The opacity of portal hypertension-related ascites correlates with the fluid's triglyceride concentration.

To determine if an elevated triglyceride concentration can explain the opacity of some cirrhotic ascites specimens, the authors measured triglyceride concentration by Coulter DACOS (Hialeah, FL) on 133 paired serum and ascitic fluid specimens. The specimens were categorized as clear or cloudy by coded visual inspection. In addition, the ascitic fluid specimens were inspected for a lipid supernatant after 48 hours of refrigeration at 4 degrees C. The ascitic fluid triglyceride concentration of the 87 clear specimens was 1.9 +/- 1.0 mmol/L compared with 7.0 +/- 4.6 mmol/L for the opalescent specimens (P less than 0.001). Only 17% of the clear specimens demonstrated any lipid layer after refrigeration, compared with 94% of opalescent specimens (P less than 0.001). The triglyceride concentrations were not significantly different between the serum samples obtained from patients with clear compared with opalescent ascites. The opacity of portal hypertension-related ascites appears to be related to the triglyceride concentration of the fluid.

The 28K protein in urinary bladder, squamous metaplasia and urine is triosephosphate isomerase.

OBJECTIVES: The objective of this study was to establish the identity of a protein found in high concentrations in squamous metaplasia of the bladder. DESIGN AND METHODS: The protein was isolated and subjected to a series of physical, chemical, and catalytic studies. RESULTS: In the normal urothelium the protein was confined to a juxtanuclear pattern on the luminal side of the umbrella cells; in squamous metaplasia and squamous cell carcinoma the protein was increased and exhibited a more diffuse intracellular distribution. The protein was found to be identical to triosephosphate isomerase (EC 5.3.1.1; TPI) with respect to its immunological properties, native and subunit molecular weights, electrophoretic mobility, catalytic activity, and amino acid sequence. CONCLUSIONS: While the basis for the altered distribution of TPI remains to be established, the increased amounts of the protein in urine or bladder tissue may be indicative of squamous metaplasia, squamous cell carcinoma, or other bladder injuries.

Nonmucinous nature of the surface material of the bladder mucosa.

The urinary bladder is lined by transitional epithelium, also known as urothelium. Some investigators have described a material known as mucin, which lines the luminal surface of the urothelium, but its nature is not well understood. The authors examined sections of bladder from rat, mouse, rabbit, and man and found that, although they reacted differently to common histochemical stains for complex carbohydrates, none showed any material that stained as mucin on the surface of the mucosa. Rather, intracellular granules that have varying staining characteristics in different animals were found on the luminal side of the urothelium. The authors speculate, based on their histochemical findings, that some form of mucin may be present in the urothelial granules in man and that studies on animals may not be applicable to man.

[Radiation myelopathy]. / Bestralingsmyelopathie.

The tolerance of the spinal cord to ionising radiation, particularly the influence of dose and fractionation, is discussed in connection with the medical history of two patients with severe neurological abnormalities, irradiated for breast cancer and Hodgkin's disease. Different forms of radiation myelopathy and the requirements for the diagnostic procedure are described.

The effects of oral agent or insulin treatments on the plasma lipoproteins and the plasma lipoprotein lipase activator in diabetic patients.

The structure and the metabolism of plasma lipoproteins are altered in diabetes mellitus. Insulin or oral agent treatments affect the lipoprotein metabolism in addition to improving hyperglycemia. However, it is not clear whether the alterations seen in lipoproteins during treatment are related to the degree of diabetic control or to the mode of diabetic treatment. The effects of insulin or oral agent treatments on the plasma lipoproteins and lipoprotein lipase activator were compared in a strictly defined non-obese, non-insulin dependent diabetic patient. Both treatment groups had similar plasma triglyceride, total cholesterol, low and high density lipoprotein cholesterol, and lipoprotein lipase activator levels. Lipoprotein lipase activator contents of the very low density lipoproteins correlated positively with their triglyceride (r = 0.803 in insulin, r = 0.828 in oral agent treated patients) and protein (r = 0.713 in insulin, r = 0.862 in oral agent treated patients) contents. The findings of this study indicated that plasma lipid levels, very low density lipoprotein compositions, and lipoprotein lipase activator contents were not significantly different in non-obese, non-insulin dependent diabetic patients treated with either oral hypoglycemic agents or insulin.

