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Cutaneous hyperpigmentation

Cotellessa C, Peris K, Onorati MT, et al (1999) The use of chemical peelings in the treatment of different cutaneous hyperpigmentation. Dermatol Surg 25 450-454... [Pg.159]

Discrete cutaneous hyperpigmentation occurred in two patients after high-dose chemotherapy with cyclophosphamide, etoposide, and carboplatin (29). [Pg.1027]

Mouton RW, Jordaan HF, Schneider JW. A new type of minocycline-induced cutaneous hyperpigmentation. Clin Exp Dermatol 2004 29 8-14. [Pg.1768]

CoteUessa C, Peris K, Eaignoli MC, Mordenti C, Giacomello RS, Chimenti S (2003) Microabrasion versus microabrasion followed by 15% trichloroacetic acid for treatment of cutaneous hyperpigmentations in adult females. Dermatol Suig 29(4) 352-356... [Pg.86]

PCBs are chloracnegens as has been demonstrated in reports in capacitor workers (Taylor et al. 1977 Tindall 1985) and in other workers (Longnecker et al. 1997). Cutaneous hyperpigmentation eye discharge and palpebral edema have also been reported (Taylor et al. [Pg.228]

Skin Cutaneous hyperpigmentation following treatment with quinine is rare [23 ]. [Pg.396]

Cutaneous hyperpigmentation is more commonly seen in patients on antimalarials such as chloroquine, hydroxychloroquine, mepacrine and mefloquine. [Pg.396]

Post-inflammatory hyperpigmentation (PIH) is the acquired presence of darker macules and patches of skin occurring at sites of previous cutaneous inflammatory conditions. The processes preceding the altered skin color include mechanical injuries, allergic reactions, primary inflammatory skin disorders, and therapeutic interventions. [Pg.177]

Post-phlebrtic syndrome, a complication of acute DVT is estimated to occur in approximately 4% of the population (213). This syndrome is characterized by persistent pain, edema, hyperpigmentation, induration of the skin, and stasis ulceration (214). The post-phlebrtic syndrome may be due to venous hypertension as a result of outflow obstruction or damage to the valves and in the cutaneous microcirculation may manifest as tissue hypoxia and lymphatic obstruction. Chronic venous insufficiency may lead to post-phlebetic syndrome. The syndrome may be the result of abnormalities in the superficial, the perforator, or the deep venous system. The diagnosis is purely clinical. The pharmacologic treament of post-phlebetic syndrome is rather limited, with pentoxifylline reported to improve the healing rate of skin ulcers. [Pg.18]

Skin and subcutaneous tissue disorders Reversible cutaneous reactions have been observed and are generally mild to moderate. Reactions are characterised by a rash including localised eruptions mainly on the feet and hands (including severe hand and foot syndrome), but also on the arms, face or thorax, and frequently associated with pruritus. Eruptions generally occur within one week after the docetaxel infusion. Severe nail disorders are characterised by hypo- or hyperpigmentation and sometimes pain and onycholysis. [Pg.201]

Dose-limiting effects are in bold type. Cutaneous reactions (sometimes severe), hyperpigmentation, and ocular toxicity have been reported with virtually all nonhormonal anticancer drugs. For adverse interactions with other drugs, see The Medical Letter Handbook of Adverse Drug Interactions, 2003. [Pg.401]

These disorders are associated with acute or cutaneous manifestations (or both). In the acute state, the presentation may include abdominal pain, constipation, hypertension, tachycardia, and neuropsychiatric manifestations. Cutaneous problems consist of photosensitivity (itching, burning, redness, swelling, and scarring), hyperpigmentation, and sometimes hypertrichosis... [Pg.686]

Systemic vinblastine (velban, others) is approved for use in Kaposi s sarcoma and advanced cutaneous T-cell lymphoma. Intralesional vinblastine also is used to treat Kaposi s sarcoma. Intrale-sional bleomycin (blenoxane, others) is used for recalcitrant warts and has cytotoxic and proin-flammatory effects. Intralesional injection of bleomycin into the digits has been associated with a vasospastic response that mimics Raynaud s phenomenon, local skin necrosis, and flagellate hyperpigmentation. Intralesional bleomycin has been used for palliative treatment of squamous cell carcinoma. Systemic bleomycin has been used for Kaposi s sarcoma (see Chapter 51 for a more complete discussion of these agents). Liposomal anthracyclines [specifically doxorubicin (doxil, CAELYX)] may provide first-line monotherapy for advanced Kaposi s sarcoma. [Pg.1089]

B. Potential sequelae include erythema multiforme, keloids, infections, cos-metio tissue damage (fat atrophy and hyperpigmentation), contractures, paresthesias, neuritis, recurrent cutaneous emptions, paralysis, and regional vasospasm with vascular insufficiency. [Pg.237]

Postinflammatory hyperpigmentation can be seen after endogenous or exogenous inflammatory conditions. Essentially any disease with cutaneous inflammation can potentially result in postinflammatory hyperpigmentation in individuals capable of producing melanin. [Pg.143]


See other pages where Cutaneous hyperpigmentation is mentioned: [Pg.717]    [Pg.1763]    [Pg.717]    [Pg.1763]    [Pg.51]    [Pg.140]    [Pg.180]    [Pg.51]    [Pg.140]    [Pg.180]    [Pg.282]    [Pg.445]    [Pg.92]    [Pg.777]    [Pg.92]    [Pg.875]    [Pg.935]    [Pg.1072]    [Pg.1704]    [Pg.1652]    [Pg.300]    [Pg.109]    [Pg.891]    [Pg.92]    [Pg.208]    [Pg.238]    [Pg.103]    [Pg.19]    [Pg.84]    [Pg.127]    [Pg.144]    [Pg.145]   


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CUTANEOUS

Cutan

Cutans

Hyperpigmentation

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