Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0023473 (chronic myeloid leukemia)
 18,916 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Hydroxyurea is an antimetabolite agent used in the treatment of myeloproliferative disorders and sickle cell anaemia. Although hydroxyurea is relatively well tolerated, adverse effects often involve skin and mucous membrane during long-term therapy. A group of 510 patients affected by chronic myeloid leukaemia from 1977 to 1998 has been considered. Only 158 patients were treated with hydroxyurea and fulfilled inclusion/exclusion criteria of this study. A spectrum of severe cutaneous and mucosal changes (inflammatory and neoplastic) was seen in about 13% of patients (21 patients out of 158) and was studied in detail. Cutaneous and mucosal atrophy were observed in all 21 patients. Skin atrophy was often characterized by numerous telangiectases, especially on legs and on sun-exposed sites (16/21). Cutaneous, mucosal and nail hyperpigmentation was evident, albeit with variable extent, in 10 of the 21 patients. Severe stomatitis and glossitis with flattening of papillae were another common finding. Five patients, who received a particularly long treatment with hydroxyurea, developed squamous-cell neoplasms on sun-exposed sites (both squamous-cell carcinomas and keratoacanthomas). Acral changes were characteristic and constant, including acral erythema (21/21), dermatomyositis-like changes on the dorsa of hands (7/21), ulcers localized on acral areas of legs, on genitalia and oral mucosae (20/21). The frequency and the variety of these muco-cutaneous changes are reported and the mechanisms by which hydroxyurea may induce this muco-cutaneous syndrome-like group of changes, are proposed.
Clin Exp Dermatol 2001 Mar
PMID:Muco-cutaneous changes during long-term therapy with hydroxyurea in chronic myeloid leukaemia. 1129 3

Although hemodialysis has permitted long-term survival of patients with renal failure, beta 2 microglobulin-derived amyloidosis is a serious complication occurring most commonly in long-term hemodialysis patients. Orthopedic manifestations are quite common, but cutaneous and lingual manifestations are relatively uncommon. We report a 56-year-old patient with lichenoid plaque type of skin eruptions and lingual papules caused by beta 2 microglobulin-derived amyloidosis. Immunohistochemical study showed that amyloid deposits were positive for anti-beta 2 microglobulin antibody, but negative for anti-advanced glycation end products antibody (anti-CML and CLE antibody). We discuss the histological and the clinical features of skin manifestations of beta 2 microglobulin-derived amyloidosis.
Eur J Dermatol
PMID:Cutaneous and lingual papules as a sign of beta 2 microglobulin-derived amyloidosis in a long-term hemodialysis patient. 1294 22

A 70-year-old Japanese man visited our clinic with the chief complaint of chilblain-like eruptions on the toes of both feet. His toes were bluish, erythematous, and swollen. Neither oral administration of vitamin E for 2 weeks nor wearing insulated socks improved the clinical manifestations. Peripheral blood examination revealed the presence of a large number of monocytic atypical cells and myeloblasts, anemia, and thrombocytopenia. In the bone marrow, monocytic cells were elevated, and myelocytic atypical cells were observed. Chromosomal analysis demonstrated Philadelphia chromosome. We diagnosed him as having a blast crisis of chronic myelocytic leukemia (CML). A biopsy specimen of the skin from the chilblain-like eruption showed infiltration of large, atypical, mononuclear cells; most of them were positive for CD68, and some of them were positive for CD14. Therefore, we concluded that the chilblain-like eruptions on his toes were specific skin lesions of a blast crisis in CML.
J Am Acad Dermatol 2004 Feb
PMID:The chilblain-like eruption as a diagnostic clue to the blast crisis of chronic myelocytic leukemia. 1472 65

Hydroxyurea is commonly used in the treatment of various myeloproliferative disorders. In conventional pediatric clinical practice, its use is limited to benign hematologic conditions such as sickle cell disease and thalassemia. Long-term hydroxyurea use is associated with various adverse mucocutaneous effects including hyperpigmentation, alopecia, leg ulcers, and lichenoid eruptions. We report a 10-year-old boy with chronic myelogenous leukemia who presented with hyperpigmentation of the skin and nails 3 months after the start of hydroxyurea therapy. Melanonychia of all 20 nails with involvement of all three mucocutaneous areas (skin, nails, and mucosa) at presentation was a unique feature in our patient. With the recently increasing pediatric use of hydroxyurea in a variety of disorders, its benign and not so uncommon cutaneous adverse effects are emphasized here.
Pediatr Dermatol
PMID:Cutaneous manifestations of hydroxyurea therapy in childhood: case report and review. 1507 51

