Assessment of disease activity and extent by magnetic resonance imaging in ulcerative colitis.

BACKGROUND: We determined whether magnetic resonance imaging (MRI) could determine the activity and site of involvement in ulcerative colitis. METHODS: Colonoscopy, double-contrast barium enema and gadodiamide-enhanced MRI were performed prospectively in six patients with ulcerative colitis, including three females aged 10-22 years, both in the active and the remission stages. RESULTS: Characteristic findings of MRI in the active stage of ulcerative colitis were loss of haustral markings and thickening and contrast enhancement of the colonic wall. In five of six patients, the site of disease distribution determined by MRI was in accordance with that determined by colonoscopy. CONCLUSIONS: Gadodiamide-enhanced MRI is a safe and useful method of determining disease activity and extent in patients with ulcerative colitis.

Correlation of serum HDL-cholesterol and LCAT levels with the fraction of ionized magnesium in children.

Correlation of serum lipids and apolipoprotein levels with serum total magnesium concentration and whole blood ionized magnesium level was determined in 47 children (14 female and 33 male; mean age, 8.7 +/- 4.2 years). Mean serum concentration of magnesium was 2.19 +/- 0.19 mg/dl, whole blood concentration of ionized magnesium 1.23 +/- 0.08 mg/dl, and fraction of ionized magnesium (ratio of whole blood ionized magnesium to serum total magnesium) 0.56 +/- 0.04. Neither serum total magnesium level nor whole blood ionized magnesium level had any correlation with serum albumin, lipid, and apolipoprotein levels. However, the fraction of ionized magnesium was significantly correlated with HDL-cholesterol (n = 46, r = 0.31, p = 0.0345), apolipoprotein A-1 (n = 41, r = 0.39, p = 0.0124), and lecithin-cholesterol acyltransferase (LCAT) (n = 20, r = 52, p = 0.0184). These results suggest that fraction of ionized magnesium is more closely linked to serum HDL-cholesterol and LCAT level than with the serum total magnesium level or whole blood ionized magnesium.

Effects of quinapril and losartan on insulin sensitivity in genetic hypertensive rats with different metabolic abnormalities.

This study was designed to investigate the effects of the angiotensin-converting enzyme (ACE) inhibitor quinapril and the angiotensin II-receptor antagonist losartan on insulin sensitivity in two types of genetic hypertensive rats with insulin resistance. Quinapril (3 mg/kg) and losartan (10 mg/kg) decreased the systolic blood pressure to almost the same extent in both spontaneously hypertensive rats (SHRs) and Dahl salt-sensitive (Dahl S) rats. Quinapril increased the glucose requirement for the euglycemic clamp test in both SHRs and Dahl S rats, whereas losartan increased it in SHRs but not in Dahl S rats. The severity of the metabolic abnormalities may be responsible for the failure of losartan to improve the insulin sensitivity in Dahl S rats because serum insulin, total cholesterol, triglyceride, and free fatty acids (FFAs) were higher in the Dahl S rats than in SHRs. A kinin antagonist, Hoe 140, inhibited the increase in the glucose requirement by quinapril without affecting the depressor effect of quinapril in SHRs. In conclusion, quinapril improved the insulin sensitivity more effectively than did losartan in the genetic hypertensive rats with insulin resistance and relatively severe metabolic abnormalities. Based on our findings, one of the mechanisms underlying the difference between quinapril and losartan may thus be endogenous kinins.

CD20-positive T-cell chronic lymphocytic leukaemia.

Although CD20 is considered to be a representative marker for B lymphocytes, the antigen is weakly expressed on a small subset of normal T lymphocytes. A 60-year-old man developed pancytopenia and hepatosplenomegaly due to clonal proliferation of atypical lymphocytes that were weakly positive for CD20. The leukaemic cells were also positive for T-cell antigens such as CD2, CD3, CD5, CD7, CD8 and T-cell receptor (TCR) Vbeta8 and for activation antigens such as CD38 and HLA-DR, but were negative for CD19, CD21, CD22, CD25. Southern blot analysis revealed rearrangement of the TCR-beta gene and a germline configuration of the immunoglobulin heavy chain gene. This is the first report of a case of clonal expansion of CD20dim T lymphocytes.

