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Skin ulcers are commonly described in the juvenile form of dermatomyositis; however, in the adult form they are rarely described. We report on a patient with adult dermatomyositis, deep cutaneous ulcers in the skin folds and livedo reticularis eruption.
Skin and serum zinc measurements have been made in patients with leprosy with and without trophic skin ulceration and in several other groups. Serum zinc concentrations were decreased in leprosy irrespective of the presence or absence of skin ulceration. Serum zinc concentrations in leprosy were also unrelated to smears positive for Mycobacterium leprae and to the clinical type of leprosy. Since a decrease of the serum zinc was also found in patients with dermatitis herpetiformis and pulmonary tuberculosis it seems likely that the decreased serum zinc in leprosy is a nonspecific metabolic consequence of chronic skin and internal disease. The mean skin zinc concentration in leprosy did not differ significantly from the corresponding value in control subjects, the lack of agreement between serum and skin concentrations being possibly related to the presence of nonexchangeable keratin-bound zinc in skin. Though the clinical significance of lowered serum zinc concentrations in leprosy is uncertain therapeutic trials of zinc treatment in leprosy with trophic skin ulceration seem justifiable.
Intractable skin ulcers that arise as secondary lesions from disease and full-thickness skin defects that result from skin tumor excision often need autologous skin grafting to close the wound. We developed an allogeneic cultured dermal substitute (CDS) to shorten the time needed to prepare a wound bed suitable for autologous skin grafting. The CDS was prepared by plating normal human fibroblasts on a spongy matrix consisting of hyaluronic acid and atelo-collagen. The allogeneic CDS was then placed on the rinsed wound surface. This procedure was repeated twice a week for up to five weeks, until the wounds were closed by autologous skin grafting. In all three cases, after CDS treatment for two to five weeks, the wound conditions became suitable for skin grafting; these conditions had not been improved by conventional topical treatments, including topical basic fibroblast growth factor (bFGF). Healthy granulation tissue developed rapidly, concomitant with wound size reduction. The present results indicate that CDS is an excellent biological wound dressing for improving wound conditions so that they are suitable for subsequent autologous skin grafting as well as for shortening the treatment duration for skin ulcers and full-thickness skin defects.
Chronic skin ulceration is a common complication of diabetes, peripheral vascular disease, and disorders that decrease mobility. Local ulcer care will be successful only if the underlying cause is correctly identified and steps are taken to reverse it. This article reviews the emergency department assessment and management of the patient with chronic skin ulceration.
Mycobacterium haemophilum has recently been recognized as a newly emerging cause of osteomyelitis in immunocompromised patients. While still uncommon, its incidence has increased significantly with the growing AIDS epidemic. Like its relative M. tuberculosis and M. intracellulare, this organism is acid-fast positive; yet unlike its more well-known counterparts, M. haemophilum requires iron-supplemented culture media and low incubation temperatures (30-32 degrees C) for growth. We describe a case of M. haemophilum osteomyelities in the distal femur of a 36-year-old HIV-positive male, who also presented with multiple skin ulcerations. In an AIDS patient with a lytic bone lesion and concomitant skin eruptions, the diagnosis of M. haemophilum should be entertained so that special culture media can be used and appropriate treatment administered.
This is the case report of a seventy-seven-year-old woman with ulcerated skin vasculitis of the lower extremities that preceded the appearance of myelofibrosis. No previous report of this association has been found in a survey of the literature.
OBJECTIVE: To evaluate concordance with compression therapy in ambulatory patients with venous leg ulcers. METHOD: This was a prospective observational survey conducted in general practice. Consecutive patients with venous leg ulcers about to receive a non-adherent primary dressing and with no contraindication to compression bandaging were selected. At the inclusion visit, size, local aspect of the ulcer and the peri-ulcer skin were scored. Patients were asked about concordance with compression and were given a questionnaire to be completed at home. If patients were seen at a three-week follow-up visit, ulcer and peri-ulcer characteristics and concordance were reassessed. RESULTS: A total of 2842 patients were included, of whom 2532 were re-evaluated at three weeks and 1397 (49%) returned their questionnaire. A compression bandage was already available for 62.9% of these patients, and 62.7% said they used it on a daily basis, 23.3% wore it one or two days per week and 13.7% wore it irregularly or never. There was a statistically significant correlation between concordance with compression and ulcer and peri-ulcer skin severity scores (p < 0.001 and p = 0.042 respectively). At the follow-up visit, concordance with compression therapy improved (80.1% were wearing it regularly). Ulcer, peri-ulcer skin severity scores and ulcer size were significantly lower (p < 0.001) when concordance with compression therapy was good. However, 65.6% of patients considered applying compression very difficult; 45% considered it very unaesthetic and 23% judge wearing it to be very painful, while 9% thought it may worsen their ulcer. CONCLUSION: On a short-term basis, concordance with compression can be substantially improved by simple measures with a clear favourable consequence on both ulcer status and peri-ulcer skin aspect when a non-adherent primary dressing is used. However, the acceptability of compression to patients is poor, and continuous effort is required to convince them of its importance.
