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24 h-urine excretion of aldosterone-18-glucuronide was determined with and without preceding paper chromatography in patients with essential hypertension (n = 50). Radioimmunoassay was performed with a highly specific antibody against aldosterone. Urine specimens determined without chromatography gave significantly higher values than aliquots which were estimated at the same time with chromatography. A highly significant correlation was found between the two methods (r = 0.91, p less than 0.0001). Without chromatography, mean over estimation in samples with concentrations in the low and middle range was on average 32 and 24% respectively, whereas aldosterone concentrations in the upper range showed a 14% over estimation. The RIA procedure for aldosterone without chromatography as here described is suitable for hypertension screening programmes to exclude known forms of primary hyperaldosteronism in which elevated aldosterone excretion rates have to be differentiated from values lying within the normal range.

Familial type III hyperlipoproteinemia is characterized by the presence of elevated plasma levels of very low density lopoproteins (VLDL) which contain an increased amount of cholesterol and by the presence of a significant amount of lipoproteins with an intermediate density between that of VLDL and low density lipoproteins (LDL); the intermediate density lopoproteins, designated IDL or Lp III, have a slower electrophoretic migration rate than VLDL, and are found in the ultracentrifugal top fraction as a contaminant. Classically, the diagnosis of type III is based on the demonstration of beta-migrating lipoproteins in the ultracentrifugal top fraction (density less than 1.006), thus "floating beta-lipoprotein". More recently, it has been proposed that an elevated VLDL-cholesterol to triglyceride ratio is diagnostic of the disorder. In the present report, we have compared the two methods for their diagnostic value and have concluded that the chemical index definition is the more reliable method for the diagnosis of type III hyperlipoproteinemia.

The combination of pulmonary emphysema and liver cirrhosis in early childhood is documented for the first time in a 31/2 year old girl with homozygous (ZZ) deficiency of a1-antitrypsin. Examination of relatives in the generation of parents and grand parents revealed 7 heterozygous (MS) and five normal members (MM). Lung function tests showed altered respiratory function in 4 out of these 7 heterozygous subjects. Measurement of trypsin inhibitory capacity in plasma gave a good correlation to the genotype, however determinations of a1-antitrypsin coincided with it to a lesser degree. A high trypsin inhibitory capacity was detected in the tears of the propositi, which was shown to be immunologically distinguishable from serum a1-antitrypsin. Similarly, antiprotease activity was demonstrated in nasal secretions. This too did not reflect the serum profile.

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Copyright of Klinische Wochenschrift is the property of Springer Nature and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

In clinical practice the acquired or de novo resistance of tumors to antitumor chemotherapy remains a big problem. However, in the past few years some progress has been made in understanding the two principal mechanisms: metabolic alterations leading to a reduced cytostatic or cytotoxic effect of drugs, and reduced accumulation of drugs within the tumor cells [15, 34, 35]. The second phenomenon is usually attributed to the ability of tumor cells to accelerate the efflux of various xenobiotics. This phenomenon is considered primarily responsible for the development of multidrug resistance (MDR). However, loss or impairment of drug uptake by the tumor cells may also contribute to resistance to antitumor drugs. This paper focusses on recent findings with hepatoma cells, which support this view. [ABSTRACT FROM AUTHOR]

In vitro binding of aldosterone to mineralocorticoid receptors on human mononuclear leukocytes (HML) and its effects on the intracellular sodium and potassium concentrations of HML have already been described. In the present paper this easily accessible human cell model was investigated in 13 patients with essential hypertension. In only four patients sodium in HML without incubation was elevated compared with the range for normal persons. A decrease of intracellular sodium or potassium occurred during incubation without aldosterone ( P<0.02). The addition of 1.4 n M aldosterone did not prevent this loss of electrolytes as observed in normal persons. Plasma renin activity and aldosterone were not correlated with the electrolyte response and were within the normal limits. The number of mineralocorticoid receptors/cell were within or close to the normal range ( n=9). The independence of intracellular electrolytes from aldosterone despite a normal number of mineralocorticoid receptors may reflect an impairment of the mineralocorticoid effector mechanism in the HML of patients with essential hypertension. [ABSTRACT FROM AUTHOR]

