Annals of clinical and laboratory science
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Ann. Clin. Lab. Sci. · Jan 2008
Case ReportsUse of bivalirudin to prevent thrombosis following orthotopic liver transplantation in a patient with Budd-Chiari syndrome and a history of heparin-induced thrombocytopenia.
Type II heparin-induced thrombocytopenia (HIT) is an immune-mediated syndrome that may arise in a time-dependent manner following heparin therapy, placing patients at significant risk for thromboembolic events. Therapy includes anticoagulation with a direct thrombin inhibitor and avoidance of heparin. ⋯ During the post-transplant graft function improvement, we observed a significant dose-effect alteration manifested by an increased bivalirudin dose requirement as factor V activity increased. This observation is an important consideration in the attempt to maintain an optimal balance between effective anticoagulation and a reduced risk of postoperative bleeding.
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Ann. Clin. Lab. Sci. · Jan 2008
Influence of Nrf2 genotype on pulmonary NF-kappaB activity and inflammatory response after traumatic brain injury.
Inflammatory response plays an important role in the pathogenesis of acute lung injury (ALI) after traumatic brain injury (TBI). Nuclear factor erythroid 2-related factor 2 (Nrf2) is a key transcription factor that plays a crucial role in cytoprotection against inflammation. The present study explored the influence of Nrf2 genotype on the production of cytokines and on activation of transcription factors in a murine TBI model. ⋯ Nrf2 (-/-) mice were shown to have a greater increase in the lung wet/dry weight ratio compared to their wild-type Nrf2 (+/+) counterparts after TBI. This exacerbation of lung injury in Nrf2 (-/-) mice was associated with increased levels of TNF-alpha, IL-1beta, IL-6, ICAM-1, and their mediator, NF-kappaB. The results suggest that Nrf2 plays an important protective role in attenuating the pulmonary inflammatory response and NF-kappaB activation after TBI.
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Ann. Clin. Lab. Sci. · Jan 2008
Progesterone administration modulates TLRs/NF-kappaB signaling pathway in rat brain after cortical contusion.
This study investigated whether progesterone administration modulates toll-like receptors (TLRs) and the nuclear factor-kappa B (NF-kappaB) signaling pathway in the injured rat brain following traumatic brain injury (TBI). Right parietal cortical contusion was made by a weight-dropping method. Male rats were given 0 or 16 mg/kg injections of progesterone at postinjury hr 1 and 6 and on days 1, 2, 3, 4, and 5. ⋯ Administration of progesterone following TBI down-regulates the cortical levels of these agents related to the TLRs/NF-kappaB signaling pathway. After progesterone administration, apoptotic TUNEL-positive cells in the injured brain were significantly decreased. In summary, post-TBI progesterone administration attenuates the TLRs/NF-kappaB signaling pathway in injured rat brain, and this may be a mechanism whereby progesterone improves the outcome following TBI.
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Ann. Clin. Lab. Sci. · Jan 2008
Case ReportsPromyelocytic blast crisis of chronic myeloid leukemia during imatinib treatment.
A 32-yr-old man with the chronic phase of chronic myeloid leukemia (CML-CP) was treated with imatinib mesylate for 6 mo. The real-time quantitative reverse transcription PCR ratio for BCR/ABL in blood mRNA (BCR/ABL RT-QPCR) decreased from an initial value of 0.0159 to a low value of 0.0012 after 3 mo, indicating complete hematologic response. ⋯ Complete remission was achieved by therapy with all-trans retinoic acid (ATRA) and high-dose imatinib mesylate. Using retrospective PML/RARalpha RT-QPCR with a bone marrow specimen obtained at the initial diagnosis of CML-CP, we quantified the mRNA ratio as 0.000321, suggesting that the clonal evolution of PML/RARalpha translocation occurred early in the CML-CP.
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Ann. Clin. Lab. Sci. · Jan 2008
Non-anion gap acidosis in asthma: clinical and laboratory features and outcomes for hospitalized patients.
Metabolic acidosis secondary to lactic acidosis may occur in acute, severe asthma and its presence suggests that respiratory muscle fatigue and tissue hypoxia play a major part in the pathogenesis. Non-anion gap metabolic acidosis (NAG acidosis) has also been reported in acute asthma but its impact on the clinical outcome has not been evaluated. The objective of this study was to evaluate the prevalence of NAG acidosis, characterize the laboratory findings, and determine its impact on clinical outcomes. ⋯ NAG acidosis was associated with a statistically significant (p = 0.028) risk of requirement for mechanical ventilation necessitating admission to the Medical Intensive Care Unit (MICU); the odds ratio for intubation for NAG acidosis compared to other groups was 3.92. No difference, however, was detected in overall length of stay (LOS) in hospital for patients with NAG acidosis vs the other groups. NAG metabolic acidosis in acute asthma may be more prevalent than expected and may be associated with more frequent need for mechanical ventilation and admission to an intensive care unit.