Digoxin-like immunoreactive substances in chronic liver disease.

Digoxin-like immunoreactive substances, which cross-react with digoxin antibody, have been found to have natriuretic effect and Na+,K+-ATPase inhibitory effect. The role of digoxin-like immunoreactive substances in chronic liver disease was studied by radioimmunoassay in 63 serum and 60 urine samples from 58 patients with chronic liver disease and compared with 16 controls. Although the mean serum digoxin-like immunoreactive substances level of compensated chronic liver disease patients (0.06 +/- 0.05 ng per ml, p less than 0.01) was higher than that of controls (0.02 +/- 0.03 ng per ml), only four patients had serum digoxin-like immunoreactive substances higher than 0.10 ng per ml. Mean serum digoxin-like immunoreactive substances level was much higher in patients with decompensated chronic liver disease who had ascites (0.32 +/- 0.17 ng per ml, p less than 0.001), hepatorenal syndrome (0.57 +/- 0.20 ng per ml, p less than 0.001) and hepatic encephalopathy (0.43 +/- 0.20 ng per ml, p less than 0.001). Five patients with recent variceal hemorrhage requiring transfusions and saline infusion had significantly increased serum digoxin-like immunoreactive substances (mean: 0.16 +/- 0.06 ng per ml, p less than 0.001) before the development of clinically detectable ascites.(ABSTRACT TRUNCATED AT 250 WORDS)

Phenytoin toxicity and hepatic encephalopathy: simulation or stimulation?

Two cases of phenytoin toxicity in patients with chronic liver disease who were taking 300 mg phenytoin daily are described. Each patient developed encephalopathy, characterized by confusion, disturbed conscious state, asterixis, and nystagmus, which was resistant to treatment with protein restriction, lactulose, and neomycin, but responsive to withdrawal of phenytoin. We suggest that the phenytoin did not precipitate hepatic encephalopathy, but caused an encephalopathy that mimicked it. We recommend that phenytoin be used cautiously in patients with liver disease, and that the drug's unbound serum level be measured if encephalopathy occurs.

Histochemical demonstration of guanase in human liver with guanine in bicine buffer as substrate.

Histochemical studies of human guanase (guanine deaminase) have seldom been undertaken, in part because of technical difficulties which result in heavy background staining. In this report, we describe a modified procedure in which the methodological inadequacies have been overcome. The modified technique has been applied to determine the intracellular and lobular distribution of guanase in normal human liver and in cases of primary biliary cirrhosis and alcoholic cirrhosis. Guanase was present within the cytoplasm of hepatocytes throughout the entire lobule. Enzyme activity was stronger on the sinusoidal side of the hepatocytes and in the periportal area. The reaction was weaker in perivenular hepatocytes. Portal components (bile ducts and veins), fibrous tissue and inflammatory cells were non-reactive, and the enzyme was absent from hepatocyte nuclei and membranes. Sections of skeletal muscle contained no guanase. The specificity of the reaction was confirmed by control tests on liver tissue and by the use of a specific inhibitor of guanase. It is concluded that the modified procedure overcomes the disadvantages inherent in the original method for guanase demonstration, allows the examination of fine cellular detail and should become a valuable histochemical tool with which to study diseases of the liver.

28K antigen in the urothelium.

