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Books on the topic 'Skin Diseases, epidemiology'

Author: Grafiati

Published: 4 June 2021

Last updated: 29 January 2023

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1

C, Williams Hywel, and Strachan David P, eds. The challenge of dermato-epidemiology. Boca Raton: CRC Press, 1997.

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2

J, Grob J., ed. Epidemiology, causes, and prevention of skin diseases. Oxford: Blackwell Science, 1997.

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3

Faber, William Richard, R. J. Hay, and B. Naafs. Imported skin diseases. 2nd ed. Chichester, West Sussex: Wiley-Blackwell, 2013.

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4

Rheumatic and skin disease. New York, N.Y: Facts on File Publications, 1988.

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5

Jo-David, Fine, and National Epidermolysis Bullosa Registry (U.S.), eds. Epidermolysis bullosa: Clinical, epidemiologic, and laboratory advances, and the findings of the National Epidermolysis Bullosa Registry. Baltimore: Johns Hopkins University Press, 1999.

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6

Beddingfield, Frederick Coston. Melanoma: A decision analysis to estimate the effectiveness and cost-effectiveness of screening and an analysis of the relevant epidemiology of the disease. Santa Monica, CA: RAND, 2002.

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7

Patlak, Margie. Mammography and beyond: Developing technologies for the early detection of breast cancer : a non-technical summary. Edited by National Cancer Policy Board (U.S.). Committee on the Early Detection of Breast Cancer and National Research Council (U.S.). Commission on Life Sciences. Washington, D.C: National Academy Press, 2001.

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8

Imported Skin Diseases. Elsevier, 2008.

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9

Hay, Roderick J., William R. Faber, and Bernard Naafs. Imported Skin Diseases. Wiley & Sons, Incorporated, John, 2012.

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10

Hay, Roderick J., William R. Faber, and Bernard Naafs. Imported Skin Diseases. Wiley & Sons, Incorporated, John, 2012.

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11

Imported skin diseases. Maarssen: Elsevier gezondheidszorg, 2006.

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12

Hay, Roderick J., William R. Faber, and Bernard Naafs. Imported Skin Diseases. Wiley & Sons, Incorporated, John, 2012.

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13

Hay, Roderick J., William R. Faber, and Bernard Naafs. Imported Skin Diseases. Wiley & Sons, Limited, John, 2012.

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14

Summers, Yvonne L. Lichen Planus: Epidemiology, Symptoms and Treatment. Nova Science Publishers, Incorporated, 2015.

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15

Maibach, Howard I., and Jacob P. Thyssen. Filaggrin: Basic Science, Epidemiology, Clinical Aspects and Management. Springer London, Limited, 2014.

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16

Maibach, Howard I., and Jacob P. Thyssen. Filaggrin: Basic Science, Epidemiology, Clinical Aspects and Management. Springer, 2016.

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17

Maibach, Howard I., and Jacob P. Thyssen. Filaggrin: Basic Science, Epidemiology, Clinical Aspects and Management. Springer, 2014.

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18

Ngatu, Nlandu Roger, and Mitsunori Ikeda. Occupational and Environmental Skin Disorders: Epidemiology, Current Knowledge and Perspectives for Novel Therapies. Springer, 2018.

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19

Ngatu, Nlandu Roger, and Mitsunori Ikeda. Occupational and Environmental Skin Disorders: Epidemiology, Current Knowledge and Perspectives for Novel Therapies. Springer, 2019.

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20

Dellavalle, Robert P. United States Skin Disease Needs Assessment: Dermatologic Clinics. Elsevier - Health Sciences Division, 2011.

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21

Maibach, Howard I., and Jurij J. Hostýnek. Nickel and the Skin: Absorption, Immunology, Epidemiology, and Metallurgy. Taylor & Francis Group, 2002.

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22

Takeshita, Junko, and Joel M. Gelfand. Epidemiology of psoriasis. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198737582.003.0002.

