ABSTRACT
We describe a patient who became cushingoid as a result of receiving steroid therapy for thrombocytopenia purpura and who then developed spinal epidural lipomatosis 4 months after he started receiving ritonavir as part of his therapy for human immunodeficiency virus infection. We believe that ritonavir may have contributed to the development of epidural lipomatosis and that clinicians should be aware of this possible association.
Subject(s)
HIV Infections/drug therapy , HIV Protease Inhibitors/adverse effects , Lipomatosis/chemically induced , Ritonavir/adverse effects , Spinal Diseases/chemically induced , Adult , Anti-HIV Agents/adverse effects , Anti-Inflammatory Agents/therapeutic use , Dexamethasone/therapeutic use , Drug Therapy, Combination , Epidural Space , HIV Infections/complications , Humans , Lipomatosis/pathology , Magnetic Resonance Imaging , Male , Purpura, Thrombocytopenic/complications , Purpura, Thrombocytopenic/drug therapy , Spinal Diseases/pathologyABSTRACT
Transformation of pneumococcus was used to detect homology among tetracycline resistance determinants of clinical isolates of Streptococcus pneumoniae. A strain of pneumococcus containing a mutated tet determinant (tet-3), of class M, integrated into the chromosome was used as a recipient in transformation experiments, where donor DNA was from the tetracycline resistant isolates. 34/34 strains appeared to have tet determinants homologous to tet-3 (i.e. tet M). Still using transformation it was possible to determine that the tet-3 transforming activity of DNA from Tn916 and S. pneumoniae BM6001 was contained in a 5 kb HincII fragment. For this purpose a transformation technique where donor DNA was directly taken from low melting point agarose gels was standardized and used.
Subject(s)
Genetic Markers , Streptococcus pneumoniae/genetics , Tetracycline/pharmacology , Transformation, Bacterial , DNA, Bacterial/genetics , Drug Resistance, Microbial , Streptococcus pneumoniae/drug effectsABSTRACT
The effect of depot parenteral injections of zinc (110 mg Zn/kg body weight) on copper metabolism in young, male rats was investigated. Individually caged rats, fed known amounts of stock diet and deionized-distilled water, were injected s.c. weekly for the first 4 weeks and biweekly for the next 17 weeks with zinc in sesame oil or the oil vehicle only. No significant differences in body weight, hemoglobin, hematocrit and fecal copper excretions were observed between treatments. However, 2 weeks after the initial injections, urinary copper excretion was elevated in the zinc-injected animals and remained elevated throughout the rest of the study. Plasma copper concentrations were significantly higher in the zinc-injected animals from week 2 to 8 of the study, and plasma zinc concentrations of these injected animals were elevated (P less than 0.05) from week 2 and throughout the remainder of the study. Zinc concentrations were significantly higher in the liver, heart, kidney and spleen (P less than 0.05) and copper concentrations were lower in the liver (P less than 0.07), kidney and spleen (P less than 0.05) of zinc-injected animals compared to the vehicle-treated control animals. The data indicate that when zinc is administered by a non-gastrointestinal route, the fecal excretion of copper, the major route of copper excretion, is not altered. Thus, a negative copper balance is not initiated by high levels of zinc administered by the depot technique, in contrast to the negative copper balance stimulated by the gastrointestinal administration of zinc.
