Biomedical subjects
Publications and source records attributed to J Faber.
One of the most typical complications following chorionic villae sampling (CVS) is vaginal bleeding shortly or some days after the intervention, resulting in abortion in some cases. We report on a case of intraplacental haematoma (pathology: massive subtotal acute haemorrhagic placental infarct), followed by acute placental insufficiency in the 29th week of pregnancy. Therefore, we decided on an emergency caesarean section.
OBJECTIVE: We investigated possible changes in the pituitary-thyroid axis after radioactive iodine (RAI) treatment of multinodular non-toxic goitre. DESIGN: Consecutive patients with multinodular non-toxic goitre, who remained euthyroid after radioactive iodine (RAI) treatment. PATIENTS: Twenty-three women with multinodular non-toxic goitre were followed after treatment with RAI. MEASUREMENTS: Free T4 index (FT4I), FT3I, free T4, SHBG (immunoradiometric assay), and a third-generation TSH assay (chemiluminetric assay) TSH were measured. RESULTS: Three weeks after RAI treatment TSH had decreased and SHBG increased (P < 0.05). Only 2/18 patients actually had suppressed TSH values, while 12/18 had values in between euthyroid and toxic levels. Trend analysis from 1.5 to 24 months after RAI treatment demonstrated a progressive increase in TSH (P < 0.01) and gradual decrease in SHBG (P < 0.02). No changes in FT4I, FT3I, or free T4 were found. CONCLUSION: A third-generation TSH assay gave detailed information about changes in thyroid status when TSH was below normal values. FT4I, FT3I, and free T4 seem to be less sensitive parameters than TSH and SHBG for recording subtle changes in thyroid status after RAI treatment of nodular non-toxic goitre. We demonstrated that changes in the pituitary-thyroid axis continue for a long time after RAI treatment of multinodular non-toxic goitre. These patients should be followed up in order to detect possible late hypothyroidism.
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It has previously been shown that long-term oral exposure to cobalt can cause goiter and myxedema. The effect of industrial cobalt exposure on thyroid volume and function was determined for 61 female plate painters exposed to cobalt blue dyes in two Danish porcelain factories and 48 unexposed referents. Thyroid volume was determined by ultrasonography. The cobalt blue dyes were used in one of two forms, cobalt aluminate (insoluble) and cobalt-zinc silicate (semisoluble). Only the subjects exposed to semisoluble cobalt had a significantly increased urinary cobalt content (1.17 micrograms.mmol-1 versus 0.13 micrograms.mmol-1, P less than 0.0001). These subjects also had increased levels of serum thyroxine (T4) and free thyroxine (FT4I) (P = 0.0001 and 0.0029, respectively), unaltered serum thyroid stimulating hormone (TSH), and marginally reduced 3,5,3'-triiodothyronine (T3), whereas thyroid volume tended to be lower (P = 0.14). The group exposed to insoluble cobalt did not differ significantly in any thyroid-related parameters. No correlation between urinary cobalt and FT4I or thyroid volume was found. The study demonstrates an effect of cobalt on thyroid hormone metabolism.
The recent literature dealing with the diagnosis of pulmonary embolism is reviewed. Clinical signs, electrocardiogram and arterial blood gases analysis are not very helpful whereas a normal level of blood D-dimers makes the diagnosis of pulmonary embolism very unlikely. Lung scanning must be interpreted carefully in parallel with chest radiography. It is most useful if the pattern is either normal or of high probability. All intermediate scans are inconclusive and need a pulmonary arteriogram. Another option in patients with good cardiorespiratory reserve is the use of repeated non-invasive investigations of the lower limbs.
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The dietary exposure to cadmium and lead of two ground-living species of small mammals, i.e., shrews Sorex araneus (Insectivora) and voles Microtus agrestis (Rodentia), was investigated and related to metal loads in target organs (kidneys and liver). The study was done in two natural areas polluted with cadmium and lead originating from urban and industrial metal sources. The average intake of cadmium by the herbivorous voles varied between 0.1 and 0.4 micrograms/g/day and of lead between 2 and 10 micrograms/g/day. The carnivorous shrews showed a considerably higher metal intake rates, i.e., cadmium 3 to 16 micrograms/g/day and lead 19 to 53 micrograms/g/day, which was largely due to the consumption of contaminated earthworms (Oligochaeta). An average cadmium intake of 15 micrograms/g/day or a lead intake of 20 micrograms/g/day corresponded with critical renal metal loads of 120 micrograms/g for cadmium and 25 micrograms/g for lead, which are indicative of adverse health effects. The renal metal loads in shrews reached the critical level, but they remained far below this level in voles. The results indicate a greater risk of toxic exposure to cadmium and lead in soricine shrews than in microtine rodents.
