Pemphigus Vulgaris: A Closer Look Pemphigus vulgaris is a serious but rare autoimmune disorder of the epithelial cells and mucosal lining of the skin. The first cases were recorded by McBride in 1771 and by Whichman in 1979. McBride was to describe the first to casualties as being caused by “bloody ichor” and “putrid ulcers”. (Jordon, 2013) However, Whichman was the one who would originally name the disease as pemphigus. The word “pemphigus” is of Greek origin which means blister or bubble. (Jordon, 2013) As the name suggests, this disease causes painful blisters or bullous erosions of the squamous epithelia and mucous membranes. It can be sub-classified based on the location of the lesions in the epidermis. Pemphigus vulgaris is considered to be one of the deep forms of the disease. The lesions appear deep into the epidermis of the skin right above the basal lamina. (Zeina, 2013) Pathology The autoimmune process that causes pathogenicity is the formation and activation of antibodies targeting the keratinocyte desmosomal cadherins or for simplicity desmosomes. The latter is responsible for the adherence of keratinocytes, and when it is targeted by these antibodies the desmosomes lose their ability to maintain keratinocytes together and the cells become detached. “Ultrastructural studies of pemphigus lesions have suggested that dissolution of desmosomes may result in the formation of blisters. This is a phenomenon known as acantholysis.” (Loannides, Lazaridou, Rigopolous, 2008) Studies have shown that the antigens responsible for this autoimmune attack have components of the actual desmosome. Two transmembrane glycoproteins have been identified. One being desmoglein ( Dsg) and desmocollin (Dsc). Both of these have three isofor... ... middle of paper ... ...glubulin isotypes correlate with disease activity, morphology, duration, and hla association in pemphigus vulgaris. Autoimmunity, 45(7), 516-526. DOI:10.3109/08916934.2012.702811 IPPF. (2013). International pemphigoid and pemphigus foundation. Retrieved from http://www.pemphigus.org/research/clinically-speaking/treatments/ Jordon, R. (2003, January 31)Pemphigus. Pemphigus:A historical perspective.Retrieved from http://www.pemphigus.org/pemphigus-a-historical-prescpective-2/ Loannides, D; Lazaridou, E; Rogopolous, D. (2008). Pemphigus. European academy of dermatology and venereology,22, 1478-1496. DOI: 10.1111/jdv.2008.22.issue-12 Lowe, S. (2007). A patient's journey: Pemphigus vulgaris. BMJ, 335, 1152. DOI: http://dx.doi.org/10.1136/bmj.39374.504884.BE Pemphigus Vulgaris Network (2014). What is pemphigus vulgaris? Retrieved from http://www.pemphigus.org.uk/
Arch Dermatol. 2007;143(1):124–125. Puchenkova, S. G. (1996). "
Barone, Eugene J., Judson C. Jones, and Joann E. Schaefer. "Hidradenitis Suppurativa." Skin Disorders. Philadelphia: Lippincott Williams & Wilkins, 2000. 21-25. Print.
Acute paronychia is clinically characterised by rapid onset of erythema, oedema, and tenderness of the proximal...
1. Goodpasture syndrome it is a unique and rare autoimmune disease characterized by a type II hypersensitivity reaction leading to formation of antiantibodies against the glomerular basement membrane (GBM). These anti-GBM antibodies attack α 3 chain of the type IV collagen cells located in the renal glomeruli and pulmonary alveoli. The result of this interaction expresses in inflammatory responses and tissue damages in the kidneys and the lungs. In the Goodpasture syndrome, the T- and B- cell activation play an important role in inducing the formation of the anti-GBM antibodies as a condition of endogenous antigen recognition on the GBM. The anti- GBM antibodies bind to the basement membrane in the kidneys inducing the release of monocytes,
“Cells Involved In Immune Responses and Antigen Recognition.” Microbiology and Immunology. Web. 18 Dec. 2011. .
This condition occurs when the immune system produce abnormal response against substances that are normally present in the body. The immune system becomes incapable in differentiating healthy body tissues and antigens, which results in the destruction of normal body tissues. This is usually characterized by hypersensitivity reaction almost identical to the response in allergic conditions. The cause of the autoimmune disorders are still unknown, however, there is a theory stating that some microorganisms or drugs may have trigger these changes. These can also affect one or multiple organs or tissues. Some of the most commonly affected are blood vessels, joints, muscles, red blood cells, skin, and connective tissues.