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Buruli ulcer, a disease caused by Mycobacterium ulcerans, causes ulcerative skin disease likely generated by a toxin that mediates apoptosis. We analyzed paraffin-embedded sections of surgically excised Buruli ulcer lesions (two ulcers and one edematous plaque) and adjacent non-lesional skin samples (n = 9) for apoptosis by an indirect immunofluorescent terminal deoxynucleotide transferase-mediated dUTP-digoxigenin nick end labeling (TUNEL) assay. All samples were stained for acid-fast bacilli (AFB) and cultured for mycobacteria, and most were analyzed with an M. ulcerans-specific diagnostic polymerase chain reaction (PCR). TUNEL (+) bodies were numerous in both ulcers and the plaque, and sparse or absent in adjacent non-lesional skin. The AFB tissue stains and cultures for M. ulcerans were positive only in the three lesions. The result of the PCR for M. ulcerans was positive in all three lesions and in four of six non-lesional tissue samples; three contained sparse TUNEL (+) bodies. An abundance of TUNEL (+) bodies in the three AFB stain (+), culture (+), and PCR (+) Buruli ulcer lesional samples, but not in nearby AFB stain (-), culture (-), and PCR (+) non-lesional skin samples, strengthen the evidence that apoptosis is an important tissue destruction mechanism in human lesions closely associated with viable M. ulcerans.
BACKGROUND: Skin ulcers with compromised healing remain a major problem for plastic and dermatological surgeons. Low incident levels of laser energy have been shown to increase the blood flow rate and volume and to accelerate the wound healing process, thus raising the possibility in augmenting treatment for skin ulcers. METHODS: Preliminary controlled experiments with a 830 nm GaAlAs diode laser in axial pattern flap survival in the rat model showed statistically significant improvement in survival for the irradiated versus unirradiated control animals. In the present study, a newly developed defocused GaAlAs diode laser (830 nm, continuous wave, 669 mW/cm(2)) was applied once or twice per week in an uncontrolled study of five patients (aged between 5 and 81 years old, average 46.6 years old, doses from 6.3 J/cm(2) to 21 J/cm(2)) with previously unresponsive ulcers of various aetiologies. RESULTS: In all five patients, the ulcers healed completely between 3 weeks and 7 months (22.8 +/- 19.3 weeks), without recurrence during a minimum 12-month follow-up. CONCLUSIONS: Defocused 830 nm diode laser therapy was well tolerated, and was very effective in the treatment of this small number of compromised skin ulcers of different aetiologies and in a large range of patient ages. Further controlled studies in larger populations are required. Defocused diode laser therapy nonetheless appears to be a very useful adjunctive method in the treatment of slow-to-heal and non-healing skin ulcers.
Skin ulceration produced by inadvertently extravasated doxorubicin is characterized by a prolonged course accompanied by severe morbidity, and it has proven to be notoriously difficult to treat. In attempts to identify possible antidotes, 11 different pharmacologic agents were tested using piglets, because their skin is anatomically similar to that of man. Among the agents studied, topical application of DMSO daily for 7 days tended to decrease the maximal diameter and accelerate healing of skin ulcers produced by intradermal doxorubicin. alpha-Tocopherol appeared to worsen the ulceration. None of the 11 agents studied prevented the development of ulcerations completely.
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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.
Skin ulcers by Leishmania (Viannia) braziliensis are often deep and irregular and are difficult to measure by just the skin surface transverse and longitudinal diameters. The proposal is to mould the cavity, after local asepsis with fresh water plus soap, with a gelatinous plastic which contains silence, potassium alginate, calcium sulphate, magnesium oxide commercialized under the name of jeltrate (Dentsply Laboratory), by solving 9.5g of jeltrate in 20ml of fresh water and applying the gel on the ulcer which solidifies in 5 minutes. This mould is then filled with a self polymerising acrylic and its volume measured either by weight (by using an analytical balance)-technique 1-or by water displacement by applying Archimeds'principle-technique 2. We show data in a field trial before and after 20 days treatment in 20 patients using three different schedules as follows: 7 received pentamidine isethionate, 7 patients received aminosidine sulphate and 6 received meglumine antimoniate. The results point out that there was a uniform reduction of ulcer volume occurred during this period in the three groups, in both technique. Regarding the therapeutic schedules we are sure that there was a significant statistical difference between the three schedules using the T Student Test, which showed that aminostdine sulphate produced a better volume reduction of the ulcer than the other drugs. Serial moulds reflect clinical billing and are a permanent record. We conclude that the measure of the volume of the skin ulceration can be useful in the therapeutic evaluation, as a practical and cheap procedure, and may be used in field trials.