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Psoriasis is a common chronic inflammatory disorder of the skin that is associated with multisystem effects. Approximately 125 million people worldwide are affected by psoriasis, nearly one quarter of whom have moderate to severe disease. The majority of patients with psoriasis have a waxing and waning course with variable periods of spontaneous disease improvement or clearance. A rapidly expanding body of epidemiologic literature suggests psoriasis to be associated with a greater comorbid disease burden than patients without psoriasis. In addition to psoriatic arthritis, cardiometabolic diseases, including metabolic syndrome and its component disorders, as well as major adverse cardiovascular events are the most common comorbidities of psoriasis; together they are the primary cause of premature mortality among moderate to severe psoriasis patients. Continued efforts to better understand currently known and identify other emerging comorbidities of psoriasis are critical.

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23

Cassidy, Jim, Donald Bissett, Roy A. J. Spence OBE, Miranda Payne, Gareth Morris-Stiff, and Madhumita Bhattacharyya. Skin cancers. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199689842.003.0023_update_001.

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Tumours of the central nervous system examines the epidemiology, aetiology, genetics and pathology of these heterogeneous tumours. Clinical presentation reflects the site of origin and rate of growth. Investigation usually comprises imaging (MRI superior to CT for most), and biopsy; requirement for additional staging depends on pathology. The treatment of low-grade gliomas may be delayed if small with few symptoms, otherwise surgery and/or radiotherapy. High grade gliomas may be managed with surgery, radiotherapy, and temozolomide chemotherapy in fit patients. Unfit patients should be offered supportive care only. Brief summaries are provided for management of ependymoma, pineal tumours, meningioma, germ-cell CNS tumours, pituitary tumours, CNS lymphoma, acoustic neuroma, medulloblastoma, and spinal cord tumours. Radiotherapy for primary CNS tumours is described along with its side effects, and chemotherapy for these diseases is reviewed. Brain metastases far outnumber primary brain tumours, with generally poor prognosis, but this relates both to the pathology and patient performance status. Appropriate treatment may include surgery, radiotherapy, and/or chemotherapy.

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24

(Editor), Jurij J. Hostynek, and Howard I. Maibach (Editor), eds. Nickel and the Skin: Absorption, Immunology, Epidemiology, and Metallurgy (Dermatology, Clinical and Basic Science). Informa Healthcare, 2002.

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25

Charles, Parish Lawrence, Millikan Larry E. 1936-, and Amer Mohamed, eds. Global dermatology: Diagnosis and management according to geography, climate, and culture. New York: Springer-Verlag, 1994.

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26

Global Dermatology: Diagnosis and Management According to Geography, Climate, and Culture. Springer, 1994.

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27

Williams, Hywel C. Atopic Dermatitis: The Epidemiology, Causes and Prevention of Atopic Eczema. Cambridge University Press, 2000.

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28

Williams, Hywel C. Atopic Dermatitis: The Epidemiology, Causes and Prevention of Atopic Eczema. Cambridge University Press, 2009.

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29

Atopic Dermatitis: The Epidemiology, Causes and Prevention of Atopic Eczema. Cambridge University Press, 2000.

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30

Williams, Hywel C. Atopic Dermatitis: The Epidemiology, Causes, and Prevention of Atopic Eczema. Cambridge University Press, 2000.

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31

Williams, Hywel C. Atopic Dermatitis: The Epidemiology, Causes and Prevention of Atopic Eczema. Cambridge University Press, 2005.

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32

Chanmugam, Arjun S., Richard Rothman, Sanjay Desai, and Shannon Putman, eds. Infectious Diseases Emergencies. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199976805.001.0001.

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Infectious Diseases Emergencies is a compact reference that summarizes the key topics of those infectious disease processes that are most commonly seen in emergency departments, clinics, and urgent care facilities. The opening section reviews principles of infectious disease management and general management of severe infections in acute and emergency environments. The following sections provide a “head-to-toe” synopsis of common infections presenting in both outpatient and acute care settings, including the following human areas: central nervous system; ear, nose, and throat; ocular; cardiovascular; pulmonary; gastrointestinal; genitourinary; skin and soft tissue; and bone and joint. The concluding sections discuss vector-borne infections, infections in special populations, bioterrorism, and finally antibiotic resistance. Each chapter covers some basic elements of the disease, epidemiology, diagnosis and tests, organisms involved, treatment, and other key issues. Concisely written and consistently organized chapters outline the most useful elements of diagnosis and treatment for easy memorization and clarity.

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33

Dermatology: Health Care Needs Assessment : The Epidemiologically Based Needs Assessment Reviews, Second Series. Radcliffe Publishing Ltd, 1997.

