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Biomedical subjects

A Lasson

Publications and source records attributed to A Lasson.

At least 55 records · Page 3Linked to original sources
PubMed1988

The postcholecystectomy syndrome: bile ducts as pain trigger zone.

Sixty-five non-icteric patients presumed to have the postcholecystectomy syndrome (PCS) were followed up for 4-13 years after their first endoscopic retrograde cholangiopancreatography (ERCP) examination, which gave normal findings. All patients, however, experienced severe pain on injection of only 1-2 ml of contrast medium over 5-10 sec into the common bile duct (CBD). Thirty-four of the 65 patients were found to have true PCS on long-term follow-up studies, whereas 31 of them had other diseases. A second ERCP also showed normal results, and the injection-related pain was preceded by an abnormal pressure rise in the CBD at manometry. The CBD acted like a pain trigger zone, and the pain reaction might be diagnostic in everyday clinical practice. In conclusion, ultrasonography is an adequate diagnostic method in non-obstructive PCS. Medical treatment is often successful. ERCP and interventional treatment should be reserved for patients with obstructive symptoms and for patients in whom all medical treatment has failed.

Biliary Dyskinesia↗
PubMed1988

Radiology in cutaneous sinuses and fistulae.

In patients with cutaneous openings, sinography and fistulography are usually performed. Fistulae in the head/neck region and perineum are seldom life-threatening while enterocutaneous fistulae involving the small bowel can be a serious threat due to loss of fluid. Radiology contributes to the preoperative examination of these patients. Fistulography outlines communications to the gastrointestinal tract, pleura, joints and other underlying crucial structures. Involved bowel segments are further demonstrated with barium examination.

Adult↗
PubMed1987

Recurrence rates after curative surgery for rectal carcinoma, with special reference to their accuracy.

Is the observed recurrence rate after curative surgery for rectal cancer always a good measure of therapeutic improvements? In an attempt to answer this question, the rates of local and distant recurrences were studied in two complete series of patients operated on for cure for rectal carcinoma. One hundred one consecutive patients were followed for five years in one series and 231 were followed for at least 18 years in the other series. The recurrence rate in the first series was 39 percent and in the second, with the longer observation time, 54 percent. The local recurrence rates were 24 and 38 percent, respectively. Both local and total recurrence rates increased with the length of the follow-up period. This was especially true for patients with combined local and distant disease. Autopsy sometimes demonstrated recurrences, clinically undiscovered. It is concluded that completeness, long follow-up, and intensive search for recurrence, including a high autopsy rate, are factors that raise both total and local recurrence rates. All these factors are important to consider when comparing results of different treatment modalities.

Adenocarcinoma↗
PubMed1987

The elimination of trypsin--alpha-macroglobulin complexes from the blood circulation in pigs during acute pancreatitis and after massive intravenous trypsin infusion.

The elimination from plasma of intravenously injected 125I-labelled trypsin-alpha-macroglobulin complexes was studied in both healthy and diseased, anaesthetized pigs. The t1/2 for the 125I-labelled complexes was 5-10 min in healthy pigs as well as in two groups of pancreatitis pigs. Pre-loading of the eliminating capacity by massive intravenous trypsin infusion, raised t1/2 to 80-100 min. Thus, the eliminating capacity seems to be saturable. Elimination of the complexes from the blood circulation occurred within 4-5 h. Even massive intravenous amounts of trypsin-alpha-macroglobulin complexes gave no demonstrable complement or kinin activation. Neither were other deleterious effects seen during the experiment or during 7 days of follow-up. The results indicate that treatment of acute pancreatitis in humans with alpha 2-macroglobulin might be possible, without any danger arising from the protease-alpha 2-macroglobulin complexes formed.

Acute Disease↗
PubMed1987

Pancreatic pseudocysts: a biochemical evaluation of proteases and protease inhibitors in plasma.

A biochemical evaluation was performed on plasma from eight patients developing a pancreatic pseudocyst during acute pancreatitis attacks and from six patients with a known pseudocyst. Patients developing an acute pancreatic pseudocyst had high levels of activated trypsin in complex with alpha 1-protease inhibitor, together with a probable activation of the kinin, complement, coagulation and fibrinolytic systems. Profound changes were also seen in several protease inhibitors, indicating consumption of the inhibitors. The changes did, however, not differ from those seen in severe acute pancreatitis attacks in which no pseudocyst developed. Patients with chronic pancreatic pseudocysts had biochemical changes similar to those seen in moderate pancreatitis attacks, without any overt cascade system activation. At convalescence, however, these patients had biochemical signs of leakage from the pancreas and an ongoing proteolytic activity.

Acute Disease↗
PubMed1986

Serum levels of immunoreactive PSTI in acute abdominal disorders, with special reference to a possible extrapancreatic PSTI production.

