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Biomedical subjects

D Berg

Publications and source records attributed to D Berg.

At least 145 records · Page 8Linked to original sources

Vancomycin-associated linear IgA dermatosis. A report of three cases.

BACKGROUND: Linear IgA dermatosis is an autoantibody-mediated, subepidermal blistering disease that is rarely associated with drug exposure. OBJECTIVE: We report the development of linear IgA dermatosis in three patients associated with the administration of vancomycin and further characterize the immunopathology. METHODS: Direct and indirect immunofluorescence assays were performed to characterize the immunoreactants, determine the subclass of the IgA deposits, and map the site of antibody deposition. RESULTS: A subepidermal blistering disease developed in all patients shortly after vancomycin was initiated, which resolved on discontinuation of the drug. Immunofluorescence studies revealed linear deposits of IgA1 only at the basement membrane zone, below the lamina lucida. Circulating IgA anti-basement membrane zone antibodies were not detected. CONCLUSION: Three patients had linear IgA dermatosis in association with the administration of vancomycin. All patients had linear deposits of IgA1 localized to the sublamina densa zone. Immunophenotypically, the disease in these patients mimics the pattern of IgA deposits seen in the majority of patients with idiopathic linear IgA dermatosis.

Aged↗

Interleukin 10: an overview.

Since the original description of interleukin-10, a wealth of information concerning its biological properties has been gathered. Studies in vitro have rapidly identified both immunostimulatory and immunosuppressive activities for IL-10. Based on these findings, in vivo studies were initiated in a variety of animal disease models to assess the importance of these activities. This review will summarize the pleiotropic properties of IL-10 and will survey current research regarding the potential of IL-10 to regulate acute and chronic inflammatory reactions.

Animals↗

Lyme disease in children: diagnosis, treatment, and prevention.

Lyme disease is a multisystem disorder that is caused by infection with Borrelia burgdorferi. In endemic areas, its occurrence is extremely common among children. The early diagnosis and treatment of Lyme disease may prevent the development of serious cardiac, rheumatological, and neurological sequelae. For this reason, a full understanding of the clinical manifestations, laboratory evaluation, and antibiotic therapy of Lyme disease is of vital importance.

Animals↗

Concomitant evaluation of efficiency, acute and delayed toxicities of combined treatment of radiation and CDDP on an in vivo model.

The efficiency, acute and delayed toxicities of different radio-chemotherapeutic combinations were assessed on an in vivo model (Krebs II ascitic carcinoma grafted to female Swiss mice). Mice were given whole abdomen irradiation (WAI) 2.5 to 10 Gy as a single dose (WAI). CDDP was given intraperitoneally at 0.5 to 4 mg/kg dose level, 12 hr before or after WAI. There was a relationship between dose of CDDP and increase of life span (ILS) of mice. However, WAI did not increase the life span. When a single dose of 2 mg/kg CDDP was given prior to a 2.5 Gy WAI, the ILS reached 47%. By contrast, it was only 37% when treatment sequence was reversed. When the WAI dose level was increased to 5 Gy, the ILS was not increased. The jejunal crypt cell number, determined 3 days after the last treatment, was not modified, regardless of the treatment sequence. There was no delayed renal toxicity. The study on the Krebs II ascites model confirms the tumor cell therapeutic potentiation without exacerbation of normal tissue damage.

Animals↗

Simultaneous administration of granulocyte-macrophage colony-stimulating factor and cytosine arabinoside for the treatment of relapsed acute myeloid leukemia.

The treatment of patients with relapsed or refractory acute myeloid leukemia (AML) with high dose cytosine arabinoside (ara-C) results in short-lived complete response rates of 30-50%. We have previously shown that entry of myeloid leukemic cells into S phase can be accelerated in vitro through the use of recombinant human granulocyte-macrophage colony-stimulating factor (rhGM-CSF), resulting in enhancement of ara-C-mediated cytotoxicity. In order to evaluate the in vivo biological and clinical effects of this strategy in patients with high risk AML, we treated three patients with either refractory or relapsed disease with a continuous infusion of rhGM-CSF (0.45 micrograms/kg/h aglycoprotein) for 18 h, followed by the institution of high dose ara-C and continuation of rhGM-CSF throughout the 4 day duration of ara-C treatment. Prior to therapy, no patient had detectable levels of circulating rhGM-CSF, and there was no evidence of GM-CSF receptor occupancy in leukemic myeloblasts. After 18 h of rhGM-CSF therapy, all patients had biologically active levels of circulating rhGM-CSF (7.9-12.0 ng/ml), and two patients showed a significant degree of leukemic GM-CSF receptor occupancy without evidence of GM-CSF receptor down-regulation. A significant rise in the S phase fraction of leukemic myeloblasts was observed at 18 h of rhGM-CSF treatment in all three patients (29-56% increment). The toxicity of combined rhGM-CSF/ara-C therapy included pericarditis and cerebellar degeneration in one patient, fever and mild renal dysfunction in two patients, and mild hepatic dysfunction in all three patients. Each patient showed a transient rise in the absolute neutrophil and blast count during rhGM-CSF/ara-C administration, followed by profound, but clinically tolerable, myelosuppression. No patient developed clinical evidence of leukostasis. There was one death related to pericardial tamponade, one death related to refractory disease, and one clinical and cytogenetic remission. These results suggest that exogenously administered rhGM-CSF is capable of rapidly mobilizing leukemic cells into S phase in vivo and theoretically should be useful in overcoming kinetic resistance to ara-C. Clinical trials of this regimen in patients with high risk AML who are not already pharmacologically resistant to ara-C are warranted.

