government. If we wish to reverse this trend and protect the patient, I can see no alternative but to follow in the steps of the junior doctors and fight the Government in the only way it understands. Just as the politicians like to take a global view, so also should the doctors. "The patient first" must include patients "past, present, and future". By allowing the Government to encourage us to lower standards and our colleagues to emigrate we do all patients a disservice.
seems that the D, cell is not the PP cell. We have conclude that the D, cell has once again been deprived of its peptide hormone.
Thus, it
to
Departments of Histology and Pharmacology, University of Lund, 223 62 Lund, Sweden
FRANK SUNDLER ROLF HÅKANSON
areas are
Royal South Hants Hospital, Southampton SO9 4PE
A. D. B. CHANT
SERUM-GASTRIN AFTER PORTAL-SYSTEMIC SHUNTING tic
SIR,-Patients with cirrhosis have an increased risk of pepulcer,’ but whether this risk is further increased by portal-
of sersystemic shunt procedures is uncertain.1 Measurement um-gastrin34and gastric acid secretion3’6in patients6 with cirrhosis and changes in acid secretion after shunting’ have given conflicting results. We have measured serum-gastrin in five patients 3-19 years after a portal-systemic shunt operation, in five cirrhotic patients without surgical shunts, and in a control group of ten healthy subjects. Venous blood-samples were taken after an overnight fast and at 5, 10, 20, and 30 min after drinking 130
ml of water into which two cubes of ’Oxo’ meat extract had been dissolved. Serum-gastrin was measured by radioimmunoassay. The patients with surgical shunts included four with cirrhosis (cases 1-4, table) and one (case 5) with extrahepatic porSTIMULATED SERUM-GASTRIN CONCENTRATION IN PATIENTS WITH AND WITHOUT PORTAL-SYSTEMIC SHUNTS AND IN CONTROLS
D1 CELL IN SEARCH OF A HORMONE SIR,—The Dl cell is characterised by its content of small (about 150 nm) granules, which but for their size, resemble those of the D cell. 1The Dl cell has been found by several workers in the gastric and duodenal mucosa, and its presence in the pancreas has also been established.’ Its function is a mystery, although it displays the typical features of polypeptide-hormone-secreting cells. It seemed that the D, cell in the gut had found its hormone when Pearse et al. localised gastric inhibitory peptide to this cell type. However, two years later gastric inhibitory peptide escaped from the D, cell and took refuge in the newly recognised K cell.4 Lately the Dl cells (now those in the pancreas) have had another peptide-hormone candidate thrust upon them, again by Pearse’s team;5 this time it is the pancreatic polypeptide (PP).6 However, there are some hard facts that should be considered before the Dl cell settles down quietly with its newfound hormone: (1) In certain species (notably cat and dog) the PP cell is identical with the F (or X) cell,2 having ultrastructural properties quite different from those of the D, cell (which is present in the pancreas of these species also). (2) Using the consecutive semithin/ultrathin section technique for defining the ultrastructure of immunoreactive cells we have shown that PP cells and D, cells are distinct from each other in species other than cat and dog.2 (3) In several species, PP cells are absent from gastric and duodenal mucosa whereas Dl cells have been found.12 (4) Bordi et al.1 have described a pancreatic tumour which contained cells having granules with the characteristics of D, cell granules. These tumour cells do not contain PP-immunoreactive material (unpublished). -
1.
Solcia, E., Capella, C., Vassallo, G., Buffa,
R. Int. Rev.
Cytol. 1975, 42,
223. 2. 3. 4. 5. 6. 7.
Larsson, L.-I., Sundler, F., Håkanson, R. Diabetologia, 1976, 12, 211. Polak, J. M., Bloom, S. R., Kuzio, M., Brown, J. C., Pearse, A. G. E. Gut, 1973, 14, 284. Buffa, R., Polak, J. M., Pearse, A. G. E., Solcia, E., Grimelius, L., Capella, C. Histochemistry, 1975, 43, 249. Heitz, Ph., Polak, J. M., Bloom, S. R., Adrian, T. E., Pearse, A. G. E. Virchows Arch. B Cell Path. 1976, 21, 259. Lin, T. M., Chance, R. E. Gastroenterology, 1974, 67, 737. Bordi, C., Bussolati, G., Ballerio, G., Togni, R. Cancer, Philadelphia, 1975, 35, 436.
(MEAN
±
S.D.)
tal-vein occlusion. The stimulated serum-gastrin concentrations were raised in the three patients with portacaval anastomosis (P.C.A.) but not in the two with splenorenal anastomosis (s.R.A.). The mean serum-gastrin for the five cirrhotic patients without surgical shunts was not significantly different from control values (table) but raised fasting and 5 and 10 min values were found in the two patients who had ascites. Lam3 found raised serum-gastrin levels in cirrhosis, but these were not further increased in five patients after splenorenal anastomosis. He suggested that the hypergastrinæmia reflected gastric hypoacidity, which in turn was produced by high levels of an acid-inhibiting hormone which the liver failed to metabolise. Our results suggest that hypergastrinsemia is more likely to follow portacaval than splenorenal anastomosis, and, if this were confirmed, it would point to the small intestine as the source of such a hormone. We thank Dr A.
for
Paton, Mr M.
Dudley Road Hospital, Birmingham B18 7QH East Birmingham Hospital, Birmingham B9 5ST 1. 2.
D.
Middleton, and Dr D. J. Parry
permission to study patients under their care. GEOFFREY NICHOLSON C. SAMPSON C. E. WOODHOUSE
Swisker, W. P., Baker, L. A., Bennett, H. D. Am. J. dig. Dis. 1955, 22, 291. Phillips, M. M., Ramsby, G. R., Conn, H. O. Gastroenterology, 1975, 68,
121. 3. Lam, S. K. Gut, 1976, 17, 700. 4. Pointer, H. Digestion, 1975, 13, 372. 5. Tabaqchali, S., Dawson, A. M. Gut, 1964, 5, 417. 6. Wilkinson, F. O. W., Riddell, A. G. Br. J. Surg. 1965,
52, 530.