Side effects of corticosteroid injections: What's new?

The risk of sepsis with a hip or knee implant does not seem to be increased by prior joint injections, as long as the injection and surgery are separated by at least two months. Calcifications have been reported after intradiscal injection in the coccygeal region for coccydynia. Complete rest for 24 hours after injection of triamcinolone hexacetonide into the knee had no effect on systemic diffusion of the product. Patients infected by HIV who are treated with ritonavir are at much greater risk for Cushing syndrome after epidural injection. Problems with menstruation after corticosteroid injection seem to be related to a transient decrease in estradiol levels, without alterations in FSH and LH levels. The risk of central serous chorioretinopathy and acute necrosis of the retina after injection is not known, even by ophthalmologists. Transient dysphonia occurs in 12% of patients receiving corticosteroid injections. The impressive Tachon's syndrome seems to be the venous counterpart to Nicolau's syndrome for arteries. Injections into C1-C2 should be abandoned because of the neurological risks. Since serious neurological events after foraminal injections could be the result of an overly fast injection into the arterialized radicular veins rather than in the arteries, only slow injections with products having a low risk of embolism or vascular complications should be allowed. Dexamethasone-based preparations seem to contain no particles or crystals, and have not induced any neurological accidents in various animal models, even after direct administration into vertebral or carotid arteries.     

Prevention of gram-negative translocation reduces the severity of hepatopulmonary syndrome

Hepatopulmonary syndrome (HPS) is characterized by intrapulmonary vascular dilatations and an increased alveoloarterial oxygen difference (AaPO(2)). These abnormalities are related to augmented pulmonary nitric oxide (NO) production, dependent primarily on increases in the expression and activity of inducible NO-synthase (iNOS) within pulmonary intravascular macrophages and, to a lesser extent, of endothelial NOS (eNOS). Production of iNOS by pulmonary intravascular macrophages might be related to translocated gut bacteria present in the pulmonary circulation. To test this hypothesis, we determined whether macrophage sequestration, lung iNOS expression and activity, and HPS severity were decreased after norfloxacin was given for 5 weeks to prevent Gram-negative bacterial translocation in rats with common bile duct ligation-induced cirrhosis. Norfloxacin decreased the incidence of Gram-negative translocation from 70 to 0% and the percentage of pulmonary microvessels containing more than 10 macrophages from 52 +/- 7 to 21 +/- 8% (p < 0.01). AaPO(2) and cerebral uptake of intravenous (99m)Tc-labeled albumin macroaggregates (reflecting intrapulmonary vascular dilatations) were intermediate to those of untreated cirrhotic and sham-operated rats. The activity and expression of lung iNOS, but not eNOS, were reduced to normal. Norfloxacin may reduce HPS severity by inhibiting Gram-negative bacterial translocation, thereby decreasing NO production by pulmonary intravascular macrophages. Bacterial translocation may be the key to the pathogenesis of HPS.     

Role of the renin-angiotensin system in primitive erythropoiesis in the chick embryo

Inactivation of the gene encoding mouse angiotensin I-converting enzyme (ACE), which converts angiotensin I into angiotensin II, results in anemia in adult animals. This anemia is corrected by angiotensin II, demonstrating the involvement of angiotensin II in adult (definitive) erythropoiesis. We investigated the possible role of the renin-angiotensin system (RAS) in primitive erythropoiesis in the yolk sac of the chicken embryo. Enzymatically active ACE was detected in the yolk sac endoderm, concomitantly with the differentiation of blood islands in the adjacent yolk sac mesoderm. The simultaneous presence of all the other components of the RAS (renin, angiotensinogen, angiotensin II receptor) in the vicinity of the blood islands suggests that this system is involved in erythropoiesis. This role was confirmed by in vivo blockade of the RAS with fosinoprilate, a specific inhibitor of chicken ACE, which decreased hematocrit by 15%. A similar decrease in hematocrit was observed following treatment with the angiotensin II receptor antagonist Sar1-Ile8-Angiotensin II, suggesting that this effect was mediated by angiotensin II. Both treatments affected hematocrit by decreasing erythroblast proliferation. Thus, the RAS, and its effector peptide angiotensin II in particular, modulates primitive erythropoiesis.