Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P04141 (granulocyte-macrophage colony-stimulating factor)
 6,790 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The hematopoietic growth factors are under investigation for the treatment of patients with chemotherapy-induced bone marrow suppression. One such trial at the University of California, Los Angeles involves chemotherapy with or without granulocyte colony-stimulating factor (G-CSF) in patients with small cell lung cancer. The authors report a case of a patient who had bullous pyoderma gangrenosum at the site of previous eczema during treatment with G-CSF. The lesions resolved promptly when the drug was discontinued. Other investigators have recently reported inflammatory complications of G-CSF and granulocyte-macrophage colony-stimulating factor (GM-CSF) but this is the first case report of biopsy-proven neutrophilic dermatosis associated with administration of a hematopoietic growth factor. Patients should be monitored for development of inflammatory processes during G-CSF therapy and this therapy should be given with caution to those patients with existing inflammatory conditions.
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PMID:Bullous pyoderma gangrenosum after granulocyte colony-stimulating factor treatment. 171 66

Newer agents of particular interest to rheumatologists are increasingly associated with vasculitis. There is now good evidence that treatment with hematopoietic growth factors, including granulocyte colony-stimulating factor and granulocyte-macrophage colony-stimulating factor, can cause or mimic vasculitides such as Sweet's syndrome and pyoderma gangrenosum. Similarly, there is strong evidence that clinical use of interferons is associated with a variety of autoimmune phenomenon rarely including vasculitis. The increased availability of testing for antineutrophil cytoplasmic antibody (ANCA) has widened the clinical spectrum of systemic vasculitides. There are now many reports that treatment with either hydralazine or propylthiouracil is associated with ANCA-positive vasculitis. A small number of case reports also implicate penicillamine and minocycline as agents capable of inducing an ANCA-associated vasculitis. Clinicians should be aware of the potential of certain drugs to cause vasculitis and especially cautious in using these agents in patients with known vasculitis.
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PMID:Drugs associated with vasculitis. 944 89

Granulocyte colony-stimulating factor (G-CSF) is a hematopoietic growth factor (HGF) with many applications in cancer therapy. The most important applications are reduction in the incidence of febrile neutropenia, acceleration of neutrophil recovery after chemotherapy or bone marrow transplantation, and mobilization of progenitor cells. Many cutaneous adverse reactions associated with HGF have been reported in recent years, including injection site reactions, pyoderma gangrenosum, Sweet's syndrome, cutaneous leucocytoclastic vasculitis, and widespread folliculitis. The presence of large histiocytes on the dermis between collagen bundles has been proposed as a characteristic histopathologic finding in cutaneous eruptions secondary to granulocyte colony-stimulating factor and granulocyte-macrophage colony-stimulating factor. We report on a patient with a high-risk ductal infiltrating carcinoma of the breast who received high-dose chemotherapy (HDC) with peripheral blood progenitor cell (PBPC) rescue. The patient received G-CSF after PBPC for a faster granulocyte recovery. She developed a cutaneous eruption located on back, buttocks, axillae, groin and sites where electrocardiography electrodes had been placed. From the histopathological point of view, the eruption was characterized by the presence of numerous large, atypical histiocytes in the dermis with several mitotic figures, mimicking involvement of the dermis by a malignant process.
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PMID:Histopathology of cutaneous reaction to granulocyte colony-stimulating factor: another pseudomalignancy. 987 Jun 76

Although most wounds heal rapidly, impaired or delayed tissue repair represents a major clinical challenge. Current therapy is directed at providing a wound with the most favorable environment in which to heal, rather than aiming to increase the rate of healing pharmacologically. Recent studies have suggested that a number of drugs may act specifically to increase healing rates. In vivo studies have demonstrated that recombinant human granulocyte-macrophage colony-stimulating factor facilitates wound contraction, causes local recruitment of inflammatory cells, and induces keratinocyte proliferation. It also activates mononuclear phagocytes, promotes migration of epithelial cells, and further regulates cytokine production. In 2 recent placebo-controlled studies involving venous leg ulceration, subcutaneous perilesional injections of recombinant human granulocyte-macrophage colony-stimulating factor were found to be significantly better than placebo in the time to complete wound healing. In other studies, recombinant human granulocyte-macrophage colony-stimulating factor was administered topically to wounds. Several case reports have also demonstrated the use of recombinant human granulocyte-macrophage colony-stimulating factor for postsurgical wounds, chronic leg ulcers of sickle cell anemia patients, and refractory pyoderma gangrenosum. Despite proper attention to wound care, some wounds fail to heal in an appropriate fashion and may become chronic. Studies of wound physiology as well as experimental and clinical evidence suggest that recombinant human granulocyte-macrophage colony-stimulating factor may promote healing of these lesions.
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PMID:Recombinant human GM-CSF in the treatment of poorly healing wounds. 1107 3

Pyoderma gangrenosum is a noninfectious neutrophilic dermatosis that usually starts with sterile pustules which rapidly progress to painful ulcers of variable depth and size with undermined violaceous borders. In 17 to 74% of cases, pyoderma gangrenosum is associated with an underlying disease, most commonly inflammatory bowel disease, rheumatological or hematological disease or malignancy. Diagnosis of pyoderma gangrenosum is based on a history of an underlying disease, typical clinical presentation and histopathology, and exclusion of other diseases that would lead to a similar appearance. Randomized, double-blinded prospective multicenter trials investigating the treatment of pyoderma gangrenosum are not available. The treatments with the best clinical evidence are systemic corticosteroids (in the initial phase usually 100 to 200 mg/day) and cyclosporine (mainly as a maintenance treatment). Combinations of corticosteroids with cytotoxic drugs such as azathioprine, cyclophosphamide or chlorambucil are used in patients with disease that is resistant to corticosteroids. The combination of corticosteroids with sulfa drugs, such as dapsone, or clofazimine, minocycline and thalidomide, has been used as a corticosteroid-sparing alternative. Limited experience has been documented with methotrexate, colchicine, nicotine, and mycophenolate mofetil, among other drugs. Alternative treatments include local application of granulocyte-macrophage colony-stimulating factor, intravenous immunoglobulins and plasmapheresis. Skin transplants (split-skin grafts or autologous keratinocyte grafts) and the application of bioengineered skin is useful in selected cases in conjunction with immunosuppression. Topical therapy with modern wound dressings is useful to minimize pain and the high risk of secondary infection. The application of topical antibacterials cannot be recommended because of their potential to sensitize and their questionable efficacy, but systemic antibacterial therapy is mandatory when infection is present. Despite recent advances in therapy, the prognosis of pyoderma gangrenosum remains unpredictable.
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PMID:Clinical management of pyoderma gangrenosum. 1197 36