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Biomedical subjects

R Dreher

Publications and source records attributed to R Dreher.

At least 19 recordsLinked to original sources
PubMed2006

[Insufficiency fractures in rheumatology. Case report and overview].

Stress fractures occur as insufficiency fractures, with a prevalence of 0.8% in patients with rheumatological illness. The main sites of insufficiency fractures are the pelvis and sacrum, parts of the tibia and fibula that are close to the joints, and the calcaneus and hip. Since the painful symptoms overlap with the clinical picture of the painful joint diseases and because of the low sensitivity of conventional diagnostic X-ray, insufficiency fractures are not diagnosed directly or their diagnosis is delayed. The high sensitivity of computer tomography, skeletal scintigraphy and nuclear magnetic resonance imaging should be exploited in the diagnosis of insufficiency fractures. The case report presented describes insufficiency fractures of the distal right tibia and fibula in an elderly female patient with rheumatoid arthritis being treated with long-term glucocorticoids. In addition to advanced age, female gender, immobility and rheumatoid arthritis requiring long-term cortisone, there are further risk factors for insufficiency fractures: fluoride treatment over many years in the past, hypovitaminosis D3, renal failure. The DXA bone density values of the neck of the femur and the lumbar vertebrae do not show any osteoporosis, and the calcium concentration in the serum is low; phosphate is raised and parathormone is normal; osteocalcin, beta crosslaps and alkaline phosphatase are raised. Bone biopsy specimens taken from the iliac crest and the proximal femur and investigated for the purpose of differential diagnosis revealed renal osteopathy with secondary hyperparathyroidism and osteomalacia. In elderly patients with kidney failure, the possibility of renal osteopathy must be considered as the possible cause of reduced bone quality with a raised risk of insufficiency fractures, even when the parathormone levels are normal. In view of the frequency of osteopathies in rheumatological patients, osteology is of enormous significance in rheumatology.

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PubMed2004

[Specialties in therapy of osteoporosis in inflammatory joint disease].

The therapeutic specialties of osteoporosis in inflammatory rheumatic diseases has gained mounting interest in the last year. The paper describes special aspects of osteoporosis in rheumatoid arthritis, ankylosing spondylitis and systemic lupus erythematodes. The problems of glucocorticoid therapy are discussed intensively with regard to the recently published recommendations for glucocorticoid-induced osteoporosis. Risk factors of osteoporosis and the therapeutic implications are demonstrated intensively as well as the modifications of the recommendations.

Arthritis, Rheumatoid↗
PubMed2000

[Osteoporosis in the male].

BACKGROUND: Osteoporotic fractures occur frequently also in men. Epidemiologic data from Germany indicate that more than 900,000 men are affected by osteoporotic fractures. Diagnosis and therapy of male osteoporosis are hampered by a lack of clinical studies. DIAGNOSIS: Risk factor analysis, conventional spine X-rays, bone densitometry and a limited number of serum and urine analyses contribute to the diagnosis of osteoporosis and the assessment of future fracture risk. Bone densitometry at the femoral neck is superior to measurements at the lumbar spine because of the high prevalence of degenerative changes at the lumbar spine in elderly men. Major risk factors for osteoporosis are hypogonadism, glucocorticoid therapy, hypercalciuria, gastrointestinal disease, and high alcohol consumption. In individual cases, bone histology or additional biochemical studies are needed to establish the cause of osteoporosis. THERAPY: Calcium and vitamin D deficits should be substituted both in prevention and treatment of male osteoporosis. Testosterone replacement therapy is effective in hypogonadism. In primary osteoporosis and in corticosteroid-induced osteoporosis, bisphosphonates (cyclical etidronate, alendronate) and fluorides are therapeutic options. CONCLUSION: Important principles in the care of men with osteoporosis are the transfer of knowledge established for postmenopausal osteoporosis and the rigorous search for secondary osteoporosis aiming at treatment of the underlying cause. Large prospective randomized trials aiming at the reduction of fracture rate in male osteoporosis are missing. They are urgently needed.

