Spontaneous pneumothorax in children with osteosarcoma: report of three cases and review of the literature.

Spontaneous pneumothorax is a rare manifestation of primary lung cancer or metastasis. It is estimated that < 1% of all cases of spontaneous pneumothorax are tumor-associated and metastatic osteogenic or soft-tissue sarcomas are associated most commonly with pneumothorax especially in the setting of cytotoxic chemotherapy or radiotherapy. In this article, we report three pediatric cases with osteosarcoma that developed spontaneous pneumothorax during chemotherapy with a review of the literature. Two of them had lung metastasis at the time of the detection of pneumothorax and the remaining patient was found to have a bronchopleural fistula. SPx is an emergency situation and early diagnosis and management can improve prognosis and quality of life of the patient however the optimal management has yet to be determined.

Human immunodeficiency virus-negative tonsil Kaposi's sarcoma and Hodgkin's disease: case report and review of the literature.

Kaposi's sarcoma (KS) is a multicentric malignant neoplastic vascular disorder characterized by multiple violet-colored nodules of the skin. The coexistence of KS with other primary malignancies, especially of the lymphoreticular system, has been frequently noted. However, the association of Hodgkin's disease with KS is a rare occurrence. In this article we present the case of a 33-year-old man with human immunodeficiency virus (HIV)-negative KS of the tonsil, occurring in the radiotherapy field for Hodgkin's disease treated 20 years ago.

Effects of neonatal monosodium glutamate and aging on morphine dependence development.

Administration of monosodium glutamate (MSG) to neonatal rats has been reported to destroy aspartatergic (ASPergic) and glutamatergic (GLUergic) neurons. Ageing has been shown to induce cell loss, a rather general CNS atrophy, and slowness in the CNS functions. On the other hand, it has been hypothesized that two of the main reasons for opiate dependence development are the blockade by opiates of the NMDA receptors and their associated upregulation and supersensitivity. Accordingly, the abstinence syndrome precipitating effect of naloxone (NL) has been assumed to be the consequences of the removal by NL of opiate from NMDA receptors without being able to prevent upregulated and supersensitive NMDA receptors from being stimulated stronger than normal. To investigate the role of the decrease in the number of NMDA receptors in the development of morphine (M) physical dependence, 4 g/kg MSG was SC injected into neonatal rats on days 2, 4, 6, 8 and 10 after birth. Their littermate controls SC received equimolar NaCl solution. Three or 14 months later, three pellets containing 75 mg base M were SC implanted into male rats treated neonatally with MSG or equimolar NaCl solution. Seventy-two hours after pellet implantation, all rats were injected with 2 mg/kg NL intraperitoneally. Some abstinence syndrome signs were counted or rated for 15 min immediately after NL injection and then statistically evaluated. The NL-precipitated abstinence syndrome was less intense in 3-month-old MSG-treated rats than in controls, most probably due to the decrease in the number of NMDA receptors in MSG-treated rats.(ABSTRACT TRUNCATED AT 250 WORDS)

Effects of MK 801 on morphine physical dependence: attenuation and intensification.

It has previously been reported that the noncompetitive NMDA receptor antagonists ketamine and dextromethorphan suppressed the naloxone-induced morphine abstinence syndrome. In addition, the previous blockade by ketamine and dextromethorphan of NMDA receptors has been shown to intensify the naloxone-elicited morphine abstinence syndrome. On the basis of this information, another noncompetitive NMDA receptor antagonist, (+)-5-methyl-10,11-dihydro-5H-dibenzo-a,d-cyclohepten-5,10-imine maleate (MK 801), was administered to rats in which two morphine-containing (75 x 2 morphine base) pellets had been implanted. The naloxone-precipitated abstinence syndrome in rats injected with 0.3 mg/kg MK 801 36 h after pellet implantation was found significantly more intense than controls whereas the abstinence syndrome in rats that received 0.1 mg/kg MK 801 before naloxone injection was less intense. The intensification by MK 801 given 36 h following pellet implantation was attributed to the further increase in upregulation and supersensitivity of NMDA receptors caused by morphine. The attenuation was explained by the blockade by MK 801 of NMDA receptors as occurred in the case of ketamine and dextromethorphan.

Effects of tizanidine on morphine physical dependence: attenuation and intensification.

It has previously been shown that subchronic and acute administration of L-asparaginase and glutaminase inhibitors D-Aspartic acid (D-ASP) and prolyl-leucyl-glycinamide (PLG) intensifies and attenuates morphine (M) physical dependence, respectively, by the inhibition of ASP and glutamic acid (GLU) production, and subsequently their normal releases. Tizanidine (TIZ) has long been known to be an alpha 2-adrenoceptor agonist and inhibitor of ASP and GLU release. Therefore, in this study TIZ has been administered subchronically during the development of M physical dependence to rats in which M-containing pellets had been implanted or acutely 30 min before naloxone (NL)-induced abstinence syndrome. The subchronic administration of TIZ intensified NL-precipitated abstinence syndrome whereas its acute administration attenuated it, as did D-ASP and PLG. On the other hand, TIZ added into the medium prevented the in vitro M-dependent-made guinea pig ileum from contracting following NL application. Furthermore, TIZ stopped the already started contraction by NL of the M-dependent ileum, which completely relaxed later. These effects of TIZ on M-dependent ileum were antagonized by the alpha 2-adrenoceptor antagonist yohimbine. The intensification by subchronic TIZ administration of abstinence syndrome was attributed to the lesser release of ASP and GLU, which resulted in the larger blockade of M of ASPergic/GLUergic receptors due to the lesser release of their endogenous agonist ASP and GLU and consequently the higher upregulation of the receptors. The attenuation by acute TIZ administration of NL-precipitated abstinence syndrome was explained with lesser release of ASP and GLU and concomitantly the lesser stimulation of the receptors.(ABSTRACT TRUNCATED AT 250 WORDS)