This paper presents an alternative view to a commonly held misconception. The extent to which the causes of human cancer can be known is less than generally believed on the basis of the formal summation of estimates on the causal role of certain carcinogenic factors that have been tabulated by Doll and Peto (1981). Here it is stressed that the factors with known causal relation in the etiology have not as yet been ascertained for up to 97% of human cancers. Currently only one-third of the cancer deaths registered in the Federal Republic of Germany can be assigned etiologically to known exogenous carcinogenic agents or lifestyle. Accordingly, the causes of less than 50% of all malignant neoplasms are known and amenable to direct causal primary prevention. This, however, does not preclude a concept of 'indirect primary prevention' which, based on the probable summation of subcarcinogenic effects of single carcinogens, enables removal from the environment of compounds that show carcinogenicity in animals, even if these compounds lack epidemiological evidence of carcinogenic activity. [ABSTRACT FROM AUTHOR]

Chronic renal failure (CRF) is characterized histologically by progressive glomerulos-clerosis (GS) and tubulo-interstitial scarring (TIS). Recently, research has focused on the study of the pathophysiology of GS. Most advances in this field have been derived from the study of various experimental models of CRF and GS in the rat. In this paper, I will review some of the concepts and hypotheses put forward to explain progressive GS and examine their relevance to glomerular scarring and CRF in humans. [ABSTRACT FROM AUTHOR]

Various endocrine and metabolic disturbances associated with long standing uremia persist after kidney transplantation or arise from the use of immunosuppressive drugs. Hyperlipidemia for long time being implicated as the cause of corticosteroids is also observed in renal transplant recipients treated with cyclosporin A monotherapy. After conversion from cyclosporin to azathioprine serum cholesterol and triglyceride concentration fall, and elevation of LDL-cholesterol may also be reversed. There is a tendency for higher HDL-cholesterol in azathioprine and prednisolone treated transplant patients. Those patients who are at risk for clinically significant cholesterol elevations can be predicted by their pretransplant lipid levels, specifically the LDL-fraction. Risk-benefit ratio of conversion and of treatment with lipid-lowering drugs, especially with lovastatin, should be carefully examined, also in view of glucose intolerance. Higher incidence of diabetes mellitus requiring insulin therapy in cyclosporin treated transplant recipients has been reported. Cyclosporin may cause toxic effects on pancreatic beta-cells resulting in inhibition of insulin secretion. High doses of cyclosporin induce inhibition of glycogen synthesis in rat liver. Glucose intolerance is reversible after reduction of cyclosporin dose or conversion to azathioprine. Therefore glucose metabolism in kidney transplant recipients treated with cyclosporin should be carefully followed. Immunosuppressive therapy may affect reproductive function, arachidonate metabolism and renin-angiotensin-aldosterone system as well as posttransplant calcium and phophate metabolism. Endocrine and metabolic abnormalities are associated with long standing uremia. After successful kidney transplantation several observations are normalized but further complications arise from the use of immunosuppressive drugs. The present paper reviews various endocrine and metabolic disturbances described following renal transplantation. [ABSTRACT FROM AUTHOR]

This paper describes an information-theoretical model developed for detection of renal allograft rejection on the basis of various laboratory data. In this report the mathematical background of the model is described in detail and the rationale of its use is discussed. An example is given for the practical application of the model in kidney grafted patients. In the 30 patients of the test collective, seven rejection episodes were diagnosed by the clinicians and vertified histologically. All seven rejection episodes were detected by the model, in the mean 2.4 days (median; 3 days) before the clinical diagnosis. [ABSTRACT FROM AUTHOR]

Twenty-nine adult patients with acute myelogenous leukemia AML who received 40 treatment courses with high dose cytosine arabinoside (HD-A), alone or combined with other cytotoxic drugs, for remission induction (RI) or postremission intensive consolidation (IC) were retrospectively analysed for types and severity of infectious complications. In this paper, we report the unusually high rate of streptococcal septicemia in our patients. Of 13 bacteremic infections in a total of 45 infectious episodes, 10 were caused by streptococci (9 viridans streptococci, 1 group B hemolytic streptococcus). Three of them were lethal. After reviewing all documented cases of streptococcal septicemia in the same study period, four additional cases among adult patients with AML were identified. Three of them have had antileukemic chemotherapy without HD-A, while one have had HD-A as a conditioning regimen for bone marrow transplantation. Only three cases were documented to occur in adult patients with AML. Patients treated with HD-A for RI or IC had a significantly lower risk of streptococcal septicemia during previous chemotherapy-associated febrile neutropenic episodes (1/55 vs 10/45; P=0.01). Neither prophylactic regimens including trimethoprim-sulfamethoxazole nor those without it were effective in preventing streptococcal septicemia. Further studies are needed to confirm these data before the value of additional or alternative prophylactic antibiotics is proven necessary. [ABSTRACT FROM AUTHOR]