UNLABELLED: Clinical, physiological and biochemical studies of PGE1 were done in a series of collagen disease patients with skin ulcer, in a foot varix patient with skin ulcer as a non-inflammatory skin ulcer control, and in two diabetics without skin ulcer as no skin ulcer controls. Intravenous infusions of prostaglandin E1 (PGE1) were given continuously at the dose of 1 ng/kg/min for 72 hours. Blood samples were collected from the cubital vein, before, during, immediately after and at seven days after PGE1 therapy. Platelet aggregations were studied by light transmittance (PRP: modified by Born's method; whole blood: modified by Tohjima's method). Platelet iPGE (immunoreactive PGE-like material) levels were assayed by radio-immunoassay. Essential fatty acid compositions of plasma, platelet and red cells, were analysed by gas chromatography. Results were as follows: (1) in all cases, complete healing of skin ulcers was observed; (2) In most cases, skin temperature increased during PGE1 treatment; (3) Platelet aggregation was higher during PGE1 treatment than before and was higher in PRP than in whole blood during PGE1 treatment; (4) The platelet basal iPGE levels were significantly decreased by PGE1 (P less than 0.025); (5) The plasma and platelet linoleic acid levels were significantly higher than before PGE1 treatment (plasma: P less than 0.05, platelets: P less than 0.025); (6) Thrombocytosis of one case of MRA was healed by the second PGE1 treatment. CONCLUSION: The inflammatory skin ulcers in collagen diseases were healed completely by continuous intravenous infusion of PGE1. This effect might be brought about by the suppression of PG metabolism, especially in platelets.
BACKGROUND: THe antimitotic agent paclitaxel is highly active in the therapy of several tumor types, including ovarian and breast cancer. The commercial formulation (Taxol) is supplied in a vehicle containing alcohol and the surfactant Cremophor EL (polyethoxylated castor oil). Whereas Phase I studies did not describe extravasation necrosis, more recent case reports have suggested that paclitaxel can cause soft tissue necrosis if inadvertently extravasated. The efficacy of various antidotal maneuvers, if any, was not known. METHODS: Dehaired, BALB/c mice were given intradermal (ID) injections of paclitaxel 0.3 mg, 0.6 mg, or 1.2 mg, or Cremophor EL, 0.1 mL, into the dorsal skin. The sites were observed thrice weekly for evidence of ulceration. Perpendicular widths of skin ulcers were measured by caliper and multiplied to yield a lesion area in cm2. The lesion area multiplied by time in days was integrated by computer to yield cumulative ulceration areas in (cm2 x days). Potential pharmacologic adjuvants were injected ID after paclitaxel. These included saline (0.05 mL), albumin (0.05 mL), hyaluronidase (15 Units), and hydrocortisone (2.5 mg). Topical adjuvants included dimethylsulfoxide solution, (0.1 mL), cooling to 8-10 degrees C or heating to 43-44 degrees C for 30 minutes after ID paclitaxel. RESULTS: Dose-dependent skin ulcers that lasted 12-17 days were created with the 3 ID paclitaxel doses. The two higher paclitaxel dose levels, 0.6 mg and 1.2 mg, were selected for antidote studies. Hyaluronidase and saline were effective ID antidotes for lesions induced by the 0.6-mg paclitaxel dose, but not for the higher paclitaxel dose of 1.2 mg (P<0.05 by analysis of variance). None of the topical adjuvants or other ID adjuvants significantly reduced paclitaxel-induced skin ulcers in the mice. CONCLUSIONS: Paclitaxel has experimental vesicant potential in the ID mouse skin model. Clinical extravasations of paclitaxel may be treated by subcutaneous injections of hyaluronidase diluted in saline.
OBJECTIVE: To report a case of skin ulceration as a result of treatment with leflunomide for rheumatoid arthritis. CASE SUMMARY: A 78-year-old white woman developed bilateral leg ulcers after 6 months of treatment with leflunomide for rheumatoid arthritis. A history of leg ulcers after methotrexate therapy had been documented. Serologic and diagnostic tests did not support an alternate process. Other medications prescribed were oral ethinyl estradiol 0.05 mg/d, felodipine 5 mg/d, and paroxetine 20 mg/d, for which no documented correlation with the skin breakdown could be made. DISCUSSION: This is the first published case describing a possible relationship between the use of the immunosuppressant agent leflunomide and skin ulceration. CONCLUSIONS: Skin breakdown and ulceration is a recognized adverse effect of drugs with immunosuppressant activity such as methotrexate. Leflunomide, a newer agent prescribed in the treatment of rheumatoid arthritis, may now be listed among the drugs in this category associated with this adverse drug effect.
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