Biomedical subjects
Publications and source records attributed to M Madsen.
SPECT brain imaging using Iofetamine HC1 I-123 (IMP) has a great potential in the evaluation of various neurologic disorders. Transverse, coronal, and sagittal sectional IMP images obtained using a single head rotating gamma camera system are correlated with corresponding normal brain slices in this atlas.
The effect of 40 mg furosemide intravenously on sodium excretion, the renin-aldosterone system and arginine vasopressin (AVP) was studied in 14 patients with the nephrotic syndrome and in 13 control subjects. Creatinine clearance (Ccr) was reduced in all patients but four. Before furosemide, AVP, but not angiotensin II (AII) or aldosterone (Aldo), was increased in the nephrotic patients. After furosemide, sodium excretion (NaE) increased less and changes in AVP, AII and Aldo were blunted in the patients. Ccr and NaE were positively correlated in the nephrotic syndrome. The reduced sodium response after furosemide in the nephrotic syndrome seems to be closely correlated to a reduced glomerular filtration rate but not to an increased activity of the renin-angiotensin-aldosterone system. The reduced response of AVP, AII and Aldo after furosemide is consistent with a lower degree of volume depletion in nephrotic patients.
An oral water load of 20 ml (kg body wt)-1 was given to seventeen patients with the nephrotic syndrome and fifteen healthy control subjects. Diuresis (D), free water clearance (CH2O), plasma concentrations of arginine vasopressin (AVP), angiotensin II (AII) and aldosterone (Aldo) were determined before and 3 times during the first 4 h after loading. In the nephrotic syndrome D was significantly lower 1-2 h after loading than in the control subjects, predominantly due to a lower CH2O (2.61 and 7.01 ml min-1 (medians), P less than 0.01). Creatinine clearance and the maximum increase in CH2O were significantly correlated in patients with the nephrotic syndrome (rho = 0.721, n = 17, P less than 0.01) and the control subjects (rho = 0.596, n = 15, P less than 0.01). AVP was reduced in both groups during loading, but AVP was clearly elevated in the patients with the nephrotic syndrome when compared to the control subjects both before (3.0 and 1.9 pmol 1(-1), P less than 0.01) and during loading. There was a significantly negative correlation between CH2O and AVP in both groups. AII and Aldo were reduced during loading, but the levels were the same in the patients and in the control group, and AII and Aldo were not correlated to CH2O. It is concluded that patients with the nephrotic syndrome excrete an oral water load more slowly than healthy control subjects, and that this phenomenon partly is due to reduced glomerular filtration rate and partly to increased AVP.
Arginine vasopressin (AVP) and serum osmolality (Sosm) were determined in plasma before and after a 24-h period of water deprivation in 19 patients with post-renal-transplant hypertension (group I), 14 patients with normal blood pressure after renal transplantation (group II), and 16 healthy control subjects (group III). Urine was collected in four periods of 6 h each for measurement of urine volume (V), urine osmolality (Uosm) and tubular capacity for reabsorption of water (Tc water). AVP and Sosm increased significantly in all groups. The AVP levels were the same in groups I and II, but higher in group I than III both before and after water deprivation. In group II, AVP was higher than in group III only after water deprivation; V was significantly reduced in all groups. In groups I and II, V, Tc water and Uosm were the same. In group III, V was significantly lower than in groups I and II in the last three 6-h periods, and in group III, Tc water was higher in the first 6-h period than in groups I and II. There was a significant positive correlation between AVP and Sosm in all groups. In conclusion, renal water excretion cannot be reduced as rapidly and to the same degree in renal transplant recipients as in control subjects because of a decreased renal capacity for reabsorption of water. The higher AVP level in the transplant recipients may be a compensatory phenomenon for the decreased responsiveness of the renal collecting ducts in the transplanted kidneys. The sensitivity of the osmoreceptors to changes in osmotic stimuli was normal.