Patients with severe bleeding complications and other side effects on conventional anticoagulants and strong indication for further anticoagulation were treated with a low molecular weight heparin fragment (Tedelparin). In this paper we report the experiences in 30 patients, who were anticoagulated 1-11 months with this compound. All patients injected themselves a dose ranging from 1 × 2,500 to 1 × 20,000 anti factor Xa units per day. Within 132 months of treatment one patient with good compliance developed thromboembolism. Four patients had bad compliance. Two of them experienced rethrombosis 1 and 8 weeks after starting therapy. Severe haemorrhages did not occur. Two patients had one minor bleeding complication each. Both patients developed several times per year severe haemorrhages with conventional anticoagulants. All excessive subcutaneous haematomas and indurations of the adipose tissue at the injection site of conventional heparin disappeared completely. Low molecular weight heparin can be regarded as an alternative anticoagulant in patients with severe bleeding and other complications on oral anticoagulants and conventional heparin. [ABSTRACT FROM AUTHOR]

Hemophilia A is the most common inherited bleeding disorder in man. The recent isolation of the hemophilia gene has led to the identification of an intragenic restriction fragment length polymorphism (RFLP) which can be used for segregation analysis in families at risk for carrying the disease. In addition, a tightly linked extragenic RFLP can also be used for these analyses. In this paper, we exemplify the usefulness of DNA analysis in genetic counseling of families at risk for hemophilia A. Although DNA analysis allows carrier detection in the majority of families, bioassays are still required for accurate diagnosis when DNA analysis is not informative. [ABSTRACT FROM AUTHOR]

In an earlier publication, we described a modified procedure for the determination of plasma catecholamine levels using high-performance liquid chromatography (HPLC), followed by amperometry. In this paper, we present our results on the variability of normal catecholamine values in plasma for noradrenaline (NA), adrenaline (A) and dopamine (DA). In 122 women and men at rest, the range for NA was 0.15-3.5 nmol/l, for A 0.01-0.8 nmol/l and for DA 0.04-4.5 nmol/l. We also describe the effects of orthostasis, intravenous catheters, food intake, cigarette smoking, age and sex on venous catecholamine levels. The efficiency of the HPLC method allowed us to check, using a large subject group, the results obtained by other authors from studies involving smaller subject groups with more expensive and time-consuming methods. [ABSTRACT FROM AUTHOR]

In connective tissue diseases, the differentiation of disease-related hematological aberrations from drug-induced cytotoxic or allergic blood-cell dyscrasias is often difficult. In this paper we report on the positive identification of an indoprofen-induced severe pancytopenia in a multidrug-treated patient with active systemic lupus erythematosus by use of a drug-specific lymphocyte transformation test. [ABSTRACT FROM AUTHOR]

The consequences of altered immunocompetence resulting from anaesthesia and surgery are potentially hazardous to the patient with malignant disease. Malnutrition also produces reduction in cell mediated immunity, a condition which is commonly incurred in patients with neoplastic disorders. Numerous agents have been claimed to stimulate the immune responses but few have proved to be of practical value. This paper reports the use variously of protease inhibitors, using Aprotinin, and post operative nutritional therapy, following major surgical resection for carcinoma - specifically as regards their influence on parameters believed to relate to cell mediated immunity. No clinical, metabolic or immunologic benefit was identified from either method of post operative stimulation of cell mediated immunity, although this study did confirm post operative depression of these parameters. The significance of these changes is unclear but there is no evidence to support an immunological mechanism for either of these approaches being of benefit in clinical practice. [ABSTRACT FROM AUTHOR]

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The present paper reviews the results of recent investigations into the influence of pregnancy and sex hormones on rheumatoid arthritis (RA) and ankylosing spondylitis (AS). Prospective patient studies have shown that pregnancy exerts a beneficial effect on the majority of RA patients, while AS patients generally have unchanged disease activity during gestation. In AS, gestational remission was confined to patients with accompanying diseases. A postpartum disease flare-up occurred commonly in both RA and AS. Blood parameters reflected mainly the biochemical changes of normal pregnancy. A decrease of circulating immune complexes has been found in RA patients remitting during pregnancy. No single serum factor or combination of serum factors responsible for gestational remission could be detected. The possible influence of α-pregnancy-associated globulin on disease activity in pregnant patients remains contradictory. Hormonal contraceptives have been found to be protective against the manifestation of RA in four of five studies. However, no beneficial effect of sex hormones on the symptoms of established RA and AS could be demonstrated. [ABSTRACT FROM AUTHOR]

