Extensor Surfaces Of Elbows Research Articles

Scabies: A Neglected Global Disease.

Scabies is a skin disease caused by an obligate human parasite mite Sarcoptes scabiei var. hominis. Children under the age of two and elderly individuals are at the greatest risk. Knowledge of this condition is important for an early diagnosis to be made and treatment to be initiated. The review aimed to familiarize physicians with the clinical manifestations, diagnosis, evaluation, and management of scabies. A search was conducted using Pubmed with the built-in "Clinical Queries" tool. The search term "Scabies" was used. The categories of "epidemiology", "diagnosis", "therapy", "prevention" and "prognosis" had a limited scope for primary clinical studies. Meta-analyses, randomized controlled trials, clinical trials, observational studies, and reviews were included. Only papers published in the English language were included. A descriptive, narrative synthesis was provided of the retrieved articles. Worldwide, scabies affects 200 to 300 million individuals annually. The average prevalence is estimated to be 5 to 10% in children of developing countries. Transmission usually occurs after close prolonged skin-to-skin contact. Classic scabies is characterized by an erythematous papular eruption, serpiginous burrows, and intense pruritus. Sites of predilection include the webs of the fingers, volar wrists, lateral aspects of fingers, extensor surfaces of elbows and knees, waist, navel, abdomen, buttocks, groins, and, genitals. A clinical diagnosis of classic scabies can be made on the basis of the history and clinical findings. Other clinical variants include crusted scabies, nodular scabies, and bullous scabies. Finding the mite, ova, or fecal pellets on microscopic examination of scrapings taken from skin lesions confirms the diagnosis of scabies infestation. For eradication of scabies mites, the drugs of choice are topical permethrin and oral ivermectin. Scabies is a highly contagious parasitic cutaneous disease that is stigmatising and debilitating. Increased awareness, accurate diagnosis, and prompt treatment are essential for the effective control of scabies and for the prevention of the spread of the disease.

Paraneoplastic Pemphigus and Autoimmune Blistering Diseases Associated with Neoplasm: Characteristics, Diagnosis, Associated Neoplasms, Proposed Pathogenesis, Treatment.

Autoimmune paraneoplastic and neoplasm-associated skin syndromes are characterized by autoimmune-mediated cutaneous lesions in the presence of a neoplasm. The identification of these syndromes provides information about the underlying tumor, systemic symptoms, and debilitating complications. The recognition of these syndromes is particularly helpful in cases of skin lesions presenting as the first sign of the malignancy, and the underlying malignancy can be treated in a timely manner. Autoimmune paraneoplastic and neoplasm-associated bullous skin syndromes are characterized by blister formation due to an autoimmune response to components of the epidermis or basement membrane in the context of a neoplasm. The clinical manifestations, histopathology and immunopathology findings, target antigens, associated neoplasm, current diagnostic criteria, current understanding of pathogenesis, and treatment options for a selection of four diseases are reviewed. Paraneoplastic pemphigus manifests with clinically distinct painful mucosal erosions and polymorphic cutaneous lesions, and is often associated with lymphoproliferative neoplasm. In contrast, bullous pemphigoid associated with neoplasm presents with large tense subepidermal bullae of the skin, and mild mucosal involvement, but without unique clinical features. Mucous membrane pemphigoid associated with neoplasm is a disorder of chronic subepithelial blisters that evolve into erosions and ulcerations that heal with scarring, and involves stratified squamous mucosal surfaces. Linear IgA dermatosis associated with neoplasm is characterized by annularly grouped pruritic papules, vesicles, and bullae along the extensor surfaces of elbows, knees, and buttocks. Physicians should be aware that these autoimmune paraneoplastic and neoplasm-associated syndromes can manifest distinct or similar clinical features as compared with the non-neoplastic counterparts.

Development of Rheumatoid Nodules after Anti-Tumor Necrosis Factor-α Treatment with Adalimumab for Rheumatoid Arthritis.

