- The Sensitivity, Specificity and Accuracy of Warning Signs in Predicting Severe Dengue, the Severe Dengue Prevalence and Its Associated Factors. [Journal Article]
- IJInt J Environ Res Public Health 2018 Sep 15; 15(9)
- Objectives: To study Malaysian dengue clinical practice guideline (CPG) warning signs (WS) in predicting severe dengue (SD) and its associated factors among confirmed cases presented to a teaching h...
Objectives: To study Malaysian dengue clinical practice guideline (CPG) warning signs (WS) in predicting severe dengue (SD) and its associated factors among confirmed cases presented to a teaching hospital in north-eastern Malaysia in 2014. Methods: A cross-sectional study was performed in February 2015 using secondary data acquired from the hospital records. There were 2607 confirmed dengue cases presented to Hospital Universiti Sains Malaysia (HUSM) in 2014. Seven hundred patients were selected after proportionate stratified random sampling conducted according to the number of cases in 12 different months in 2014. Data were collected and analysed using SPSS version 22.0. Results: Severe dengue outcomes represented 4.9% of cases. The prevalence of any of WS in SD was 91.2%. The most common WSs prior to SD were persistent vomiting (55.9%), and abdominal pain/tenderness (52.9%). The most sensitive warning sign in detecting SD was abdominal pain (59%). Specificity of individual WS were generally good, especially of clinical fluid accumulation (99%), hepatomegaly (98%) and mucosal bleeding (93%). Factors associated with SD were persistent vomiting (Adjusted odds ratio (aOR)): 2.41), mucosal bleeding (aOR: 4.73) and haematocrit rise with rapid platelet drop (aOR: 2.74). Conclusion: A focus on sensitivity, specificity, predictive values and association of a number of particular WS should be emphasized in order to better predict severe dengue outcomes.
- Pulmonary Metastasis in Infantile Choriocarcinoma: Successful Outcome. [Journal Article]
- IPIndian Pediatr 2018 Aug 15; 55(8):699-700
- Infantile choriocarcinoma is usually fatal without appropriate treatment.
Infantile choriocarcinoma is usually fatal without appropriate treatment.
- Undifferentiated embryonal sarcoma of the liver in adult patient: A report of two cases. [Journal Article]
- AHAnn Hepatobiliary Pancreat Surg 2018; 22(3):269-273
- Primary sarcomas of the liver are unusual neoplasms developing in adults. They constitute a heterogeneous group of neoplasms including undifferentiated embryonal sarcoma. Patients usually present wit...
Primary sarcomas of the liver are unusual neoplasms developing in adults. They constitute a heterogeneous group of neoplasms including undifferentiated embryonal sarcoma. Patients usually present with an abdominal mass and abdominal pain. Case 1: A 53-year-old woman presented with abdominal pain. Computed tomography showed an occupying mass in the right lobule and an intra-auricular multi-lobulated mass suggestive of a secondary deposit. Biopsy of the hepatic lesion revealed undifferentiated embryonal sarcoma. Despite radiotherapy and supportive measures, her overall status progressively worsened until cardiac arrest. Case 2: A 41-year-old woman presented with hepatomegaly. Abdominal imaging showed cystic lesions in the right hepatic lobule with multiple septae. The patient underwent extended right hepatectomy and a histopathological study reported high-grade undifferentiated embryonal sarcoma. Two years after surgery, a new cystic lesion in the surgical site was recorded and chemotherapy was scheduled. The lesion remained stable for three years when disease progression was observed and second-line chemotherapy was initiated. Although undifferentiated embryonal sarcoma of the liver has poor prognosis, early diagnosis is essential to increase the chances of survival. Currently, surgical resection and chemotherapy are the primary treatment modalities.
- [Clinical and genetic analysis of an infant with progressive familial intrahepatic cholestasis type II]. [Journal Article]
- ZDZhongguo Dang Dai Er Ke Za Zhi 2018; 20(9):758-764
- Progressive familial intrahepatic cholestasis type II (PFIC-2) is an autosomal recessive disorder caused by biallelic variants of ABCB11 gene. This paper reports the clinical and laboratory features ...
