[Hyperemesis as an individuation attempt--a case report].
Explore the source record for details and available documents.
Biomedical subjects
Publications and source records attributed to L Winkler.
Explore the source record for details and available documents.
We evaluated posttransplantation growth, bone maturation, and adult height in 20 adolescents who had received kidney transplants at the age of 10.5 to 17 years. Nine patients (five male, four female) were treated with cyclosporine and low-dose prednisolone, and 11 children (six male, five female) were treated with azathioprine and high-dose prednisolone. The cumulative dose of steroids after transplantation was significantly lower in the cyclosporine-treated group. Bone age, according to the radius-ulna-short bones method of Tanner and Whitehouse, was almost the same in both groups at the time of transplantation (15.0 and 14.6 years for male subjects, 13.3 and 13.1 years for female subjects). Predicted adult height (Tanner-Whitehouse Mark II-method of Tanner et al) and target height were estimated at transplantation. Adult height was defined as achieved when bone age in male subjects had reached 18 years and, in female subjects, 16 years. Bone maturation of the cyclosporine-treated patients occurred at a normal rate (0.92 bone-age years per chronologic year), whereas the azathioprine-treated group exhibited a significantly slower rate (0.56 bone-age years per chronologic year). The growth rate per year for the cyclosporine-treated group was more than double that of the azathioprine-treated group (3.0 cm vs 1.4 cm). The adult height of the cyclosporine-treated group exceeded the predicted adult height by a mean of 1.3 cm, but the azathioprine-treated group missed it by 3.9 cm. Target heights could not be achieved in any group. Kidney function was significantly lower in the cyclosporine- vs the azathioprine-treated group, but no patients suffered from severe renal insufficiency. We conclude that cyclosporine and low-dose prednisolone are associated with normal bone maturation and a better prognosis for final height in children with renal transplants.
The association of various unsystematic aneuploidies with premature centromere division (PCD) was observed in a patient with conspicuous clinical features and combined immunodeficiency. Trisomies and monosomies of almost all autosomes and gonosomal aberrations were found separately or in combination in a majority of the proband's lymphocytes and fibroblasts. The chromosome number varied from 44 to 50. A high proportion of the metaphases showed PCD or had the appearance of C-anaphases. These findings probably represent a new mutant affecting mitosis and causing mosaic aneuploidies.
Eight children with terminal renal insufficiency on continuous ambulatory peritoneal dialysis were followed for 12 months to evaluate laboratory parameters of mineral ion and bone metabolism. Calcium carbonate (range 47-295 mg/kg body weight per day) was given in combination with low doses of either vitamin D or 1,25(OH2D3. Blood urea nitrogen and serum phosphate concentrations remained well controlled throughout the observation period. A significant increase in serum calcium levels from 2.35 +/- 0.18 to 2.61 +/- 0.22 mmol/l (mean +/- SD) was observed during the first 6 months. Alkaline phosphatase activity and mid-C-regional parathyroid hormone, both indirect parameters of bone metabolism, revealed no evidence of severe secondary hyperparathyroidism. Our data indicate that calcium carbonate may be sufficient to induce relative hypercalcaemia in uraemic children, and thus reduce the risk of developing renal osteodystrophy. Unwanted side-effects of vitamin D preparations, i.e. increased intestinal phosphate absorption and hypercalcaemia after successful renal transplantation, may thus be avoided.
Fourteen patients (aged 5.9-22.1 years) undergoing continuous ambulatory or cycling peritoneal dialysis were treated with recombinant human erythropoietin (rhEPO), which was given intravenously once a week at a dosage of 300 units/kg. The mean haematocrit level increased from 18.5% to 27.5% and the reticulocyte count from 19% to 62% within 1 month. After an average time of 3.1 months rhEPO dosage could be adjusted to 100 units/kg per week to keep the haematocrit level at 30%. Only 1 patient had an exacerbation of hypertension, which required a dosage reduction; other side-effects were not noted.
In 14 nonobese patients after acute pancreatitis and with normal oral glucose tolerance, the response of insulin, C-peptide, and pancreatic glucagon after 100 g of oral glucose was assessed. The curves of insulin and C-peptide were significantly raised compared with those of controls, and no difference was found between the response of patients with a negative (n = 8) and a positive (n = 6) family history of type II diabetes. The curves of pancreatic glucagon did not differ from those found in controls. Our results indicate that a normal response to glucose after recovery from an attack of acute pancreatitis is maintained at the cost of increased insulin secretion.
A methodical base for estimation of apolipoprotein AI (apo AI) in the serum using a monoclonal antibody in a non-competitive ELISA is described. The technical approach is adjusted to commercial materials of the DDR industry. The assay allows to determine apo AI within the range of 5-100 micrograms apo AI/I. The Vk was 4% (within), and 8% (day to day). The monoclonal antibody used is directed against a native epitope which is fully exposed in the serum. Application of the SUMAL system further improves the practicability of the method. The assay should be suitable particularly for the recognition of epitopes of apo AI in serum HDL fractions associated with an atherogenic risk. The values obtained by the ELISA correspond to those measured turbidimetrically using polyclonal antibodies.
