Cutaneous syndrome

Some skin damage frequently accompanies ARS. However, the cutaneous syndrome can also result from localized acute radiation exposure to the skin, usually from direct handling of radioactive sources or from contamination of the skin or clothes (2,8) (see Figs. 4.1 and 4.2) With localized exposure, even with high doses, the victim frequently survives, because the whole body usually does not receive the localized dose. However, if a patient with localized radiation induced cutaneous injury has also received whole body irradiation from an external source, the cutaneous damage increases the risk for death from the whole body exposure (2). Patients with the hematopoietic syndrome due to whole body irradiation will recover more slowly, if at all, from cutaneous injury due to bleeding, infection and poor wound healing (2). 

Paraneoplastic autoimmune syndromes. Autoimmune diseases that are caused by tumour-induced perturbations of the immune system with damaging effects on various organ systems (e.g. cancer-associated retinopathy, paraneoplastic neurological syndromes, paraneoplastic cutaneous syndromes). In most cases, autoantibodies generated by antitumour immunity are responsible for the tissue injury. 

Wright P (1975) Untoward affects associated with practolol administration oculomuco-cutaneous syndrome. Br Med J 1 595-598... 

Patients with Stevens—Johnson syndrome or toxic epidermal necrolysis due to antiepileptic drugs have been compared with patients with antiepileptic drug-related hypersensitivity syndrome the results are shown in Table 1 [79 ]. The authors concluded that these cutaneous syndromes may share some clinical and laboratory features. 

Winkelmann, R. K., Perry, H. O. and Achor, R. W. (1963). Cutaneous syndromes produced as side effects of triparanol therapy. Arch. Dermatol, SI, 312... 

Inflammatory and immune diseases Autoimmune disease (A,I), asthma (A), osteoarthritis (I), rheumatoid arthritis (I), septic shock (A,I), infections (A,I), familial cold auto-inflammatory syndrome (I), Muckle Wells syndrome (I), chronic infantile neurological cutaneous and articular syndrome/neonatal onset multisystemic inflammatory disease (CINCA/NOMID) (I), Crohn s disease (I), gout (I), acute renal failure (A,l)... 

Denileukin diftitox is a combination of the active sections of interleukin 2 and diphtheria toxin. It binds to high-affinity interleukin 2 receptors on the cancer cell (and other cells), and the toxin portion of the molecule inhibits protein synthesis to result in cell death. The pharmacokinetics of denileukin diftitox are best described by a two-compartment model, with an a half-life of 2 to 5 minutes and a terminal half-life of 70 to 80 minutes. Denileukin diftitox is used for the treatment of persistent or recurrent cutaneous T-cell lymphoma whose cells express the CD25 receptor. Side effects include vascular leak syndrome, fevers/chills, hypersensitivity reactions, hypotension, anorexia, diarrhea, and nausea and vomiting. 

Ramos-Casals, M., Anaya, J. M., Garcia-Carrasco, M. et al. Cutaneous vasculitis in primary Sjogren syndrome classification and clinical significance of 52 patients. Medicine (Baltimore) 83 96-106, 2004. 

Hypersensitivity Anaphylactoid purpura, anaphylaxis, angioneurotic edema, myocarditis, pericarditis, polyarthralgia, pulmonary infiltrates with eosinophilia, systemic lupus erythematous exacerbation, urticaria hypersensitivity syndrome (cutaneous reaction, eosinophilia, and one or more of the following Hepatitis, pneumonitis, nephritis, myocarditis, pericarditis, fever, lymphadenopathy). Muscuioskeietai - ArVr ra g a, arthritis, bone discoloration, joint stiffness and swelling, myalgia, polyarthralgia. 

Dermatological reactions Patients have rarely developed serious cutaneous reactions, such as Stevens-Johnson syndrome, during treatment with voriconazole. Photosensitivity Voriconazole has been infrequently associated with photosensitivity skin reaction, especially during long-term therapy. It is recommended that patients avoid strong, direct sunlight during voriconazole therapy. 