Serum bone gamma-carboxyglutamic acid-containing (Gla) protein (BGP) was measured before and with initially 2 weeks, later 4-8 weeks intervals for 20-58 weeks during treatment of patients with hyperthyroidism (n = 10) and hypothyroidism (n = 4). Biochemical euthyroidism was obtained in the hyperthyroid patients after a median of 3 weeks (range 1-8 weeks), and in the hypothyroid patients after a median of 17 weeks (range 10-27 weeks). Serum BGP levels closely followed the thyroid state, being high respectively low in the hyperthyroid and hypothyroid state and reaching a stable plateau just at the time biochemical euthyroidism was obtained. These data suggest that osteoblastic activity is enhanced in hyperthyroidism and reduced in hypothyroidism, and that normalization occurs in close conjunction with the normalization of the thyroid state, without any delay, indicating a direct effect on the function of the excisting osteoblasts by the thyroid hormones.
Total and free concentrations of T4 and rT3 in serum and cerebrospinal fluid were estimated by ultrafiltration in 12 patients with unipolar endogenous depression before and after electroconvulsive treatment. Recovery from depression resulted in a decrease in CSF concentrations of free T4 (median) (26.2 to 21.4 pmol/l, p less than 0.02) and free rT3 (14.1 to 12.3 pmol/l, p less than 0.05). Concentrations of free T4 in the cerebrospinal fluid were lower than those in serum (p less than 0.02), the ratio being 0.6. In contrast, levels of free rT3 in the cerebrospinal fluid were considerably higher than those found in serum (p less than 0.01), the ratio being 25. These ratios did not change following recovery from depression. In 9 patients with nonthyroidal somatic illness, concentrations of free T4 and rT3 in the cerebrospinal fluid were similar to those found in patients with endogenous depression, whereas 4 hypothyroid patients and one hyperthyroid patient had considerably lower and higher, respectively, concentrations of both free T4 and rT3. In conclusion, levels of free T4 and free rT3 in the cerebrospinal fluid are increased during depression compared with levels after recovery, probably reflecting an increased supply of T4 from serum and an increased production of rT3 from T4 in the brain. The data also suggest that the transport of iodothyronines between serum and the cerebrospinal fluid is restricted.
In the course of 12 years the authors subjected to clinical EEG and stereo-EEG (SEEG) 72 patients (66 epileptics with the diagnosis of psychomotor epilepsy and grand mal) and six psychotic patients suffering from schizophrenia. With the exception of five epileptics and two psychotic patients all subjects had epileptic foci in the amygdalohippocampal complex (AHK). After coagulation of these foci marked improvement of the fits and the mental state occurred in half the patients. During EEG and SEEG recording the authors used different activation methods (hyperventilation through the nose and mouth, sleep, listening to music) and above all direct electric stimulation (ES) of one of the AHK. Secondary epileptic foci had, as a rule, more spikes and a lower threshold for ES than primary ones which contained more delta and slow theta waves. The ES led as a rule to an emotional response, such as anxiety and fear, more rarely to illusions, depersonalization and oneiroid hallucinations and twice to a hedonic response of non-sexual character. The purpose of ES was to assess the site from where it is possible to start the original aura or typical parox. The authors considered these foci, consistent with data in the literature, as the leading focus and it was subsequently coagulated. The authors investigated the reactivity and vigility by the patient's response to sound (the patient had to press a button) and by an interview with the patient. It was revealed that in isolated discharges of the spikes and waves in the scalp electrodes, i.e. in the neocortex, reactivity is lacking. In isolated discharges in the AHK the reactivity was satisfactory, but as a rule anxiety developed. It is thus possible to divide consciousness into emotional consciousness with its site in the AHK, i.e. in the limbic system, and rational consciousness which is a function of the neocrotical system. Congenital changes of consciousness such as vigility or sleep are described as "states" of consciousness. The rational or emotional aspect of behaviour is described as "type" of consciousness. Under normal conditions the states of consciousness alternate periodically and are sharply defined, the types of consciousness are closely linked and are difficult to separate. Under pathological conditions the "states" of consciousness differ less markedly and the "types" of consciousness are in dissociation. Thus obnubilation, depersonalization, illusions, pathic affects etc. develop, as a rule as part of the epileptiform or psychotiform syndrome.