Progressive familial intrahepatic cholestasis type II (PFIC-2) is an autosomal recessive disorder caused by biallelic variants of ABCB11 gene. This paper reports the clinical and laboratory features of a pediatric patient with PFIC-2. The patient was a 2.4-month-old male infant with jaundice and hepatomegaly as the main clinical manifestations. The serum levels of total bilirubin, direct bilirubin and total bile acids were increased, while the serum γ-glutamyl transpeptidase (GGT) level was normal. Next generation sequencing revealed two missense variants, c.1493T>C(p.Ile498Thr) and c.1502T>G(p.Val501Gly), in the ABCB11 gene of the patient, which were inherited from his father and mother, respectively. The latter was a novel variant which was predicted to be pathogenic by using a variety of bioinformatic tools, and the affected p.Val501 residue was highly conserved in 112 homologous peptides.
- [YAP induces chromosomal instability in liver cancer patients]. [Journal Article]
- PPathologe 2018 Sep 11
- CONCLUSIONS: These results reveal a new oncogenic mechanism of the Hippo/YAP signaling pathway and identify YAP and FOXM1 as potential targets for targeted therapies.
- Outbreak of Tuberculosis caused by Mycobacterium bovis in a cattery of Abyssinian cats in Italy. [Journal Article]
- TETransbound Emerg Dis 2018 Sep 04
- Mycobacterium bovis is a re-emerging zoonosis; it was diagnosed in five Abyssinian cats in a breeding cattery in Italy. The infection entered the cattery with an imported kitten (cat A); it had a sus...
Mycobacterium bovis is a re-emerging zoonosis; it was diagnosed in five Abyssinian cats in a breeding cattery in Italy. The infection entered the cattery with an imported kitten (cat A); it had a suspected bite wound on its leg that had been treated at a veterinary clinic in Kiev, Ukraine, which is probably where it became infected with M. bovis. When the kitten arrived in Italy there were four cats in the cattery; an adult female, her two kittens, and a kitten imported from Russia. These were all healthy, and had no outdoor access. All five cats developed tuberculous interstitial pneumonia; in cat A this occurred six weeks after importation, the others were diagnosed four to six weeks later. Three cats were euthanised with deteriorating pneumonia while two cats remained clinically well on antibiotic therapy (marbofloxacin, doxycycline and azithromycin). The latter cases were euthanised after five weeks, as required by Italian law once M. bovis infection was suspected. Changes consistent with tuberculosis on gross post-mortem examination included mesenteric and mediastinal lymphadenopathy, splenomegaly and hepatomegaly, and the presence of disseminated focal white lesions on the cut surface of the spleen, liver and lungs. Visible acid-fast bacteria (cats A, B and C) were confirmed as Mycobacterium tuberculosis complex by PCR (cats A, B, C, D and E), refined to Mycobacterium bovis (cats A, B and D), spoligotype SB0950 (cats A and D). This article is protected by copyright. All rights reserved.
- Clinical features and treatment of primary autoimmune hemolytic anemia in childhood. [Journal Article]
- TATransfus Apher Sci 2018 Aug 08
- CONCLUSIONS: Primary AIHA is an acute illness mostly self-limiting or requiring short-term steroid therapy. Rarely, it might be resistant to immunosuppressive treatment and be mortal.
- Treatment of polycystic liver disease. Update on the management. [Journal Article]
- JVJ Visc Surg 2018 Aug 23
- Polycystic liver disease (PLD) may consist of autosomal dominant PLD or isolated PLD without renal impairment. The natural history of liver cysts is to increase in size and number, causing progressiv...
Polycystic liver disease (PLD) may consist of autosomal dominant PLD or isolated PLD without renal impairment. The natural history of liver cysts is to increase in size and number, causing progressive disease that can lead to very large and incapacitating hepatomegaly. Only symptomatic hepatomegaly (pain, inability to eat, weight loss, dyspnea) or cystic complications such as infection or intracystic hemorrhage should be treated. The treatment of PLD thus covers a wide range of therapeutic options, ranging from non-intervention to liver transplantation, including needle aspiration evacuation with injection of sclerosant, laparoscopic fenestration and fenestration by laparotomy combined with liver resection. The choice between these different treatments depends on the symptomatology, the intrahepatic extension of the lesions and the patient's general condition. Hepatic resection is commonly chosen since the vast majority of PLD consists of multiple small cysts that are impossible or difficult to fenestrate. Since cysts are inhomogeneously distributed in the hepatic parenchyma with most areas less affected, the preservation of this less-involved territory allows liver regeneration relatively free of cysts. Hepatectomies for PLD are technically difficult because the planes and the vascular and biliary structures are compressed by the cysts. Liver transplantation, whether isolated or associated with renal transplantation, is indicated in cases of severe malnutrition and/or end-stage renal disease or if the volume of remnant parenchyma is insufficient and suggests failure of a partial hepatectomy.
