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Biomedical subjects

S Ritland

Publications and source records attributed to S Ritland.

At least 19 recordsLinked to original sources
PubMed1992

Hilar lymphadenopathy associated with Chlamydia pneumoniae infection.

A 27-year-old man with an acute Chlamydia pneumoniae infection and hilar lymph node involvement is reported. Further investigation gave no evidence of sarcoidosis or other known cause of enlarged hilar nodes. Serological tests proved an acute infection with C. pneumoniae Thus, an infection with C. pneumoniae may lead to enlargement of the hilar lymph nodes, and infection with this microorganism should be included in the differential diagnostic considerations in patients with hilar lymphadenopathy.

Adult↗
PubMed1979

Liver copper content in patients with inflammatory bowel disease and associated liver disorders.

In 45 patients with inflammatory bowel disease (9 with Crohn's disease and 36 with ulcerative colitis) and associated liver disorders, increased liver copper content (above 100 microgram/g dry weight) was found in 14 (31%). These patients represented about 50% of the patients with either biliary cirrhosis or pericholangitis. Four of the patients had levels regarded as compatible with hepatolenticular degeneration (greater than 250 microgram/g dry weight). In patients with chronic active hepatitis or non-specific changes in liver tissue, normal levels were found. The patients with Crohn's disease also had normal levels. Plasma ceruloplasmin was normal or increased in all. Determination of urinary copper output gave little diagnostic information. Alkaline phosphatases were markedly increased in most of the patients with increased liver copper concentration. In patients with ulcerative colitis and enhanced alkaline phosphatases, elevated liver copper content should be suspected and chelation therapy should be considered.

Adult↗
PubMed1979

The fortune of a capacious spinal canal.

Injury to the spine may be either osseous, neural, or both. The neurological deficit may or may not be a reflection of the severity of the osseous injury. Patients having wide canals are more likely to have less neurological dysfunction than those having narrow canals.

Adolescent↗
PubMed1978

The effect of lipoprotein lipase and hepatic lipase on the electrophoretic mobility of lipoprotein-X.

Lipoprotein-X containing plasma from a patient with familial lecithin:cholesterol acyltransferase (LCAT) deficiency, was used as substrate and incubated with postheparin plasma or partly purified lipases. LP-X could not be demonstrated by agar gel electrophoresis after incubation with postheparin plasma from a healthy subject, from a patient with chronic active hepatitis deficient in hepatic lipase, or with partly purified lipoprotein lipase. After incubation a marked increase in free fatty acids (FFA) was observed. In contrast LP-X was still present after incubation when postheparin plasma deficient in lipoprotein lipase or partly purified hepatic lipase was added to the substrate. Only minor changes in the concentration of FFA occurred. After addition of oleic acid to the substrate LP-X could not be demonstrated by agar gel electrophoresis. However, in the isolated low density lipoproteins, LP-X like particles were still present as viewed by electron microscopy. Our results strongly suggest that the change in electrophoretic mobility of LP-X was induced by the release of FFA. This was achieved by lipoprotein lipase, but not by hepatic lipase.

Adult↗
PubMed1978

Oesophageal variceal bleeding in Felty's syndrome associated with nodular regenerative hyperplasia.

Four patients with Felty's syndrome developed massive upper gastrointestinal bleeding due to oesophageal varices. The underlying hepatic pathology in all 4 was nodular regenerative hyperplasia. This appears to be a difficult histological diagnosis to make, having been initially reported as normal on percutaneous biopsy or as fibrosis or cirrhosis on wedge biopsy. This series brings the total number of cases reported in the English literature of this association to 12, suggesting a definite symptom complex. The portal hypertension seems to be due to a combination of increased splenic blood flow and postsinusoidal resistance. The clinical importance of this syndrome is that the appropriate therapy for bleeding oesophageal varices appears to be shunt procedure such as a splenorenal shunt with splenectomy, which should be well tolerated.

Aged↗
PubMed1978

Chromogenic substrate assay of plasma prekallikrein. With a note on its site of biosynthesis.

A method for assaying plasma prekallikrein has been developed applying the chromogenic substrate Chromozym PK. Different variables have been investigated, and the final assay system was found to give a reproducible and reliable assay procedure. A normal value of 99.0 +/- 18% was found, the coefficient of variation being 7.9. Studies on material from patients with various liver diseases indicated that the main site of prekallikrein biosynthesis is the liver.

Adult↗
PubMed1977

The electrophoretic mobility of lipoprotein X in postheparin plasma.

After incubation whole plasma and low density lipoproteins (LDL) taken before and 10 min after intravenous administration of heparin, from a patient with primary biliary cirrhosis and a patient with familial lecithin:cholesterol acyltransferase (LCAT) deficiency, have been tested for the presence of lipoprotein X (LP-X) by agar gel electrophoresis. LP-X was present in preheparin whole plasma and LDL. No precipitation lines on the cathodal side of the wells, indicating the absence of LP-X, were seen after electrophoresis of postheparin plasma and LDL. Immunodiffusion revealed the presence of apo-beta-lipoproteins and LP-X in preheparin as well as postheparin LDL. After gel filtration three subfractions and similar patterns were observed in the preheparin and postheparin LDL. Electronmicroscopical examination of the intermediate subfractions showed LP-X-like particles in preheparin and postheparin samples. These observations indicate a changed electrophoretic mobility in agar gel of postheparin LP-X, giving a false negative LP-X test by the conventional agar gel electrophoresis.

Electrophoresis, Agar Gel↗
PubMed1977

Hepatic copper content, urinary copper excretion, and serum ceruloplasmin in liver disease.

Increased liver copper concentration and raised serum ceruloplasmin were demonstrated in primary biliary cirrhosis and disorders of the biliary tract, and occasionally in chronic active hepatitis and cirrhosis of the liver. Eight of 13 patients with primary biliary cirrhosis had liver copper content as high as seen in patients with hepatolenticular degeneration (is greater than 250 mjg/g dry weight). Normal liver content was found in patients with acute hepatitis, steatosis of the liver, hepatic amuloidosis, haemochromatosis, and Gilbert's syndrome. The urinary copper excretion was increased (is greater than 75 mjg/24 h) in half the patients with primary biliary cirrhosis and occasionally in the other patient groups. Serum ceruloplasmin was raised in more than half of all patients, and none had levels below the reference range. Raised heaptic copper content did not always coincide with enhanced urinary copper excretion, but was significantly correlated with this parameter and also with ceruloplasmin, alkaline phosphatases, and vitamin-K-dependent clotting factors, but not with ALAT. Combination of laboratory data, as found in typical cases of hepatolenticular degeneration, was not observed in this study, including 66 patients.

Acute Disease↗
PubMed1976

Changes in the concentration of lipoprotein-X during incubation of postheparin plasma from patients with familial lecithin: cholesterol acyltransferase (LCAT) deficiency.

The concentration of lipoprotein-X (LP-X) has been studied in six patients with familial lecithin:cholesterol acyltransferase (LCAT) deficiency before and after the administration of heparin. In preheparin plasma, LP-X was present in all the patients, the concentrations ranging from 40 to 251 mg/100 ml. When postheparin plasma samples were incubated at 37 degrees C for 4 hours, LP-X could not be detected, whereas it was still present before incubation. LCAT activity was absent in the preheparin as well as in the postheparin samples. Accordingly, the changes in the concentration of LP-X could not be attributed to alterations in plasma LCAT activity. An increase in lysolecithin and a decrease in lecithin was observed during incubation of postheparin plasma samples.

Acyltransferases↗