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Background: Acute malnutrition is broadly classified as severe acute malnutrition (SAM) or moderate acute malnutrition (MAM). It affects almost 20 million children worldwide, with majority of the cases in developing countries. In ...
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Background: Acute malnutrition is broadly classified as severe acute malnutrition (SAM) or moderate acute malnutrition (MAM). It affects almost 20 million children worldwide, with majority of the cases in developing countries. In Africa, it was estimated that about 5%–15% of deaths in children age ranging from 0 to 59 months are due to SAM. Therefore, this study sought to determine common clinical features and outcome in children with acute malnutrition. Methods: A retrospective descriptive study was conducted at the Federal Medical Centre Birnin Kudu, Jigawa State. Case files of patients admitted into the Emergency Pediatric unit and Ppediatric Medical Ward over the period of 1 year (January–December 2017) with a diagnosis of acute malnutrition were reviewed. Results: There were 123 cases of acute malnutrition during the study period: 53 (43.1%) males and 70 (56.9%) females. There were 103 (83.7%) cases of SAM and 20 (16.3%) cases of MAM. Among the SAM cases, there were 70 (56.9%) cases of marasmus, 10 (8.1%) cases of kwashiorkor, and 23 (18.7%) cases of marasmic kwashiorkor. Infection was the most common morbidity associated with SAM. Relatively death was mostly witnessed in the marasmic kwashiorkor subgroup (17.4%). However, majority of the subjects who spent 1–2 weeks on admission were discharged without complications, while death occurred mostly in those who spent <7 days on admission and this observation was statistically significant (Fisher's exact = 32.351, P = 0.001). Conclusion: Marasmus remains the most common form of SAM, and infection is a common comorbidity; however, majority of our cases were discharged without any noticeable complication.
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Background: Acute kidney injury (AKI) and acute hyperglycemia are associated with unfavorable outcomes. The impact of acute hyperglycemia on the development of AKI after acute myocardial infarction (AMI), however, remains unclear....
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Background: Acute kidney injury (AKI) and acute hyperglycemia are associated with unfavorable outcomes. The impact of acute hyperglycemia on the development of AKI after acute myocardial infarction (AMI), however, remains unclear. This study was undertaken to assess the relationship between admission glucose and incidence of AKI after AMI. Methods and Results: This study consisted of 760 patients with AMI admitted to the National Cerebral and Cardiovascular Center within 48 h after symptom onset. Blood sample was obtained on admission and repeated sampling was done at least every 1 or 2 days during the first week. AKI was diagnosed as increase in serum creatinine ≥0.3 mg/dl or ≥50% within any 48 h. Ninety-six patients (13%) had AKI during hospitalization for AMI, and these patients had higher in-hospital mortality than those without AKI (25% vs. 3%, P<0.001). Patients with AKI had higher plasma glucose (PG) on admission than those without (222±105 mg/dl vs. 166±69 mg/dl, P<0.001). The incidence of AKI increased as admission PG rose: 7% with PG <120 mg/dl; 9% with PG 120-160 mg/dl; 11% with PG 160- 200 mg/dl; and 28% with PG >200 mg/dl (P<0.01). On multivariate analysis admission PG was an independent predictor of AKI (odds ratio, 1.10; 95% confidence interval: 1.03-1.18, P=0.02). Conclusions: Admission hyperglycemia might have contributed to the development of AKI in patients with AMI.
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After acute necrotizing pancreatitis (ANP), a pancreatic fistula may occur from disconnected pancreatic duct syndrome (DPDS) where a segment of the pancreas is no longer in continuity with the main pancreatic duct. To study the ou...
