Biomedical subjects
Publications and source records attributed to J Haas.
Tumor recurrences can be detected earlier than in former times by new biochemical and radiological methods. Recurrences could be suspected in 35 (30.4 per cent) of 115 oncological patients 6 months before their clinical manifestation by determination of elevated levels of tumor markers in the serum. In the following time in all cases the suspicion could be proved with computed tomography.
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In spite of dietary treatment, the infants of pregnant patients with abnormal glucose tolerance have hyperinsulinism and diabetogenic fetopathy in 10 to 36% of cases. Those patients, who require insulin to prevent from fetopathy cannot be reliably selected by maternal parameters such as blood glucose and glycosylated hemoglobin values. We recommend the measurement of amniotic fluid insulin between the 28 and 32 weeks of pregnancy to differentiate whether the fetus is compromised or not. Subjects with values above the 97th centile require insulin therapy. Inadequate insulin dosage or delayed fetal hyperinsulinism can be discovered by checking the amniotic fluid insulin level at 33 to 36 weeks. In a total of 88 gestational diabetic patients 19 had raised amniotic fluid insulin levels indicating the onset of diabetic fetopathy at an early stage. Diabetic patients with raised amniotic fluid insulin levels needed large doses of insulin, namely 64.6 +/- 29.5 (Mean +/- SD) U/24 h. This treatment reduced mean blood glucose levels from 98 +/- 9 (Mean +/- SD) mg/dl to 82 +/- 10 mg/dl and was sufficient to prevent from diabetic fetopathy.
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The degree of androgynism (A) in women can be assessed via clinical data and by determining the levels of testosterone (T), dehydroepiandrosterone sulfate (DHEA-S) and testosterone binding globulin (TBG) in the blood. The determination of the "free androgen index" (FAI), the ratio of total T and TBG, helpful in estimating the level of free T in serum, conveys valuable additional information: in case of FAI below 1, a mild kind of A without elevation of free testosterone can be assumed. However, severe A with elevation of free testosterone and absolute hyperandrogynism is associated with FAI values above 1. In 63 women with signs of A the parameters mentioned above and the FAI were used to determine the degree of severity of A. These data were compared with the corresponding data of a control group. It could be shown that in women whose A was due to idiopathic hirsutism the increased level of bonded T played a causal role. The mean FAI in this group was 0.41. In contrast, in women with POC syndrome and androgynous cycle disturbances, the absolute hyperandrogynism with elevation of free T levels predominated. In these groups the mean FAI was above 1. However, women with male pattern bolding as single sign of A did not exhibit any significant difference in comparison to the control group. In this disease, the increased response of androgen receptors in the skin despite normal androgen levels seems to play a causal role. Two cases of androgen producing ovarial tumours and one case of adrenogenital syndrome were analysed separately.
In Central Europe and in South Africa duodenal ulcer disease has been reported to occur twice as often in migrant workers as in the indigenous population. To investigate the reasons for this phenomenon the joint effect of occupation and nationality on the prevalence of gastric and duodenal ulcer was studied in a survey of 73,000 active members of the German workforce. Non-ulcer dyspepsia and gastric, but not duodenal, ulcer were found more frequently in migrant than in indigenous workers. Manual workers were more prone to develop gastric and duodenal ulcer and non-ulcer dyspepsia than sedentary workers. The seemingly increased prevalence of duodenal ulcer in migrant workers observed by other authors may be due to migrant workers being employed predominantly in manual labour which bears a twofold risk of developing duodenal ulcer.
The efficacy of two chemotherapy regimens for recurrent and inoperable squamous cell carcinoma of the head and neck is reported. All patients had failed prior surgery and/or radiotherapy. 23 patients (group A) were treated with Cisplatin 120 mg/m2 and Adriamycin 60 mg/m2. 21/23 were evaluable for tumour response. The overall response rate (RR) was 28.5% (6/21, 2 CR and 4 PR). Methotrexate 250 mg/m2 with Leucovorin-Rescue 5 X 10 mg/m2 and 5-Fluorouracil 600 mg/m2 were administered to 28 patients. In 26 evaluable patients a RR of 38.4% (10/26, 5 CR and 5 PR) was achieved. The responders in groups A and B had a median survival of 98 and 85.5 weeks respectively and the non-responders 27 weeks in both groups. Nausea, vomiting and alopecia were common and severe in the DDP/ADM group. The major toxic effect of MTX/5-FU was neutropenia with two associated deaths from septicemia, although subjective side-effects were almost completely absent. MTX/5-FU can be recommended for the palliative treatment of recurrent squamous head and neck cancer because of an acceptable response rate, good subjective tolerance and the possibility of outpatient treatment.