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PubMed1997

Insufficiency and stress fractures of the long bones occurring in patients with rheumatoid arthritis and other inflammatory diseases, with a contribution on the possibilities of computed tomography.

In patients with long standing rheumatoid arthritis and other rheumatoid disorders, stress fractures and insufficiency fractures are not uncommon. The cause may be osteoporosis due to rheumatoid arthritis, corticosteroid therapy, joint stiffness, and deformity of the joints caused by the inflammatory process. Also, unaccustomed exercise after reconstructive joint surgery may be a cause of fractures in these patients. Fractures can be documented on conventional X-ray-pictures and tomograms. Computed tomography can show the medullary extent of these fractures and gives, in several cases, additional information showing the combination of insufficiency fractures with fragmentations of parts of the involved bone. Reconstructive surgery with total joint replacement may be another cause of the development of these fractures. This unaccustomed increase in ambulation may lead to stress fractures in other joints of the same extremity or of contralateral extremity. Pain beginning in joint of the lower extremity in a patient with chronic rheumatoid arthritis should, besides arthritis, raise the possibility of a stress fracture. Also with cases of angular deformity of a joint and unaccustomed exercise after reconstructive surgery patients stress fractures may be seen and can be established by Plainfilm, Computed Tomography scintimetric bone scanning and MRI.

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PubMed1990

Traditional and new types of spondarthritis with special consideration of spondylodiscitis.

In rheumatology the so-called "seronegative spondarthritis" is a group of diseases characterized by the presence of HLA-B 27. This group includes the typical ankylosing spondylitis as well as atypical spondylopathies such as those occurring in psoriasis, Reiter's disease and chronic inflammatory enteropathies, which attack mainly the spine and secondarily the peripheral joints. In some severe cases, non-infectious, sterile spondylodiscitis was observed. These can lead to instability and fracture, followed by pseudarthrosis of the involved segment of the spine. In contrast to these traditional spondarthritides three new types are marked by the lack of HLA-B 27. 1) "Spondarthritis hyperostotica pustulo-psoriatica" (F. Schilling), a very rare variation of psoriatic spondylopathy, sometimes accompanied by spondylodiscitis. 2) Arthritis and spondarthritis in acne fulminans. 3) Destructive arthropathy and spondylopathy in long-term hemodialysis, occasionally occurring with spondylodiscitis, a very new type of spondarthritis. The amyloid B (beta-2-micro-globulin), discovered only four years ago, plays a dominant role in the pathogenetic chain of this disease. Details of the etiology of these very impressive diseases are presented. Destructive spondylodiscitis will no doubt be a challenge to neurosurgeons.

Acne Vulgaris↗
PubMed1987

The association reaction of yeast alcohol dehydrogenase with coenzyme is partly diffusion-controlled in solvents of increased viscosity.

The steady-state kinetics of the yeast and liver alcohol dehydrogenase catalyzed reduction of aldehydes were examined in solvent mixtures of increased viscosity. This was done to investigate the effects of diffusion control on the fast association of NADH with the enzymes. Both glycerol and sucrose were unsatisfactory as viscosogens, as they inhibited the enzyme, but poly(ethylene glycol)/water mixtures were satisfactory. The 5-fold faster reaction of yeast alcohol dehydrogenase with NADH is partly diffusion controlled, whereas the slower liver alcohol dehydrogenase reaction showed no diffusion effects. These results are consistent with a yeast alcohol dehydrogenase active site that has relatively little steric hindrance to NADH binding. It is estimated that contributions to this association reaction from diffusion control and chemical activation control are equal at a solvent viscosity of 10 cP. Thus, under physiological conditions of increased viscosity the NADH association may be significantly affected by diffusion effects. In order to estimate accurately the maximum diffusion-controlled rate constant from diffusion theory, the diffusion coefficients of NADH were measured in poly(ethylene glycol)/water mixtures and were found to vary inversely as the solvent viscosity raised to the power of 0.5. The non-Stokesian behaviour of molecules as large as NADH in polymer/water mixtures may be a serious limitation to the routine use of poly(ethylene glycol) as a viscosogen for diffusion studies.