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After acute necrotizing pancreatitis (ANP), a pancreatic fistula may occur from disconnected pancreatic duct syndrome (DPDS) where a segment of the pancreas is no longer in continuity with the main pancreatic duct. To study the outcome of patients treated using Roux-Y pancreatic fistula tract-jejunostomy for DPDS after ANP. Between 2002 and 2011, patients treated for DPDS in the setting of endoscopic retrograde cholangiopancreatography (ERCP) or magnetic resonance cholangiopanreatography (MRCP) documented main pancreatic duct disruption with Roux-Y pancreatic fistula tract-jejunostomy. In all, seven patients with DPDS were treated. The median age was 62 years (range 49-78) and five were men. The cause of ANP was gallstones (2), alcohol (1), ERCP (1) and idiopathic (3). Pancreatic necrosectomy was done in six patients. Time from onset of pancreatitis to fistula drainage was 270 days (164-365). Pancreatic fistulae arose from DPDS in the head/neck (4) and body/tail (3). Patients had a median fistula output of 140 ml (100-200) per day before surgery. The median operative time was 142 min (75-367) and estimated blood loss was 150 ml (25 to 500). Patients began an oral diet on post-operative day 4 (3-6) and were hospitalized for a median of 7 days (5-12). The median follow-up was 264 days (29-740). Subsequently, one patient required a distal pancreatectomy. After surgery, three patients required oral hypoglycaemics. No patient developed pancreatic exocrine insufficiency. Internal surgical drainage using Roux-en-Y pancreatic fistula tract-jejunostomy is a safe and definitive treatment for patients with DPDS. ? 2011 International Hepato-Pancreato-Biliary Association.
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OBJECTIVE: The aim of our study was to elucidate the clinical characteristics of alcoholic-hyperlipidemic etiologically complex acute pancreatitis. PATIENTS AND METHODS: We reviewed complete data from 233 patients with acute pancr...
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OBJECTIVE: The aim of our study was to elucidate the clinical characteristics of alcoholic-hyperlipidemic etiologically complex acute pancreatitis. PATIENTS AND METHODS: We reviewed complete data from 233 patients with acute pancreatitis treated in our hospital during the period January 2017-January 2022. They were divided into three groups according to etiology: alcoholic acute pancreatitis (AAP), hyperlipidemic acute pancreatitis (HLAP), and alcoholic-hyperlipidemic acute pancreatitis (AHAP). General clinical data, co-morbidities, laboratory results, imaging data, and disease severity were analyzed and compared between groups. RESULTS: The proportion of male individuals in the AHAP group was significantly higher than that in the HLAP group (p0.05). CONCLUSIONS: The clinical characteristics of patients in the AHAP, AAP and HLAP groups were different, and the patients in the AHAP group were more likely to have a moderate to severe disease course, with longer hospital stay. As a new AP classification concept, AHAP would offer high significance for diagnosis, treatment, and prognosis.
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Although cases of acute cholecystitis, acute pancreatitis, and acute appendicitis following dengue virus infections have been documented, very few large-scale studies have investigated the postdengue risk of these acute abdominal ...
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Although cases of acute cholecystitis, acute pancreatitis, and acute appendicitis following dengue virus infections have been documented, very few large-scale studies have investigated the postdengue risk of these acute abdominal conditions.This retrospective population-based cohort study included all patients with laboratory-confirmed dengue from 2002 to 2015 in Taiwan and 1:4 nondengue individuals matched by age, sex, area of residence, and symptom onset time. Multivariate Cox proportional hazards regression models were used to investigate the short-term (≤ 30 days), medium-term (31–365 days), and long-term (> 1 year) risks of acute cholecystitis, pancreatitis, and appendicitis after dengue infection, adjusted for age, sex, area of residence, urbanization level, monthly income level, and comorbidities. Bonferroni correction was used for multiple testing; E-values were used to assess the robustness of the results to unmeasured confounding.This study included 65,694 individuals with dengue and 262,776 individuals without dengue. Patients with dengue had a significantly increased risk of acute cholecystitis (adjusted hazard ratio (aHR) 60.21; 95% CI 29.11–124.54; P < 0.0001, E-value = 119.92) and acute pancreatitis (aHR 17.13; 95% CI 7.66–38.29; P < 0.0001, E-value = 33.75) within the first 30 days postinfection compared to those without dengue, but this increased risk was not present after that. The incidence rates of acute cholecystitis and pancreatitis in the first 30 days were 18.79 and 5.27 per 10,000, respectively. No increased risk of acute appendicitis was observed among patients with acute dengue infection.This study was the first large epidemiological study to show a significantly increased risk of acute cholecystitis and pancreatitis among patients with dengue during the acute phase of dengue infection, while no such association was observed for acute appendicitis. Early identification of acute cholecystitis and pancreatitis in patients with dengue is crucial for preventing fatal complications.