The degree of apo E sialylation in VLDL from serum of diabetics and controls was determined by densitometric scanning of the pherograms after isoelectric focusing of the VLDL proteins including treatment with neuraminidase. The distribution pattern of sialylation within the groups of patients and controls followed a Gaussian type. A significantly elevated level of sialylated apo E could be demonstrated in IDDM and NIDDM as compared to the controls. No correlation was found between the apo E phenotype and the diabetic state. From the correlation analysis including the parameters degree of sialylation, age, duration of diabetic state, and blood glucose pattern no significant results were obtained except a significant but only week correlation (r less than 0.3) between sialylation, age, and blood glucose in IDDM patients. Possible consequences of the elevated apo E sialylation in diabetes mellitus are discussed.
To get insight into the low density lipoprotein (LDL)-apoB flux in the rat fetus near term and in the early postnatal period, homologous apoE-free 125I-labeled LDL was injected into the umbilical vein of the rat fetus immediately after Caesarean section. Since the serum LDL-apoB spontaneously declined after birth, a time-dependent two-pool model was used to calculate the flux rates in the neonate from the specific activities of LDL-apoB up to 15 h post partum. An approximate value of LDL-apoB flux in the fetus at birth was obtained by extrapolation of the kinetic data to the time of injection of the tracer. The data revealed that the turnover of LDL-apoB in the fetus (18.6 micrograms LDL-apoB/h per g body weight) exceeded that in the adult rat (0.4 microgram/h per g body weight) by at least one order of magnitude. Even 15 h after delivery, the LDL-apoB influx amounted to 2.5 micrograms/h per g body weight. The fractional catabolic rate of LDL-apoB in the fetus at term (0.39, h-1) slightly exceeded that in the adult animal (0.15, h-1) and reached the adult level within the first 3 h after birth and remained constant thereafter. In the rat fetus, LDL-apoB flux greatly exceeds that of VLDL-apoB. The data support the view of a direct synthesis and secretion of LDL, most probably by the fetal membranes.
A 2-day-old girl developed a severe lactic acidosis with a normal lactate/pyruvate ratio and hyperammonaemia. Plasma arginine and citrulline levels were below the limit of detection. In muscle total pyruvate dehydrogenase complex (PDHC) and pyruvate decarboxylase (E1) activities were reduced to a fraction of lower control values. The acute neonatal period was bridged with peritoneal dialysis, dichloroacetate therapy, supplements of arginine and branched chain amino acids, a complete vitamin B complex and lipoic acid. Lactate homeostasis responded to pharmacological supplements of lipoic acid. At age 1 year the child was hypotonic, showed severe developmental retardation, optic atrophy and cranial dysmorphism. She died aged 1 year 8 months with signs of respiratory paralysis but with normal lactate levels under assisted breathing. Pathological findings at autopsy were suggestive of Leigh syndrome, interstitial pneumonia and extensive fatty infiltration of hepatocytes. Regression analysis of data from 187 plasma amino acid determinations from the patient over a period of 1 year 8 months revealed a persistent-imbalance involving alanine, glutamic acid, glutamine, proline, citrulline and branched chain amino acids. Aspects of acute and long-term therapy in this patient and some implications of the imbalances in plasma amino acids are discussed.
About 50% of the individuals with a coronary risk show lipid levels within the normal range. Therefore, apolipoprotein profiles could be better risk indicators than TC or TG. Apolipoproteins generally discussed in this context are apo A1, apo B, and apo E. Their diagnostic validity, however, is ambigously evaluated. The individual iso-protein pattern of apo E is important for the differential diagnosis of the type III hyperlipidemia with its strong predisposition for premature atherosclerosis. Moreover, the extent of the apo E sialylation seems to be important because the modification of apo E by sialic acid alters its metabolism. Our date provide evidence that in IDDM and NIDDM the degree of apo E sialylation is increased. Concerning apo A1 and B we tried to find out parameters suitable for the prediction of the coronary risk both in the hyperlipidemic and the normolipidemic state. 64 male survivors of a myocardial infarc"ion and 60 matched controls were included in the study (group I). From group I a supopulation showing non-pathological values for TC and TG was selected (group II with 31 survivors and 44 controls). The diagnostic validity of the parameters apo A1, apo B, TC, HDL-C, apo A1/apo B, TC/apo B, HDL-C/apo B, TG, TG/apo A1, TG/HDL-C, TC-HDL-C/apo B determined by calculation of their sensitivities, specificities, efficiencies, and predictive values. Only the parameters TC/apo B, HDL-C/apo B, and apo B were suitable in the order given for detection of the coronary risk. Using the TC/apo B ratio 71-76% of the controls and 79% of the survivors could be exactly reclassified independent of the group they belonged to.(ABSTRACT TRUNCATED AT 250 WORDS)
Explore the source record for details and available documents.