The concentration of the pancreatic secretory trypsin inhibitor (PSTI) was measured in serum from 360 patients with acute abdominal diseases. Elevated levels were found in acute pancreatitis, cholangitis, choledocholithiasis, acute cholecystitis, pancreatic pseudocyst, malignancy, renal failure and in several different inflammatory conditions not connected with the pancreas. The results suggest the possibility of an extra-pancreatic production of PSTI, especially since the changes seen over time do not favour leakage or reabsorption as the cause of the high PSTI levels seen in acute pancreatitis. PSTI rather behaves as an acute phase reactant, as judged from the parallelism in the reaction pattern with antichymotrypsin.

Acute Disease↗
PubMed1986

Consumptive coagulopathy, fibrinolysis and protease-antiprotease interactions during acute human pancreatitis.

Twenty-seven attacks of acute human pancreatitis of different severity were analysed concerning clinical outcome and activation of the coagulation and fibrinolytic systems. Consumptive coagulopathy was suggested by decreased platelet counts, decreased prothrombin values and consumption of fibrinogen during the first days in severe attacks. Factor X was slightly decreased the first 5 days in all attacks. Increased fibrinolysis was suggested by decreased plasminogen values in severe attacks. Fibrinogen degradation products were seen in 40% of the patients in blood and in 100% of the patients in the peritoneal fluid. The four main protease inhibitors of the two systems all showed protease-antiprotease complexation and lower functional than quantitative values. Plasma levels of antithrombin III and alpha 2-macroglobulin were low, while the levels of C1-inhibitor and alpha 2-antiplasmin were high. Functional levels of all the four protease inhibitors were almost zero in the peritoneal fluid in severe attacks. It is concluded that severe acute pancreatitis results in both consumptive coagulopathy and in increased fibrinolysis. A local antiprotease deficiency is seen in the peritoneal cavity and high levels of protease-antiprotease complexes are also seen in plasma. All these changes are closely correlated to the severity of the disease and may probably determine the clinical outcome of the acute attack.

Adult↗
PubMed1986

Kinin activation and protease inhibitors in acute pancreatitis in man.

The changes in the protease inhibitors and in the kallikrein-kinin system were analysed in 19 attacks of acute pancreatitis in man and correlated to the severity and clinical course of the disease. Functional alpha 2-macroglobulin was 5% in peritoneal fluid and 32% in blood in severe attacks. Functional Cl inactivator was zero in the peritoneal fluid, while values were normal in blood. High levels of complexes between alpha 1-proteinase inhibitor and trypsin were found during the first 6 days of illness in severe attacks, especially in the peritoneal fluid. Prekallikrein, kininogen and kallikrein inhibition were significantly lower in blood in severe attacks than in moderate or mild attacks. These changes were even more pronounced in the peritoneal fluid, where kallikrein-like activity was above normal, while kininogen and kallikrein inhibition were zero in severe attacks. Both high and low molecular weight kininogen were decreased, denoting an activation also by kininogenases other than plasma kallikrein. In conclusion, kinin activation was demonstrated in acute pancreatitis, especially in the peritoneal fluid. Kinin activation and protease inhibitory activity were closely correlated to the severity and clinical course of the disease. Tryptic activation of the kinin system seems probable at the low alpha 2-macroglobulin levels found in severe attacks, according to our earlier in vitro studies.

Acute Disease↗
PubMed1986

Elevated pancreatic secretory trypsin inhibitor levels during severe inflammatory disease, renal insufficiency, and after various surgical procedures.

Elevated levels of immunoreactive pancreatic secretory trypsin inhibitor (PSTI) were found in serum from patients with perforated duodenal ulcer, bacterial peritonitis, urosepticemia, pneumonia, acute renal failure, and also after different surgical procedures. The extent of the trauma seemed to determine the maximal level of PSTI. The increase found paralleled the changes seen in the acute-phase protein antichymotrypsin. There was, however, almost no increase in trypsinogen, thought to be produced together with PSTI in the acinar cells of the pancreas. In conclusion, there is evidence that PSTI is probably also produced somewhere outside the pancreas, in agreement with recent immunohistochemical data. This production may be part of a general acute-phase reaction. Thus, PSTI may have a more general inhibitory function against trypsin-like protease release in tissue injury, instead of being a purely local trypsin inhibitor in the pancreatic gland.

Acute Kidney Injury↗
PubMed1986

Leukocyte elastase alpha 1-proteinase inhibitor complexes may diagnose pancreatic abscesses early.

Complexes of alpha 1-proteinase inhibitor and leukocyte elastase could be demonstrated by crossed immunoelectrophoresis of the peritoneal fluid from four patients who developed a pancreatic abscess during an attack of pancreatitis. No such complexes were seen in 69 patients with acute pancreatitis without an abscess. The complexes were demonstrable 2-3 days before the abscess was clinically evident. They may thus be diagnostically and therapeutically important. The appearance of these complexes denotes the liberation of large amounts of leukocyte elastase. This may help explain the pathophysiology and high mortality of the pancreatic abscess, since leukocyte elastase is known to cause degradation of all components of connective tissue and also degradation and activation of many components within the different cascade systems.