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Infected necrotizing pancreatitis is a challenging condition to treat because of the profound inflammatory response these patients undergo which can then be exacerbated by interventions. Treatment of this condition has evolved in ...
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Infected necrotizing pancreatitis is a challenging condition to treat because of the profound inflammatory response these patients undergo which can then be exacerbated by interventions. Treatment of this condition has evolved in timing of intervention as well as method of intervention and includes less invasive options for treatment such as percutaneous drainage and endoscopic drainage, in addition to less invasive endoscopic and video-assisted or laparoscopic debridements. The precise optimal treatment strategy for these patients is an ongoing topic of discussion and may be different for each patient as this is a heterogenous condition.
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Summary Advances in the classification of acute leukaemias have led to improved outcomes for a substantial fraction of patients. However, chemotherapy resistance remains a major problem for specific subsets of acute leukaemias. He...
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Summary Advances in the classification of acute leukaemias have led to improved outcomes for a substantial fraction of patients. However, chemotherapy resistance remains a major problem for specific subsets of acute leukaemias. Here, we propose that a molecularly distinct subtype of acute leukaemia with shared myeloid and T cell lymphoblastic features, which we term acute myeloid/T‐lymphoblastic leukaemia ( AMTL ), is divided across 3 diagnostic categories owing to variable expression of markers deemed to be defining of myeloid and T‐lymphoid lineages, such as myeloperoxidase and CD 3. This proposed diagnostic group is supported by (i) retained myeloid differentiation potential during early T cell lymphoid development, (ii) recognition that some cases of acute myeloid leukaemia ( AML ) harbour hallmarks of T cell development, such as T‐cell receptor gene rearrangements and (iii) common gene mutations in subsets of AML and T cell acute lymphoblastic leukaemia (T‐ ALL ), including WT 1, PHF 6, RUNX 1 and BCL 11B . This proposed diagnostic entity overlaps with early T cell precursor ( ETP ) T‐ ALL and T cell/myeloid mixed phenotype acute leukaemias ( MPAL s), and also includes a subset of leukaemias currently classified as AML with features of T‐lymphoblastic development. The proposed classification of AMTL as a distinct entity would enable more precise prospective diagnosis and permit the development of improved therapies for patients whose treatment is inadequate with current approaches.
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Acute pancreatitis begins as acute pancreatic injury and may generate a systemic inflammatory response that evolves into multiorgan failure, leading to death. Multiple inciting factors such as toxins (alcohol), gallstones, or endo...
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Acute pancreatitis begins as acute pancreatic injury and may generate a systemic inflammatory response that evolves into multiorgan failure, leading to death. Multiple inciting factors such as toxins (alcohol), gallstones, or endoscopic retrograde cholangiopancreatography result in a cascade of events beginning with the intra-acinar activation of zymogens and the release of cytokines and other proinflammatory mediators. Their release is a major determinant of the systemic inflammatory response and distant organ failure. Attempts to attenuate the severity of acute pancreatitis by blocking specific inflammatory mediators have had limited success. This review is divided into experimental acute pancreatitis and clinical acute pancreatitis. The distinction is maintained because although animal models of disease have helped define the pathogenesis of acute pancreatitis, they do not completely reproduce the clinical syndrome of human acute pancreatitis or guarantee equal success of therapies in humans. < copyright > 2002 Lippincott Williams & Wilkins, Inc.
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