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G Bos

Publications and source records attributed to G Bos.

27 records · Page 2Linked to original sources
PubMed1979

Raised total thyroxine and free thyroxine index but normal free thyroxine. A serum abnormality due to inherited increased affinity of iodothyronines for serum binding protein.

2 people from different families had high levels of serum-thyroxine (T4) and a high free T4 (FT4) index but a normal serum triiodothyronine (T3) and serum-reverse-T3 (rT3). The abnormal serum thyroid hormone profile appeared to be inherited in an autosomal dominant manner. Serum-FT4 in affected relatives was normal. The increases in serum-T4 and FT4 index are explained on the basis of an observed increase in affinity of T4 for thyroxine-binding globulin, thyroxine-binding prealbumin, and albumin. The FT4 index did not reflect the true concentration of circulating free T4 in these cases. Thyroid function in the propositi was normal and the results of T4, T3, and rT3 kinetic studies accorded with increased binding of T4 by serum proteins and normal binding of the other iodo-thyronines. This "euthyroid high total T4, normal T3 syndrome" should be kept in mind during diagnostic evaluation of thyroid function.

Female↗
PubMed1978

Lowering of serum 3,3',5-triiodothyronine thyroxine ratio in patients with myocardial infarction; relationship with extent of tissue injury.

Serial measurements of haematocrit (Ht), plasma thyroxine (T4), triiodothyronine (T3) and alpha-hydroxybutyrate dehydroxygenase (alpha-HBDH) were performed in patients following myocardial infarction (MI). Infarct size was estimated by mathematical analysis of the change in plasma alpha-HBDH activity with time. After an initial small increase Ht decreased 12% until day 9 and remained constant thereafter. Serum T4 did not change during the entire study. Serum T3 decreased to 66% at day 9 and then returned to normal within 2 months. These figures are expressed relative to determinations in the first blood sample obtained within 12 h after MI. A significant correlation between the lowest serum T3/T4 ratio and infarct size was observed. These observations suggest that in these patients the peripheral conversion of T4 into T3 is reduced. This was accompanied by an increased production of reverse T3 as evidenced by observations in one patient.

Aged↗
PubMed1977

Acute-phase proteins from the liver and enzymes from myocardial infarction; a quantitative relationship.

In 14 patients with acute myocardial infarction (M.I.) not having any other disease, the possible quantitative relationship between enzymes from M.I. and changes in concentration of acute phase reactants coming from the liver were studied. The patients were followed up until 1 1/2 years after M.I. and comparison of baseline-protein values took place using a control group of 18 healthy individuals. Quantitation of protein changes was done by planimetric determination of the area under the concentration curve and by taking peak values. The myocardial infarction was quantitatively estimated by mathematical analysis of the time course of alpha-hydroxybutyrate dehydrogenase (alpha-HBDH) plasma concentrations and by taking peak values. A quantitative relationship with enzymatic infarct size was found for haptoglobin, alpha1-acid glycoprotein, alpha1-antitrypsin, C-reactive protein, fibrinogen and E.S.R. Albumin and transferrin did not show a negative quantitative relationship with enzymatic infarct size. Humoral factors originating from the site of tissue injury and evoking in proportion a positive acute phase reaction by the liver are probably the basis for this observed quantitative relationship.

Acute Disease↗
PubMed1976

Liver reaction to tissue injury: do therapeutic measures trigger the acute phase reaction?

In 30 healthy people we investigated the hypothesis that therapeutic measures trigger the acute phase reaction. In order of severity we analyzed: (1) the effects of an intramuscular injection of 2.5 ml 0.14 molar NaCl (6 patients), (2) the effects of an indwelling venous catheter for 24 h (7 patients), and for 72 h (8 patients), (3) the effects of cardiac catheterization (arterial and venous catheterization) carried out in 9 patients. In clinical investigations of the acute phase reaction, an intramuscular injection and a 24- or 72-h indwelling catheter, brought in by venipuncture, are acceptable because they do not provoke an acute phase reaction. A venous cutdown associated with an arterial puncture is not acceptable because this injury evokes a positive acute phase reaction. This was also observed in two patients who developed phlebitis during a 24-h indwelling venous catheter. Only a positive acute phase reaction was found, not a negative one.

Acute Disease↗
PubMedDate not supplied

LDL oxidative modifications in well- or moderately controlled type 2 diabetes.

BACKGROUND: The aim of the study was to examine, by measurement of specific indicators of free radical-mediated oxidation of LDL, whether there is evidence of increased in vivo oxidation of LDL in type 2 diabetic patients, and to investigate their associations with carotid intima media thickness (IMT). METHODS: In native LDL, we quantified five different products of LDL oxidation reflecting various stages of LDL oxidative modification in 38 individuals with well- or moderately controlled type 2 diabetes (HbA(1c) </= 8.5%) and 38 gender-matched subjects with normal glucose metabolism. Baseline conjugated dienes (BCD), 7-OH-glycero-phosphocholine (7-OH-GPC), lyso-phosphatidylcholine (lyso-PC), and ketocholesterol were determined in LDL, and circulating in vivo oxidized apolipoprotein B100 (Ox-apoB) was measured in plasma. The IMT of the carotid artery was measured by ultrasound. RESULTS: Borderline higher carotid IMT values were observed in individuals with diabetes (0.88 +/- 0.14 vs 0.83 +/- 0.11 mm, p = 0.06). LDL-ketocholesterol (45.5 +/- 19.4 vs 37.1 +/- 13.8 nmol/mmol LDL-cholesterol, p < 0.05) and Ox-apoB (25.3 +/- 5.5 vs 22.2 +/- 5.8 U/mmol LDL-cholesterol, p < 0.05) were significantly increased in diabetic patients. The concentration of BCD, 7-OH-GPC and lyso-PC in LDL did not differ between diabetic patients and control subjects. No significant correlations were demonstrated between the measured indicators of LDL oxidation and carotid IMT. CONCLUSION: Levels of BCD, 7-OH-GPC and lyso-PC, that is, intermediary products of LDL oxidation, were not significantly elevated, but ketocholesterol and Ox-apoB, that is, stable end products of the oxidation process, were increased in diabetic patients. We conclude that in vivo oxidation of LDL is increased, even in subjects with well- or moderately controlled type 2 diabetes.

Aged↗
PubMedDate not supplied

The influence of plasma volume changes on enzymatic estimation of infarct size.

In 18 patients, myocardial injury was estimated by mathematical analysis of the rise in plasma activity of alpha-hydroxybutyrate (alpha-HBDH) dehydrogenase as observed by multiple sampling after admission. This enzyme represents the lactate dehydrogenase isoenzymes LDH1 and LDH2. Changes in plasma volume were assessed by determining hematocrit values at the same time as the enzyme activities. Infarct size was expressed in IU/liter of plasma and in grams of heart muscle per liter of plasma (g/liter). Significant changes in plasma volume, reflected in hematocrit changes, occurred (average 12%): 10 patients without pulmonary edema showed an average change of 7%; for the group of eight patients with pulmonary edema, the change was 17%. When calculated infarct size was not correlated for plasma volume changes, a significant overestimation occurred (11.7%, range 0.7-29.7%). In the subgroup of patients with pulmonary edema the mean overestimation was 15.8%, and in patients without pulmonary edema, the mean overestimation was 8.5%. It is concluded that plasma volume changes after an acute myocardial infarction have to be taken into account when infarct size is calculated on the basis of plasma enzyme levels.

Creatine Kinase↗