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34

Dr, Stevens Andrew, Raftery James Professor, and Wessex Institute for Health Research and Development, eds. Dermatology: Health care needs assessment : the epidemiologically based needs assessment reviews, second series. Oxford: Radcliffe Medical Press, 1997.

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35

Török, M. Estée, Fiona J. Cooke, and Ed Moran. Immunodeficiency and HIV. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199671328.003.0024.

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This chapter covers primary and secondary immunodeficiency, antibody deficiency syndromes, selective T-cell deficiency, infections in asplenic patients and transplant recipients, neutropenic sepsis, HIV epidemiology, natural history, and classification, initial evaluation of the HIV patient, skin, oral, cardiovascular, neurological, and pulmonary complications, HIV gastrointestinal, liver, and kidney disease, HIV infection and malignancy, as well as HIV prevention.

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36

Stuart, Philip E., Lam C. Tsoi, Caely A. Hambro, and James T. Elder. Genetics of psoriasis. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198737582.003.0005.

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Psoriasis is an immune-mediated inflammatory disease (IMID) characterized by skin inflammation, epidermal hyperplasia, increased risk of arthritis, and cardiovascular morbidity. Substantial evidence indicates that psoriasis is driven by abnormal interactions between cells of the innate and adaptive host defence systems, including keratinocytes, dendritic cells, and T-cells, resulting in a dysregulated immune response and markedly increased epidermal proliferation. The precise aetiology of psoriasis remains unknown. Here, we review how innate and adaptive host defence responses are regulated by genetic factors that modulate the overall risk of psoriasis and dictate whether the disease affects the skin and/or the joints. Specifically, we review the epidemiologic basis for considering psoriasis as a genodermatosis, summarize knowledge derived from linkage and association studies of cutaneous psoriasis (PsC) and psoriatic arthritis (PsA), and attempt to relate genetic and immunologic discoveries in a pathogenetic framework that may eventually allow prediction of the development of PsA in psoriatic individuals.

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37

Pearson, Andrew. Tularaemia. Oxford University Press, 2011. http://dx.doi.org/10.1093/med/9780198570028.003.0031.

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Tularaemia is a plague-like bacterial disease of animals (particularly rodents, hares, and rabbits) and man caused by five subspecies of Francisella. Two subspecies predominate: F. tularensis tularensis in North America and F. tularensis holarctica throughout the northern hemisphere. F. tularensis occurs in persistent natural foci causing localized epidemics and sporadic cases in man.Francisella tularensis subspecies tularensis was described originally as causing a more virulent form of tularaemia than was seen in Europe. More recently recognized are subpopulations of Francisella tularensis subspecies tularensis which have markedly different virulence for man. These have been designated A1a, A1b and A2. Infections resulting from type A1b have been shown to have an attributable mortality of 24% as compared to 4% for tularaemia caused by A1a types.F. tularensis is one of the most potent bacterial pathogens affecting humans with an infective dose from 1 to 10 organisms. The incubation period is usually 3–5 days (range from 1–21 days). Onset of disease is abrupt, with fever, chills, fatigue, general body aches, and headache. When the bacteria are acquired through skin or mucous membranes, tender regional node enlargement may become conspicuous. When bacteria are inhaled, the infection will result in deep lymph node enlargement.The clinical epidemiology of human infection is complex since it relates to one of four modes of transmission of the agent harboured in multiple hosts from diverse ecosystems. Clinical presentation of the human disease is indicative of both the mode of transmission and often the source of infection in a specific ecosystem. Tularaemia presenting as ulceroglandular disease results from either vector-borne infection from mosquito or tick bites or occurs as a result of animal contact from bites, hunting or from skinning hares or muskrats. Oropharyhgeal and typhoidal infections predominate in waterborne outbreaks of F. tularensis holarctica. Pulmonary or influenza disease results from airborne transmission associated with either farmers moving rodent contaminated hay or laboratory acquired infection. An intentional aerosol release of F. tularensis tularensis would be expected to result in clinical manifestations similar to those recognized in natural respiratory tularaemia. Both vector-borne and airborne transmission of F. tularensis may both be associated with florid skin manifestations as a presenting symptom of tularaemia. Pulmonary or typhoidal forms of the tularaemia may occur as a complication of localized infection.

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