Biomedical subjects
Publications and source records attributed to J Hafner.
We have shown that ethanol in concentrations of 0.0001%-10% significantly enhances 3H-thymidine uptake in cultured human mammary carcinoma cell line MCF-7. Methanol only enhances 3H-thymidine uptake in a concentration of 0.01%.
OBJECTIVE: To determine whether hospital employee biological hazardous exposure rates varied with time of day or increased with time interval into shift. METHODS: This was a retrospective occurrence report review conducted at a university hospital with an emergency medicine residency program. Health care worker biological hazardous exposure data over a 30-month period were reviewed. Professional status, date, time, and type of exposure (needlestick, laceration, splash), time interval into shift of exposure, and hospital location of exposure were recorded. Hourly employee counts and risky procedure counts were matched by location with each reported exposure, to determine hourly rates of biological hazardous exposures. RESULTS: Analysis of 411 recorded exposures demonstrated that more people were exposed between 9:00 AM and 11:00 AM (p < 0.05), yet the exposure risk did not vary significantly when expressed as the number of exposures per worker or per procedure. Of the 393 exposures with data describing time interval into shift when the exposure occurred, significant numbers of exposures occurred during the first hour and at shift's end [when corrected for exposures per worker (p < 0.05) or exposures per procedure (p < 0.05)]. CONCLUSION: While the number of exposures are increased in the AM hours, the exposure rate (as a function of workers or procedures) does not vary with time of the day. However, the exposure rate is increased during the first hour and last 2 hours of a shift. Efforts to increase worker precautions at the beginning and end of shifts are warranted.
Treatment of leg ulcers should consider two aspects, i.e. the exact underlying condition (main cause and contributing factors) and local conditions. Compression therapy remains the corner-stone of the therapeutic concept. A compression of 35 mmHg at the distal calf improves insufficient venous function. A systolic ankle pressure of < or = 80% of blood pressure (ankle-arm-index < or = 0.8) requires reduction of compression therapy. At an ankle pressure below 80 mmHg compression should not be used. If superficial reflux is the major cause of chronic venous insufficiency, vein stripping should be considered. Contributing diseases like heart insufficiency, anemia or diabetes may require general medical care. Local contributing factors like reduced mobility of the ankle joint and lymphostasis may require physical therapy, and calcification of the wound bed should be excised. Local treatment considers ulcer bed and border. The ulcer bed needs debridement and moist wound care. Infection is treated with systemic antibiotics, according to the antibiogram. Tetanus immunization is required for all leg ulcer patients. Some centers report good results with endoscopic subfascial decision of perforator veins, paratibial fasciotomy and excision of fibrous tissue. Local application of recombined growth factors is currently under clinical evaluation. Adjuvant pharmacotherapy plays a minor role in the treatment of venous leg ulcers. An efficient treatment of the underlying cause combined with optimal wound care are the key to therapeutic success.
In the management of leg ulcers two aspects should be considered, i.e. the exact underlying condition (main cause and contributing factors) and local conditions. Concomitant peripheral arterial occlusive disease must systematically be excluded. Effective compression therapy (35 mmHg pressure at the distal calf) is the corner-stone in treatment of venous leg ulcers. Superficial venous reflux can be the major cause of chronic venous insufficiency. Careful examination of reflux patterns helps to distinguish between indications for conservative treatment and indications suitable for surgical treatment. To what extent the stripping of varicose veins and/or endoscopic subfascial perforator vein discision really improves the outcome and prevents recurrence still remains to be shown in controlled trials. Local treatment considers ulcer wound bed and border. Modern synthetic wound dressings follow the concept of moist wound healing whilst local application of growth factors is currently under clinical evaluation. Management of eczema includes avoidance of potent or known allergens, patch tests in severe cases with suspicion of contact dermatitis and an adapted local therapy.
We report a case with segmental arterial calcification and atheromatosis of the superficial femoral artery in a patient with venous angiodysplasia (Klippel-Trenaunay syndrome). Pathogenesis remained unclear. A short hemodynamically significant stenosis within the calcified segment was treated by angioplasty requiring high balloon pressure and was complicated by an arterio-venous fistula. This fistula could successfully be closed by a dacron-covered endovascular prosthesis (Cragg-stent). There is little experience with covered stents to close arterio-venous shunts and our case may encourage further use in this indication.
The combination of oral anticoagulants with antiplatelet agents has been advocated as particularly efficient in prophylaxis of arterial thromboembolism. The indications at issue are nonrheumatic chronic atrial fibrillation, mechanical and biological heart valve prostheses, coronary artery disease, coronary stents and peripheral arterial occlusive disease. However, such a combined prophylaxis might also be associated with a higher bleeding risk. Clinical trials addressing administration of coumarines with antiaggregants are rare and inhomogeneous. The present article reviews the literature on oral anticoagulants combined with aspirin in the prevention and treatment of arterial thromboembolism and draws a comparison to oral anticoagulation alone and aspirin alone, respectively. It clearly shows that this potentially dangerous combination should not be recommended in most indications until specifically designed trials have addressed its benefit-to-risk ratio.