- A peculiar case of Campylobacter jejuni attenuated aspartate chemosensory mutant, able to cause pathology and inflammation in avian and murine model animals. [Journal Article]
- SRSci Rep 2018 Aug 22; 8(1):12594
- An attenuated Campylobacter jejuni aspartate chemoreceptor ccaA mutant caused gross pathological changes despite reduced colonisation ability in animal models. In chickens, the pathological changes i...
An attenuated Campylobacter jejuni aspartate chemoreceptor ccaA mutant caused gross pathological changes despite reduced colonisation ability in animal models. In chickens, the pathological changes included connective tissue and thickening of the mesenteric fat, as well as the disintegration of the villus tips in the large intestine, whereas in mice, hepatomegaly occurred between 48-72 hours post infection and persisted for the six days of the time course. In addition, there was a significant change in the levels of IL-12p70 in mice infected with the C. jejuni ccaA mutant. CcaA isogenic mutant was hyper-invasive in cell culture and microscopic examination revealed that it had a "run" bias in its "run-and-tumble" chemotactic behaviour. The mutant cells also exhibited lower level of binding to fucosylated and higher binding to sialylated glycan structures in glycan array analysis. This study highlights the importance of investigating phenotypic changes in C. jejuni, as we have shown that specific mutants can cause pathological changes in the host, despite reduction in colonisation potential.
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- Paradoxical Protective Effect of Perfluorooctanesulfonic Acid Against High-Fat Diet-Induced Hepatic Steatosis in Mice. [Journal Article]
- IJInt J Toxicol 2018 Aug 22; :1091581818790934
- Perfluorooctanesulfonic acid (PFOS) is a persistent organic pollutant with worldwide bioaccumulation due to a very long half-life. Perfluorooctanesulfonic acid exposure results in significant hepatic...
Perfluorooctanesulfonic acid (PFOS) is a persistent organic pollutant with worldwide bioaccumulation due to a very long half-life. Perfluorooctanesulfonic acid exposure results in significant hepatic effects including steatosis, proliferation, hepatomegaly, and in rodents, carcinogenesis. The objective of this study was to determine whether PFOS exposure exacerbates nonalcoholic fatty liver disease and nonalcoholic steatohepatitis pathogenesis. Eight-week-old male C57BL/6 J mice (n = 5 per group) were fed ad libitum normal chow diet (ND) alone, 60% high-fat diet (HFD) alone, ND + PFOS, and HFD + PFOS (0.0001% w/w (1 mg/kg) of PFOS) for 6 weeks. Both HFD alone and the ND + PFOS treatment induced significant adiposity and hepatomegaly, but the HFD + PFOS treatment showed a marked protection. Oil Red O staining and quantitative analysis of hepatic lipid content revealed increased hepatic steatosis in ND + PFOS and in HFD alone fed mice, which was prevented in HFD + PFOS treatment. Further studies revealed that ND + PFOS treatment significantly affected expression of lipid trafficking genes to favor steatosis, but these changes were absent in HFD + PFOS group. Specifically, expression of CD36, the major lipid importer in the cells, and peroxisome proliferator-activated receptor gamma (PPARγ), its major regulator, were induced in HFD + no treatment (NT) and ND + PFOS-fed mice but remained unchanged in HFD + PFOS mice. In conclusion, these data indicate that coadministration of PFOS with HFD mitigates steatosis and hepatomegaly induced by HFD and that by PFOS fed in ND diet via regulation of cellular lipid import machinery. These findings suggest dietary lipid content be considered when performing risk management of PFOS in humans and the elucidation of PFOS-induced hepatotoxicity.