Alcohol Dehydrogenase↗
PubMed1986

[Pathogenesis and therapy of rheumatoid inflammation].

By initial 3H-thymidine labelling an enhanced monocyte proliferation in the bone marrow of patients with rheumatoid arthritis is demonstrated. The significant monocyte proliferation correlates positively with the erythrocyte sedimentation rate but shows a negative correlation with age. The high significance of the mononuclear phagocyte (MNP) system in the pathogenesis of rheumatoid arthritis is seriously underlined by the experimental findings in our allergic arthritis model. Benoxaprofen as an inhibitor of the lipoxygenase pathway and of the inflammatory monocyte influx significantly suppresses the experimental allergic synovitis. These findings stress upon the important role of the MNP-system in the pathogenesis of rheumatoid arthritis and demonstrate the significance of the monocytes/macrophages as an important target-cell system for antirheumatic drugs.

Adolescent↗
PubMed1985

Functional domains of colicin M.

The structure of colicin M of Escherichia coli was studied with regard to its organization into functional domains. A proteolytic fragment with an Mr of 24,000 was isolated which comprised the carboxyterminal portion of the protein. It adsorbed to the outer membrane receptor protein and inhibited killing of cells by colicin M and by phage T5 that uses the same receptor. The fragment killed cells when the outer membrane was rendered permeable to macromolecules for a short time by the osmotic shock procedure. It is concluded that the fragment contains the receptor binding site and the active center but is lacking the sequence required for transport into cells. The carboxy-terminal amino acid sequence-Lys-Arg of the fragment was identical to that obtained from colicin M. Release of lysine and arginine led to inactivation of colicin M. The sequence of the first 39 amino acids of the amino terminal end of colicin M was determined.

Amino Acid Sequence↗
PubMed1983

[Immunomodulation with symptomatically effective antirheumatic agents].

As antigen-presenting and/or monokine-secreting cells, macrophages play a major role in immunoregulation. Proteases of macrophage origin (cathepsin G, elestase , thrypsin and pronase) act on cell surfaces of different cell lines, inducing cell activation, e.g. of B-lymphocytes. T-lymphocytes might be stimulated by the activating factor LAF. Other macrophage products (CSF, FIM ) control monocyte production in bone marrow. While lymphocytes are the target cell lines for classical immunosuppressive agents, mononuclear phagocytes are kept for the major cell population affected by antiinflammatory drugs. The presented study outlines the significance of the mononuclear-phagocyte-system in antiinflammatory drug research. The inhibiting potency of antiinflammatory drugs on the monocyte-macrophage cell line as an additional immunoregulatory principle should be discussed.

Animals↗
PubMed1983

[Immunomodulation by symptomaticly active antirheumatic agents].

As antigen-presenting and/or monokine-secreting cells, macrophages play a major role in immunoregulation. Proteases of macrophage origin (cathepsin G, elestase, thrypsin and pronase) act on cell surfaces of different cell lines, inducing cell activation, e.g. of B-lymphocytes. T-lymphocytes might be stimulated by the activating factor LAF. Other macrophage products (CSF, FIM) control monocyte production in bone marrow. While lymphocytes are the target cell lines for classical immunosuppressive agents, mononuclear phagocytes are kept for the major cell population affected by antiinflammatory drugs. The presented study outlines the significance of the mononuclear-phagocytesystem in antiinflammatory drug research. The inhibiting potency of antiinflammatory drugs on the monocyte-macrophage cell line as an additional immunoregulatory principle should be discussed.

Animals↗
PubMed1982

Origin of synovial type A cells during inflammation. An experimental approach.