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BACKGROUND: Uremic small-artery disease with medial calcification and intimal hyperplasia can lead to life-threatening skin necrosis or acral gangrene. It is a distinct complication of chronic renal failure that must be differentiated from soft-tissue calcification. An increased calcium-phosphate product and secondary hyperparathyroidism are the main underlying conditions. The benefit of parathyroidectomy is controversial. OBJECTIVE: This article is based on a literature search to determine prognostic factors and, in particular, the benefit of parathyroidectomy. METHODS: The literature on uremic small-artery disease (so-called calciphylaxis) was reviewed (full data set: 104 cases, including five of our own). The therapeutic benefit of parathyroidectomy and the relation between prognostic predictors (localization, dialysis, and transplant) and outcome were analyzed. The relation between diabetes and acral gangrene was also examined. Further epidemiologic data on the reviewed group of patients were established. RESULTS: Thirty-eight of 58 patients who underwent parathyroidectomy survived compared with 13 of 37 patients who did not undergo parathyroidectomy (p = 0.007, n = 95). Forty of 53 patients with distal localization of necrosis survived compared with 11 of 42 patients with proximal pattern (p < 0.00001; n = 95). Dialysis and kidney transplantation followed by immunosuppression showed no relation to disease outcome. No association was found between diabetes and acral gangrene (p = 0.50). CONCLUSION: Uremic small-artery disease is a distinct complication of chronic renal failure. Its recognition and early diagnosis should allow more effective treatment. In our retrospective study parathyroidectomy was significantly related to survival. Only a randomized, controlled, prospective trial (parathyroidectomy vs conservative treatment of secondary hyperparathyroidism) can establish the value of parathyroidectomy in uremic small-artery disease.
Minor nail trauma may cause bluish discoloration of the nail, while tangential skin trauma on the heel can result in a so-called black heel. To rule out melanoma in such clinical situations, a biopsy is needed to reveal homogeneous eosinophilic masses deposited under the nail plate or within it (transepidermal elimination). Most dermatopathologists attempt to demonstrate the presence of hemoglobin in these eosinophilic masses with Prussian blue stain, which typically remains negative. In our experience, these traumatically induced blood deposits are always situated in avascular spaces, devoid of degrading phagocytes. Consequently, a histochemical stain for these deposits should be directed specifically toward hemoglobin, not hemosiderin. In the dermatopathologic literature, the various techniques to detect hemoglobin deposits in tissue sections are not well-known. We would like to emphasize benzidine stain, a highly selective and efficient method to demonstrate the presence of hemoglobin deposits in histologic sections. To date, benzidine stain has not been utilized to characterize splinter hemorrhage (subungual hematoma). Of concern, the use of benzidine in histopathology laboratories is restricted because this agent is a known carcinogen, while the non-mutagenic derivative, 3,3',5,5'-tetramethylbenzidine, does not stain histologic sections. Patent blue V, a completely different and less specific agent, stains hemoglobin an intense blue-green.
Relapsing eosinophilic perimyositis is a rare entity. Only 11 cases have been reported in the literature. We describe a patient with relapsing myopathy, peripheral blood eosinophilia and cutaneous manifestations, who had histopathological features of eosinophilic perimysial inflammation. His disease responded to moderate doses of glucocorticosteroids, and pursued an apparently benign course. Serum levels of eosinophilic cationic protein correlate with disease activity, and may be helpful in monitoring treatment. The features of this case are compared with those of other hypereosinophilic syndromes. It appears to be part of the spectrum of eosinophilic myositis.
2 workers at an aircraft factory were employed in a plasma sparying unit. Soon after they were equipped with new semisynthetic working suits, they started to complain of pruritic eruptions after heavy exposure to metal dust. They noted that the dust was not as easily blown off the clothes by pressurized air as previously. Clinical findings consisted of discrete macular and papular lesions, partly follicular, on the ventral and medial thighs. Atopy score, IgE level and a standard series of prick tests ruled out atopic disposition. Patch tests revealed no reactions. A diagnosis of occupational airborne irritant contact dermatitis from metal dust was therefore made. To elucidate the role of the working suit, extensive physical investigations of the physical properties of the textile were performed. Microscopic pictures at low magnification showed more dust particles on the semisynthetic working suit, compared to the former pure cotton suit. This impression could not be confirmed by particle count because of too uneven particle distribution at higher magnification. Hairiness of the 2 textiles was low and ruled out irritation by the semisynthetic textile itself. No difference in electrostatic properties between the 2 working suits could be established either. Both textiles showed high static electrical propensity. When use of the semisynthetic overall was discontinued, the patients reported no recurrence.(ABSTRACT TRUNCATED AT 250 WORDS)
Skin symptoms in renal disease occur in a series of rare inherited or acquired diseases affecting the kidneys as well as the skin (amyloidosis, vasculitis, angiokeratoma diffusum corporis Fabry) (table 1). Chronic renal failure, regardless of its origin, often causes important skin symptoms, such as pruritus, the typical complexion with elastosis seen in uremic patients, porphyria cutanea uremica, metastatic calcifications, skin necrosis due to uremic small arteries disease with medial calcification and intimal hyperplasia, perforating dermatoses, nail lesions and symptoms of the oral mucosa (table 2). The following article reviews the pathogenesis and the limited possibilities of treatment for skin symptoms in chronic renal failure.
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