Fligh doses of rifampin (greater than 600 mg) given once or twice weekly have resulted in a high incidence of adverse reactions including the following Flu-like syndrome hematopoietic reactions cutaneous, Gl, and hepatic reactions shortness of breath shock renal failure asymptomatic elevations of liver enzymes rash. Rifabutin... 

Cutaneous reactions such as rash or Stevens-Johnson syndrome are also consist with initiation through protein haptenation, although in this case dendritic cell activation/ migration and T-cell propagation are involved [31]. Other immune mediators such as cytokines, nitric oxide and reactive oxygen species which may be linked to the formation of reactive metabolites may also be implicated, as may specific processes occurring at the level of the keratinocyte. 

Hypersensitivity reactions, such as pruritus, cutaneous vasculitis, and thrombocytopenia, are seen in some patients, and an immune-mediated systemic flulike syndrome with thrombocytopenia also has been described. Rifampin imparts a harmless red-orange color to urine, feces, saliva, sweat, tears, and contact lenses. Patients should be advised of such discoloration of body fluids. 

Contraindications Hypersensitivity to pimecrolimus or any component of the formulation, Netherton s syndrome (potential for increased systemic absorption), application to active cutaneous viral infections. 

The standard dosage, 25 mg/kg (maximum 1.5 g) twice daily, should be given after meals. Tablets should be chewed. For strongyloides infection, treatment is for 2 days. Cure rates are reportedly 93%. A course can be repeated in 1 week if indicated. In patients with hyperinfection syndrome, the standard dose is continued twice daily for 5-7 days. For cutaneous larva migrans, thiabendazole cream can be applied topically, or the oral drug can be given for 2 days (although albendazole is less toxic and therefore preferred). 

As mentioned above, gas has been widely used and it is a powerful vesicant agent. In the form of vapor, it damages the respiratory tract. Eyes become temporarily blind and the skin in contact with the substance becomes inflammatory. The sweaty zones of skin are the most damaged as well as sensitive mucous membranes. If no treatment is applied, the cutaneous reaction provokes blisters full of liquid after 4-8 h. Spread in the form of particles, the gas penetrates the respiratory tract and destroys the mucous membranes with a respiration distress syndrome. Lungs suffer from emphysemae and edema due to the presence of fluids, which may cause a death similar to a drowning if the dose is too strong. 

Mutations in the gene for p53 also cause tumors in more than 90% of human cutaneous squamous cell carcinomas (skin cancers) and about 50% of all other human cancers, p53 is defective. Those very rare individuals who inherit one defective copy of p53 commonly have the Li-Fraumeni cancer syndrome, in which multiple cancers (of the breast, brain, bone, blood, lung, and skin) occur at high frequency and at an early age. The explanation for multiple tumors in this case is the same as that for Rb mutations an individual bom with one defective copy of p53 in every somatic cell is likely to suffer a second p53 mutation in more than one cell in his or her lifetime. 

Other bothersome side effects are related to specific agents. Niacin, for instance, is often associated with cutaneous vasodilation and a sensation of warmth when doses are administered, but administering an extended-release form of this drug can reduce these sensations.71 99 Some fairly serious problems, including liver dysfunction, gallstones, and pancreatitis, can occur with many antihyperlipidemia drugs, but the incidence of these side effects is rare. Cardiovascular problems such as arrhythmias, blood dyscrasias, and angioneurotic syndrome may also occur with fibric acids. 

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. 

Cutaneous T-Cell Lymphoma Mycosis Fungoides and Sezary Syndrome... 

M12. McDuffie, F. C., Sams, W. M., Maldonado, J. E., Andreini, P. H., Conn, D. L., and Samayoa, E. A., Hypocomplementemia with cutaneous vasculitis and arthritis. Possible immune complex syndrome. Mayo Clin. Proc. 48, 340-348 (1973). 

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. 

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