Biomedical subjects
Publications and source records attributed to W M Sams.
Eight patients with livedo vasculitis of four to 30 years' duration that was unresponsive to a variety of medications were treated with pentoxifylline. Three patients experiences complete healing and remained free of active lesions while receiving the drug, four noted much improvement, and one had no change.
Peripheral blood mononuclear cells were obtained from 20 untreated condyloma acuminatum patients and from an equal number of sex- and age-matched controls and assayed for cell surface antigen expression, natural killer activity, and lymphokine production. Patient peripheral blood mononuclear cells had significantly lower helper-to-suppressor T-cell ratios (Leu3/Leu2) (P less than 0.05) and significantly higher percentages of Leu 2+ Tac+ cells (activated suppressor/cytotoxic cells) (P less than 0.05) and Leu 2+ OKM1+ cells (suppressor cells) (P less than 0.01). Natural killer activity of condyloma acuminatum patients was significantly lower (P less than 0.05) than that of controls. Production of interleukin-2 and interferon gamma, but not interferon alpha, was significantly (P less than 0.01) decreased in condyloma acuminatum patients. There was an inverse correlation between the in vitro production of interleukin-2 and interferon gamma and the percentage of Leu 2+ OKM1+ cells (suppressor) (P less than 0.01). Thus, patients with condyloma acuminatum differ from controls by demonstrating decreased natural killer-cell activity, decreased production of lymphokines which enhance natural killer-cell activity (i.e., interferon gamma and interleukin-2), and an increased proportion of T cells with a suppressor phenotype.
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Bullous systemic lupus erythematosus is a newly recognized form of systemic lupus erythematosus characterized by a skin eruption clinically and histologically resembling dermatitis herpetiformis and responsive to dapsone. We report on a patient with bullous systemic lupus erythematosus who initially presented with lesions clinically resembling erythema multiforme, experienced exacerbation of her disease with dapsone, and had detectable circulating autoantibodies to the epidermolysis bullosa acquisita antigen.
Chronic sun exposure can result in numerous changes in human skin, particularly the skin of fair-skinned individuals. These changes include wrinkling, elastosis, actinic keratoses, irregular pigmentation, telangiectasia, and skin cancer. Most of these alterations had formerly been considered to be caused by UVB wavelengths, which are the wavelengths probably most responsible. However, a number of recent studies have demonstrated that UVA can also cause burning, elastosis, and skin cancer. Thus, individuals exposed to intense UVB from sunlight coupled with intense UVA from suntan parlors are likely at increased risk.
Human hypersensitivity angiitis is an immune complex disease in which patients present with palpable purpuric lesions of the skin and may often have multiple organ involvement. The antigen may be derived from an infectious organism such as the hepatitis virus, streptococcus, or a drug, and complexes with antibody. Under circumstances of vascular turbulence or vessel wall dilatation this complex may become fixed, activating the complement sequence with elaboration of chemotactic factors for neutrophils. These cells release lysosomal enzymes resulting in vessel wall destruction. Red blood cells leak into the tissue producing purpura and the inflammatory infiltrate accounts for the palpability. Although many patients have skin lesions only, others may have involvement of joints, gastrointestinal tract, kidneys, and even the lungs. The central question in the pathogenesis of this disease is why the immune complex is so selective in its site of deposition. Part of the reason must be related to the lattice formation of a particular complex, while other reasons are related to host factors of altered vascular permeability, integrity of clearance mechanisms or even a genetically determined defect of the phagocytic system.
Nail abnormalities secondary to systemic disease are important to the dermatologist because they are readily examined and may be the initial signal that systemic disease may be present. Some of the abnormal nail findings represent part of a symptom complex that may be useful in physical diagnosis. The knowledge of the correct onychopathologic etiology may give the patient the correct nail prognosis and may prevent institution of possible incorrect lengthy and costly treatment regimens. In this article, nail signs are grouped according to the characteristics of the change and according to systemic diseases producing signs.
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Immunocompromised patients are more susceptible to unusual pathogens. The case of an immunocompromised patient who presented with cellulitis as the only manifestation of disseminated cryptococcosis is reported. The literature on cryptococcal cellulitis is reviewed.
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In vivo suppression of neutrophil chemotaxis in humans by orally and topically administered tetracycline (TCN) was examined using both modified Boyden chamber and skin chamber assays. Chemoattractants were derived from serum complement and bacterial culture supernates. The results showed that oral TCN caused significant suppression of neutrophil chemotaxis when measured by both assays and both sources of chemoattractant. Furthermore, application of a commercially available topical preparation containing TCN caused local suppression of chemotaxis as measured by the skin chamber assay. These results show that TCN does suppress neutrophil migration in vivo, and they provide support for an anti-inflammatory effect of TCN mediated in part by suppression of neutrophil chemotaxis.