We have been investigating the nature of the mucosal lining of human urinary bladder. Surface material was obtained from bladders at autopsy and used for biochemical analysis. Western immunoblotting and tissue immunochemistry identified a molecule of Mr 28,000 (28K) which is present within surface cells of the urothelium (umbrella cells). Antiserum to 28K stained sections of the bladder of two patients with squamous cell carcinoma of the bladder and other patients with squamous metaplasia. We consider 28K to be a component of the normal human bladder surface that is increased in patients with squamous metaplasia and may also be present in squamous cell carcinoma of the bladder.

Differentiation in human amniotic fluid cell cultures: I: Collagen production.

The collagen produced by differentiated cells cultured from human amniotic fluid was characterized in two ways. By chain composition and by 4-hydroxyproline:3-hydroxyproline isomer ratio, the collagen synthesized by F-type (fibroblast) cells was indistinguishable from that made by cultured fetal dermal fibroblasts. The predominant cells in young amniotic fluid cultures, termed AF-type, produced collagen with a lower isomer ratio, resembling that of basement membrane collage. The chain composition, as determined by chromatography on carboxymethyl cellulose, varied for different cultures of the AF-type, but the major pattern was consistent with that of basement membrane collagen. On the basis of these characteristics, F cells are of fibroblast origin, whereas most AF cells are of a different origin either endothelial or epithelial. Other evidence (Megaw et al., 1977) suggests an epithelial origin for AF cells.

Correlation of urinary lactic dehydrogenase with polymorphonuclear leukocytes in urinary tract infections in patients with spinal cord injuries.

A number of indirect methods have been developed to determine the site of urinary tract infection, including the measurement of LDH in urine [1]. Although LDH has been thought to be from the kidneys, it has also been noted that leukocytes could contribute LDH isoenzymes 4 and 5 [2]. Seventeen patients with injured spinal cords and significant bacteriuria were included in this study. Urine specimens obtained by urethral catheter were cultured, and PMNLs identified with Sternheimer-Malbin stain were counted in a hemacytometer. A positive test for antibody-coated bacteria and the lack of patient response to five to 10 days of antibiotic therapy were used as an indication of upper urinary tract infection. Levels of LDH isoenzymes 4 and 5 (cathodal) correlated with the number of PMNLs in the urine (r = 0.63, P less than 0.01). There was no correlation of PMNLs with LDH isoenzymes 1 and 2 (r = 0.18). In addition, there was no correlation of LDH isoenzymes 4 and 5 with the level of urinary tract infection. These results suggest that the PMNLs in the urine are the source of the LDH isoenzymes 4 and 5.

Increase in fibronectin in the deep dermis of involved skin in progressive systemic sclerosis.

The distribution and amount of fibronectin in both involved and uninvolved skin from scleroderma patients and controls were compared by indirect immunofluorescence. A marked increase in fibronectin was found in the deep dermis of involved scleroderma skin, while the subepidermal papillary regions of all specimens revealed little variation in fibronectin content. The districution of the accumulated fibronectin appeared to parallel that of the accumulated collagen in the involved reticular dermis.

28 K in squamous metaplasia of the bladder in patients with spinal cord injury.

Antibody to 28 K was used to examine sections of bladder biopsies obtained by cystoscopy from 14 patients with spinal cord injury (SCI). Most of the biopsies were obtained from patients with indwelling catheters during the investigation for possible malignancy. Sections of bladder were stained by the streptavidin procedure. The 28 K in the normal transitional epithelium of the bladder was in the superficial cells (umbrella cells). All the biopsies from patients with indwelling urethral catheters showed areas of squamous metaplasia usually associated with evidence of chronic inflammation. Cystitis cystica glandularis was also seen in one patient. Staining was most marked in the areas of squamous metaplasia with intracellular granular staining. The basal layers were not well stained. With marked squamous metaplasia, there was a superficial hyperkeratotic layer that stained variably and often did not stain at all. Staining was less marked in areas of hyperplasia, regenerating urothelium, and cystitis cystica glandularis. These findings raise the possibility that the presence of 28 K glycoprotein in the tissues or released into the urine may be used as an indicator of squamous metaplasia and chronic inflammation of the bladder.