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Biomedical subjects

U Gresser

Publications and source records attributed to U Gresser.

At least 37 records · Page 2Linked to original sources
PubMed1993

Deposits of paraprotein in small vessels as a cause of skin ulcers in Waldenström's macroglobulinemia.

A 71-year-old man presented with epistaxis and large ulcers on arms and legs. A monoclonal IgM-kappa gammopathy and high levels of cryoglobulins were found. Histology of the affected skin showed deposits of paraprotein in the small vessels, causing luminal obstruction. This in turn caused ischemic skin lesions, which were successfully treated with cortisone (fluocortolone 100 mg/day every second day) and cyclophosphamide (100 mg/day).

Aged↗
PubMed1992

Familial synovial chondromatosis combined with dwarfism.

In a family with synovial chondromatosis affecting at least three, presumably five members, the articular disorder was combined with dwarfism. The persons with joint disorders were below the third percentile in body height, but family members with normal articular function had normal height. We believe this to be the first description of a combination of synovial chondromatosis with genetically caused dwarfism.

Adolescent↗
PubMed1991

Muscle metabolism and red cell ATP/ADP concentration during bicycle ergometer in patients with AMPD-deficiency.

6 patients with AMPD-deficiency and 6 control subjects performed exercise on a bicycle ergometer until heart rate was 200 minus age. During exercise the increase of ammonia plasma concentrations was reduced in AMPD-deficient patients compared with that of control subjects. Plasma concentrations of lactate, pyruvate, inosine, hypoxanthine and xanthine increased during exercise in both groups. The concentrations of lactate, inosine and hypoxanthine were lower in AMPD-deficient patients during exercise, the difference was not significant. In AMPD-deficient patients the ATP-concentrations of red blood cells increased during exercise in contrast to control subjects, whereas the ADP amount did not change significantly. Our data suggest that in AMPD-deficient-patients AMP is mainly reduced to adenosine during exercise resulting in decreased ammonia concentrations. The increased concentrations of ATP in red blood cells may be the consequence of increased phosphorylation.

AMP Deaminase↗
PubMed1991

Effects of oral ribose on muscle metabolism during bicycle ergometer in AMPD-deficient patients.

Three patients with AMP deaminase deficiency (AMPD deficiency) performed exercise on a bicycle ergometer with increasing work load without and with administration of ribose (3 g p.o. every 10 min, beginning 1 h before exercise until the end). The patients performed exercise until heart rate was 200 minus age. Maximum capacity was not increased by administration of ribose, but postexertional muscle stiffness and cramps disappeared almost completely in 2 of 3 AMPD-deficient patients. Plasma concentrations of lactate and inosine were increased in AMPD-deficient patients after oral administration of ribose. Our data suggest that ribose may both serve as an energy source and enhance the de novo synthesis of purine nucleotides.

AMP Deaminase↗
PubMed1991

[Indications for sonography and follow-up studies. Initial results of a prospective study].

Ultrasonic examinations of the abdomen may result in expensive secondary imaging examinations. This prospective study was conducted in collaboration with the Zentralinstitut Köln. The first aim of our study was to compare the results of abdominal sonography in three different patient groups: The first group was comprised of patients referred for a medical check-up, the second group of patients referred because of upper abdominal pain and the third group of patients with generalized atherosclerosis. The second aim was to correlate sonographic findings (classified in three degrees of severity), with subsequently induced diagnostic procedures in the three groups. 2719 patients were enrolled, 2393 (88%) in group 1, 286 (11%) in group 2 and 40 (1%) in group 3. A total of 1792 abnormal findings were diagnosed. 65.6% of the findings in group 1, 65.7% in group 2 and 88% in group 3 were abnormal. Up to now, the findings led to a nearly equal number of subsequent diagnostic procedures in groups 1 and 2. The preliminary results show that abdominal sonography may be as effective in patients for a check-up as in patients referred because of a well-defined indication. Patients with defined abdominal symptoms show more abnormal sonographic findings than patients on a check-up. Higher costs resulting from subsequent examinations deserve critical assessment in the individual patient.

Abdomen↗
PubMed1990

Identification of a splice mutation at the adenine phosphoribosyltransferase locus in a German family.