Abscess↗
PubMed1986

Disseminated intravascular coagulation and antiprotease activity in acute human pancreatitis.

The coagulation and fibrinolytic systems were analysed parallel to the clinical evaluation in 27 attacks of acute human pancreatitis of different severity. Consumptive coagulopathy was evident from decreased platelet counts, decreased prothrombin values and consumption of fibrinogen during the first days in severe attacks. Fibrinolysis was suggested by decreased plasminogen values and the presence of fibrinogen degradation products. All main protease inhibitors of the two systems showed protease-antiprotease complexation and lower functional than quantitative values. Functional levels of the protease inhibitors were almost zero in the peritoneal fluid in severe attacks. It is concluded that severe acute pancreatitis results in consumptive coagulopathy and fibrinolysis together with a local antiprotease deficiency. All the changes are closely correlated to the severity of the disease.

Acute Disease↗
PubMed1985

Correlation among complement activation, protease inhibitors, and clinical course in acute pancreatitis in man.

Changes in complement levels and protease inhibitors were measured in plasma/serum and peritoneal fluid during 15 attacks of acute pancreatitis. The abnormalities found in the complement system and the protease inhibitors were most pronounced in severe attacks, especially in the peritoneal fluid. Depressed levels of C1q, C3, properdin, and factor I were found in blood on admission in severe attacks. A decrease during the first days of illness was found for C1q, C3, C4, properdin, factor I, and factor H levels in blood. There was a discrepancy between the low C1q and the high C1r and C1s levels in blood. Complexes of C1r-C1s-C1 inactivator and factor B conversion products were found, especially in the peritoneal fluid, denoting an activation of the complement system. High levels of trypsin in complex with alpha 1-protease inhibitor were found, both in blood and in peritoneal fluid, denoting the liberation of active trypsin in acute pancreatitis. The levels of the functional alpha 2-macroglobulin were low, especially in the peritoneal fluid. It is concluded that both classical and alternative complement activation take place in acute pancreatitis, starting in the peritoneal cavity. The magnitude of activation depends on the severity of the disease. Trypsin-induced activation of complement components may explain some of these changes.

Acute Disease↗
PubMed1985

The value of 5-hydroxyindolacetic acid analysis in urine. A clinical and cost-benefit study.

The clinical value and the cost-benefit of 5-hydroxyindolacetic acid in urine (5-HIAA/u) measurements in diagnosing carcinoid tumours were analysed. During a 5-month period a total of 1397 analyses yielded 62 patients with elevated 5-HIAA/u levels, of which 28 patients had previously been operated on for a carcinoid tumour. Only one carcinoid tumour was found to have been diagnosed on the evidence of elevated 5-HIAA/u levels. In patients previously operated on for carcinoid tumour, elevated leves of 5-HIAA/u did not influence their treatment. Several border-line values were probably due to a temporary decline in hepatic function or to substances interfering with the analytical methods used. It is concluded that 5-HIAA/u measurements are of limited clinical value.

Carcinoid Tumor↗
PubMed1985

Thrombosis in the superior mesenteric artery simulating acute pancreatitis. A case report.

A case of thrombosis in the superior mesenteric artery simulating acute pancreatitis, but causing intestinal gangrene, is described. The possibility of other simulating diseases must always be considered when non-operative peritoneal lavage is used as a treatment of acute pancreatitis. Bacteriological examination of the peritoneal fluid might be beneficial. Laparotomy is indicated when there is a marked discrepancy between the general condition of the patient and the objective clinical signs of pancreatitis.

Adult↗
PubMed1984

Changes in the kallikrein kinin system during acute pancreatitis in man.

Changes in the kallikrein-kinin system were analysed in 19 attacks of acute pancreatitis in man and correlated to the severity and clinical course of the disease. Prekallikrein, kininogen and kallikrein inhibition were significantly lower in blood in severe attacks than in moderate or mild attacks. These changes were even more pronounced in peritoneal fluid, where kallikrein activity was above normal, while kininogen and kallikrein inhibition were nil in severe attacks. Both high and low molecular weight kininogen were decreased, denoting an activation also by kininogenases other than plasma kallikrein. These changes indicate an activation of the kallikreinkinin system in acute severe pancreatitis in man, especially in the abdominal cavity. Although there is a great deal of evidence for activation of the kinin system in experimental shock states in animals (1-4), there are to date rather few studies showing that such an activation takes place in human acute pancreatitis. This lack of clinical studies is mainly explained by the difficulty in measuring activated components of the system, especially since these components are rapidly inactivated in different ways in vivo (5).

Acute Disease↗