Hydroxyurea is a chemotherapeutic agent used to treat myeloproliferative disorders and other non-neoplastic conditions. Cutaneous side-effects have been described in long-term therapy with hydroxyurea and include xerosis, hyperpigmentation, skin atrophy, erythema, alopecia, skin tumours and ulceration of the skin, particularly of the legs. We present a 71-year old patient with chronic myelocytic leukemia (CML) who developed extremely painful ulcers on the hands and heels as well as skin tumours while on long-term therapy with hydroxyurea. The ulcers were resistant to therapy but healed three months after discontinuation of hydroxyurea therapy.
Eur J Dermatol
PMID:Cutaneous ulcerations on hands and heels secondary to long-term hydroxyurea treatment. 1535 75

Interferon-alpha can exacerbate existing psoriasis and induce de novo psoriasis and psoriatic arthritits. The exact underlying mechanism is not very well understood. It is not a contraindication to treat patients with pre-existing psoriasis with interferon-alpha. In these patients interferon-alpha should be used with care and only if the potential benefits justify the potential risk. Control of psoriasis prior to initiation of interferon-alpha and simultaneous antipsoriatic therapy while on interferon-alpha are essential. We would like to report a 61-year-old male patient with stable psoriasis for over 20 years, who experienced exacerbation of his psoriasis after receiving interferon-alpha for chronic myeloid leukemia. The association between the interferon-alpha therapy and the exacerbation of his psoriasis was only recognized on rechallenge at the stage he was referred to our department.
J Drugs Dermatol
PMID:Psoriasis exacerbated by interferon-alpha in a patient with chronic myeloid leukemia. 1577 81

Pegylated interferon alfa-2b is a formulation of recombinant human interferon conjugated with polyethylene glycol. Compared with standard interferon alfa injections, this preparation has a longer half-life allowing for once-weekly injections and superior antiviral efficacy in the treatment of hepatitis C when used in combination with ribavirin. Cutaneous side effects caused by interferon are well known. Cutaneous necrosis as a result of interferon alfa is an infrequent complication with unknown pathogenesis, in which a cutaneous local immune-mediated inflammatory process might be involved. We report 5 patients (3 patients with chronic hepatitis C treated with pegylated interferon alfa-2b in association with oral ribavirin and two patients with chronic myelocytic leukemia) who developed local cutaneous reactions at sites of injection after the administration of weekly subcutaneous injections of pegylated interferon alfa-2b at different doses. The ulcers slowly healed with local therapy, but two patients required dose modification of the pegylated interferon alfa-2b and one patient required treatment withdrawal. We review the literature on previously reported cases of cutaneous necrosis after injection of standard interferon alfa or pegylated interferon alfa-2b and discuss the different pathophysiologic mechanisms that might be involved.
J Am Acad Dermatol 2005 Jul
PMID:Cutaneous necrosis after injection of polyethylene glycol-modified interferon alfa. 1596 22

