Biomedical subjects
Publications and source records attributed to Lloyd E King.
Isolated penile and scrotal elephantiasis presents a diagnostic and therapeutic challenge. We report a case of chronic penile and scrotal elephantiasis caused by indolent Chlamydia trachomatis infection. The patient improved modestly with long-term doxycycline.
Alopecia areata is an autoimmune disease that targets actively growing (anagen) hair follicles in humans, mice, rats, dogs, horses, and cattle. C3H/HeJ mice spontaneously develop alopecia areata from 5 mo of age and older in females and later in males. Frequency of disease approached 20% in a colony by 18 mo of age. C57BL/6J mice do not develop alopecia areata. A segregating F2 population of female mice (n=1096) was generated from crossing these two strains. Alopecia areata (n=138) and clinically normal (n=214) mice were genotyped at 12 mo of age using 211 microsatellite probes. The peak logarithm of odds ratio score on mouse chromosome 17 (10.9) was around marker D17Mit134 at 16.9 cM from the centromere. The mouse histocompatibility locus, H2, the mouse equivalent of human leukocyte antigen in humans, was a likely candidate. Twelve-month-old C3H.SW-H2b/SnJ mice (C3H/HeJ congenic mice in which the H2k purported susceptibility locus was replaced with the H2b purported resistance locus) did not develop alopecia areata, supporting this locus as being important in alopecia areata. A suggestive linkage was also found on mouse Chromosome 9 (logarithm of odds ratio score 2.0) around D9Mit206, 20 cM from the centromere. The interval on mouse Chromosome 17 contains several orthologous genes potentially associated with human alopecia areata.
A potentially contributing factor to the development and chronicity of pyoderma gangrenosum is infection with the relatively recently characterized human pathogen, Chlamydia pneumoniae. C pneumoniae is an obligate intracellular bacterium that can infect endothelial, monocyte, and smooth muscle cells and is associated with cardiopulmonary diseases. A case of serologically, polymerase chain reaction-positive, immunohistochemically, and culture-documented viable C pneumoniae organisms in a chronic pyoderma gangrenosum ulcer is reported, a finding that has not been described previously.
Alopecia areata is a suspected autoimmune hair loss disease. In a rodent model, alopecia areata can be induced in normal haired C3H/HeJ mice by transfer of skin grafts from mice with spontaneous alopecia areata. At weeks 2, 4, 6, and 10 after surgery, grafted mice were euthanized, skin collected and processed for histology, and RNA extracted. Age-matched sham-grafted mice, and mice with and without spontaneous alopecia areata, were similarly processed. For comparison, skin biopsies from alopecia areata and androgenetic alopecia affected humans were also collected. Skin mRNA processed to cDNA was analyzed using Affymetrix mouse 11K and human 6800 gene chip(R) array technology. Microarray results indicated 42 known genes upregulated or downregulated during onset of mouse alopecia areata consistent with an inflammatory cell-mediated disease pathogenesis involving antigen presentation, costimulation, and a T helper 1 lymphocyte response. In contrast, 114 genes, many regulating immunoglobulin response, were altered late in disease development. In alopecia areata affected humans, 95 genes were significantly modulated. As confirmation of microarray analysis results, lymph node and spleen cells from alopecia areata affected mice injected into normal haired littermates transferred the alopecia areata phenotype. Alopecia areata onset could be inhibited in skin-grafted mice by modulation with B7.1- and B7.2-specific monoclonal antibodies. In addition, depletion of CD4+ CD8+ expressing cells in chronic alopecia areata affected mice using monoclonal antibodies permitted hair regrowth. The results consistently demonstrated the importance of an immune cell-mediated disease mechanism in alopecia areata pathogenesis and suggested targeting antigen-presenting cells and reactive lymphocytes may be effective in alopecia areata treatment.
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BACKGROUND: Chronic diabetes-related foot ulcers result from predisposition, tissue injury, and inadequate reparative mechanisms. Standard care for diabetes-related foot ulcers includes weight off-loading, pressure-relieving footwear, aggressive surgical debridement, and frequent dressing changes. Graftskin is a recently developed living skin construct. OBJECTIVE: To compare Graftskin and standardized wound care to standardized wound care alone in the treatment of difficult to heal diabetes-related neuropathic foot ulcers, and to assess the handling and application characteristics of Graftskin. METHODS: A university dermatology clinic was part of a 24-center prospective, randomized, controlled, parallel group comparative trial of Graftskin for the treatment of difficult to heal neuropathic diabetes-related foot ulcers. Patients were randomly assigned to treatment with Graftskin with aggressive debridement and standardized wound care, or aggressive debridement and standardized wound care alone. Blinding was not feasible due to device visibility during application. RESULTS: Five of nine patients (56%) treated with Graftskin therapy had complete healing. Three of eight control patients (37%) had complete healing. CONCLUSION: Graftskin as an adjunct to aggressive debridement and standardized wound care appears to be a valuable treatment adjunct in patients with difficult to heal diabetes-related neuropathic foot ulcers. The application learning curve was steep and the ease of application exceptional.
Basal cell carcinomas (BCCs) typically occur in middle-aged to elderly patients but less commonly in younger ones. In our experience, most BCCs seen in patients younger than 40 years are found in women. We evaluated 30 women with biopsy-proven BCC and 30 control patients matched for sex, age, and skin type to determine potential risk factors for this population. Tanning bed visits, pack-years of cigarette smoking, recreational sun exposure, number of blistering sunburns, and use of sunscreens were determined for both groups. Among patients with a BCC, the histologic type of tumor, site of involvement, method of treatment, follow-up period, incidence of recurrence, and presence of actinic keratoses were also evaluated. Patients with a BCC had a statistically greater number of pack years of smoking (P =.045), and a greater percentage of these women had experienced blistering sunburns (P =.028). Although women with a BCC had, on average, almost twice as many tanning salon visits (152.2 vs 83.1), this was not statistically significant. Sunscreen use and amount of recreational ultraviolet light exposure were essentially equal between the two groups. Young women with a BCC are more likely to have a past or current history of cigarette smoking and blistering sunburns. Repeated exposure to tanning beds may also be a contributory factor.
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Pyoderma gangrenosum is a rare, chronic ulcerative skin disease. It is a diagnosis of exclusion, after ruling out other causes of cutaneous ulceration. The etiology of pyoderma gangrenosum is poorly understood but is likely multifactorial. We describe 2 families affected by ulcerative pyoderma gangrenosum. This familial clustering suggests a possible genetic role in the development of pyoderma gangrenosum in some cases.