Acute Disease↗

The laboratory diagnosis of Lyme disease.

Growing awareness of Lyme disease, caused by the tickborne spirochete Borrelia burgdorferi has led to a marked increase in laboratory procedures to help in its diagnosis. Despite the frequent ordering of serologic tests specific for Lyme disease, there remains confusion in the accurate interpretation of these tests. Because of the important cutaneous manifestations of B burgdorferi infection, dermatologists should understand the role of the laboratory in Borrelia-related conditions. This article reviews laboratory techniques available for the diagnosis of Lyme disease. The role of histologic findings and culture, the sensitivity, specificity, and reproducibility of commonly used serologic tests, the effects of disease duration and treatment on serologic results, and the future of laboratory diagnosis are described.

False Positive Reactions↗

[Venous constriction by local administration of ruscus extract].

The venoconstrictive action of the topical application of Ruscus extract was evaluated in a randomized, double-blind study involving 18 healthy volunteers, using duplex B-scan ultrasonography. Within 2 1/2 hours of the application of 4 to 6 g of a cream containing 64 to 96 mg Ruscus extract, the diameter of the femoral vein decreased by an average (median) of 1.25 mm, while placebo (base of the cream) was associated with a diameter increase of 0.5 mm (means) (p = 0.014). The decrease in venous diameter reflects good percutaneous absorption of the active substance. To date, venoconstrictive action has been demonstrable only indirectly with the aid of plethysmographic methods; it has now been measured directly under orthostatic conditions.

Administration, Topical↗

Comparative study of the incorporation of ellipticine-esters into low density lipoprotein (LDL) and selective cell uptake of drug--LDL complex via the LDL receptor pathway in vitro.

Esters of elliptinium with stearic (ST-NME), palmitic (PAL-NME) or oleic (OL-NME) acids, a series of lipophilic derivatives of ellipticine, were synthetized, in order to evaluate their incorporation into Low Density Lipoprotein (LDL). Among the three derivatives, OL-NME shows the most potent incorporation (83 micrograms/mg protein LDL) compared to ST-NME (37 micrograms/mg protein LDL) and PAL-NME (58 micrograms/mg protein LDL). The size of OL-NME-LDL was determined by size distribution particles, showing their homogeneity compared to native LDL. When culture normal human fibroblasts were incubated with [125I]LDL incorporated drug, they bound to the LDL receptor with the same affinity as native LDL and were internalized and degraded intracellularly. The presence of excess native LDL inhibited the cellular uptake and degradation of [125I]drug-LDL. We have used [125I]acetyl-LDL as a probe for a binding site on macrophages that mediated the uptake and degradation of chemically altered or denatured LDL. Mouse peritoneal macrophages were shown to take up and degrade [125I]acetyl-LDL at rates that were greater than those for the uptake and degradation of native [125I]LDL and [125I]drug-LDL. The in vitro cytotoxic test on L1210 murine leukemic cells demonstrated that the complex was cytotoxic and was more effective than the free drug. This cytotoxic activity of the drug-LDL complex depends on the LDL high affinity receptor since the addition of native LDL reduces the killing power. In contrast, methylated LDL, which does not bind to the LDL receptor, has no effect on it. We conclude that it is possible to incorporate a large amount of cytotoxic drug into LDL without modifying their cellular metabolism via the high affinity LDL receptor pathway. It indicates also that the delivery of lipophilic drugs using LDL might provide distinct advantages over the use of synthetic carriers.

Alkaloids↗

Studies on the ascorbic acid metabolism of callitrichid monkeys by 14C isotope excretion technique.

Recently it has been found that the two monkey species Callithrix jacchus and Saguinus fuscicollis, both belonging to the same New World monkey family Callitrichidae and held in the same colony under identical conditions, had extremely different serum ascorbate levels. To examine the ascorbic acid metabolism the 14C-excretion of orally given 1-14C-ascorbic acid was studied under conditions of marginal and abundant vitamin C supply and under intentional stress. There were large differences in the mode of 14C excretion between low and high ascorbate supply. The differences were smaller between stress/no stress conditions intraindividually than between the two species, but they were in the same manner. In comparable trials S. fuscicollis reacted such that a higher status of stress can be supposed in this species.

Animals↗

[Ultrasound of the knee joint: normal values and changes in rheumatoid arthritis].

The bursa suprapatellaris, infrapatellaris, the patella tendon, condylar cartilage, menisci and fossa poplitea were examined sonographically in 56 healthy persons in defined sections. References for normal findings are given. The examination of 22 patients with rheumatoid arthritis revealed joint effusions, Baker cysts, synovial hypertrophy, intraarticular septae and changes in the echogenicity of the synovial fluid.

Adult↗

Sweating in ectodermal dysplasia syndromes. A review.

Ectodermal dysplasia syndromes are currently classified based on constellations of clinical features, a major one of which is the presence or absence of normal sweating. The evaluation of sweating in these disorders has not been performed in a standardized manner, as is shown here in this literature review of a sampling of ectodermal dysplasia syndromes. Accurate evaluation of sweating is important not only in enabling more effective diagnosis and classification of patients with these syndromes, but also in aiding genetic counseling by potential detection of carrier states. A review of the variety of sweat tests currently in use is presented.

Ectodermal Dysplasia↗