Surgical specimens from 14 cases of early invasive squamous carcinoma of the vulva were extensively examined with serial sections to evaluate methods of tumor volume measurement. Using mathematical formulas, three-dimensional parameters were calculated from two-dimensional measurement. A technique of simplified volume estimation was developed and the results correlated with the status of the regional nodes.
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A fatal syndrome characterized by progressive clinical deterioration with unexplained thrombocytopenia, renal dysfunction, cholestasis, and ascites developed in certain infants throughout the United States who had received E-Ferol, an intravenous vitamin E supplement. We reviewed the clinical course of all 36 infants from one (index) nursery who had received E-Ferol, which contains 25 units per milliliter of dl-alpha-tocopheryl acetate solubilized with 9% polysorbate 80 and 1% polysorbate 20. The syndrome was recognized in eight of the 36 infants; affected infants had a lower birth weight (less than 1,200 g) and had received a higher total dose of E-Ferol for longer periods than the unaffected cases. We reviewed autopsy-derived tissue from 20 infants (six from the index nursery and 14 from three other collaborating nurseries) who had received the intravenous vitamin E preparation in a reported dose of 25 to 137 units/kg/day for six to 45 days between October 1983 and March 1984. The hepatic histology in the affected cases indicated a progressive injury characterized initially by Kupffer cell exfoliation, central lobular accumulation of cellular debris, and centrally accentuated panlobular congestion. Prolonged exposure to E-Ferol was associated with progressive intralobular cholestasis, inflammation of hepatic venules, and extensive sinusoidal veno-occlusion by fibrosis. We propose that vasculocentric hepatotoxicity is the basis for the observed clinical syndrome that represents the cumulative effect of one or more of the constituents of E-Ferol.
To investigate whether the elevation of factor VIII coagulant activity observed in children with poor control of diabetes is due to increased levels of the factor VIII coagulant moiety of the factor VIII complex or reflects activation of the factor VIII coagulant moiety, factor VIII coagulant activity (VIII C), factor VIII coagulant antigen (VIII C:Ag), and factor VIII-related antigen (VIII R:Ag) were determined in 75 insulin-dependent children. All children were without signs of vascular disease based on negative funduscopy, negative fluorescein angiography, normal serum creatinine levels, and absence of proteinuria. Children with poor actual control of diabetes had significantly higher VIII C values than did children with good actual control of diabetes based on HbA1 values, but VIII C:Ag values did not differ in children with good or poor actual control of diabetes. A significant elevation of VIII C over VIII C:Ag values was observed in children with poor actual control of diabetes, but no elevation of VIII C over VIII C:Ag was found in children with good actual control. VIII R:Ag values were higher in children with poor actual control. VIII C, VIII C:Ag, and VIII R:Ag did not differ significantly in children with short or long duration of clinical diabetes. Our observation of significantly higher VIII C values than VIII C:Ag levels strongly suggests intravascular activation of the factor VIII coagulant moiety during poor diabetes control. The process leading to activation of the coagulant moiety seems to be different from the process leading to the elevation of the other moiety of the factor VIII complex, the factor VIII-related antigen, in diabetic subjects.
Six cases of posttraumatic hematomas in areas of the chest wall are reported, four of them were found subpleural and two extrapleural. Radiological signs and differential diagnostic possibilities are discussed.