Dear Editor: A 40-year-old male presented with 4 months history of multiple various sized erythematous to violaceous subcutaneous nodules on both extensor surfaces of elbows, which was partially movable and showed no symptoms (Fig. 1A). He was diagnosed as rheumatoid arthritis (RA) 7 years ago. A variety of therapeutic options, such as systemic corticosteroid, antimalarial drug, nonsteroidal anti-inflammatory drugs (NSAIDs), and methotrexate, were prescribed to control RA activity. However, they all failed to show symptomatic improvement. After that, the patient started adalimumab, a human monoclonal antibody to tumor necrosis factor (TNF)-α, 40 mg injection every other week with concomitant systemic corticosteroid, methotrexate and a NSAID. Adalimumab injection improved signs and symptoms of RA gradually. However, the multiple subcutaneous nodules occurred in the extensor sides of the elbows two months after adalimumab injection. A skin biopsy was performed and it showed dense fibrinoid deposits in deep dermis. At high magnification, large palisading granulomas surrounding degenerated connective tissue and fibrin were noticed and infiltrating inflammatory cells were mostly composed of lymphocytes and histiocytes. Mucin deposition was rarely observed. Overall, it was consistent with rheumatoid nodule (Fig. 1B, C). The patient didn't receive any treatment, and there was no change in the lesion at the follow-up visit. Fig. 1 (A) Multiple various sized erythematous to violaceous subcutaneous nodules on both extensor surfaces of elbows. (B) Biopsy showed dense fibrinoid deposits in deep dermis (H&E, ×100). (C) Biopsy showed palisading granulomas surrounding ... Rheumatoid nodule development is extremely rare side effect of TNF-α antagonists and only two cases after etanercept and adalimumab injection have reported so far. However, in the previous report caused by adalimumab injection, rheumatoid nodule was diagnosed by only ultrasonogram1. Thus, to our knowledge, this is the first report of rheumatoid nodules confirmed by histopathologic diagnosis following the treatment with adalimumab. Rheumatoid nodules are one of the most common extra-articular manifestations of RA, usually associated with severe disease activity. Macrophage is the main infiltrating inflammatory cell in both rheumatoid nodule and synovial membrane of RA and they show similar expressions of proinflammatory cytokines such as TNF-α, and interleukin-1 receptor antagonist (IL-1Ra)2. However, in this case, rheumatoid nodules were developed when the signs and symptoms of RA had been gradually improving by the adalimumab. There are several differences between rheumatoid nodule and synovial membrane of RA. Rheumatoid nodules lack infiltrating B cells, plasma cells, and organized lymphoid structures. In addition, E-selectin expression, IL-1 level are higher and TNF-α concentration is significantly lower in the rheumatoid nodule compared to the synovial membrane of RA3, which suggests that development of rheumatoid nodules might be less influenced by TNF-α. One study with TNF-α knockout mice demonstrated abnormally low TNF-α level might induce an exaggeration of the effects driven by other inflammatory mediators4. Therefore, it could be considered that excessive TNF-α suppression could induce the development of rheumatoid nodules. Furthermore, anti-TNF-α treatments increase peripheral blood counts which are thought to be related to reduced cell traffic to the inflamed joint in RA5. Thus it is conceivable that these migratory cells infiltrate other inflamed tissues and form rheumatoid nodules. So herein, we report a case with great interest which could be one of the example and supporting clinical evidence of the paradoxical effects of anti-TNF-α treatment.

Scabies: A Review of Diagnosis and Management Based on Mite Biology

Scabies is a contagious parasitic dermatitis that is a significant cause of morbidity, especially outside of the United States. Scabies is diagnosed most often by correlating clinical suspicion with the identification of a burrow. Although scabies should be on the differential for any patient who presents with a pruritic dermatosis, clinicians must consider a wide range of diagnostic possibilities. This approach will help make scabies simultaneously less over- and underdiagnosed by clinicians in the community. Atypical or otherwise complex presentations may necessitate the use of more definitive diagnostic modalities, such as microscopic examination of KOH prepared skin scrapings, high-resolution digital photography, dermoscopy, or biopsy. Scabies therapy involves making the correct diagnosis, recognizing the correct clinical context to guide treatment of contacts and fomites, choosing the most effective medication, understanding how to use the agent properly, and following a rational basis for when to use and reuse that agent. Although the development of new therapeutic agents is always welcome, tried and true treatments are still effective today. Permethrin is the gold standard therapy, with malathion being an excellent topical alternative. Ivermectin is an effective oral alternative that is especially useful in crusted scabies, patients who are bed ridden, and in institutional outbreaks. Despite the availability of effective therapeutics, treatment failures still occur, mostly secondary to application error (ie, failure to treat the face and scalp or close contacts, failure to reapply medication) or failure to decontaminate fomites. Because increasing resistance to scabies treatments may be on the horizon, we propose that standard of care for scabies treatment should involve routine treatment of the scalp and face and re-treating patients at day 4 on the basis of the scabies life cycle to ensure more efficient mite eradication. Practitioners should attempt to treat all close contacts simultaneously with the source patient. To eradicate mites, all fomites should be placed in a dryer for 10 minutes on a high setting, furniture and carpets vacuumed, and nonlaunderables isolated for a minimum of 2 days, or, for those who wish to be rigorous, 3 weeks.

Exfoliative dermatitis after undecylenic acid therapy for psoriasis.

Perlman 1 and Milberg 2 reported good results from the use of undecylenic acid by mouth in the treatment of psoriasis and neurodermatitis. Perlman restated his belief in its value at the meeting of the American Academy of Dermatology and Syphilology in Chicago in December 1949. Among the side effects of the drug, exfoliative dermatitis was reported by Behrman. 3 I had a similar case, herewith reported. REPORT OF CASE A white man aged 33 had mild psoriasis of the extensor surfaces of elbows and knees for the past seven years. His general health had always been good. With the exception of his psoriasis, his past history was noncontributory. On July 15, 1949 his family physician prescribed for him undecylenic acid. After the patient had taken nine capsules daily for two weeks, he began to feel nauseated and to vomit. He noticed red blotches on his face, chest and back.