17 research outputs found
613 cases of splenic rupture without risk factors or previously diagnosed disease: a systematic review
Background
Rupture of the spleen in the absence of trauma or previously diagnosed disease is largely ignored in the emergency literature and is often not documented as such in journals from other fields. We have conducted a systematic review of the literature to highlight the surprisingly frequent occurrence of this phenomenon and to document the diversity of diseases that can present in this fashion.
Methods
Systematic review of English and French language publications catalogued in Pubmed, Embase and CINAHL between 1950 and 2011.
Results
We found 613 cases of splenic rupture meeting the criteria above, 327 of which occurred as the presenting complaint of an underlying disease and 112 of which occurred following a medical procedure. Rupture appeared to occur spontaneously in histologically normal (but not necessarily normal size) spleens in 35 cases and after minor trauma in 23 cases. Medications were implicated in 47 cases, a splenic or adjacent anatomical abnormality in 31 cases and pregnancy or its complications in 38 cases.
The most common associated diseases were infectious (n = 143), haematologic (n = 84) and non-haematologic neoplasms (n = 48). Amyloidosis (n = 24), internal trauma such as cough or vomiting (n = 17) and rheumatologic diseases (n = 10) are less frequently reported. Colonoscopy (n = 87) was the procedure reported most frequently as a cause of rupture. The anatomic abnormalities associated with rupture include splenic cysts (n = 6), infarction (n = 6) and hamartomata (n = 5). Medications associated with rupture include anticoagulants (n = 21), thrombolytics (n = 13) and recombinant G-CSF (n = 10). Other causes or associations reported very infrequently include other endoscopy, pulmonary, cardiac or abdominal surgery, hysterectomy, peliosis, empyema, remote pancreato-renal transplant, thrombosed splenic vein, hemangiomata, pancreatic pseudocysts, splenic artery aneurysm, cholesterol embolism, splenic granuloma, congenital diaphragmatic hernia, rib exostosis, pancreatitis, Gaucher's disease, Wilson's disease, pheochromocytoma, afibrinogenemia and ruptured ectopic pregnancy.
Conclusions
Emergency physicians should be attuned to the fact that rupture of the spleen can occur in the absence of major trauma or previously diagnosed splenic disease. The occurrence of such a rupture is likely to be the manifesting complaint of an underlying disease. Furthermore, colonoscopy should be more widely documented as a cause of splenic rupture
ICB3E Induces INOS Expression by ROS-Dependent JNK and ERK Activation for Apoptosis of Leukemic Cells
The role of c-Jun N terminal Kinase (JNK) has
been well documented in various cellular stresses where it
leads to cell death. Similarly, extracellular signal-regulated
kinase (ERK) which was identified as a signalling molecule
for survival pathway has been shown recently to be
involved in apoptosis also. Recently we reported that
ICB3E, a synthetic analogue of Piper betle leaf-derived
apoptosis-inducing agent hydroxychavicol (HCH), possesses
anti-chronic myeloid leukemia (CML) acitivity in
vitro and in vivo without insight on mechanism of action.
Here we report that ICB3E is three to four times more
potent than HCH in inducing apoptosis of leukemic cells
without having appreciable effects on normal human
peripheral blood mononuclear cells, mouse fibroblast cell
line NIH3T3 and monkey kidney epithelial cell line Vero.
ICB3E causes early accumulation of mitochondria-derived
reactive oxygen species (ROS) in K562 cells. Unlike HCH,
ICB3E treatment caused ROS dependent activation of both JNK, ERK and induced the expression of iNOS leading to
generation of nitric oxide (NO). This causes cleavage of
caspase 9, 3 and PARP leading to apoptosis. Lack of
cleavage of caspase 8 and inability of blocking chimera
antibody to DR5 or neutralizing antibody to Fas to reverse
ICB3E-mediated apoptosis suggest the involvement of only
intrinsic pathway. Our data reveal a novel ROS-dependent
JNK/ERK-mediated iNOS activation pathway which leads
to NO mediated cell death by ICB3
Tuberculosis and cardiovascular disease: linking the epidemics
The burden of tuberculosis and cardiovascular disease (CVD) is enormous worldwide. CVD rates are rapidly increasing in low- and middle-income countries. Public health programs have been challenged with the overlapping tuberculosis and CVD epidemics. Monocyte/macrophages, lymphocytes and cytokines involved in cellular mediated immune responses against Mycobacterium tuberculosis are also main drivers of atherogenesis, suggesting a potential pathogenic role of tuberculosis in CVD via mechanisms that have been described for other pathogens that establish chronic infection and latency. Studies have shown a pro-atherogenic effect of antibody-mediated responses against mycobacterial heat shock protein-65 through cross reaction with self-antigens in human vessels. Furthermore, subsets of mycobacteria actively replicate during latent tuberculosis infection (LTBI), and recent studies suggest that LTBI is associated with persistent chronic inflammation that may lead to CVD. Recent epidemiologic work has shown that the risk of CVD in persons who develop tuberculosis is higher than in persons without a history of tuberculosis, even several years after recovery from tuberculosis. Together, these data suggest that tuberculosis may play a role in the pathogenesis of CVD. Further research to investigate a potential link between tuberculosis and CVD is warranted