Some epidemiologic features of female breast cancer in the GDR and the Estonian SSR are compared on the basis of data from the cancer registries. From 1968 to 1980 68,626 new breast cancer cases were reported in the GDR and 3,768 in Estonia. Age-standardized incidence rates were consistently higher in the GDR. Increasing rates were present in both regions. The ratios of left to right sided lesions were 1.07 and 1.15 for the GDR and Estonia, respectively. Overall, 95.2% of breast cancers in the GDR and 80.6% in Estonia were histologically verified. Although some differences in stage at diagnosis were reported these may reflect classification practices. There was no evident change in stage at diagnosis over this time period. During 1968-1980 treatment with combined radical surgery and radiotherapy declined in both regions in favor of radical surgery alone. Some suggestions for future collaborative research are proposed.
Apolipoprotein A-IGiessen is a variant form of apo A-I that is displaced from the corresponding normal A-I isoforms on isoelectric focusing gels by a single charge unit towards the cathode [Utermann et al. (1982) J. Biol. Chem. 257, 501-507]. Three subjects heterozygous for the variant were detected in one family. The percentage of the total A-I in plasma represented by the A-IGiessen in these subjects ranged over 25-30%. The variant and normal major A-I isoforms from the proband (Y.J.) were purified by preparative isoelectric focusing and cleaved with CNBr. Analytical focusing of CNBr fragments demonstrated a charge difference between CB3Giessen and normal CB3. Sequence analysis of CB3Giessen revealed that a proline existing in normal A-I was replaced by an arginine in the variant A-I at residue 143. The ability of the mutant A-I to activate purified lecithin:cholesterol acyltransferase was determined in vitro. The cofactor activity of [Arg143]apolipoprotein A-I was about 60-70% of that demonstrated by control A-I. Residue 143 is in a putative beta-turn between two of the repeating amphiphilic helices in apolipoprotein A-I and may be a critical determinant of the protein's structure and function.
A group of 51 patients treated surgically for ovarian carcinoma was randomly subdivided to test the efficacy of lithium carbonate in the prevention of leucopenia during systemic chemotherapy. In 26 patients receiving sequential lithium carbonate the side effect of myelosuppression was mitigated and the leucocyte count during treatment, which determines the dosage of the cytostatic drugs, was significantly higher in this group. It was, thus, possible to reduce the number of cytostatic courses of treatment in the lithium group in comparison with the treatment courses in the 25 control patients. Lithium therapy had to be discontinued due to side effects in seven patients, which were then excluded from the trial.
An apolipoprotein (apo) A-I variant that has a relative charge of -1 compared to normal apo-A-I on isoelectric focusing gels has been identified in five unrelated families as a result of screening a large number of individuals. The cause of the electrophoretic abnormality has been examined by analyzing the variant apo-A-I structure. The evidence suggests that a single amino acid, lysine 107, has been deleted in the variant apo-A-I of all affected individuals studied from these families, with the remainder of the variant apo-A-I sequence being unaffected. The deletion of this single basic amino acid residue is sufficient to account for the charge difference between the variant and normal apo-A-I as seen on isoelectric focusing gels. This variant, previously referred to as A-I-Marburg or A-I-Münster-2, can now be designated by the structural abnormality apo-A-I(Lys107----0). The evidence from extensive pedigree analysis suggests the likelihood that the deletion mutant gene is allelic to the normal apo-A-I gene. At the same time, the kindred analyses have failed to yield a lipid abnormality that can be unequivocally related to the presence of this deletion mutant of apo-A-I. However, all subjects expressing apo-A-I(Lys107----0) also express normal apo-A-I, so that any abnormality caused by the variant apo-A-I might be adequately compensated for by the normal apo-A-I. To examine directly the functional consequence of the lysine deletion, the isolated variant was tested in vitro for its ability to activate lecithin:cholesterol acyltransferase, the principal cholesterol-esterifying enzyme in plasma. It was found that apo-A-I(Lys107----0) is deficient in its ability to activate lecithin:cholesterol acyltransferase, having only 40-60% of the cofactor activity of normal apo-A-I. The cofactor activity of the pro-apo-A-I component of the variant was also reduced to about 60% of either normal A-I or normal pro-apo-A-I. The functional defect is probably related to a disruption in the secondary and/or tertiary structure of the protein caused by the deletion of lysine 107 in the primary structure.
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