The history of urticaria is a fascinating account of mankind gradually growing to understand human diseases. The process starts with the many different names this disease has been given to in the past. The school of Hippocrates in 4th century BC recognized urticaria with nettles. The roman school instead focused on its burning sensation and is where Plinius named it uredo. In the 10th century, Hali Ben Abbas used the name essera because it means mountain or elevation, alluding that the welt is above skin level. In 18th century, Zelder called it urticatio, and in 1792, urticaria was the accepted name. A couple of words have been made during recent times but they did not clearly distinguish the disease from the other skin diseases. Some writings of the 16th century can be rediscovered indicating that strawberries and shellfish were implicated as a cause for urticaria. There were many other theories that tried to explain the causes of the formation of these raised welts. Many stated that certain foods were the reason but slowly doctors discovered that it is not just food that triggers urticaria.
Other lesions, such as eczema, body lice, insect bites, fungal infections, poison ivy, and various forms of dermatitis can make a person susceptible to this infection.... ... middle of paper ... ... The New York Times.
Graves’ disease is considered an auto immune disorder. It is also a hyperthyroid disorder that leads to the over activity of the thyroid gland. Graves’ disease is a condition that occurs when the immune system mistakenly attacks healthy tissue. Many people suffer from symptoms. This paper will talk about the causes of the disease, research that has been conducted and how it can be treated.
Psoriasis and psoriatic arthritis are two symptoms of a single disease caused by an overactive immune system attacking the skin and joints of the affected individual. The “t-cells” or white blood cells that fight infection within your body are also the cause of psoriasis. Psoriasis is characterized by red patches of inflamed skin with a build-up of silvery-white colored dead skin or scale. Psoriatic arthritis is similar to rheumatoid arthritis as it is an inflammation of the joints. This inflammation can cause pain, stiffness, and even disfigurement. The same white blood cells attacking the skin are also attacking the cartilage in the joints. However, what is causing the white blood cells to attack the skin and joints is still unclear.
Psoriasis is an autoimmune disease that affects 125 million people world wide according to the World Psoriasis Day consortium. The origin of psoriasis is unknown, but many doctors and researches believe that genetics, along with environmental factors, trigger a hyperactive reaction of the immune system that leads to the relatively harmless, yet uncomfortable skin disease. The response of the immune system induces skin cells to multiply and mature rapidly, causing the skin cells to accumulate on top of each other and as a result, the skin becomes red, scaly, itchy, and forms thick patches on the skin. Despite that this disease is the most frequent auto-immune disease in the world, there is no cure for it. Not only is there no cure for psoriasis, but this disease can lead to other problems depending on the severeness of the disorder for example: psoriatic arthritis. However, this chronic disease has several treatment options that if used correctly and in a timely manner, will reduce and lessen the symptoms.( Although there is no cure for psoriasis, understanding how it begins, recognizing the symptoms, and learning about treatment options can enhance the quality of life for a person diagnosed with psoriasis.)
The second layer of the skin is called the dermis and is also known as the middle layer. The dermis is what holds the body together. The dermis has layers to it as well as the epidermis. There are two layers to the dermis, the papillary layer and the reticular layer. The cells of the dermis are fibroblast, macrophages, mast cells, and scattered white blood cells (wbc’s). the dermis is richly supplied with nerve fibers and BV;s. dermal BV’s is also a part of the integumentary system, dermal BV,s have converging and diverging vessels that ar...
Schepis, Carmelo, Donatella Greco, and Corrado Romano. "Cardiofaciocutaneous (CFC) Syndrome." Australasian Journal of Dermatology 40.2 (1999): 111-13. Print.
Psoriasis is a chronic skin disorder, easily identified by its symptoms of white, scaly skin and red lesions, though not so easily cured or understood. In psoriasis, skin cells mature faster than the body can shed them, causing a buildup. Although there are many theories as to what the cause of such a disease might be – genetics, stress, or other triggers – no one is quite sure why the disease occurs, or what could be a possible way to fully cure it. In this essay we will explore the symptoms, types, and effects of this condition, and also some of the known treatments.
5.) Mylonakis, M.D., Eleftherios. PPD skin test. 10 June 2006 MedlinePlus. 26 July 2006 .