Development Of Skin Ulcers Research Articles

Prostatic Infarction Involving the Urinary Sphincter, an Association with Pyoderma Gangrenosum

A 70-year-old man presented with haematuria and restrictive urinary symptoms 7 years after a transurethral prostatectomy (TURP). Onset of symptoms coincided with development of a large skin ulcer on his back. A diagnosis of pyoderma gangrenosum was made based on clinical signs and histopathology. On repeated cystoscopy the urethral sphincter was obliterated by necrotic tissue, suspicious for malignancy. Histopathology revealed only necrotic tissue consistent with infarction of the prostate and sphincter. This clinical presentation with infarction of the prostate and sphincter, concurrent with development of skin ulcers, was consistent with pyoderma gangrenosum affecting the prostatic urothelium and sphincter. Previous prostatic surgery may have predisposed our patient to development of pyoderma gangrenosum in the area of the prostate.

Protection against experimental Aeromonas salmonicida infection in carp by oral immunisation with bacterial antigen entrapped liposomes

Liposome-entrapped atypical Aeromonas salmonicida antigen was prepared to investigate the potential protective efficacy for A. salmonicida infection. Carp ( Cyprinus carpio) were immunised orally with liposome-entrapped A. salmonicida antigen. After immunisation, significantly higher antigen-specific antibodies were detected in serum, intestinal mucus and bile than non-immunised control group. Furthermore, immunised carp were challenged by immersion with 1 × 10 6 cfu ml −1 of A. salmonicida for 60 min. Of the eight non-immunised carp, three carp died (62.5% survival), whereas five out of six (83.5%) immunised survived. Furthermore, the development of skin ulcers was significantly inhibited in carp immunised with liposomes containing A. salmonicida antigen. These results suggest that liposomes containing A. salmonicida antigen have the potential for the induction of a protective immune response against atypical A. salmonicida infection and also suggest the possibility of developing a vaccine that may ultimately be used for the prevention of fish diseases.

Cutaneous ulceration caused by methotrexate

Methotrexate has been associated with the development of skin ulceration in small numbers of patients with psoriasis. We describe a 58-year-old man with a 15-year history of plaque-type psoriasis. He had been treated with methotrexate therapy (15 mg orally per week for 32 weeks) and had ulcers develop within psoriatic plaques on both elbows, on the mucosal aspect of the lower lip, and in an appendectomy scar on the right lower quadrant of the abdomen. Ulcers healed upon discontinuation of methotrexate, but the scar eroded again upon reintroduction of methotrexate.

Skin ulcers in fish: Pfiesteria and other etiologies.

Skin ulcers on fish are one of the most well-recognized indicators of polluted or otherwise stressed aquatic environments. In recent years, skin ulcer epidemics have been either experimentally or epidemiologically linked to exposure to a number of xenobiotic chemicals as well as to biotoxins. Some of these agents, such as toxins produced by the dinoflagellate alga Pfiesteria, have led to serious concerns about the health of aquatic ecosystems, such as estuaries along the east coast of the United States. However, a number of other risk factors besides Pfiesteria have been shown to damage epithelium and may also play important roles in skin ulcer pathogenesis. In addition, increasing evidence indicates that not only may skin damage occur via direct contact with toxins, but it may also be induced indirectly from physiological changes that result from exposure not only to toxins but also to other environmental stressors, such as pH and temperature extremes. The multifactorial pathways that operate at both the ecological and the organismal levels as well as the nonspecific response of the skin to insults make it very challenging to link epidemic skin ulcers to any single cause in natural aquatic populations. Consequently, using pathology to unequivocally identify the specific cause of a lesion (eg. Pfiesteria exposure) is not a valid approach. Only with an increased understanding of the basic mechanisms leading to skin damage (including development of specific biomarkers for specific toxins), along with a better understanding of ecological processes operating in these environments, will we be able to discern the relative importance of various risk factors in skin ulcer development.

Targeted gene disruption demonstrates that P-selectin glycoprotein ligand 1 (PSGL-1) is required for P-selectin-mediated but not E-selectin-mediated neutrophil rolling and migration.

P-selectin glycoprotein ligand 1 (PSGL-1) is a mucin-like selectin counterreceptor that binds to P-selectin, E-selectin, and L-selectin. To determine its physiological role in cell adhesion as a mediator of leukocyte rolling and migration during inflammation, we prepared mice genetically deficient in PSGL-1 by targeted disruption of the PSGL-1 gene. The homozygous PSGL-1-deficient mouse was viable and fertile. The blood neutrophil count was modestly elevated. There was no evidence of spontaneous development of skin ulcerations or infections. Leukocyte infiltration in the chemical peritonitis model was significantly delayed. Leukocyte rolling in vivo, studied by intravital microscopy in postcapillary venules of the cremaster muscle, was markedly decreased 30 min after trauma in the PSGL-1-deficient mouse. In contrast, leukocyte rolling 2 h after tumor necrosis factor alpha stimulation was only modestly reduced, but blocking antibodies to E-selectin infused into the PSGL-1-deficient mouse almost completely eliminated leukocyte rolling. These results indicate that PSGL-1 is required for the early inflammatory responses but not for E-selectin-mediated responses. These kinetics are consistent with a model in which PSGL-1 is the predominant neutrophil P-selectin ligand but is not a required counterreceptor for E-selectin under in vivo physiological conditions.

Historical perspective: the neurotrophic theory of skin ulceration.

Though nearly forgotten, the neurotrophic theory was very much a part of mainstream medical thinking during the mid-nineteenth century. This theory stated that all bodily organs are maintained by special nutritional factors secreted by the central nervous system. Development of skin ulceration in the face of neurologic injury became a model for the theory, and controversy involved two great neurologists of the time, Jean Martin Charcot and Edouard Brown-Séquard. As the neurotrophic theory fell into disfavor, interest in decubitus ulcers waned as well. Today, pressure sores remain a major epidemiologic problem for the growing population of frail elderly persons in both acute and long-term care settings. Because of the increased mortality, morbidity, and cost associated with these lesions, attention needs to be refocused on research and education concerning the decubitus ulcer.

Transcutaneous oxygen tension and capillary morphologic characteristics and density in patients with chronic venous incompetence.

The transparent oxygen electrode, recently developed by Huch and his co-workers, permits monitoring of transcutaneous oxygen tension (tcPO2) at defined sites on the capillaroscopic image obtained by videomicroscopy. This combined system has been applied to study the nutritional skin capillaries of patients with chronic venous incompetence (CVI). The results of 44 studies in 17 patients with CVI demonstrated a direct correlation between tcPO2 and density and morphologic characteristics of the superficial capillaries. The mean tcPO2 was 47.7 +/- 14.4 mm Hg at the site of incompetent perforating veins of the ankle without major trophic changes. There was no statistically significant difference between the mean values obtained in patients and control subjects (56.8 +/- 9.9 mm Hg). Videomicroscopic examination revealed dilated and tortuous capillaries surrounded by halo formations. In areas of hyperpigmentation, induration, and hyperkeratosis, significantly decreased mean tcPO2 (22.5 +/- 7.0 mm Hg; p less than .001) corresponded to reduced capillary density (less than 10 capillaries/mm2). In avascular skin areas (scar tissue, white atrophy) tcPO2 was measured at 0 mm Hg. No capillaries, or a greatly reduced number, were visible at such sites, resulting in a distance between capillary and cathode tip of the oxygen sensor of greater than 100 micron. The combined system of tcPO2 measurement and simultaneous videomicroscopy gives new pathophysiologic information on the development of skin ulcers and may be useful for the objective comparison of different therapeutic modalities at the microcirculatory level.