Acute Lymphocytic Leukemia (ALL)

Acute Lymphocytic Leukemia (ALL)

Acute lymphocytic leukemia (ALL) is a fast-growing cancer of a type of white blood cells called lymphocytes. These cells are found in the bone marrow and other parts of the body. Acute lymphocytic leukemia (ALL) occurs when the body produces a lar…

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Febrile neutrophilic dermatosis

<h1>Febrile neutrophilic dermatosis</h1>

Sweet’s syndrome (SS), or acute febrile neutrophilic dermatosis[1][2] is a skin disease characterized by the sudden onset of fever, an elevated white blood cell count, and tender, red, well-demarcated papules and plaques that show dense infiltrates by neutrophil granulocytes on histologic examination.

The syndrome was first described in 1964 by Robert Douglas Sweet. It was also known as Gomm-Button disease in honour of the first two patients Sweet diagnosed with the condition.[3][4][5]


  • 1 Signs and symptoms
  • 2 Cause
    • 2.1 Systemic diseases
    • 2.2 Associations
  • 3 Diagnosis
    • 3.1 Laboratory studies
    • 3.2 Definition
  • 4 Treatment
  • 5 See also
  • 6 References
  • 7 External links

Signs and symptoms[edit]

Pustular lesions with central necrosis on the left leg of a patient with Sweet’s syndrome associated with Crohn’s disease.

Punch biopsy of a skin lesion showing neutrophilic infiltration in the dermis, with no evidence of vasculitis (same patient with Crohn’s disease).

Acute, tender, erythematous plaques, nodes, pseudovesicles and, occasionally, blisters with an annular or arciform pattern occur on the head, neck, legs, and arms, particularly the back of the hands and fingers. The trunk is rarely involved. Fever (50%); arthralgia or arthritis (62%); eye involvement, most frequently conjunctivitis or iridocyclitis (38%); and oral aphthae (13%) are associated features.[citation needed]


SS can be classified based upon the clinical setting in which it occurs: classical or idiopathic SS, malignancy-associated SS, and drug-induced SS.[6]

Systemic diseases[edit]

SS is a reactive phenomenon and should be considered a cutaneous marker of systemic disease.[6] Careful systemic evaluation is indicated, especially when cutaneous lesions are severe or hematologic values are abnormal. Approximately 20% of cases are associated with malignancy, predominantly hematological, especially acute myelogenous leukemia (AML). An underlying condition (streptococcal infection, inflammatory bowel disease, nonlymphocytic leukemia and other hematologic malignancies, solid tumors, pregnancy) is found in up to 50% of cases. Attacks of SS may precede the hematologic diagnosis by 3 months to 6 years, so that close evaluation of patients in the “idiopathic” group is required.

There is now good evidence that treatment with hematopoietic growth factors — including granulocyte colony-stimulating factor (G-CSF), which is used to treat AML, and granulocyte-macrophage colony-stimulating factor — can cause SS.[citation needed] Lesions typically occur when the patient has leukocytosis and neutrophilia but not when the patient is neutropenic. However, G-CSF may cause SS in neutropenic patients because of the induction of stem cell proliferation, the differentiation of neutrophils, and the prolongation of neutrophil survival.


Although it may occur in the absence of other known disease, SS is often associated with hematologic disease (including leukemia), and immunologic disease (rheumatoid arthritis, inflammatory bowel disease, Behçet’s syndrome).

A genetic association has been suggested,[7] but no specific genetic link has been identified.


The clinical differential diagnosis includes pyoderma gangrenosum, infection, erythema multiforme, adverse drug reactions, and urticaria.[citation needed] Recurrences are common and affect up to one third of patients.

Laboratory studies[edit]

Studies show a moderate neutrophilia (less than 50%), elevated ESR (greater than 30 mm/h) (90%), and a slight increase in alkaline phosphatase (83%). Skin biopsy shows a papillary and mid-dermal mixed infiltrate of polymorphonuclear leukocytes with nuclear fragmentation and histiocytic cells. The infiltrate is predominantly perivascular with endothelial-cell swelling in some vessels, but vasculitic changes (blood clots; deposition of fibrin, complement, or immunoglobulins within the vessel walls; red blood cell extravasation;inflammatory infiltration of vascular walls) are absent in early lesions.

Perivasculitis occurs secondarily, because of cytokines released by the lesional neutrophils. True transmural vasculitis is not an expected finding histopathologically in SS.


Sweet described a disease with four features: fever; leukocytosis; acute, tender, red plaques; and a papillary dermal infiltrate of neutrophils. This led to the name acute febrile neutrophilic dermatosis. Larger series of patients showed that fever and neutrophilia are not consistently present.[citation needed] The diagnosis is based on the two constant features, a typical eruption and the characteristic histologic features;[citation needed] thus the eponym “Sweet’s syndrome” is used.