Current evidence strongly supports the theory that the lesions of pemphigus are due to binding of pemphigus antibody to an antigen in or near the epidermal cell membrane, which causes a release of at least one enzyme which results in dissolution of the intercellular attachments and acantholysis. Similarly, strong evidence supports the hypothesis that pemphigoid blisters are due to binding of antibody at the basement membrane, followed by activation of complement and release of anaphylatoxins which activate tissue mast cells to release eosinophil chemotactic factor. These eosinophils then release tissue-destructive enzymes and reactive oxygen intermediates directly onto the basement membrane zone, with loss of dermoepidermal adherence and formation of blisters.
Giant cell arteritis is a systemic disease usually occurring in patients in the fifth decade or older, more often in women. Dermatologic manifestations are rare but, when found, are usually expressed as scalp ulcerations or blanching associated with gangrene of the tongue. The dermatologist should be familiar with the entity because it is often more severe when associated with scalp necrosis, and prompt intervention with corticosteroids can prevent catastrophic sequelae.
Two patients with established systemic lupus erythematosus developed bullous dermatoses clinically suggestive of bullous pemphigoid (BP). Direct immunofluorescence demonstrated linear staining at the dermoepidermal junction for IgG and C3 in a pattern typical for BP. However, immunoelectron microscopy demonstrated deposits of IgG largely below the basal lamina, with little if any deposit present within the lamina lucida. These findings are consistent with systemic lupus erythematosus (SLE) and effectively rule out BP. In addition, the leukocyte attachment assay, an in vitro assay of the functional activity of tissue-deposited immune complexes, demonstrated strong attachment of leukocytes to the dermoepidermal junction of patients' skin, suggesting that the immune reactants were functional immune complexes of possible importance to the pathogenesis of the bullous lesions. To our knowledge, this is the first time that immunoelectron microscopy has been performed on skin from patients suspected of manifesting concurrent SLE and BP. Our findings cast doubt on previous such reports by demonstrating the existence of a bullous form of SLE resembling BP both clinically and by direct immunofluorescence.
Previous immunofluorescent studies showing deposits of immunoglobulin and complement at the cutaneous basement membrane zone have provided evidence supporting a role for immune complexes in the pathogenesis of bullous pemphigoid. In this study the functional activity of the deposits has been examined using leukocyte attachment, a method for detecting and quantitating the biological activity of complement-activating immune complexes in tissues. When peripheral blood leukocytes suspended in serum complement were incubated with cryostat sections of lesional and adjacent normal-appearing skin from 9 patients with pemphigoid, skin from 11 normal controls and lesional skin from 14 nonpemphigoid disease controls there was significantly greater attachment of leukocytes to the basement membrane zone of lesional bullous pemphigoid skin compared to normal-appearing pemphigoid skin and skin of both control groups. A significant reduction in attachment in the absence of serum complement suggested the reaction was dependent on activation of complement by tissue-deposited complexes. Although leukocyte attachment was greater in lesional than normal-appearing pemphigoid skin, a comparison of the incidence and intensity of cutaneous IgG and complement immunofluorescence between the 2 groups showed no significant differences. Furthermore, no correlation between leukocyte attachment and serum titers of immunoglobulin G or complement-binding anti-basement membrane zone antibodies was observed. These results suggest that immune reactants in lesional pemphigoid skin are functional complement-activating immune complexes, that differences exist between the activity of complexes in lesional and normal-appearing pemphigoid skin and may explain why lesions develop at some sites and not others.
In this study, an in vitro model of immune complex-mediated basement membrane zone separation caused by periphigoid antibodies, serum complement, and peripheral blood leukocytes is described. When cryostat sections of fresh-frozen normal human skin were treated with either of 4 bullous pemiphigoid sera containing complement-activating anti-basement membrane zone antibodies and subsequently incubated at 37 degrees C with normal human peripheral blood leukocytes and fresh human serum, leukocytes attached to 96% of the basement membrane zone in 100% of sections. Sixty-seven percent of the sections developed focal areas of basement membrane zone separation resembling dermal-epidermal separation described in early pemphigoid lesions. In control sections in which either leukocytes, pemphigoid antibody or fresh human serum were omitted, significantly less leukocyte attachment and basement membrane zone separation occurred. Evidence that leukocytes caused separation was supported by an absolute requirement for viable leukocytes during incubation, a high correlation between leukocyte attachment and separation and experiments showing that leukocytes attached to the basement membrane zone were activated. This study provides the first in vitro evidence directly supporting a functional role for immune-complex mediated inflammation in the pathogenesis of basement membrane zone separation and blisters in bullous pemphigoid.