The authors present their experience with a number of drugs which are not antiepileptics nor antipsychotic drugs but influence the cholinergic and noradrenergic system and glucose and protein metabolism of neurons. Their efficiency in severe epileptics with psychic changes is about 60%. Standard epileptic treatment, mono- and polytherapy, failed completely in these patients. To the authors' "modulating" and "nootropic" therapy applies the same what applies to stereotactic treatment of epilepsy, i.e. that treatment must be started before the epileptic or psychotic process becomes chronic. Epileptogenesis is divided into the following stages: 1. insulation of the brain and development of a lesion (trauma, asphyxia, infection), 2. A. latency, an epileptic focus develops in the lesion, 2. B. latency, secondary and tertiary epileptic foci develop, in particular in the corpus amygdaloideum, hippocampus and fronto-orbital area and from there frequently also psychic changes arise, 2. C. the focus acts also on the thalamo-cortical reverbation circle and gradually "teaches" it epileptic discharges which sometimes can be followed on the EEG, although this stage is still in the latent period, i.e. clinically inapparent. 2. D. modulating structures of the stem fail, REM, i.e. paradox sleep, diminishes. Because these stages resemble those in the development of some psychoses, the psychogenesis of this epileptogenesis is similar; in schizophrenia the deepest stage of NONREM sleep declines. In this stage of epilepsy the inhibitory protective influence of noradrenergic, serotoninergic and dopaminergic (?) systems disappears. The 3rd stage is manifestation of clinical attacks or psychotic behaviour which may be enhanced by some provocation, e.g. alcohol, sleep deprivation, psychic stress, which influence emotivity and the sleep profile. With regard to these stages (insulation, latency, manifestation) treatment should be provided. In the 1st and 2nd stage "nootropic and modulating" treatment should be administered to a greater extent.
Cheyne-Stokes respiration is a respiratory dysrhythmia which is encountered frequently in pathological situations as well as in certain physiological situations. Observed in antiquity it is only recently that the pathophysiological mechanisms have been more precisely understood. For a long while there has been controversy as to whether the origin is primarily circulatory or neurological. The value of Cheyne-Stokes respiration as a clinical sign should be defined in relation to the clinical situation in which it arises. It should be regarded as a sign of instability of respiratory control occurring physiologically in sleep and pathologically in certain diseases.
The increased serum thyroxine (T4) levels in endogenous depression (ED) might be due to an increased production or a reduced degradation of T4. We therefore performed turnover studies of radiolabeled T4 and 3,5,3'-triiodothyronine (T3) in 6 patients with ED and 8 age-matched healthy controls. In ED, the median daily production of T4 was 130 nmol/day/70 kg, (range 100-186 nmol/day/70 kg) and elevated compared to control values which were 99 nmol/day/70 kg (range 85-142 nmol/day/70 kg) (p less than 0.05), whereas that of T3 was similar in the two groups. Serum thyrotropin (TSH) levels (0.90 mU/liter, 0.18-2.15 mU/liter) were elevated in ED compared to a group of 7 L-T4-treated hypothyroid subjects with similar production and serum levels of T4 and T3 (0.11 mU/liter, 0.07-1.10 mU/liter) (p less than 0.02). The data show that increased serum T4 levels in ED are secondary to an increased thyroidal production of T4, which is at least partly due to inappropriately high serum TSH levels.
A 74-year-old patient presented with congestive heart failure and continuous periodic breathing. Left ventricular ejection fraction was 20% and the lung-to-brain circulation time was prolonged to 35 s. We report on the phasic changes of the patient's arterial blood gas tensions and on the periodic fluctuations of pulmonary artery pressures and cardiac output that we observed during Swan-Ganz catheterisation.
Fifty-one children with hemiparetic cerebral palsy underwent clinical, EEG and CT examinations to assess mental performance, laterality of CP and incidence of epilepsy, 80 per cent of the children had epileptic abnormalities on EEG, but less than half had clinical signs of epilepsy. Clinical paroxysms were more frequent in those with right-sided hemiparesis. Focal or epileptic EEG changes were usual in those with right-hemisphere involvement, but unless clinical paroxysms developed, these had no bearing on mental performance. Lower IQ was found in the patients with clinical epilepsy--in nearly all cases with left-sided hemiparesis and in half of those with right-sided hemiparesis.
