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Biomedical subjects

M Fliegner

Publications and source records attributed to M Fliegner.

4 recordsLinked to original sources

[Antibiotics, purpura and ulcers: a leukocytoclastic vasculitis after clarithromycin].

HISTORY AND CLINICAL FINDINGS: A 47- year-old woman presented with palpable purpura of both lower limbs after taking six tablets of clarithromycin for pneumonia. INVESTIGATIONS: Apart from mild microhematuria there were no other signs of organ involvement. Histology of a skin biopsy revealed a hypersensitivity vasculitis. TREATMENT AND COURSE: A hypersensitivity vasculitis due to clarithromycin was the cause of the purpura. The course of this hypersensitivity vasculitis was severe and protracted over weeks with formation of deep ulcerative skin lesions. CONCLUSION: Clarithromycin may be the cause of a hypersensitivity vasculitis: often the course of the disease is mild, but it may also lead to severe local complications. The diagnosis of hypersensitivity vasculitis can be made in a patient over 16 years of age if there is the combination of a triggering substance, purpura and leukocytoclastic vasculitis. The most important step is immediate withdrawal of the causative agent. A beneficial effect of treatment with steroids on prognosis is not proven.

Anti-Bacterial Agents↗

[17 year old patient with acute abdominal pain, hematochezia and exanthema].

A 17-year old adolescent presented with abdominal pain, petechial lesions, arthralgia, and hematochezia. Abdominal ultrasound showed a suspicious ileocecal region and a lower endoscopy revealed the picture of an ileitis terminalis. The diagnosis of Purpura Henoch Schoenlein was made and confirmed by skin-biopsy showing a leucocytoclastic vasculitis. This case report demonstrates the various clinical symptoms of Purpura Henoch Schoenlein and its clinical course.

Abdominal Pain↗

[Splice site mutations and atherosclerosis: mechanisms and prediction models].

Nucleotide variants in genes of the lipid metabolism influence the risk of premature atherosclerosis. Ten percent of all single nucleotide substitutions in these genes involve splice sites. The effects of these changes on mRNA splicing and phenotypic severity, however, are not inherently obvious from the nucleotide sequence. This review presents various genes of lipid metabolism with splicing mutations known to influence the risk of premature atherosclerosis. Mechanisms of pre-mRNA splicing are illustrated and different models for prediction of the effect of nucleotide substitutions on splice-site function are presented. The role of information theory-based models is emphasized along with its role for prediction of splice-site function and phenotypic severity of atherosclerosis.

Age Factors↗

P-glycoprotein expression in normal and reactive bone marrows.

The expression of mdr1 gene product P-glycoprotein (P-gp) was investigated in 53 normal and reactive bone marrows by means of immunocytochemistry, using the monoclonal antibody (mAb) C219 and the alkaline phosphatase anti-alkaline phosphatase method. In a limited number of patients, data were confirmed by using the mAb MRK16 or a polymerase chain reaction assay for mdr1 gene expression. There was no history of prior chemotherapy or any malignancy in this group. Bone marrow aspirates were obtained as part of a routine diagnostic programme in bone marrow donors or in patients presenting with a variety of diagnoses such as unexplained gammopathy, fever, anaemia, other changes in peripheral blood smear, rheumatoid arthritis, vasculitis, or urticaria pigmentosa. Morphologically the bone marrow was normal in 23 patients, a megaloblastic erythropoiesis was seen in two patients and unspecific changes were seen in 28 patients. Twenty-seven of 53 samples were found to be positive for P-gp expression with the percentage of positive cells ranging from 2%-80% (mean = 24%). With a cutoff point of 10%, five of 23 normal (22%) and 13 of 28 reactive bone marrows (46%) were considered positive for P-gp expression. There was no obvious correlation between diagnosis or age and P-gp expression. Additional staining for the early surface marker CD-34 was performed in 12 samples, with none of them revealing more than 1% positivity. Since P-gp expression has so far been described only in CD-34 positive bone marrow cells, data suggest that P-gp expression may be reinduced in CD-34 negative cells under conditions which remain to be determined.

ATP Binding Cassette Transporter, Subfamily B, Mem↗