Date: 26 November 2013
Secondary metabolites, structure diagram: Trivial name – Emodin/Archin/Emodol/Frandulic Acid
Copyright: n/a
Notes:
Species: A. aureus, A. sclerotiorum, A. terreus, A. wentiiSystematic name: 9,10-Anthracenedione, 1,3,8-trihydroxy-6-methyl- (9CI)Molecular formulae: C15H10O5Molecular weight: 270.237Chemical abstracts number: 518-82-1Selected references: Kiriyama, Noriki; Nitta, Keiichi; Sakaguchi, Yoshiaki; Taguchi, Yasuhisa; Yamamoto, Yuzuru (Fac. Pharm. Sci., Kanazawa Univ., Kanazawa, Japan). Chem. Pharm. Bull., 25(10), 2593-601 (English) 1977.Toxicity: Mean lethal dose of emodin orally administered to 1-day-old DeKalb cockerels was 3.7 mg/kg.BACKGROUND: Emodin, a widely available herbal remedy, was evaluated for potential effects on pregnancy outcome. METHODS: Emodin was administered in feed to timed-mated Sprague-Dawley (CD) rats (0, 425, 850, and 1700 ppm; gestational day [GD] 6-20), and Swiss Albino (CD-1) mice (0, 600, 2500 or 6000 ppm; GD 6-17). Ingested dose was 0, 31, 57, and approximately 80-144 mg emodin/kg/day (rats) and 0, 94, 391, and 1005 mg emodin/kg/day (mice). Timed-mated animals (23-25/group) were monitored for body weight, feed/water consumption, and clinical signs. At termination (rats: GD 20; mice: GD 17), confirmed pregnant dams (21-25/group) were evaluated for clinical signs: body, liver, kidney, and gravid uterine weights, uterine contents, and number of corpora lutea. Fetuses were weighed, sexed, and examined for external, visceral, and skeletal malformations/variations. RESULTS: There were no maternal deaths. In rats, maternal body weight, weight gain during treatment, and corrected weight gain exhibited a decreasing trend. Maternal body weight gain during treatment was significantly reduced at the high dose. In mice, maternal body weight and weight gain was decreased at the high dose. CONCLUSIONS: Prenatal mortality, live litter size, fetal sex ratio, and morphological development were unaffected in both rats and mice. At the high dose, rat average fetal body weight per litter was unaffected, but was significantly reduced in mice. The rat maternal lowest observed adverse effect level (LOAEL) was 1700 ppm; the no observed adverse effect level (NOAEL) was 850 ppm. The rat developmental toxicity NOAEL was > or =1700 ppm. A LOAEL was not established. In mice, the maternal toxicity LOAEL was 6000 ppm and the NOAEL was 2500 ppm. The developmental toxicity LOAEL was 6000 ppm (reduced fetal body weight) and the NOAEL was 2500 ppm. Copyright 2004 Wiley-Liss, Inc.
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25/04/90 After itraconazole treatment. Major improvement, defined as a complete response, after 10 weeks therapy with itraconazole.
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Image A. Chest x-ray shows a single nodule in the left mid lung field.
Image B. This emphasises how chest x-rays in this context underestimate the extent of disease. The most anterior nodule has ground glass surrrounding the nodule, a halo sign. This diagnostic feature is missed on plain chest X-rays.
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Chest X ray after 4 days, prior to treatment, showing massive increase in volume of lesion (Fig 2)
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Image A. This patient, aged 25 years developed a non productive cough and dyspnoea in the context of late-stage AIDS, CMV disease with ganciclovir-induced neutropenia and receiving corticosteroids. His chest radiograph shows fine bilateral reticular lower-lobe shadowing. He then developed gastro-intestinal bleeding with a gastric ulcer which showed hyphae on biopsy. He then developed blindness of one eye and the globe of his eye perforated. Hyphae were seen and Aspergillus cultured from the vitreous aspirate.
Image B. This radiograph, taken 25 days after the first and 3 days before death, shows of fine bilateral lower-lobe reticular shadows progressing to nodules in all lung zones.
This patient was reported as patient 3 in Denning DW, Follansbee S, Scolaro M, Norris S, Edelstein D, Stevens DA. Pulmonary aspergillosis in the acquired immunodeficiency syndrome. N Engl J Med 1991; 324: 654-662.
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Further details
Image A. Bronchoscopy revealed Aspergillus on culture.
Image B. The ability of Aspergillus to cause pulmonary infarction, probably through direct angioinvasion in this case, is characteristic.
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(Fig 1) Chest radiograph with ‘classical’ appearance of a pulmonary infarction – a wedge-shaped lesion peripherally set against the pleura.
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Large soft left upper-lobe shadow of focal invasive pulmonary aspergillosis in leukaemia, that was missed on earlier radiographs but apparent retrospectively. Variable density of the lesion suggests cavitation, which would be clearly visible on a CT scan of the thorax.
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Severe unilateral invasive aspergillosis of the left lung, with complete consolidation of the left lower-lobe and reticular shadowing extending up into the left upper lobe. The right lung appears normal.
