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Biomedical subjects

H Nuutinen

Publications and source records attributed to H Nuutinen.

26 records · Page 2Linked to original sources
PubMed1993

Cholesterol crystallization-promoters in human bile: comparative potencies of immunoglobulins, alpha 1-acid glycoprotein, phospholipase C, and aminopeptidase N1.

Concanavalin A (Con A)-binding glycoproteins accelerate the rate of cholesterol crystal formation as a prelude to gallstone formation. Immunoglobulins (IgM, IgA, and IgG), aminopeptidase N (APN), phospholipase C (pcPLC), and alpha 1-acid glycoprotein from this Con A fraction have all been proposed as candidate promoters. We immunopurified each of the six putative promoters and examined their comparative effects by adding equal amounts to a cholesterol crystal growth assay. The effects of immunoabsorptive removal of each of the specific candidate promoters from native bile were also compared. In additional studies, the potency of these proteins was in the following order: IgM > IgA = AAG > IgG. APN and pcPLC showed no effect on cholesterol crystal growth at their apparent physiological concentrations. In subtractive experiments, only a minor loss (< 10%) of net promoting activity from that of the whole Con A-bound fraction was observed after immunoabsorptive removal of pcPLC, APN, or immunoglobulins. Total removal of AAG, however, showed a far greater loss (/33%) of the net promoting activity. These data indicate that AAG accounts for the greatest portion of net biliary Con A-bound promoting activity derived from currently defined and well-identified glycoproteins. However, more than 60% of total Con A-binding promoting activity remains unaccounted for, indicating the presence of other important and still unidentified promoters in human bile.

Aminopeptidases↗
PubMed1992

Triple therapy of Helicobacter pylori infection in peptic ulcer. A 12-month follow-up study of 93 patients.

This study was undertaken to evaluate the success of triple therapy in peptic ulcer patients and ulcer relapses. One hundred and one consecutive Helicobacter pylori-positive peptic ulcer patients were assigned to an open trial with 2 weeks of treatment with colloidal bismuth subcitrate, amoxicillin, and metronidazole. At the 6-week follow-up only 1 duodenal ulcer was unhealed of 57 active ulcers, and H. pylori was found to be eradicated in 84% of the 100 subjects. The sensitivity to metronidazole was determined from 71 pretreatment strains of H. pylori. Eradication of H. pylori succeeded in 89% of the patients with metronidazole-susceptible strains and in 61% of patients with metronidazole-resistant strains (p < 0.03). All 16 patients in whom the treatment failed to eradicate the organism had metronidazole-resistant strains after treatment. The ulcer relapse rate was low. At the 12-month follow-up of 93 patients only 1 of the 84 H. pylori-negative patients (including 4 patients after new successful therapy) had relapsing ulcers (2 asymptomatic episodes), and 1 had H. pylori reinfection, whereas 3 of the 9 bacteria-positive patients relapsed (p = 0.002); at the 2-year control 2 more patients had ulcer relapses. The eradication of H. pylori infection clearly prevents relapses of peptide ulcer, but the success of triple therapy depends on the frequency of pretreatment metronidazole-resistant H. pylori strains.

Administration, Oral↗
PubMed1991

Low prevalence of hepatitis C antibodies in chronic liver disease in Finland.

High prevalence of hepatitis C antibodies (anti-HCV) have been found in the Middle- and Southern European countries in connection with chronic liver diseases. In a study of Finnish chronic liver disease patients no anti-HCV antibodies were found in 22 autoimmune chronic active hepatitis, in 5 chronic persistent hepatitis and in 38 alcoholic liver disease patients. 2/30 primary biliary cirrhosis patients were anti-HCV positive. As a comparison 3/9 patients with acute community acquired non-A non-B hepatitis and 28/48 i.v. drug addicts had anti-HCV antibodies. The results indicate that HCV infections in Finnish chronic hepatitis patients are rare.

Adult↗
PubMed1983

Determinants of blood acetaldehyde level during ethanol oxidation in chronic alcoholics.