Twenty members of a family with adult hypophosphatasia were examined clinically and biochemically. Severe caries causing early loss of permanent teeth was the only clinical symptom which could be attributed to hypophosphatasia. None of them had a history of defective bone mineralization, rachitic skeletal alterations, and recurrent pseudofractures or fractures. An iliac crest bone biopsy of the proposita showed a normal finding corresponding to the age of the patient. Four family members in two subsequent generations were affected, thus suggesting an autosomal dominant inheritance. Their serum and leukocyte alkaline phosphatases were reduced. The phosphoethanolamine (PEA) excretion in the urine was increased to a level which suggests a heterozygote state. The serum alkaline phosphatase activity could be ascribed to the liver isoenzyme fraction. This was shown by polyacrylamide electrophoresis, by inhibition studies with organ-specific inhibitors, heat inactivation, inhibition by antibodies, and treatment with neuraminidase. The proposita had an unexplained, diffuse fatty infiltration of the liver. Thus, not only alterations of bone but also of liver metabolism in hypophosphatasia should be considered. The variety of adult hypophosphatasia described in this paper is characterized by the lack of severe bone abnormalities, the apparently autosomal dominant inheritance, and the reduction of bone and intestinal isoenzyme in the serum. Our study suggests that hypophosphatasia is a heterogenous disorder which includes both severe and clinically mild forms. [ABSTRACT FROM AUTHOR]

Hypertension, hyperlipidaemia and cigarette smoking are major risk factors in coronary heart disease. Since many antihypertensive drugs alter plasma lipid levels it is a subject of current discussion that these agents may increase associated coronary risk and therefore offset the beneficial effects of lowering blood pressure. The purpose of this paper is to review clinical and experimental data in the literature on the influence of antihypertensive drugs on lipid metabolism. The thiazides hydrochlorothiazide and chlorthalidone cause an elevation of plasma triglycerides and very low density lipoprotein (VLDL) but have little effect on total cholesterol, low density lipoprotein (LDL) and high density lipoprotein (HDL). The unspecific beta-blockers, e.g. propranolol, do not affect total cholesterol and LDL but increase total triglycerides and VLDL and decrease HDL. The changes of plasma lipids and lipoproteins caused by cardio-selective beta-blockers, e.g. atenolol and metoprolol, and unspecific beta-blockers with intrinsic sympathomimetic activity (ISA), e.g. oxprenolol and pindolol, appear to be qualitatively similar but less pronounced. The alpha-blocker prazosin reduces total triglycerides and slightly lowers total cholesterol. The concentration of VLDL plus LDL decreases while HDL may increase. Only very few studies have been reported on the effects of other antihypertensive drugs, e.g. clonidine, hydralazine, on plasma lipids. Several experimental studies reveal that antihypertensive agents exert direct effects on triglyceride and cholesterol metabolism. Although the pathophysiological mechanisms and the significance of the alterations of lipid metabolism induced by antihypertensive drugs are not yet clear, the following guidelines for the clinical use of these agents are recommended: (1) before initiating drug treatment in hypertensive patients, blood lipid levels should be measured to exclude a preexisting hyperlipidaemia, (2) during long-term therapy with antihypertensive agents, lipoprotein fractions should be controlled in order to reconsider the therapeutic regime if major alterations of blood lipid levels are observed. [ABSTRACT FROM AUTHOR]

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Copyright of Klinische Wochenschrift is the property of Springer Nature and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Klinische Wochenschrift is the property of Springer Nature and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Klinische Wochenschrift is the property of Springer Nature and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Klinische Wochenschrift is the property of Springer Nature and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Klinische Wochenschrift is the property of Springer Nature and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Klinische Wochenschrift is the property of Springer Nature and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Klinische Wochenschrift is the property of Springer Nature and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Klinische Wochenschrift is the property of Springer Nature and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Klinische Wochenschrift is the property of Springer Nature and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Antineutrophil cytoplasmic autoantibodies (ANCA) specific for constituents of neutrophil primary granules and monocyte lysosomes have been demonstrated in various vasculitic disorders. The staining pattern in indirect immunofluorescence microscopy using alcohol-fixed neutrophils as substrate allows distinction among 3 types of ANCA: 1) classic anti-neutrophil cytoplasmic antibody (cANCA, formerly known as ACPA); 2) a type with a perinuclear/nuclear staining pattern produced when alcohol-fixed neutrophils are used as substrate (pANCA); and 3) a mixture of both of the above types (xANCA, also described recently as pANCA). Most cANCA are directed against proteinase 3 ('Wegener's autoantigen'). Some pANCA have specificity for myeloperoxidase and are associated with idiopathic crescentic glomerulonephritis ('renal vasculitis') and other systemic vasculitides exhibiting a paucity of immune deposits in blood vessels. In addition to being a useful serological marker, ANCA appear to be directly involved in the pathogenesis of systemic vasculitis. ANCA can activate cytokine-primed granulocytes and monocytes to undergo a respiratory burst and degranulation. This effect leads to vasculitis through the attachment of these cells to the vascular endothelium primed by cytokine-induced expression of adhesion molecules (E-LAM 1) on the endothelium. Thus, the release of toxic oxygen radicals and lytic enzymes is capable of causing vascular damage. In the present paper we report on the main target antigens and on the history, nomenclature, laboratory methods, and ethiopathological implication of ANCA. Additional pathophysiological aspects of ANCA and/or autoreactive T cells and immmunoregulatory events are also discussed. [ABSTRACT FROM AUTHOR]

