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Ann Pharmacother 2002 Jul-Aug;36(7-8):1293; discussion 1294
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PMID: 12086569, UI: 22081423
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Ann Pharmacother 2002 Jul-Aug;36(7-8):1171-4
Medical Oncology Department, University Hospital La Fe, Valencia, Spain. segura_ang@gav.es
BACKGROUND: Metastatic renal cell carcinoma (MRCC) has been characteristically unresponsive to chemotherapy. In lieu of an effective regimen, interleukin-2 (IL-2) and interferon alfa are considered drugs of choice to treat this cancer. Subcutaneous IL-2 is safe and well tolerated, with a mortality rate <3%. OBJECTIVE: To report a case of cutaneous and hematologic toxicity in a patient treated with IL-2. CASE SUMMARY: A 67-year-old woman received radiotherapy and immunotherapy for cancer that had metastasized to the bone and lungs. IL-2 was part of the regimen. After 5 days of treatment with IL-2, the patient developed a hemorrhagic lesion that progressed to toxic epidermal necrolysis, as well as grade 4 pancytopenia. She died 10 days after treatment was begun. At the time of death, leukocytes were 0.3 x 10(3)/mm(3), platelets 10 x 10(3)/mm(3), and hemoglobin 6.8 mg/dL. DISCUSSION: Cutaneous IL-2 adverse effects are frequent, but generally mild and reversible. The adverse hematologic effects are usually transitory and pancytopenia is not frequent. The severity of cutaneous and hematologic toxicity experienced by our patient has rarely been reported. CONCLUSIONS: The use of IL-2 in bedridden patients with performance status >2 must be given on an individualized basis. If radiotherapy over extensive areas of the body is needed, the use of IL-2 must be postponed until radiotherapy is completed.
PMID: 12086549, UI: 22081403
Br J Dermatol 2002 Sep;147(3):624-5
PMID: 12207623, UI: 22197370
Br J Dermatol 2002 Sep;147(3):619-21
PMID: 12207621, UI: 22197368
Br J Dermatol 2002 Sep;147(3):618-9
PMID: 12207620, UI: 22197367
Br J Dermatol 2002 Sep;147(3):617-8
PMID: 12207619, UI: 22197366
Br J Dermatol 2002 Sep;147(3):598-601
Department of Dermatology, Vrije Universiteit Medical Centre, PO Box 7057, 1007 MB Amsterdam, The Netherlands. remcovandoorn@hotmail.com
We report the cutaneous side-effects of ZD1839 (Iressa), a new anticancer agent that acts by inhibiting epidermal growth factor (EGF) receptor signal transduction. Three patients receiving ZD1839 developed an eruption consisting of follicular papules and pustules in an acneiform distribution as well as diffuse fine scaling of the skin. Additionally, hair growth abnormalities were noted in two patients. Histologically, a superficial purulent folliculitis and disordered differentiation with focal parakeratosis were seen. The follicular eruption appeared to respond favourably to treatment with tretinoin cream and minocycline. The cutaneous adverse effects of ZD1839 are similar to those of other EGF receptor-targeted agents and result from direct interference with the functions of EGF receptor signalling in the skin.
PMID: 12207609, UI: 22197356
Br J Dermatol 2002 Sep;147(3):558-62
Department of Dermatology, University of Heidelberg, Vosstrasse 2, D-69115 Heidelberg, Germany. Benjamin_Durani@med.uni-heidelberg.de
Sweet's syndrome was first described in 1964. It is characterized by an acute onset of non-pruritic, painful reddish nodules on the head and neck, chest and/or the upper limbs, mostly accompanied by fever, general malaise and leucocytosis. Histopathological examination shows a diffuse dermal neutrophilic infiltrate. The pathogenesis is still not fully understood, and different diseases have been shown to be associated with this syndrome. However, although still very rare, there is an increase of reports on Sweet's syndrome induced by drugs. We describe a 30-year-old man who experienced acute neutrophilic dermatosis after systemic treatment with minocycline. Additionally, there is a strong possibility that the same patient developed a drug-induced Sweet's syndrome after oral administration of tetracycline and doxycycline.
PMID: 12207601, UI: 22197348
Hum Exp Toxicol 2002 Jan;21(1):49-54
Laboratory of Toxicology, Medical School, University of Crete, Heraklion, Greece. aris@med.uoc.gr
Two cases of severe fenthion intoxication are presented. The first is a case of a psychiatric patient who attempted suicide with ingestion of the compound, and the second case was of a child exposed to the chemical agent by air spraying. Both patients were treated in the intensive care unit with atropine and pralidoxime and finally survived. Fenthion blood levels on admission were 2.7 and 0.95 microg/mL, respectively. Different concentrations of pralidoxime were added to the first patient's poisoned serum in order to assess in vitro the effect of pralidoxime on cholinesterase reactivation. The clinical and toxicological data of the poisonings are discussed, as well as the potential therapeutic use of pralidoxime in organophosphate intoxication.
