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Results for “Capillary Fragility”

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PubMed1982

[Plasmocytoma-associated bullous hemorrhagic amyloidosis of the skin].

Case report of a 70-year-old woman with plasmocytoma-associated bullous "amyloid purpura" and a lambda light-chain IgA paraproteinemia. Cutaneous hemorrhage with blisters, erosions, and milia in the intertriginous areas were the main clinical features. Amyloid deposits in the walls of blood vessels, and the pericollagenous affinity of the amyloid in the dermis are likely to be responsible for the increased capillary fragility, i.e., the hemorrhagic tendency and the infrapapillary blisters. A differentiation from epidermolysis bullosa acquisita and porphyria cutanea tarda is possible by means of the histological level of the blisters.

Aged↗
PubMed1977

A haemorrhagic bullous eruption of the hands caused by phenylbutazone: a report of 3 cases.

Three patients developed a haemorrhagic eruption on the hands after taking phenylbutazone. The reaction appeared within two weeks of taking the drug and is probably an allergic capillaritis. All patients showed generalised capillary fragility with a positive Hess test which became negative within a week of stopping the drug. A mechanism is suggested for the development and distribution of the blisters.

Adult↗
PubMed1997

High-throughput analysis of fragile X (CGG)n alleles in the normal and premutation range by PCR amplification and automated capillary electrophoresis.

Fragile X syndrome is caused by expansion of a (CGG)n trinucleotide repeat within the 5' untranslated region of the FMR1 gene transcript. The disease is reliably diagnosed by Southern blotting, but this method constitutes a significant workload and requires large samples. Therefore, for large research or screening projects in which a large majority of the samples will be normal, a more rapid and less expensive method is needed. We present a method for accurate, high-throughput analysis of the FRAXA (CGG)n region in the normal and premutation range. The method is based on polymerase chain reaction (PCR) amplification of DNA extracted from whole blood or eluted from dried blood spots on filter-paper, followed by automated capillary electrophoresis and detection by multicolour fluorescence. This method allows a throughput of 144 samples in 48 h, with an intra-assay accuracy in size determination of 0.2-1.8 bp. We performed a blind reanalysis of samples from 30 patients, previously analysed by Southern blotting or PCR with radioactive labelling. In this study normal and premutation alleles, ranging from 28-121 (CGG)n repeats, were correctly determined with respect to number of (CGG)n repeats. All full-mutation alleles and one large premutation allele in a sample of a heterozygote failed to amplify. The method was used to determine the distribution of FRAXA (CGG)n repeats in the Danish population.

Alleles↗
PubMed2002

Increased fragility of pulmonary capillaries in newborn rabbit.

The pulmonary capillaries of neonatal lungs are potentially vulnerable to stress failure because of the complex changes in the pulmonary circulation that occur at birth. We perfusion fixed the lungs from nine anesthetized newborn rabbits at capillary transmural pressures (P(tm)) of 5 +/- 5, 10 +/- 5, and 15 +/- 5 cmH(2)O. Normal microscopic appearances were seen at P(tm) values of 5 +/- 5 and 10 +/- 5 cmH(2)O, but massive airway edema was observed in lungs perfused at a P(tm) of 15 +/- 5 cmH(2)O. Consistent with this, no disruptions of the alveolar epithelium were observed at P(tm) values of 5 +/- 5 cmH(2)O, but mean values of 0.11 and 1.22 breaks/mm epithelium were found at P(tm) of 10 +/- 5 and 15 +/- 5 cmH(2)O, respectively (P < 0.05 for 5 +/- 5 vs. 15 +/- 5 cmH(2)O). These pressures are in striking contrast to those in the adult rabbit in which, by a similar procedure, a P(tm) of 52.5 cmH(2)O, is required before stress failure is consistently seen. We conclude that stress failure of pulmonary capillaries in newborn rabbit lungs can occur at P(tm) values of less than one-third of those that are required in adult lungs.

Age Factors↗
PubMed2004

Bleeding and bruising in patients with Ehlers-Danlos syndrome and other collagen vascular disorders.

Easy bruising and bleeding are not only characteristic manifestations of clotting and platelet disorders, they are also prominent features in some heritable collagen disorders, such as the Ehlers-Danlos syndromes (EDS). The EDS comprise a heterogeneous group of connective tissue diseases sharing clinical manifestations in skin, ligaments and joints, blood vessels and internal organs. Most EDS subtypes are caused by mutations in genes encoding the fibrillar collagens type I, III and V, or in genes coding for enzymes involved in the post-translational modification of these collagens. Easy bruising is, to a variable degree, present in all subtypes of EDS, and is because of fragility of the capillaries and the perivascular connective tissues. Vascular fragility affecting medium-sized and large arteries and veins is typically observed in the vascular subtype of EDS, caused by a molecular defect in collagen type III, an important constituent of blood vessel walls and hollow organs. Extensive bruising, spontaneous arterial rupture, leading to severe internal bleeding or premature death, and rupture of hollow organs, such as the intestine or the gravid uterus are predominant features of this subtype. Haematological studies including evaluation of clotting factors, platelet aggregation and bleeding time are usually normal in patients with EDS, except for the Hess test (Rumple-Leede test), which may be abnormal, indicating capillary fragility. In some forms of EDS confirmation of the clinical diagnosis and subtype is possible with biochemical and molecular studies.

Blood Vessels↗