We analyzed the blood alcohol and acetaldehyde concentrations in nine alcoholics and four healthy nonalcoholic controls during and after an intravenous infusion of a high and a low dose of alcohol. In the alcoholics, the mean rates of plasma ethanol disappearance were significantly higher than in nonalcoholic controls. In the control subjects, the blood acetaldehyde levels were, in general, below the detection limit (less than 0.5 microM), but in sharp contrast to this, an elevated blood acetaldehyde during ethanol infusion was found in 6/9 alcoholics. Peak blood acetaldehyde values were higher after the high than the low dose of alcohol. Fructose infusion significantly enhanced the rate of plasma ethanol disappearance both in controls and in alcoholics, and this was usually associated with a significant elevation of blood acetaldehyde level. The maximal specific activities (expressed as milliunits/mg og protein) of alcohol, lactate, and aldehyde dehydrogenases in liver were significantly lower in alcoholics than in controls. Even more importantly, the peak blood acetaldehyde correlated negatively with the activity of hepatic "low-Km" aldehyde dehydrogenase. Our results suggest that the main reason for blood acetaldehyde elevation seen in these chronic alcoholics is their impaired capacity to metabolize acetaldehyde. This may be further accentuated by the increased rate of ethanol oxidation.

Acetaldehyde↗
PubMedDate not supplied

Elevated blood acetate as indicator of fast ethanol elimination in chronic alcoholics.

The concentration of acetate was determined in the hepatic and peripheral blood of 10 chronic alcoholics and six healthy non-alcoholic controls after a peroral dose of ethanol (0.8 g/kg b.wt.). The blood acetate concentration was significantly higher in the hepatic vein than peripherally and remained at a rather constant level both in alcoholics and controls during the course of ethanol elimination. However, the level of acetate was significantly (p less than 0.005) higher in alcoholics than in controls both in the hepatic vein (1.79 and 1.15 mM) and peripherally (0.91 and 0.52 mM) (alcoholics and controls respectively). The alcoholics also eliminated ethanol 54% faster than the controls (159 mg/kg b.wt./hr and 103 mg/kg b.wt./hr; alcoholics and controls respectively). Furthermore a highly significant correlation was found between the rate of ethanol elimination and blood acetate level both in the hepatic (r = 0.877, p less than 0.001) and in the peripheral vein (r = 0.799, p less than 0.001). Our results suggest that an increased level of blood acetate during ethanol oxidation may be used as an indicator of enhanced ethanol elimination.

Acetates↗
PubMedDate not supplied

Hemorrhagic gastropathy in epidemic nephropathy.

A patient with epidemic nephropathy (NE) and with gastrointestinal symptoms and hemorrhagic gastropathy prompted us to study further 10 consecutive patients with NE. Gastroscopy was carried out within 1 to 4 weeks after the beginning of the symptoms, and in every case a hemorrhagic gastropathy was observed. Hemorrhagic lesions were more marked, the shorter the elapsed time interval from the beginning of symptoms. Hemorrhagic changes were always more prominent in the proximal than in the distal part of the stomach. In 7 of 10 patients lesions were also observed in the duodenum. Colonoscopy was done in one patient and it showed similar spotty hemorrhages, suggesting that hemorrhagic lesions were not limited to the gastroduodenal mucosa only. Histological studies disclosed that the hemorrhagic lesions were associated with edema in the lamina propria, but without inflammatory changes. Follow-up gastroscopy in three patients 3 to 8 weeks later showed disappearance of hemorrhagic lesions in every patient. Thus, these results show for the first time that hemorrhagic gastropathy is a common finding in NE, and it may explain the abdominal symptoms and gastrointestinal bleeding in some of these patients. However, the mechanism of the hemorrhagic lesions needs further exploration.

Adult↗
PubMedDate not supplied

Increased blood acetate: a new laboratory marker of alcoholism and heavy drinking.

Blood acetate concentration of 51 intoxicated patients was measured and compared to conventional laboratory markers of chronic alcoholism. Mean blood acetate concentration of 23 chronic alcoholics and 17 heavy drinkers was significantly (p less than 0.0005) higher than that of 53 nonalcoholic volunteers or 11 occasional drinkers. Blood acetate level was completely independent of blood ethanol concentration ranging from 0.20 to 2.90 promille. Blood acetate was elevated in 65% of both chronic alcoholics and heavy drinkers. Gammaglutamyltransferase was abnormal only in 35%, aspartate aminotransferase in 21% and mean corpuscular volume in 12% of heavy drinkers. Combination (acetate + gammaglutamyltransferase) correctly detected 87% of alcoholics and 71% of heavy drinkers. During ethanol oxidation the upper normal limit of blood acetate is 0.75 mM. The specificity of increased blood acetate is as high as 92%. Increased blood acetate is indicative for metabolic tolerance to alcohol and it may be so far the most sensitive and specific laboratory marker of chronic alcoholism and heavy drinking.

Acetates↗