Platelet-activating factor (PAF) is transformed in vivo rapidly into the biologically inactive lyso-PAF. This reaction as well as lipid parameters were quantified in serum from 40 survivors of myocardial infarction and 36 healthy controls matched for age and body weight. The PAF-degrading capacity was 23% (p less than 0.001) higher in patients compared with the control group. Using the degradation of PAF as an univariate discriminator more than 70% of subjects were classified correctly. This is comparable with the discriminatory value of the best lipid variables, apolipoprotein B and HDL-cholesterol. Statistically significant differences in the degradation of PAF were found also by comparing subgroups which were matched for plasma levels of total cholesterol, VLDL/LDL-cholesterol or apolipoprotein B. The ratio by 48% (p less than 0.0001) in the case group was identified as an additional good discriminator between both groups. In contrast, platelet aggregation tests which were performed in acetylsalicyclic acid treated platelet-rich plasma discriminated poorly between patients and controls.
All diabetic patients suffering from the disease for at least 20 years and living in the closed area of the Erfurt district in 1970 have been followed prospectively since that time. In 47 of them still alive in 1985, i.e. after more than 35 years of diabetes, serum lipid and apolipoprotein concentrations were measured and compared to those of non-diabetic subjects without cardiovascular diseases (n = 47) pair-matched by sex, age, and body weight. In males (n = 27) significantly (p less than 0.01) higher levels of HDL cholesterol and apolipoprotein A-I as well as lower concentrations of triglycerides and a lower total cholesterol/HDL cholesterol risk ratio than in nondiabetic control subjects could be found. In long-term diabetic females (n = 20), apolipoprotein A-I levels were also increased (p less than 0.02). Trends in HDL cholesterol and triglycerides were similar to those found in males but did not reach statistical significance. Higher concentrations of total cholesterol (p less than 0.02), LDL cholesterol (P less than 0.05), and apolipoprotein B (p less than 0.02), however, did not fit in with a beneficial lipoprotein pattern. The frequency of pathological lipoprotein patterns was not higher than among the non-diabetic control subjects (32% and 40%, respectively). According to these findings an antiatherogenic lipoprotein pattern might be considered, at least in males, as one of the determinants causing the multifactorial event of long-term survival in diabetes.
Follow-up data of all 208 long-term diabetics (duration of the disease at least 20 years) living in the closed area of the Erfurt district in 1970 had demonstrated the importance of lipoprotein pattern for longevity. Now the dependence of lipoprotein levels on both the diabetes-related conditions nephropathy and glycaemic control has been examined in 47 of them, still alive in 1985 that means 35 or more years after the onset of diabetes. Glycaemic control was assessed by measuring the glycosylated haemoglobin (n = 44). Diabetic nephropathy was assumed in case of persistent proteinuria. Poor glycaemic control (n = 16) was associated with increased levels of atherogenic lipoproteins as reflected by higher concentrations of total cholesterol, LDL cholesterol, apolipoprotein B, and triglycerides, as well as a changed HDL composition indicated by a decreased HDL cholesterol/apolipoprotein A--I ratio. Higher ratios of total cholesterol to HDL cholesterol and apolipoprotein B to apolipoprotein A--I point to an increased risk of developing atherosclerotic diseases in poorly controlled diabetics. 86% of the well controlled long-term diabetics had non-pathological values of LDL cholesterol, triglycerides, apolipoprotein B, HDL cholesterol, and apolipoprotein A--I but only 31% of the poorly controlled patients did so. Diabetic nephropathy in the absence of chronic renal failure (n = 10) was characterized by higher values of LDL cholesterol, triglycerides, total cholesterol/HDL cholesterol, and apolipoprotein B/apolipoprotein A--I. 80% of the subjects with a pathological lipoprotein pattern were proteinuric or in poor glycaemic control or both. Therefore, it is concluded that prevention of these two conditions might help to delay atherosclerosis via its beneficial influence on lipoprotein metabolism.
Explore the source record for details and available documents.
In fetal rats at term LDL carries 75% of the total serum cholesterol, whereas in adult ones this value amounts to 20% only. Using a time-dependent two pool model the flux rates for LDL cholesterol can be calculated for the newborn. The data reveal that at birth the LDL cholesterol flux is 15-20 times higher than in the adult. During the first 2 h of postnatal life the FCR drops down from 0.4 at birth to values measured in the adult. Since at least 75% of LDL is of another origin than VLDL, a direct hepatic LDL synthesis is postulated for the newborn. The liver contributes to about 30% of the total LDL uptake which is mainly realized by a receptor-dependent mechanism, even though the fetus and the newborn exhibit markedly elevated LDL serum concentrations.
Platelet-activating factor (PAF) is a naturally occurring phospholipid that exerts diverse biological activities. In the present study the degradation of PAF as well as lipid concentrations were measured both in plasma from 28 patients suffering from peripheral vascular disease and 18 healthy volunteers of comparable age. Beside some changes of the lipoprotein pattern it was also found that the capacity to degrade PAF is significantly elevated in the patient group. In view of this finding the question arises whether there is any link between the degradation of PAF and the development of atherosclerosis.