scholarly journals A case of hepatic paragonimiasis was misdiagnosed as hepatocellular carcinoma with rupture and haemorrhage

2021 ◽  
Vol 49 (6) ◽  
pp. 030006052110126
Author(s):  
Wen-Xiang Jin ◽  
Tie-Han Li ◽  
Hong Zhu ◽  
Lei Zhu

Paragonimiasis is a disease caused by parasitic infections that mainly involve the lungs. However, it can also produce ectopic infections, such as when the parasites invade the liver, brain and subcutaneous tissue, which then cause different symptoms. This current case report describes a 55-year-old male patient with hepatic paragonimiasis that was misdiagnosed as liver cancer with rupture and haemorrhage. The initial computed tomography findings suggested ruptured liver cancer. The patient underwent laparoscopic right hemihepatectomy. Postoperative pathological analysis resulted in a diagnosis of hepatic paragonimiasis. The patient recovered well postoperatively and was treated with 25 mg/kg praziquantel orally three times a day for 3 days after discharge with good efficacy. In this present case, the rupture and haemorrhage of the liver mass made it difficult for the treating physicians to consider hepatic paragonimiasis, which lead to the initial misdiagnosis of this patient. Although paragonimiasis is very rare, medical staff should be vigilant and have a comprehensive understanding of the different diseases that can cause liver masses so that misdiagnosis can be avoided.

2019 ◽  
Vol 18 (4) ◽  
pp. 112-115
Author(s):  
N. V. Merzlikin ◽  
L. U. Petrov ◽  
V. F. Tskhai ◽  
E. A. Pshenichnikova ◽  
A. P. Sarueva

Background. Hepatocellular carcinoma is the most common liver cancer and is a leading cause of cancerrelated death worldwide. Its aggressiveness and extensive dissemination lead to a poor patient prognosis. The 5-year survival rate does not exceed 15 %. Despite advances in imaging techniques, its curable rate remains low, because signs and symptoms of liver cancer do not usually appear until the late stages. There is no standard curative treatment for advanced liver cancer.Description. We present the case of a 56- year-old female patient with stage T3N0M0 hepatocellular carcinoma. The patient had a tumor of 20 cm in diameter and 2400 g in weight. The patient underwent right hemihepatectomy and cryodestruction of the liver stump along the resection margin. No evidence of tumor recurrence was found with a follow-up of 12 years.Conclusion. Cryodestruction of the liver stump along the resection margin increases the potential for a higher cure rate in patients with hepatocellular carcinoma, even in cases of extensive organ damage in the absence of metastasis and tumor ingrowth into surrounding organs. 


2019 ◽  
Vol 24 (04) ◽  
pp. 163-164
Author(s):  
Cornelia Fietz

Huo J et al. Comparative Effectiveness of Computed Tomography-Versus Ultrasound-Guided Percutaneous Radiofrequency Ablation Among Medicare Patients 65 Years of Age or Older With Hepatocellular Carcinoma. Value Health 2019; 22(3):284–292 Die Inzidenz des Leberzellkarzinoms hat sich in den letzen 20 Jahren mehr als verdoppelt. 2018 wurden in den USA mehr als 31 600 neue Fälle registriert, knapp die Hälfte dieser Patienten war älter als 65 Jahre. Die damit verbundenen jährlichen Kosten werden auf 455 Millionen US Dollar geschätzt. Für fortgeschrittene, inoperable Fälle steht die Radiofrequenzablation als Therapieoption zur Verfügung, die Ultraschall- oder Computertomographie-gestützt durchgeführt werden kann. Die Autoren vergleichen die Effektivität beider Bildgebungstechniken für das Verfahren.


1987 ◽  
Vol 23 (5) ◽  
pp. 758
Author(s):  
Y Lee ◽  
J H Park ◽  
B I Choi ◽  
B H Lee ◽  
C H Suh ◽  
...  

2019 ◽  
Vol 20 (10) ◽  
pp. 785-798 ◽  
Author(s):  
Yigan Zhang ◽  
Huaze Xi ◽  
Xin Nie ◽  
Peng Zhang ◽  
Ning Lan ◽  
...  

Objective: Our study aims to detect the sensitivity of the new biomarker miR-212 existing in serum exosomes along with other hepatocellular carcinoma biomarkers such as AFP (alpha-fetoprotein), CA125 (carbohydrate antigen-ca125), and Hbx protein in the diagnosis of HBV-related liver diseases. We also aim to study the roles of these biomarkers in the progression of chronic hepatitis B and provide scientific data to show the clinical value of these biomarkers. Methods: We selected 200 patients with HBV-infection (58 cases of chronic hepatitis B, 47 cases of hepatocellular carcinoma, 30 cases of compensatory phase cirrhosis, and 65 cases of decompensatory phase cirrhosis), 31 patients with primary liver cancer without HBV infection, and 70 healthy individuals as the control group. The expression level of serum AFP and CA125 was detected with electrochemiluminescence immunoassay. The expression level of the Hbx protein was detected with ELISA. Meanwhile, the expression level of miR-212 in serum was analyzed with RT-qPCR. We collected patients’ clinical information following the Child-Pugh classification and MELD score criterion, and statistical analysis was made between the expression level of miR-212 and the collected clinical indexes. Lastly, we predicted the target genes of the miR-212 and its functions using bioinformatics methods such as cluster analysis and survival prediction. Results: Compared to the control group, the expression level of miR-212 in HBV infected patients was remarkably increased (P<0.05), especially between the HBV-infection Hepatocellular carcinoma group and the non-HBVinfection liver cancer group (P<0.05). The expression of miR-212 was increased in patients’ Child-Pugh classification, MELD score, and TNM staging. Moreover, the sensitivity and specificity of miR-212 were superior to AFP, CA125, and HBx protein. Conclusion: There is a linear relationship between disease progression and expression level of miR-212 in the serum of HBV infected patients. This demonstrates that miR-212 plays a significant role in liver diseases. miR-212 is expected to be a new biomarker used for the diagnosis and assessment of patients with HBV-infection-related liver diseases.