A 74-year-old woman with chronic auricular fibrillation, arterial hypertension, hypercholesterolemia, ischemic cardiopathy, and peripheral arteriopathy presented with purpuric lesions on the lower limbs (Fig. 1) and, to a lesser extent, on the anterior area of the chest. The mucous membranes were not affected. In 1989, she was diagnosed with anemia that evolved until 1998, when a bone marrow biopsy revealed a myelodysplastic syndrome unclassified in French-American-British Group (FAB). The patient has required periodic transfusions since February 1999. A skin biopsy of the purpuric lesions revealed a leukocytoclastic vasculitis; the lesions cleared with topical corticosteroid treatment. In May 1999, the patient presented with inflammatory and painful lesions localized on the vulva (Fig. 2), which had evolved over several days, without fever. No lesions were observed in other locations. A cutaneous biopsy showed an intense dermal edema and a diffuse and polymorphous dermal infiltrate involving the follicular structures. Exocytosis, spongiosis, and mucin deposits, demonstrated by Alcian blue stain, were observed in the follicular epithelium. Mature neutrophils were predominant in the dermal infiltrate, but a small number of eosinophils and immature cells were also present (Fig. 3). The myelogenous origin of the immature lining cells was further confirmed by positive staining of intracytoplasmic granules with naphthol-ASD chloroacetate sterase (Leder's stain). Vasculitis was not observed. Routine laboratory tests revealed 3030 leukocytes/mm(3) (60% neutrophils), a hemoglobin level of 8.4 g/dL, and 92,000 platelets/mm(3). Treatment with 30 mg/day of prednisone was started, and the lesions cleared slowly within 4 weeks. A new bone marrow biopsy in September 1999 showed a similar appearance to that taken in 1998. The patient died in January 2000 as a result of pneumonia with cardiac and respiratory failure. A 66-year-old man presented with a febrile syndrome that had evolved over 5 days, and painful and pruritic cutaneous lesions on the face and posterior neck (Fig. 4). Three months before, the patient was diagnosed with chronic myelogenous leukemia in acceleration phase. Examination revealed an edematous and erythematous face with pustular lesions on the surface, also involving the neck and the upper part of the back. The histopathologic examination revealed an intense edema and abscesses in the dermis. The infiltrate of these lesions was composed of mature neutrophils with the presence of abundant immature cells with a myelogenous aspect (Fig. 5). Analytical studies revealed 26,130 leukocytes/mm(3) (42% blasts). No specific treatment for Sweet's syndrome was administered and the lesions showed an improvement within 5 days. Eight days after admission, the patient died as a result of acute hemorrhage, before treatment for leukemia was initiated.
Int J Dermatol 2005 Aug
PMID:Concurrent Sweet's syndrome and leukemia cutis in patients with myeloid disorders. 1610 72

Imatinib mesylate (IM) represents the first-line treatment for chronic myeloid leukemia (CML). We hereby relate 3 cases of an IM-induced pityriasis rosea (PR)-like cutaneous eruption. Patients developed an erythematous, slightly pruritic, macular skin eruption, with many lesions having a peripheral collarette of desquamation, confined to the trunk, limbs, and arms with a vaguely dermatomal diffusion. The histologic findings suggested a reactive process to the drug. Full dermatological recovery was obtained after IM discontinuation, but lesions reappeared upon restoring therapy, suggesting the drug-related nature of the rash. To our knowledge this is the first reported PR-like cutaneous eruption to IM.
J Am Acad Dermatol 2005 Nov
PMID:Pityriasis rosea-like eruption during treatment with imatinib mesylate: description of 3 cases. 1622 99

Advanced glycation end products (AGEs) form non-enzymatically from reactions of proteins with reducing sugars. In the skin, AGEs were reported to accumulate in dermal elastin and collagens and to interact nonspecifically with the cell membrane of dermal fibroblasts. Therefore, AGEs may influence the process of skin aging. We investigated the presence of the AGE receptor RAGE in skin and the influence of AGEs on receptor expression and the formation of extracellular matrix (ECM). Sections of sun-protected and sun-exposed skin were analyzed with monoclonal antibodies against (RAGE), heat-shock protein 47, factor XIIIa, CD31, and CD45. RAGE was mainly expressed in fibroblasts, dendrocytes, and keratinocytes and to a minor extent in endothelial and mononuclear cells. Human foreskin fibroblasts (HFFs) highly expressed RAGE on the protein and mRNA level when analyzed by quantitative Western blotting and real-time PCR. Incubation of HFFs with the specific RAGE ligand Nepsilon-(carboxymethyl)lysine-modified BSA (CML-BSA) and tumor necrosis factor-alpha resulted in significant upregulation of RAGE expression. CML-BSA induced a mildly profibrogenic pattern, increasing connective tissue growth factor, transforming growth factor-beta (TGF-beta) 1, and procollagen-alpha1(I) mRNA, whereas expression of matrix metalloproteinase (MMP)-1, -2, -3, and -12 was unaffected. We conclude that in HFFs, AGE-RAGE interactions may influence the process of skin aging through mild stimulation of ECM gene expression.
J Invest Dermatol 2006 Feb
PMID:The receptor for advanced glycation end products is highly expressed in the skin and upregulated by advanced glycation end products and tumor necrosis factor-alpha. 1637 60


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