PubMed Health⌕ Search

PubMed · 7071172

Sclerous atrophic cellulitis.

Abstract

The author deals only with the sclerous subcutaneous inflammation caused by venous stasis. There is no clear distinction between inflammation, and tissular sclerosis, the final stage of its development. There may be a certain lesional reversibility. The term "scleroinflammatory cellulitis" is therefore quite apt. Physiopathology. Pathology venous reflex results in a flood of proteins in the interstitial tissue, and this shows in signs of tissular pain, especially at the level of the hypoderm and dermis (anatomical reasons). Clinical. This is most often in the case of women with varicose affections or with post-phlebitic syndromes causing a painful, inflamed plaque, on the surface of the inside leg, at the junction of the middle and lower thirds. As well as the inflammation of this area, adhesion to the subjacent layers and induration are also confirmed. Venous dilations may be detected at the centre of this scleroinflammatory plaque. To begin with, the skin is red and taut, but later becomes dry and atrophic. It is prone to eczema and sometimes to ulceration. The development of subcutaneous inflammation is marked by sudden manifestation of inflammation which may be extensive and results in circular suffing, in extreme cases. Varicose sclerosis can provoke sudden manifestations of inflammation and especially if the technique is faulty (excessive dosage, lack of compression, insufficient compression). Treatment. 1. Local. Bandaging and walking are imperative. The bandage must be compressive, immovable, durable, and should be reinforced as necessary at the site of the induration, by latex rubber pads. Once the object of these slightly or non-elastic pads has been achieved they can be replaced by elastic contention. 2. General. Corticoids and phenylbutazone in short courses of treatment. Other products constitute auxiliary remedies. Thermal cures are always indicated in difficult cases. Medical treatment is often enough. In certain perverse cases a surgical treatment may be required, such as hypodermal resection and ligation of the perforants. Grafts (Vigoni). Certain severe cases remain unresponsive to all treatment and in such cases it is regrettable that suitable treatment was not administered at an earlier stage.

Explore related subjects

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

H Chatard. Sclerous atrophic cellulitis.. https://pubmed.ncbi.nlm.nih.gov/7071172/

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related citations

Multiple sclerosis.

Multiple sclerosis (MS) is a demyelinating disease of the central nervous system that commonly leads to inflammatory and atrophic brain pathology, often causing cognitive impairment. MS-associated cognitive impairment was first described over a century ago. However, with the advent of standardized neuropsychological testing and quantitative brain imaging, the frequency, quality, and correlates of cognitive impairment are better understood. Dementia is rare in MS, although it is known to occur in 10 to 25% of patients. Our data suggest a frequency of 22% among clinic attendees. In addition to the cognitive impairments evident in MS dementia, changes in personality and social behavior also occur. For example, some patients develop euphoria sclerotica and marked deficiency in social empathy, conditions that in combination with executive dysfunction cause considerable hardship for patients and caregivers. These neuropsychiatric manifestations of MS dementia are correlated with magnetic resonance imaging indicators of brain atrophy, including ventricle enlargement, neocortical volume, and normalized whole brain volume. Recent developments in pharmacological treatment for disease progression and management of cognitive symptoms hold promise for patients suffering from the degenerative aspects of MS.

Atrophy↗

Inflammation, atrophy, and gastric cancer.

The association between chronic inflammation and cancer is now well established. This association has recently received renewed interest with the recognition that microbial pathogens can be responsible for the chronic inflammation observed in many cancers, particularly those originating in the gastrointestinal system. A prime example is Helicobacter pylori, which infects 50% of the world's population and is now known to be responsible for inducing chronic gastric inflammation that progresses to atrophy, metaplasia, dysplasia, and gastric cancer. This Review provides an overview of recent progress in elucidating the bacterial properties responsible for colonization of the stomach, persistence in the stomach, and triggering of inflammation, as well as the host factors that have a role in determining whether gastritis progresses to gastric cancer. We also discuss how the increased understanding of the relationship between inflammation and gastric cancer still leaves many questions unanswered regarding recommendations for prevention and treatment.

Atrophy↗