Cancers ◽  
2021 ◽  
Vol 13 (11) ◽  
pp. 2560
Author(s):  
Luis G. Guijarro ◽  
Patricia Sanmartin-Salinas ◽  
Eva Pérez-Cuevas ◽  
M. Val Toledo-Lobo ◽  
Jorge Monserrat ◽  
...  

New evidence suggests that insulin receptor substrate 4 (IRS-4) may play an important role in the promotion of tumoral growth. In this investigation, we have evaluated the role of IRS-4 in a pilot study performed on patients with liver cancer. We used immunohistochemistry to examine IRS-4 expression in biopsies of tumoral tissue from a cohort of 31 patient suffering of hepatocellular carcinoma (HCC). We simultaneously analyzed the expression of the cancer biomarkers PCNA, Ki-67, and pH3 in the same tissue samples. The in vitro analysis was conducted by studying the behavior of HepG2 cells following IRS-4 overexpression/silencing. IRS-4 was expressed mainly in the nuclei of tumoral cells from HCC patients. In contrast, in healthy cells involved in portal triads, canaliculi, and parenchymal tissue, IRS-4 was observed in the cytosol and the membrane. Nuclear IRS-4 in the tumoral region was found in 69.9 ± 3.2%, whereas in the surrounding healthy hepatocytes, nuclear IRS-4 was rarely observed. The percentage of tumoral cells that exhibited nuclear PCNA and Ki-67 were 52.1 ± 7%, 6.1 ± 1.1% and 1.3 ± 0.2%, respectively. Furthermore, we observed a significant positive linear correlation between nuclear IRS-4 and PCNA (r = 0.989; p < 0.001). However, when we correlated the nuclear expression of IRS-4 and Ki-67, we observed a significant positive curvilinear correlation (r = 0.758; p < 0.010). This allowed us to define two populations, (IRS-4 + Ki-67 ≤ 69%) and (IRS-4 + Ki-67 > 70%). The population with lower levels of IRS-4 and Ki-67 had a higher risk of suffering from multifocal liver cancer (OR = 16.66; CI = 1.68–164.8 (95%); p < 0.05). Immunoblot analyses showed that IRS-4 in normal human liver biopsies was lower than in HepG2, Huh7, and Chang cells. Treatment of HepG2 with IGF-1 and EGF induced IRS-4 translocation to the nucleus. Regulation of IRS-4 levels via HepG2 transfection experiments revealed the protein’s role in proliferation, cell migration, and cell-collagen adhesion. Nuclear IRS-4 is increased in the tumoral region of HCC. IRS-4 and Ki-67 levels are significantly correlated with the presence of multifocal HCC. Moreover, upregulation of IRS-4 in HepG2 cells induced proliferation by a β-catenin/Rb/cyclin D mechanism, whereas downregulation of IRS-4 caused a loss in cellular polarity and in its adherence to collagen as well as a gain in migratory and invasive capacities, probably via an integrin α2 and focal adhesion cascade (FAK) mechanism.


2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Seiga Komiyama ◽  
Takahiro Yamada ◽  
Nobuyuki Takemura ◽  
Norihiro Kokudo ◽  
Koji Hase ◽  
...  

AbstractLiver cancer is the fourth leading cause of cancer-related death. Hepatocellular carcinoma (HCC) is a primary liver cancer that results from chronic hepatitis caused by multiple predisposing factors such as viral infection, alcohol consumption, and non-alcoholic fatty liver disease. Accumulating studies have indicated that dysfunction of the gut epithelial barrier and hepatic translocation of gut microbes may be implicated in the pathogenesis of HCC. However, the translocated bacteria in HCC patients remains unclear. Here, we characterised tumour-associated microbiota in patients with liver cancer and focused on HCC. We observed that the number of amplicon sequence variants in tumour-associated microbiota was significantly higher compared with that in non-tumour regions of the liver. The tumour-associated microbiota consisted of Bacteroidetes, Firmicutes, and Proteobacteria as the dominant phyla. We identified an unclassified genus that belonged to the Bacteroides, Romboutsia, uncultured bacterium of Lachnospiraceae as a signature taxon for primary liver cancer. Additionally, we identified Ruminococcus gnavus as a signature taxon for HCC patients infected with hepatitis B and/or hepatitis C viruses. This study suggests that tumour microbiota may contribute to the pathology of HCC.


Cells ◽  
2021 ◽  
Vol 10 (7) ◽  
pp. 1715
Author(s):  
Macus Hao-Ran Bao ◽  
Carmen Chak-Lui Wong

Hypoxia, low oxygen (O2) level, is a hallmark of solid cancers, especially hepatocellular carcinoma (HCC), one of the most common and fatal cancers worldwide. Hypoxia contributes to drug resistance in cancer through various molecular mechanisms. In this review, we particularly focus on the roles of hypoxia-inducible factor (HIF)-mediated metabolic reprogramming in drug resistance in HCC. Combination therapies targeting hypoxia-induced metabolic enzymes to overcome drug resistance will also be summarized. Acquisition of drug resistance is the major cause of unsatisfactory clinical outcomes of existing HCC treatments. Extra efforts to identify novel mechanisms to combat refractory hypoxic HCC are warranted for the development of more effective treatment regimens for HCC patients.


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