PMID: 12046724, UI: 22041652
Int J Dermatol 2002 May;41 Suppl 1:16-20
Department of Medicine, Section of Dermatology, University of Arizona Health Sciences Center, Arizona, USA.
PMID: 12087814, UI: 22083150
Med J Aust 2002 Oct 7;177(7):362-3
School of Medicine, James Cook University, PO Box 3080, North Mackay, QLD 4740, Australia. pjfenner@ozemail.com.au
We report the first of two recent deaths from Irukandji syndrome. A 58-year-old male tourist was stung on the face and chest by an unidentified jellyfish in shallow water off the Whitsunday Islands, Queensland. He developed muscle cramps, sweating, anxiety, nausea and hypertension, and died 30 hours later from intracerebral haemorrhage.
PMID: 12358578, UI: 22247113
Toxicol Sci 2002 Jul;68(1):220-5
Department of Pharmacology and Toxicology, National Food Safety and Toxicology Center, Institute for Environmental Toxicology, B440 Life Sciences, Michigan State University, East Lansing 48824, USA.
Aflatoxin B(1) (AFB(1)) is a fungal toxin that causes both acute hepatotoxicity and hepatocellular carcinoma in humans and experimental animals. Previous studies demonstrated that a small, noninjurious dose of bacterial lipopolysaccharide (LPS) augments the hepatotoxicity of AFB(1) through activation of inflammatory cells and production of soluble inflammatory mediators (Barton et al., 2000b, 2001). This study was conducted to examine the effect of LPS on the dose-response relationship for AFB(1)-induced liver injury. Male Sprague-Dawley rats (250-350g) were treated with AFB(1) (0.1 mg/kg-6.3 mg/kg, ip) and 4 h later with a noninjurious dose of E. coli LPS (7.4 x 10(6) EU/kg, iv). Twenty-four h after AFB(1) administration, hepatic parenchymal cell injury was estimated from elevations in serum alanine aminotransferase and aspartate aminotransferase activities. Injury to intrahepatic bile ducts was evaluated from increased serum gamma-glutamyl transferase and alkaline phosphatase activities. Based on benchmark dose (BMD) analysis, the AFB(1) BMD for parenchymal cell injury was decreased 10-fold by LPS cotreatment, whereas AFB(1) BMDs for bile duct injury were decreased nearly 20-fold. The data suggest that concurrent inflammation renders the liver considerably more sensitive to the hepatotoxic effects of AFB(1).
PMID: 12075124, UI: 22070710
Toxicol Sci 2002 Jul;68(1):9-17
Center for Drug Evaluation and Research, U.S. Food and Drug Administration, Rockville, Maryland 20857, USA.
The NMDA receptor has been widely investigated in recent years as a target for the pharmacological management of seizures, pain and a variety of neurological disorders. Its role in normal central nervous system (CNS) activity and development, as well as in the development of CNS abnormalities and neurodegeneration has also been of interest. The NMDA receptor is one of three pharmacologically distinct subtypes of ionotropic receptor channels that are sensitive to the endogenous excitatory amino acid, L-glutamate. The ontogeny of the NMDA receptor, a multiple tetrameric and heteromeric channel complex with at least six known subunits, is controlled by three gene families and varies in developmental profile with species and regional brain area. NMDA receptors play a role in excitatory synaptic transmission, in the activity-dependent synaptic plasticity underlying learning and memory, and in pre- and postnatal CNS development, including brain cell differentiation, axonal growth and degeneration of unused neurons. The results of recent studies suggest that sustained alteration of NMDA receptor activation during critical periods of development may have deleterious effects on normal CNS development and function. Neonatal rats administered the NMDA receptor antagonists 2-amino-5-phosphonovalerate (AP5) and MK-801 during the first two weeks of life develop abnormal axonal arborization in the retinal connections to the superior colliculus, interfering with normal visual responses. Results from monkey studies suggest that chronic developmental exposure to high doses of a NMDA antagonist, remacemide, has pronounced and long-lasting effects on learning. Recent findings indicate that if NMDA receptors are blocked during a specific period in neonatal life (first two weeks postnatally in the rat), massive apoptotic neurodegeneration results, due not to excitotoxic overstimulation of neurons but to deprivation of stimulation. These observations require further laboratory evidence and support in order to establish their relevance to drug-induced human neurodevelopmental concerns. It is necessary to investigate the relevance of these findings in other animal species in addition to the rat, most notably, nonhuman primates, where neuronal cytoarchitecture and development are significantly different than the rodent but more like the human.
PMID: 12075105, UI: 22070691