ABSTRACT
Background: Anastomotic leakage (AL) is still the most annoying postsurgery complication after colorectal resection due to its serious complications up to death. Limited data were available regarding differences in AL incidence, management, and consequences for different types of colorectal resection. The aim of the present work was to evaluate differences in incidence of AL, incidence of postoperative complications, and length of hospital stay in a large number of patients who underwent elective colorectal resection for management of colorectal lesions. In addition to detect when and what type of reoperation for management of AL occur after colorectal resection. Patients: All 250 included patients underwent elective surgeries for colorectal resection with performance of primary anastomosis for management of colorectal neoplastic and non-neoplastic diseases in the period between May 2016 and July 31, 2021. We followed the patients for 90 days; we registered the follow-up findings. Results: the rates of AL occurrence were variable after the different procedures. The lowest rate of AL occurrence was found in patients who underwent right hemicolectomy, then in patients who underwent sigmoidectomy, left hemicolectomy, transversectomy and anterior resection (p= 0.004). A stoma was frequently performed during reoperation (79.5%) which was significantly different between different procedures: 65.5% in right hemicolectomy, 75.0% in transversectomy, 85.7% in left hemicolectomy, and 93.0% in sigmoid resection (p< 0.001). Conclusion Rates, types, time of occurrence and severity of AL vary according to the type of colectomy performed and selective construction of stoma during AL reoperation is currently safely applied with comparable mortality rates for patients who did and who did not have a stoma after reoperation. (AU)
Subject(s)
Humans , Male , Female , Postoperative Complications , Colonic Neoplasms/surgery , Anastomotic Leak/epidemiology , Reoperation , Health Profile , Risk Factors , Treatment Outcome , Neoplasm StagingABSTRACT
Thioacetamide (TAA) is one of the common fungicidal agents that induce liver injury varying from inflammation, necrosis, and fibrosis to cirrhosis. Many recent studies reported the beneficial effect of probiotics and silymarin on hepatotoxicity regardless the causative agents. Therefore, the present study aimed to evaluate the ameliorative role of probiotics and/or silymarin on TAA induced hepatotoxicity in rats via histological, and immunohistochemical methods. Twenty five male albino rats were used for this experiment and were divided into five groups (n=5 rats/group); group I acts as negative control, group II was orally administrated distilled water for six weeks, then injected with TAA (200 mg/kg b.wt./ 5 ml physiological saline/ I.P.) twice a week for another six weeks, group III was treated with probiotics at a dose of 135 mg/ kg b.wt. orally in drinking water daily for six weeks, then injected with TAA (dosage of group II), twice weekly for another six weeks, group IV was treated with silymarin at a dose of 200 mg/ kg b.wt orally 4 times per week for six weeks, then injected with TAA (dosage of group II), twice weekly for another six weeks and group V was treated with combination of both probiotics and silymarin, at the same dosage in groups III and IV respectively then injected with TAA (dosage of group II), twice weekly for another six weeks. Histologically, TAA induced hepatocytes degeneration, inflammatory cells infiltration, and pseudolobular parenchyma as well as, high apoptosis and low proliferation rates that were proved by immunohistochemical staining for caspase 3 and ki-67 respectively. Probiotics and/or silymarin improved the histological feature of hepatocytes, reduced apoptosis and stimulated proliferation. Based on these results, we concluded that the use of probiotics and silymarin combination ameliorates the hepatotoxic effect of TAA in rats more than the use of probiotics or silymarin alone.
La tioacetamida (TAA) es uno de los agentes fungicidas más comunes que inducen lesiones hepáticas que varían desde inflamación, necrosis y fibrosis hasta cirrosis. Muchos estudios recientes informaron el efecto beneficioso de los probióticos y la silimarina sobre la hepatotoxicidad independientemente de los agentes causantes. Por lo tanto, el presente estudio tuvo como objetivo evaluar el papel paliativo de los probióticos y / o silimarina en la hepatotoxicidad inducida por TAA en ratas a través de métodos histológicos e inmunohistoquímicos. Para este experimento se usaron veinticinco ratas albinas y se dividieron en cinco grupos (n = 5 ratas / grupo); el grupo I se usó como control negativo; en el grupo II se administró por vía oral agua destilada durante seis semanas y luego se inyectó TAA (200 mg / kg b.wt./ 5 ml solución salina fisiológica / IP) dos veces por semana durante otras seis semanas; el grupo III se trató con probióticos, dosis diaria de 135 mg / kg b.wt. por vía oral en agua potable, durante seis semanas y luego fue inyectado con TAA (dosis del grupo II), dos veces por semana durante otras seis semanas; el grupo IV se trató con silimarina, con una dosis de 200 mg / kg b.wt por vía oral 4 veces por semana durante seis semanas, luego se inyectó TAA (dosificación del grupo II), dos veces por semana durante otras seis semanas; y el grupo V, se trató con una combinación de ambos probióticos y silimarina con la misma dosis que en los grupos III y IV, respectivamente, luego fueron inyectados con TAA (dosificación del grupo II), dos veces por semana durante otras seis semanas. Histológicamente, la TAA indujo la degeneración de los hepatocitos, la infiltración de células inflamatorias y el parénquima pseudolobular, así como también una apoptosis alta y tasas de proliferación bajas que se probaron mediante tinción inmunohistoquímica para caspasa 3 y ki-67, respectivamente. Los probióticos y / o la silimarina mejoraron la característica histológica de los hepatocitos, redujeron la apoptosis y estimularon la proliferación. En base a estos resultados, concluimos que el uso de la combinación de probióticos y silimarina mejora el efecto hepatotóxico del TAA en ratas más que el uso de probióticos o silimarina individualmente.