Five families were studied in which cranial diabetes insipidus occurred. In the pedigrees presented, the disease clearly followed an autosomal dominant mode of inheritance. Linkage analysis was performed in one large family by calculating lod scores for linkage between loci for cranial diabetes insipidus and 18 polymorphic markers and chromosome heteromorphisms. No significant genetic linkage was found and only one of the polymorphic markers gave a positive hint of linkage. A water deprivation test was performed in nine patients from three of the families and in healthy control subjects. The plasma concentration of arginine vasopressin was very low or undetectable in the patients, and unlike the control subjects did not increase significantly during water deprivation. Arginine vasopressin and serum osmolality (Sosm) were significantly positively correlated in the controls, but not in the patients. The results indicated that an arginine vasopressin-level lower than 2 pg/ml strongly suggests a diagnosis of cranial diabetes insipidus if at the same time Sosm is higher than 295 mosmol/kg. Studies with different intranasal dosages of 1-deamino-D-arginine-vasopressin (DDAVP) given once or twice a day showed that 20 micrograms effectively reduced urinary output and that administration once a day could be sufficient.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Human Purified Protein Derivative of tuberculin- (PPD-) specific cytotoxic cells have been detected in cultures of peripheral blood mononuclear cells stimulated for 6 days with PPD. These cytotoxic cells are demonstrated by their ability to lyse PPD-pulsed autologous monocyte target cells, but not unpulsed targets. In a series of checkerboard experiments each involving 3-5 randomly combined donors, effector cells from 35 donors have been tested in autologous and 130 allogeneic combinations. Analysis of results from the pooled allogeneic combinations reveals that HLA-B - and even more pronounced HLA-DR - antigen sharing correlates positively to high lysis. No effect of HLA-A antigen sharing is found. A more detailed analysis shows that the effect of HLA-B sharing may be fully accounted for by HLA-B-DR linkage disequilibrium. The results thus indicate that cell-mediated PPD specific cytotoxicity is HLA-restricted. Further, the correlation to HLA-DR sharing indicates that the restriction element in this system in all probability is a class II antigen.
In a previous study employing conventional immunological marker analysis we found that 17% of high grade malignant lymphomas were devoid of cytoplasmic and membrane immunoglobulin and also sheep erythrocyte receptors. Cryostat sections from 24 of these cases (four of low grade and 20 of high grade malignancy) were stained with a panel of 30 monoclonal antibodies and six polyclonal antisera using a sensitive immunoperoxidase method. All tumours expressed the leucocyte common antigen (detected by monoclonal antibody 2D1) and all lacked epithelial cytokeratin (monoclonal antibody LE61), confirming their haematopoietic origin. All but one of the lymphomas expressed antigens characteristic of either B cells (17 cases) or T cells (six cases), while one case (morphologically a centroblastic lymphoma) had an unusual dual phenotype in which strong staining for T6 (marker of immature T cells) was associated with expression of the pan B lymphocyte antigens detectable with To15, anti-B1, anti-Leu12. This case was therefore classified as a B cell lymphoma showing aberrant expression of the T6 antigen. The pan B cell antibodies (To15, anti-B1, anti-Leu12) all appeared highly specific and sensitive, but the simultaneous use of all three monoclonal antibodies was necessary to detect the B cell nature in each of the 18 lymphomas. A wider panel of monoclonal antibodies was required to detect T lymphomas since these often disclosed atypical and restricted phenotypes. To15 and UCHT1 were the most reliable antibodies for the detection of B and T cell neoplasms, respectively. We conclude that most, if not all, "non-B, non-T" lymphomas are of either B or T lymphocyte origin and that monoclonal antibodies provide indispensable tools in their classification and diagnosis.
In 14 patients with pulmonary sarcoidosis and 14 matched controls we studied peripheral blood lymphocyte and monocyte counts, distribution of T and B lymphocytes, the functional helper:suppressor T cell balance, the antibody-dependent cell-mediated cytotoxicity of monocytes (monocyte ADCC), and the capacity of peripheral monocytes to generate angiotensin converting enzyme (ACE) in culture. Apart from lymphopenia in sarcoidosis patients we found a normal lymphocyte subset distribution and no evidence of increased suppressor T cell activity, using a PWM driven proliferative assay. The patients exhibited a normal monocyte count, but the proportion of monocytes was increased in sarcoidosis. Patients with active sarcoidosis had a significantly increased monocyte ADCC which was positively correlated with raised serum ACE. Peripheral monocytes had a measurable, but low ACE activity, which was modestly higher in active sarcoidosis than in controls. We could not reproduce earlier reported results on a glucocorticoid induced ACE synthesis from cultured human monocytes.