Plasma endothelin-1 levels of children with cirrhosis.

We measured plasma concentration of endothelin-1 in three children with Byler's disease, five with biliary atresia after portoenterostomy, and nine controls. No patients had ascites or hepatorenal syndrome. Plasma endothelin-1 levels were significantly higher in patients with Byler's disease than in the controls (5.19 +/- 0.90 versus 1.81 +/- 0.19 pg/ml, respectively; p < 0.01), but were normal in operated biliary atresia. Urinary concentrations of N-acetyl-beta-D-glucosaminidase (NAG) were significantly higher in the patients with Byler's disease than in controls. Plasma endothelin-1 level correlated significantly with serum concentration of bile acid (r = 0.91; p < 0.01) and urinary concentration of NAG (r = 0.92; p < 0.01). We conclude that plasma endothelin-1 levels are high in patients with severe biliary cirrhosis and that endothelin-1 may partially contribute to development of renal injury in cirrhosis.

Magnesium status, serum HDL cholesterol, and apolipoprotein A-1 levels.

To determine the relationship between low magnesium status and lipids, we divided 27 patients with microscopic hematuria and normal renal function into two groups according to magnesium retention, as measured by a magnesium-loading test, and compared their serum lipid and apolipoproteins. Patients with low magnesium status (n = 7) had significantly lower levels of cholesterol, HDL cholesterol, and apolipoprotein A-1 than those with normal magnesium status (n = 20); however, there were no significant differences between the groups in serum concentrations of magnesium and apolipoprotein B. These data suggest that magnesium deficiencies are associated with low serum concentration of HDL cholesterol and apolipoprotein A-1.

Intracranial calcifications associated with nephrogenic diabetes insipidus.

A 6-year-old boy with nephrogenic diabetes insipidus (NDI) and intracranial calcification is reported. The calcifications were symmetrical and located in the basal ganglia and in the subcortical regions of the frontal, temporal, parietal and occipital lobes. Episodes of hyperosmolality during infancy are considered to be one of the causes of intracranial calcification in NDI. However, other unknown factors may be involved, because up to now there have been no reports of intracranial calcification in patients with central diabetes insipidus.

Evidence that cyclosporine causes both intracellular migration and inappropriate urinary excretion of magnesium in rats.

We determined the effects of cyclosporine on calcium, magnesium, and potassium metabolism in rats. Thirty Sprague-Dawley rats were randomized into three groups of ten animals each--control rats given olive oil, rats given cyclosporine at a dosage of 5 mg/kg daily, and rats given 15 mg/kg daily for four weeks. Urinary excretion of calcium, magnesium, and potassium was determined before and after 2 and 4 weeks of cyclosporine therapy. All rats were sacrificed after 4 weeks of therapy, and calcium, magnesium, and potassium concentrations in serum and tissues were determined. Serum magnesium levels were significantly lower in the cyclosporine-treated groups than in the control group, but there was no significant difference between the control and either of the cyclosporine-treated groups with regard to total urinary excretion of magnesium after four weeks of treatment. Magnesium content in the kidney, muscle, and liver was significantly higher in the 15 mg/kg group than in the control group. Calcium content in the kidney and liver was significantly higher as well. Potassium content in any type of tissue was similar in the three groups. We conclude that the intracellular migration of magnesium plays an important role--as does impaired renal conservation of magnesium--in the pathogenesis of cyclosporine-induced hypomagnesemia and that there is a discrepancy between magnesium and potassium metabolism in cyclosporine-treated rats.

Pathogenesis of cyclosporine-induced hypomagnesemia.

We studied the pathogenesis of cyclosporine-induced hypomagnesemia in five patients with nephrosis. Serum magnesium concentrations and urinary excretion of magnesium were reduced by the therapy. In contrast, the magnesium concentrations in mononuclear blood cells were increased. We conclude that short-term use of cyclosporine induces an intracellular shift of magnesium and causes hypomagnesemia.