Systemic corticosteroids such as (prednisone) can produce rapid improvement and are the “gold standard” for treatment.[citation needed] The temperature, white blood cell count, and eruption improve within 72 hours. The skin lesions clear within 3 to 9 days. Abnormal laboratory values rapidly return to normal. There are, however, frequent recurrences. Corticosteroids are tapered within 2 to 6 weeks to zero.

Resolution of the eruption is occasionally followed by milia and scarring. The disease clears spontaneously in some patients. Topical and/or intralesional corticosteroids may be effective as either monotherapy or adjuvant therapy. Oral potassium iodide or colchicine may induce rapid resolution.

Patients who have a potential systemic infection or in whom corticosteroids are contraindicated can use these agents as a first-line therapy. In one study, indomethacin, 150 mg per day, was given for the first week, and 100 mg per day was given for 2 additional weeks. Seventeen of 18 patients had a good initial response; fever and arthralgias were markedly attenuated within 48 hours, and eruptions cleared between 7 and 14 days.

Patients whose cutaneous lesions continued to develop were successfully treated with prednisone (1 mg/kg per day). No patient had a relapse after discontinuation of indomethacin. Other alternatives to corticosteroid treatment include dapsone, doxycycline, clofazimine, and cyclosporine. All of these drugs influence migration and other functions of neutrophils.

See also[edit]

  • Chloroma
  • List of cutaneous conditions
  • Periodic fever syndrome – also known as autoinflammatory diseases or autoinflammatory syndromes.


  • ^ Mustafa NM, Lavizzo M (2008). “Sweet’s syndrome in a patient with Crohn’s disease: a case report”. J Med Case Reports. 2: 221. doi:10.1186/1752-1947-2-221. PMC 2503996 . PMID 18588703. 
  • ^ James, W; Berger, T; Elston D (2005). Andrews’ Diseases of the Skin: Clinical Dermatology (10th ed.). Saunders. p. 145. ISBN 0-7216-2921-0. 
  • ^ synd/3019 at Who Named It?
  • ^ Sweet RD (1964). “An acute febrile neutrophilic dermatosis”. Br. J. Dermatol. 76: 349–56. doi:10.1111/j.1365-2133.1964.tb14541.x. PMID 14201182. 
  • ^ Cohen, Phillip R (2007). “Sweet’s syndrome – a comprehensive review of an acute febrile neutrophilic dermatosis”. Orphanet Journal of Rare Diseases. 2 (34). doi:10.1186/1750-1172-2-34. PMC 1963326 . PMID 17655751. Retrieved 4 Jan 2011. 
  • ^ a b Cohen PR (2007). “Sweet’s syndrome–a comprehensive review of an acute febrile neutrophilic dermatosis”. Orphanet J Rare Dis. 2: 34. doi:10.1186/1750-1172-2-34. PMC 1963326 . PMID 17655751. 
  • ^ Parsapour K, Reep MD, Gohar K, Shah V, Church A, Shwayder TA (July 2003). “Familial Sweet’s syndrome in 2 brothers, both seen in the first 2 weeks of life”. J. Am. Acad. Dermatol. 49 (1): 132–8. doi:10.1067/mjd.2003.328. PMID 12833027. 
  • External links[edit]

    Reactive neutrophilic dermatoses


    • Acute erythema nodosum
    • Marshall syndrome
    • Neutrophilic eccrine hidradenitis
    • Pyogenic arthritis–pyoderma gangrenosum–acne syndrome
    • Rheumatoid neutrophilic dermatitis
    • Superficial granulomatous pyoderma
    • Sweet’s syndrome-like dermatosis
    • Vesicopustular dermatosis


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    Triamcinolone acetonide

    <h1>Triamcinolone acetonide</h1>

    (Learn how and when to remove this template message)

    Triamcinolone acetonide is a synthetic corticosteroid used topically to treat various skin conditions, to relieve the discomfort of mouth sores and intra-articularly by proceduralists to treat various joint conditions.[1] In nasal spray form, it is used to treat allergic rhinitis. It is a more potent derivative of triamcinolone, and is about eight times as potent as prednisone.[2]

    It is also known under the brand names Kenalog (topical) and Volon A as an injection, to treat allergies, arthritis, eye diseases, intestinal problems, and skin diseases. There are possible risks from an injection. It has been known to cause fat and muscle loss at an injection site, leaving a large divot bone deep.[3]

    In 2014, the FDA made triamcinolone acetonide an over-the-counter drug in the United States in nasal spray form under the brand name Nasacort.[4]


    • 1 Medical uses
    • 2 Contraindications
    • 3 Pharmacology
      • 3.1 Pharmacodynamics
    • 4 Chemistry
    • 5 Veterinary use
    • 6 See also
    • 7 References

    Medical uses[edit]

    Triamcinolone acetonide as an intra-articular injectable has been used to treat a variety of musculoskeletal conditions. When applied as a topical ointment, applied to the skin, it is used to mitigate blistering from poison ivy, oak, and sumac,[citation needed]. When combined with Nystatin, it is used to treat skin infections with discomfort from fungus, though it should not be used on the eyes, mouth, or genital area.[5] It provides relatively immediate relief and is used before using oral prednisone. Oral and dental paste preparations are used for treating aphthous ulcers.