The clinical success of organ transplantation depends to a large degree on the immunological acceptance of the grafted organ. This paper summarizes from an immunological point of view the recent progress that has been made to improve graft acceptance, and discusses some future aspects in the field. Over the last few years, major emphasis has been put on the development of new immunosuppressive drugs, including FK 506, rapamycin, and Deoxyspergualin. Together with monoclonal antibodies against defined T-cell surface antigens, there are now new and effective means available to prevent or treat rejection episodes. Progress has also been made in the field of HLA typing, where the introduction of molecular biology-based methods significantly increased the accuracy of HLA class II typing. The ultimate goal of transplantation immunology is the induction of (donor-) specific tolerance. While some protocols are effective in inducing peripheral tolerance in experimental animals, these regimens are at present not yet applicable in the clinical situation. To overcome the shortage of donor organs, alternative strategies are currently being considered. Among these, xenotransplantation may eventually prove successful, despite the massive immunological problems such as, e.g., the presence of preformed xenoreactive antibodies. [ABSTRACT FROM AUTHOR]

Familial defective apolipoprotein B-100 (FDB) is a recently identified dominantly inherited genetic disorder, which leads to increased serum levels of low density lipoprotein (LDL) cholesterol with reduced affinity for the LDL receptor. This genetic disorder is characterized by defective binding of the apolipoprotein B-100 (apo B-100), which is virtually the sole protein constituent of LDL, to the LDL receptor. The defective binding results from a G to A mutation at amino acid 10708 in exon 26 of the apolipoprotein B (apo B) gene creating a substitution of glutamine for arginine in the codon for amino acid 3500. It is postulated that FDB can exhibit the same clinical features as familial hypercholesterolemia (FH) caused by a defective LDL receptor. The purpose of this paper is to report on an individual with a defective LDL and a defective LDL receptor. The clinical features of this individual were the same as in the family members with either defective LDL or a defective LDL receptor: premature arcus lipoides, tendon xanthomata, and premature atherosclerosis. Although the clinical features were present to the same degree as in individuals with either defect the prognosis and treatment of such an individual could be different. [ABSTRACT FROM AUTHOR]

Synthetic human and ovine corticotropin-releasing hormone (hCRH, oCRH) are commonly used as a diagnostic tool of the hypothalamo-pituitary-adrenal axis. In this paper reports about side effects after various modes of CRH-application are analyzed and compared to our corresponding data of human studies with hCRH and oCRH. Generally, CRH is well tolerated after single administration and interval-application of standard doses, although minor side effects appear sometimes after higher doses (>200 μg hCRH, oCRH) of CRH-bolus-injections. Predominantly the cardiovascular system (e.g. tachycardia, hypotension, flushing) is affected; neuropsychological symptoms are only seen sporadically (e.g. dizziness). Long term continuous infusion (several hours) of low CRH-doses (hCRH, oCRH) are well tolerated but side effects appear (see above) when cumulated doses of 200 μg-300 μg/h are given. Standard doses of hCRH and oCRH are also well tolerated in severely ill patients; it has to be considered that higher doses may provoke marked side effects in persons with neurologic disorders, in subjects with coronary heart disease and in patients with endocrinological disorders of the pituitary-adrenal axis, especially in those subjects in whom the blood-brain-barrier may have been damaged (e.g. head injury, intracranial operation). Single hCRH- and oCRH-bolus-injections in standard doses have a very low rate of complications, 'non-standard' doses should provisionally be used only in clinical studies with well designed safety-precautions. [ABSTRACT FROM AUTHOR]

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Copyright of Klinische Wochenschrift is the property of Springer Nature and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Klinische Wochenschrift is the property of Springer Nature and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Klinische Wochenschrift is the property of Springer Nature and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)