Several patients with nontoxic goiter have reduced serum TSH levels, as measured with new sensitive assays. Whether this is a sign of subclinical hyperthyroidism, thus having the potential of adverse effects on different organs with time, is not known. We have measured serum levels of 2 markers of thyrometabolic status at the tissue level, bone gamma-carboxyglutamic acid-containing protein (BGP), reflecting the function of osteoblasts, and sex hormone-binding globulin (SHBG), reflecting the function of hepatocytes, in 44 patients (41 women and 3 men) with nontoxic goiter (11 diffuse and 33 nodular goiters; serum T4, T3, free T4, and free T3 levels had been normal and stable for at least 0.5 yr). Serum TSH levels ranged from normal to unmeasurably low values (less than 0.05 mU/L). Serum TSH levels correlated negatively to serum BGP levels (r = -0.60; P less than 0.001). Due to the postmenopausal surge in serum BGP levels, premenopausal women (n = 21) were tested separately without changing the significance (r = -0.53; P less than 0.02). Expressing serum BGP values as a percentage of the mean value in control subjects of the same age and sex did not change the correlation (r = -0.63; P less than 0.001). Six patients had serum BGP levels above the normal range, and patients with reduced serum TSH levels (less than 0.45 mU/L; n = 12) had significantly enhanced serum BGP levels [median, 1.53 nmol/L (range, 1.02-4.24) vs. 1.23 nmol/L (0.62-3.71); P less than 0.05]. Serum TSH also correlated negatively to serum SHBG levels (r = -0.56; P less than 0.001; women alone: r = -0.58; P less than 0.001). Eight patients had serum SHBG levels above the normal range, and patients with reduced serum TSH levels had significantly enhanced serum SHBG levels, expressed as a percentage of the mean control value for the relevant sex [203% (range, 75-288) vs. 120% (42-317); P less than 0.01]. It is concluded that the lower serum TSH levels in patients with nontoxic goiter, the higher are serum BGP and SHBG levels. This suggests a progressively generalized (not only pituitary) tissue overexposure to thyroid hormones, the lower the serum TSH levels. Therefore, the finding of a reduced serum TSH level in patients with nontoxic goiter might reflect supraphysiological levels of T4 and/or T3, which could possibly be harmful.
Serum levels of procollagen III N-peptide (PIIINP) and hyaluronic acid (HA) reflect secretion of procollagen III and HA from fibroblasts, a cell type sensitive to thyroid hormones. Serum PIIINP and HA concentrations were measured in different thyroid function states, the former by two different assays, one detecting intact and aggregated PIIINP (PIIINP assay) and another detecting low mol wt degradation products of PIIINP as well (Fab-PIIINP assay). Two thirds of 28 hyperthyroid patients had elevated serum PIIINP values (mean, 192% in the PIIINP assay and 243% in the Fab-PIIINP assay) compared to age- and sex-matched controls (P less than 0.001). Normalization was seen after medical treatment (n = 16). In contrast, serum HA levels increased from 49 +/- 30 to 68 +/- 37 ng/mL (P less than 0.01) when a euthyroid state was achieved. Hypothyroid patients (n = 23) had increased serum HA levels (mean, 162%; P less than 0.05), which normalized after L-T4 treatment (71 +/- 50 before and 41 +/- 20 ng/mL after treatment (n = 16; P less than 0.02). L-T4 treatment also increased serum PIIINP levels significantly. Subjects with familial dysalbuminemic hyperthyroxinemia (n = 8), representing a situation with elevated circulating levels of T4 due to enhanced protein binding, and patients with nontoxic goiter with serum TSH levels ranging from 3.6-0.05 mU/L had normal serum levels of PIIINP and HA. Our data suggest that the secretion of procollagen III and that of HA from fibroblasts are influenced differently by thyroid hormones, since the secretion of procollagen III seems enhanced by thyroid hormones, whereas the secretion of HA seems reduced. Neither euthyroidism with enhanced serum T4 levels (familial dysalbuminemic hyperthyroxinemia) nor euthyroidism with reduced serum TSH levels (nontoxic goiter) seems associated with alterations at the connective tissue level.