Case report 516: Lumbar vertebral chordoma causing sclerosis of affected vertebra (3rd lumbar vertebra).
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Biomedical subjects
Publications and source records attributed to A Adam.
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Of 27 patients with primary sclerosing cholangitis, 4 were found on investigation and subsequently at operation to have gross lobar atrophy. The disease was particularly severe in the hilar region. Three of the four patients were asymptomatic prior to the onset of jaundice. The presence of atrophy precipitated laparotomy to exclude cancer in two cases. Marked disparity in size between liver lobes precluded a hilar approach to relieve extrahepatic obstruction in two patients. Prolonged follow-up excluded coincident malignant disease. Selective liver atrophy should be considered part of the disease spectrum in primary sclerosing cholangitis.
Twenty-seven of 135 patients with malignant hilar stricture who had associated liver atrophy or hypertrophy or both were treated by the percutaneous insertion of an endoprosthesis in the hypertrophied lobe only. The procedure was successful in 25 patients. Three patients died within 30 days of drainage. Procedure-related nonfatal complications occurred in seven patients. Effective decompression was accomplished in 21 patients, with complete relief of jaundice in 15. Late complications were experienced by 10 patients. The median total hospital stay was 22 days. Thirteen patients survived from 6 weeks to 12 months (median 5 months), 8 were alive from 3 to 18 months (median 8 months), and 1 patient was lost to follow-up. On the available evidence, we suggest that the preoperative demonstration of the atrophy-hypertrophy complex in jaundiced patients with irresectable hilar cancer is an indication for nonoperative therapy. Patients without the atrophy-hypertrophy complex and those with the complex but associated nonneoplastic disease are likely to fare better with surgical decompression and direct mucosa-to-mucosa anastomosis.
Two 125I-labelled aryl-azide derivatives of MDP have been synthesized. Photoaffinity labelling experiments demonstrated cell surface binding sites for muramylpeptides on activated B-lymphocytes and intracellular muramylpeptides binding protein(s) of 40-45 kD in rat alveolar macrophages.
A case is described in which Lipiodol, selectively injected into the hepatic artery as part of the investigation of a patient with hepatocellular carcinoma, was retained at the site of a previous liver biopsy leading to the false positive diagnosis of a daughter nodule. This has not been previously described.
We have developed a sensitive and specific radioimmunoassay which allows the detection of human glandular kallikrein in biologic fluids at a level of 40 pg/ml. The antisera did not recognize human plasma kallikrein and glandular kallikrein from other species including marmoset. Furthermore the antibody did not bind pro-kallikrein but was specific for the trypsin activated kallikrein. The antibody inhibited the kininogenase activity of standard kallikrein incubated with human kininogen. However active kallikrein inhibited by inhibitors bound at the active site is still detectable, indicating that the antibody is specific for the structure of the active form but not for the active site. In normotensive subjects, daily urinary kallikrein excretion increased with age until 30, then a decrease was observed. In renal transplanted recipients a progressive increase of the active form was found. A low concentration of immunoreactive active kallikrein was detected in lymphatic fluids of patients suffering from acute pancreatitis treated by lymphatic drainage; although this kallikrein is the active immunoreactive form, a very weak kininogenase activity was measured, suggesting a partial inhibition by anti-proteases. These data provide complementary evidence for the physiological and pathological role of glandular kallikrein.
1. The content of kinins and T-kininogen (the third kininogen) in exudates induced by the subcutaneous implantation of saline-soaked sponges have been measured by radioimmunoassay in normal Wistar rats and in Brown Norway rats from a strain which is deficient in high and low molecular weight kininogens. 2. In both strains, sponge implantation induced a rise of T-kininogen in plasma with subsequent accumulation in the sponge exudate. This accumulation correlated with the extravasation of plasma proteins during the first 6 h. Bioassays showed that the T-kinin moiety was retained in T-kininogen. 3. In Wistar rats, a large release of immunoreactive kinins up to a mean value of 6.4 ng ml-1 was observed during the first 6 h and on the second day after the implantation. In Brown Norway rats, the kinin level in the exudates did not exceed 0.53 ng ml-1. 4. Of the kinins present during the first 6 h in the exudates withdrawn from Wistar rats, 60% were identified by high performance liquid chromatography as bradykinin. 5. The volume of the exudate induced by the implantation of dry sponges was smaller in Brown Norway rats than in Wistar rats. 6. We conclude that the role of T-kininogen in this kind of exudate was mainly the inhibition of thiol proteinases and not the release of T-kinin. In Wistar rats, bradykinin acts as a pro-inflammatory factor during the first hours and may play a role during the healing process.