We examined the molecular basis of adenine phosphoribosyltransferase (APRT) deficiency in homozygous-deficient, identical twin brothers who were born to non-consanguineous German parents. DNA was isolated from blood, and the APRT gene was amplified by PCR, subcloned into M13, and sequenced completely. A single T insertion between bases 1831-1832 or 1832-1833 was identified. This alters the consensus sequence at the exon 4 - intron 4 spice donor site and leads to aberrant splicing. The same mutation has been described previously in two affected brothers from Belgium, and the Indianapolis group has also identified it in two other, unrelated Caucasian patients. Thus, this mutation may be a common cause of APRT deficiency in the Caucasian population.

Adenine Phosphoribosyltransferase↗
PubMed1990

Uric acid levels in southern Germany in 1989. A comparison with studies from 1962, 1971, and 1984.

Since 1962 our group has performed four studies on uric acid values in blood donors in southern Germany (Bavaria). Uric acid levels in men have increased over the years, from 4.86 mg/dl in 1962 to 6.00 mg/dl in 1971, 5.60 mg/dl in 1984, and 5.90 mg/dl in 1989. Levels in women have increased slightly, from 4.05 mg/dl in 1962 to 4.35 mg/dl in 1971, 4.10 mg/dl in 1984, and 4.16 mg/dl in 1989. Women aged 51 to 60 years had significantly higher uric acid levels than those in the fourth decade. In women treated with oral contraceptives uric acid levels were significantly lower than in other women of the same age. Hypouricemia (uric acid levels less than or equal to 2.0 mg/dl) was observed in three women, none of whom had a history of medication. Hyperuricemia exists when uric acid levels are greater than or equal to 6.5 mg/dl. In 1989 2.6% of the female blood donors and 28.6% of the males were hyperuricemic, with an increased risk of gout, nephrolithiasis, and nephropathy.

Adult↗
PubMed1990

[Hyperuricemia--does modern therapy improve life expectancy?].

Today hyperuricaemia and gout are likewise seen in every population of the western industrial world and have been increasing since the fifties. As known from number of studies hyperuricaemia often occurs in connection with hyperlipoproteinaemia, obesity, diabetes mellitus, arterial hypertension and atherosclerosis. Up to now it was not clear whether one disease caused the other. In 1988 Abbot could prove that among men, those afflicted by gout as compared to those without gout experienced a 60% excess of coronary heart disease. Therefore, patients with gout should receive a regular thorough cardiovascular evaluation. Furthermore risk factor levels which predispose to coronary heart disease, arterial hypertension and gout should be reduced. There is a significant positive correlation between the plasma uric acid levels and the prevalence of attacks of gouty arthritis and nephrolithiasis. It is possible to avoid gouty arthritis, tophi and nephrolithiasis with a consequent diet and medical treatment. Unfortunately, many patients interrupt therapy during intervals free of pain. The consequence is that even today the complications of hyperuricaemia cause days of inability to work and to earn one's living, despite of modern therapy. Hyperuricaemia not sufficiently treated reduces the quality of life through attacks of gout, chronic gout and nephrolithiasis as well as life expectancy caused by nephropathy, arterial hypertension and atherosclerosis. This is of special importance because of the frequency of gout and hyperuricaemia in our population. An early diagnosis, a consistent therapy and a thorough monitoring could stop an increase of this disease and prolong life expectancy for those who have gout and the other attendant diseases.

Cause of Death↗
PubMed1990

Variation of benzbromarone elimination in man--a population study.

The plasma benzbromarone concentration-time profile in a healthy subject who retained the compound much longer than other individuals is described. The data suggested that determination of the 24 h plasma concentration of the parent drug after a single oral dose of 100 mg benzbromarone would be an appropriate procedure to determine the elimination phenotype. Based on this procedure, 148 of 153 healthy individuals (97%) in a population study were found to eliminate benzbromarone rapidly. In one subject the 24 h benzbromarone plasma concentration was very similar to that observed in the individual who had been more fully characterized. Four participants gave intermediate results. The data are compatible with a bimodal or trimodal distribution of different benzbromarone elimination phenotypes.

Adult↗