Beneficial effects of dietary intervention on serum lipid and apolipoprotein levels in obese children.

Effects of weight reduction on serum levels of lipids and apolipoproteins were measured in 13 obese children (seven girls, six boys). Mean weight loss of 8.4% of the initial body weight was achieved after 4 weeks of energy intake restriction and exercise. Serum total cholesterol (5.46 +/- 1.01 mmol/L) and triglyceride (2.08 +/- 0.52 mmol/L) levels were significantly high compared with control values before treatment and were significantly reduced to 4.32 +/- 0.75 and 1.31 +/- 0.42 mmol/L, respectively, after treatment. Serum high-density lipoprotein cholesterol level (1.03 +/- 0.23 mmol/L) was significantly low and unchanged after treatment (0.94 +/- 0.25 mmol/L). Serum apolipoprotein A-I level (0.039 +/- 0.009 mmol/L or 111 +/- 0.26 g/L) was normal before treatment and significantly reduced, to 0.032 +/- 0.007 mmol/L or 0.92 +/- 0.19 g/L, after weight reduction. Serum apolipoprotein B level (0.00019 +/- 0.00007 mmol/L or 1.07 +/- 0.21 g/L) was significantly high before treatment and decreased to the normal range after treatment (0.00014 +/- 0.0009 mmol/L or 0.76 +/- 0.24 g/L). The ratio of apolipoprotein B to apolipoprotein A-I (1.09 +/- 0.29) was significantly high on admission and decreased significantly to 0.64 +/- 0.12 after treatment. Serum apolipoprotein E level (0.0014 +/- 0.0006 mmol/L or 0.05 +/- 0.02 g/L) was normal and decreased to 0.0008 +/- 0.0002 mmol/L or 0.03 +/- 0.01 g/L after treatment. In conclusion, weight reduction achieved by energy intake restriction and exercise had beneficial effects on serum lipid and apolipoprotein concentrations for the prevention of future atherosclerosis.

A neonatal case of apolipoprotein C-II deficiency.

A neonatal case of apo C-II deficiency with hypertriglyceridaemia and xanthomas is presented. The patient responded well to a special diet formula containing medium-chain triglycerides (MCT). This is the first case of apo C-II deficiency to be discovered during the neonatal period.

Relationships between excessive blood cell proliferation and neural crest cells in suckling mice.

In suckling mice injected intraperitoneally with mitomycin C, endotoxin, hydrocortisone and androgen, excessive, proliferation of blood cells was found in the blood vessels and in the sites where neural crest cells and non-staining spindle shaped neural crest cells may be present. It is speculated that these phenomena may be related with the cell surface properties of neural crest cells in the G1 phase of the cell cycle through the system mediated by cyclic AMP, and that the non-staining spindle-shaped neural crest cells in the blood vessels may be the hemopoietic stem cells.

Effects of isoproterenol on postnatal tooth development in mice with special reference to neural crest derivatives.

In the lower incisors of mice injected with isoproterenol during postnatal development, cell groups or cell masses formed in the pulp showed spiral or concentric figures composed of atypical cells. Among these cells were spindle-shaped non-staining neural crest cells and spaces caused by the death of the spindle-shaped neural crest cells. In the pulp and future periodontal ligament, compact intertwining patterns of elongated spindle-shaped cells, representing non-staining neural crest cells were seen. In the periodontal ligament, the elongated spindle-shaped cells grew parallel to the ligament's long dimension. In both pulp and periodontal ligament, the cells lost 'contact inhibition', and further the histological figures resembled melanoma.

Uptake of ions in neural crest derivatives of the small intestine of rats during active transport of calcium.

In the uptake of Ca++ ions in the neural crest derivatives of the small intestine of rats during active transport of calcium, the neural crest derivatives and mast cells of senescent rat small intestine, incubated at 45 degrees C, showed elevated uptake of CA++ ions and increased cell death compared to younger rats.