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Eleven patients with benign strictures (after choledochojejunostomy, n = 10; chronic pancreatitis, n = 1) and 16 with malignant biliary strictures (cancer of the pancreas, n = 7; cholangiocarcinoma, n = 5) were treated with a self-expanding metallic biliary stent. The patients with benign disease had failed treatment with surgical reconstruction and transhepatic balloon dilation. All patients had immediate relief of jaundice and cholangitis. In a follow-up period of 6-21 months, nine of the 11 patients with benign disease had no difficulties with infection, pruritus, or recurrent jaundice. In patients with malignant strictures, the stent produced relief of biliary obstruction unless recurrent tumor invaded the bile ducts. With careful patient selection, this stent appears to be useful in the management of biliary obstruction, particularly in benign disease.
Acute renal failure (ARF) was induced in rat following a single injection of sodium chromate. A transient polyuria and a 10-fold decrease in glomerular filtration rate was immediately observed after sodium chromate administration. Urinary sodium and potassium excretion were reduced within 24 h and remained decreased for 8 to 10 days. Progressive recovery of normal renal functions, mainly electrolyte excretion and filtration rate was observed 12 days after sodium chromate administration. Urinary kallikrein excretion (UKE) was decreased only 48 h after sodium chromate administration. However the proportion of the active and inactive form excreted was unchanged. UKE remained also at a reduced level for 8 to 10 days and returned progressively to base-line level. The kallikrein content in the tissue was significantly increased immediately after sodium chromate administration and recovered normal values 12 days later. The increase of kallikrein in the tissue is more likely unspecific due to impaired protein transport than a specific stimulation of renal kallikrein biosynthesis. The decreased UKE may indicate a distal tubular reversible dysfunction in this ARF model. These reductions in electrolyte excretion, glomerular filtration and UKE were associated with selective morphological lesions. Whereas the glomeruli were intact, important damages affected proximal tubule cells which appeared necrotic and showed presence of vacuoles, liquefaction of cytoplasmic material and lost of microvilli. Less marked lesions were however observed in distal tubules, particularly large vacuoles were present at the apical poles of the tubule cells, the sites of kallikrein secretion. These distal damages may be involved in the increase of tissue concentration and in the decrease of UKE.(ABSTRACT TRUNCATED AT 250 WORDS)
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Large scale purification of human active urinary kallikrein is described. The final preparation was found homogeneous by means of SDS Page electrophoresis, amino acid composition and N-terminal analysis. The apparent molecular weight, determined on SDS Page electrophoresis, was 4.4 X 10(4). Comparative inhibition studies of the kininogenase and the amidase activities pointed out differences in the sensitivity of these two activities. Sodium inhibited amidase activity whereas kininogenase activity required the presence of this cation. In contrast, kininogenase activity was more sensitive to cadmium inhibition than amidase activity. Antibody against purified kallikrein did not completely inhibit amidase activity in crude urine. These discrepancies are consistent with the existence of several amidase activities in urine and also with possibly distinct catalytic sites on the same molecule, accordingly consideration of the methodology used appears very important when comparing results from different studies.
Recent advances in catheter and guidewire technology have allowed interventional radiologists to refine and extend methods of percutaneous hepatobiliary intervention. Liver biopsy can be followed by embolization of the track with steel coils to prevent bleeding. Biliary obstruction can be managed with self-expanding metallic endoprostheses with decreased occlusion and migration rates.
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The immune response of murine B cells, which requires the presence of various cytokines, was stimulated by N-acetylmuramyl-L-alanyl-D-isoglutamine. A novel monokine involved in this effect has been partially purified from the conditioned medium of peritoneal macrophages by using affinity chromatography on Blue-Sepharose and high-performance liquid chromatography. Hydrophobic interaction chromatography was highly efficient in removing almost all protein contaminants. The resulting biologically active material exhibited heterogeneity in ion-exchange chromatography, and apparent isoelectric points between 5.2 and 5.5 on chromatofocusing. Its apparent molecular weight, as determined by size-exclusion filtration, was about 35,000. Preliminary results on the kinetics of appearance of intracellular biological activity suggested that the monokine could also be obtained from cytoplasmic extracts.
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Plasma prekallikrein and kininogens were assayed by specific enzymatic and immunological methods in cirrhotic patients with terminal liver failure and during oestrogenic impregnation. In cirrhotic patients plasma levels of these substances were significantly lowered and they correlated negatively with necrosis enzymes. A highly significant positive correlation was found between coagulation factor values and the levels of prekallikrein and kininogens. During oestrogenic impregnation the levels of the constituents of the kallikrein-kinin system were significantly increased when compared with reference values. These findings indicate that plasma concentrations of prekallikrein and kininogens are dependent upon liver synthesis capacity.