In a consecutive series of 102 patients with no jaundice and with symptoms of cholecystolithiasis, the predictions from both ultrasonography and cholecystography were compared with the final diagnosis. The accuracy of both examinations was high. However, in 38 per cent, single dose oral cholecystography failed to visualize the gallbladder whereas ultrasonography was conclusive in all patients. Judged by a simple scoring system, ultrasonography obtained a significantly better score than cholecystography (p less than 0.01) and an insignificantly better score than combined oral and intravenous cholecystography (0.05 less than p less than 0.1). Ultrasonography is recommended as the primary investigation in suspected instances of cholecystolithiasis.
Explore the source record for details and available documents.
The difficulty of obtaining an accurate diagnosis in nodules of the thyroid gland without operation and histologic examination is well documented. Surgical intervention has therefore been recommended, though opinions differ concerning the indications for surgery. Experience from 276 patients operated on for thyroid gland nodules is reported in the present paper. The decision to operate was based on a standard schedule with relatively wide indications for surgery. Complete hemithyroidectomy was performed in all surgically managed cases. The accuracy of preoperative diagnosis was evaluated against the histologic findings. Experience of hemithyroidectomy as the standard procedure is also reviewed. The incidence of malignancy with this active policy was 9% in the series as a whole and 12% in solitary adenoma of the thyroid. Total thyroidectomy was routinely performed when malignancy was demonstrated; 24% of the malignancies were bilateral. Although fine-needle biopsy and clinical evaluation were entrusted only to experienced investigators, the results confirmed earlier reports that no hitherto available diagnostic procedure can adequately distinguish malignant from benign thyroid lesions without surgery. The value of scintigraphic thyroid scan in the preoperative assessment seemed to be insufficient to warrant its use. No persistent complications arose from hemithyroidectomy. Complete hemithyroidectomy is always the operation of choice in such cases since, should be histologic examination show malignancy, the requisite additional surgery will not involve a thyroid lobe with previous surgical interference.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
The aim of the study was to investigate the rationale of the current indications for fetal chromosome analysis. 5372 women had 5423 amniocentesis performed, this group constituting a consecutive sample at the chromosome laboratory, Rigshospitalet, Copenhagen from March 1973 to September 1980 (Group A + B). Pregnant women 35 years of age, women who previously had a chromosomally abnormal child, families with translocation carriers or other heritable chromosomal disease, families where the father was 50 years or more and women in families with a history of Down's syndrome (group A), were compared to women having amniocentesis, although considered not to have any increased risk of fetal chromosome abnormality (1390 pregnancies, group B). They were also compared with 750 consecutive pregnancies in women 25-34 years of age, in whom all heritable diseases were excluded (group C). The risk of unbalanced chromosome abnormality in group A (women with elevated risk) is significantly higher than in group B + C (women without elevated risk) (relative risk 2.4). Women with a known familial translocation and women 40 years or more have a relative risk of 5.7 of having an unbalanced chromosome abnormality compared with women without elevated risk. Spontaneous abortion rate and prematurity rate did not differ from rates expected without amniocentesis. It is concluded that current indications may be characterized as a mixture of evident high risk factors and factors with only a minor influence on risk. Indications for amniocentesis should therefore be reconsidered. Because it must be considered impractical and ethically wrong to limit amniocentesis to the two mentioned real high risk groups, and illogical to continue to present policy, which is not based on clearcut evidence, the possibility of offering amniocentesis to all who want it, is discussed. Screening for chromosome disease in all pregnancies is not without problems, but may be reasonable in some localities.
One hundred unrelated, randomly chosen, consecutive patients with otosclerosis, verified by operation, were typed for HLA-A, -B, -C antigens. No significant association between HLA-A, -B, -C antigens and otosclerosis was found.