Subject(s)
Animals , Male , Rats , Silymarin/administration & dosage , Thioacetamide/toxicity , Probiotics/administration & dosage , Chemical and Drug Induced Liver Injury/drug therapy , Immunohistochemistry , Chemical and Drug Induced Liver Injury/pathology , Liver/drug effectsABSTRACT
Background: lupus nephritis [LN] is an inflammation of the kidney caused by systemic lupus erythematosus [SLE], a disease by the immune system. Anti-C1q antibodies have been found in many different systemic autoimmune diseases, they are strongly linked to immune complex disorder most prominently SLE and severe rheumatoid arthritis and have been suggested to be closely associated with lupus nephritis [LN]. Generally anti-dsDNA antibodies have been acknowledged as an important tool in the diagnosis of SLE, however their predictive value as to the activity of the disease remains controversial, on the contrary anti-C1q antibodies appear to have a clear-cut relationship with renal complications of SLE not only have they been shown to play a pathogenic role in the development of lupus nephritis but also their serum levels correlate with the presence of active proliferation lupus nephritis
Aim of the study: this study aimed to investigate association between serum titer of anti-C1q antibody and disease manifestation of SLE
Methodology: the study was carried out in three different groups: healthy group, rheumatoid arthritis group and lupus nephritis group. All groups were subjected to determination of anti-C1q antibody, blood urea nitrogen [BUN] and serum creatinine
Results: there was no significant difference in BUN levels between the normal and rheumatoid arthritis groups in contrast there was a highly significant difference in BUN between the normal and lupus groups also, between the rheumatoid arthritis and lupus nephritis groups [p<0.001]. No significant difference was detected in serum creatinine levels between the normal and rheumatoid arthritis groups in there was a highly significant difference in serum creatinine between the normal and lupus groups and also between the rheumatoid arthritis and lupus nephritis groups [p<0.001]. No significant difference was realized in serum anti-C1q antibodies levels between the normal and rheumatoid arthritis groups in contrast there was a highly significant difference in serum anti-C1q antibodies between the normal and lupus groups and also between rheumatoid arthritis and lupus nephritis groups [p<0.001]. In the control group and rheumatoid arthritis groups, only BUN showed a highly significant positive correlation with serum creatinine concentration [r=0.906, r=0.404] and [P<0.001, P<0.05] respectively, while in lupus nephritis group, BUN showed a highly positive correlation with serum creatinine concentration [r=0.773, P<0.001] also serum creatinine concentration showed a positive concentration with serum anti-C1q antibody [r=0.513, P<0.05]
Conclusion: the present study suggested that anti-C1q antibody might be a new parameter for the development of lupus nephritis since the increased of anti-ds DNA antibody and hypocomplementemia [C3 and C4] are serological markers of SLE activity, but they are not enough to identify which organ may be affected, while anti-C1q antibody either alone or in combination with other serological markers could give information of the diagnosis of a renal flare with 100% sensitivity and specificity
ABSTRACT
Hepcidin is a small, cysteine-rich cationic peptide produced by hepatocytes. There is a single human hepcidin gene; whose essential role in iron homeostasis was confirmed by identifying homozygous frameshift or nonsense mutations in affected individuals with severe Juvenile hemochromatosis. IL-6 may be the mediator of hepcidin induction by inflammation. Hypoferremia is a common response to systemic infections or generalized inflammatory disorders, anemia of chronic disease occurs in patients with acute and chronic immune activation and represents an important clinical problem. The study will attempt to determine the hepatic hepcidin expression levels in patients with chronic hepatitis C virus infection. Fifty patients with chronic hepatitis C virus infection [CHCV], their age between [20- 55] years, selected from the National Hepatology and Tropical Medicine Research Institute were included in this study, before interferon and Ribavirin therapy, and ten healthy individuals were included to serve as controls. All the patients and controls were subjected to the following history, clinical examination, abdominal ultrasonography and collection of blood samples for routine laboratory investigations. CBCs and serological assay for serum ferritin, iron, transferrin [s-TFR] levels, Liver biopsy for hepcidin mRNA levels and iron deposits in liver by [PCR] polymerase chain reaction. All subjects gave written informed consent for enrolment in the study, which was approved by the Research Ethical Committee of the General Organization for Teaching Hospitals and Institutes. Liver biopsy was taken from healthy subjects during abdominal surgery. Our results revealed that hepatic hepcidin expression is considered highly valid marker in case of CHCV infection. Our study concluded that there's a highly significant inverse correlation between hepcidin versus liver iron, serum iron and serum transferrin but there's no significant correlation versus ferritin. Hepcidin measuring and manipulating hepcidin levels will, in the future, have a role in diagnosing and treating any number of iron related disorders. Hepcidin itself has antimicrobial properties of uncertain importance so that careful clinical trials will be required to define appropriate indications of hepcidin antagonists