    As an intravitreal injection, triamcinolone acetonide has been used to treat various eye diseases and has been found useful in reducing macular edema.[6] Drug trials have found it to be as efficient as anti-VEGF drugs in eyes with artificial lenses over a two-year period. A systematic review did not find any evidence of any benefit in preventing vision loss in eyes treated with triamcinolone acetonide over placebo, for patients with age-related macular degeneration.[7]

    Uncommonly, intramuscular injection of triamcinolone acetonide may be indicated for the control of severe or incapacitating allergic states for which conventional treatments have failed, such as asthma, atopic dermatitis, contact dermatitis, perennial or seasonal allergic rhinitis, serum sickness, and transfusion and drug hypersensitivity reactions.


    As with all immunosuppressant drugs, triamcinolone acetonide should not be taken by persons suffering from infectious diseases, either currently or in recuperation or soon thereafter. Contact with infectious persons should be avoided during the entire course of treatment. Users who contract an infection during their regimen should contact their doctors to discuss whether to discontinue triamcinolone acetonide.

    Triamcinolone acetonide should not be taken if the patient is also taking any other steroid or immunosuppressant, or if they have recently undergone any medical procedures involving the administration of steroids (e.g. nerve block).[citation needed]

    Evidence suggests that usage of traimcinolone acetonide or other steroids to treat macular edema increases the risk of increasing intraocular pressure in patients.[8]

    Many drugs have been demonstrated to increase triamcinolone acetonide concentration in the blood to well above the intended level. Patients should inform doctors about any other drugs they are taking.[citation needed]

    Triamcinolone acetonide should not be used by those with tuberculosis or untreated fungal, bacterial, systemic viral or herpes simplex infections without consulting a doctor first.



    Triamcinolone acetonide is a corticosteroid. It is specifically a glucocorticoid, or an agonist of the glucocorticoid receptor.


    See also: List of corticosteroids

    Triamcinolone acetonide, also known as 9α-fluoro-16α-hydroxyprednisolone 16α,17α-acetonide or as 9α-fluoro-11β,16α-17α,21-tetrahydroxypregna-1,4-diene-3,20-dione cyclic 16,17-acetal with acetone, is a synthetic halogenated cyclic ketal pregnane corticosteroid.[9] It is the C16α,17α acetonide of triamcinolone.[9]

    Veterinary use[edit]

    Triamcinolone acetonide is also used in veterinary medicine as an ingredient in topical ointments and in topical sprays for control of pruritus in dogs.[10] A series of injections with triamcinolone acetonide or another corticosteroid may reduce keloid size and irritation. It is used as a preinductor and/or inductor of birth in cows. It is also used in the horse racing industry, it being a banned substance if found in a horse’s system on race day.[11]

    See also[edit]

    • Topical steroid relative strength groupings list


  • ^ Triamcinolone Acetonide Drug information from MedLine Plus
  • ^ Nasacort medication leaflet
  • ^ “Kenalog injection,” Web M.D.
  • ^
  • ^ “Nystatin And Triamcinolone (Topical Route)”. Mayo Foundation for Medical Education and Research. Retrieved 18 May 2016. 
  • ^ Grover DA, Li T, Chong CCW (2008). “Intravitreal steroids for macular edema in diabetes”. Cochrane Database Syst Rev (1): CD005656. doi:10.1002/14651858.CD005656.pub2. PMC 3804331 . PMID 18254088. CS1 maint: Multiple names: authors list (link)
  • ^ Geltzer A, Turalba A, Vedula SS (2013). “Surgical implantation of steroids with antiangiogenic characteristics for treating neovascular age-related macular degeneration”. Cochrane Database Syst Rev (1): CD005022. doi:10.1002/14651858.CD005022.pub3. PMC 4269233 . PMID 23440797. CS1 maint: Multiple names: authors list (link)
  • ^ Gewaily D, Muthuswamy K, Greenberg PB (2015). “Intravitreal steroids versus observation for macular edema secondary to central retinal vein occlusion”. Cochrane Database Syst Rev. 9 (9): CD007324. doi:10.1002/14651858.CD007324.pub3. PMC 4733851 . PMID 26352007. 
  • ^ a b J. Elks (14 November 2014). The Dictionary of Drugs: Chemical Data: Chemical Data, Structures and Bibliographies. Springer. pp. 1228–. ISBN 978-1-4757-2085-3. 
  • ^ GENESIS® (triamcinolone acetonide) Topical Spray Drug information
  • ^ Champion Hurdle favourite Yanworth failed drug test
  • Antiglucocorticoids

    • Antagonists: Aglepristone
    • Ketoconazole
    • Mifepristone
    • Ulipristal acetate

    Synthesis modifiers

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    Mineralocorticoids and antimineralocorticoids
    List of corticosteroids

    See also
    Receptor/signaling modulators
    Glucocorticoids and antiglucocorticoids
    Mineralocorticoid receptor modulators
    List of corticosteroids




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