Antigen-induced hypersensitivity arthritis in guinea pigs leads to histopathological changes in the synovial membrane similar to those seen in rheumatoid arthritis. Until recently, the characteristic lining-cell hyperplasia was believed to be mainly due to proliferation of synoviocytes. The validity of this hitherto predominating concept might be refused by our experimental cell-kinetic data, which demonstrate a pronounced participation of cells of the bone marrow-derived mononuclear phagocyte system in inner multilayer formation of the inflamed synovium. This view of the response of the synovium as a bone marrow-dependent reaction is strongly supported by whole-body irradiation experiments, which indicated that hyperplasia of the lining cell of the synovium is absent in animals with an induced cell depletion of the bone marrow.

Animals↗
PubMed1981

Structural and functional properties of colicin M.

Colicin M of Escherichia coli Cl139 was isolated in pure form. It consisted of a single polypeptide with a molecular weight of 27,000 +/- 2,000. Colicin M lysed sensitive cells of E. coli but had to act continuously up to the point when lysis commenced (after 20 min). Colicin M was largely resistant to hydrolysis by trypsin except when adsorbed to cells. Within 4 to 5 min after addition of colicin M, cells could be rescued by trypsin or sodium dodecyl sulfate. Later, colicin M was apparently inaccessible to these inactivating agents. Killing of cells by colicin M required Ca2+ ions. Cells could be rescued with ethylene glycol-bis(beta-aminoethyl ether)-N,N'-tetraacetate (EGTA) immediately before the onset of lysis. Under these conditions, colicin M remained bound to the cells, and it became again sensitive to trypsin. We conclude that under the influence of EGTA colicin M is removed from its site of action and becomes again accessible to trypsin at the cell surface.

Calcium Chloride↗
PubMed1981

Significance of cell kinetic studies in experimental allergic arthritis: participation of monocytes in injury and recovery of the inflamed synovial membrane.

Experimental allergic arthritis in guinea pig has been investigated as a model of immunosynovitis. The course of synovial injury and recovery is quantitatively estimated by microscopic and autoradiographic evaluation. Using 3-H-thymidine pulse and prelabeling techniques it has been shown, that bone marrow derived monocyte-macrophage cells play a major role in the histopathogenesis of this form of arthritis. Cell kinetic studies during the initiation of experimental synovitis support the hypothesis, that so-called lining cell hyperplasia is predominantly due to infiltration by blood monocytes, which during the stage of recovery contribute to a secondary lining cell layer. The early bone and cartilage erosions are additional lesions, which appear to be dependent on the monocyte-macrophage system.

Animals↗
PubMed1981

[Histological classification of rheumatoid synovitis compared with cell-kinetics and morphology of experimental immune synovitis (author's transl)].

During the course of the experimental immune arthritis of the guinea pig four phases can be distinguished: I=fibrinopurulent, partly ulcerative synovitis, II=granulocytic activee granulomatous synovitis, III=lymphocytic activ granulomatous synovitis, IV=synovitic sequelae with subintimal fibrosis. On the basis of cell-kinetic studies with initial and systemic labelling with 3H-thymidine of the synovial membrane and of the bone marrow it could be demonstrated that in this model the infiltrating cells as well as the structural cells belong to the monocyte-macrophage system. The typical multilayer of the lining cells of this immune synovitis therefore seems to be mainly as a type A cell hyperplasia of bone marrow derived cells instead of a local proliferation of the lining cells. Clinical cases of various joint diseases are described including symptoms, X-ray findings and histopathological studies. Depending on the stage of the clinical course and the number, localization and activity of the macrophages within the synovial membrane the reaction pattern can be classified in a new way using the categories mentioned above in the experimental model. Thus the classical picture of rheumatoid arthritis corresponds to the synovitis of the subintimal type. The polyarthritic syndrome which mostly is pathogenetically unclear in contrast is designated as synovitis of the intimal type. The same holds true for the activated arthrosis.

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