Acute diffuse peritonitis secondary to a seminal vesicle abscess: A case report.

BACKGROUND: Seminal vesicle abscess (SVA) is the manifestation of a relatively rare urinary system infection. In response to urinary system inflammation, an abscess forms in special locations. However, acute diffuse peritonitis (ADP) induced by SVA is unusual. CASE SUMMARY: We report a case of a left SVA in a male patient complicated with pelvic abscess, ADP, multiple organ dysfunction syndrome, infectious shock, bacteremia, and acute appendiceal extraserous suppurative inflammation as a result of a long-term indwelling urinary catheter. The patient received a course of morinidazole + cefminol antibiotics but showed no obvious relief, so the perineal SVA underwent puncture drainage and abdominal abscess drainage + appendectomy was performed. The operations were successful. After the operation, anti-infection, anti-shock, and nutritional support treatments were continued and various laboratory indicators were regularly reviewed. The patient was discharged from the hospital after recovery. This disease is a challenge for the clinician because of the unusual spreading path of the abscess. Moreover, appropriate intervention and adequate drainage of abdominal and pelvic lesions are necessary, especially when the primary focus cannot be determined. CONCLUSION: The etiology of ADP varies, but acute peritonitis secondary to SVA is very rare. In this patient, the left SVA not only affected the adjacent prostate and bladder but also spread retrogradely through the vas deferens, forming a pelvic abscess in the loose tissues of the extraperitoneal fascia layer. Inflammation involving the peritoneal layer led to ascites and pus accumulation in the abdominal cavity, and appendix involvement led to extraserous suppurative inflammation. In clinical practice, surgeons need to consider the results of various laboratory tests and imaging examinations to make comprehensive judgments involving the diagnosis and treatment plan.

Asymptomatic gastric adenomyoma and heterotopic pancreas in a patient with pancreatic cancer: A case report and review of the literature.

BACKGROUND: Gastric adenomyoma (GA) is a rare submucosal benign neoplasm that occurs mostly in the gastric antrum and is often misdiagnosed. No standard treatment has been established for this disease in cases of malignancy. CASE SUMMARY: A 75-year-old woman with a 10-year history of hypertension was admitted to the Emergency Department of our hospital complaining of paroxysmal exacerbation of acute abdominal pain for 1 d with no apparent cause. Enhanced computed tomography and magnetic resonance imaging indicated a mass in the caudal pancreas, cholecystitis, and cholecystic polypus. Gastrointestinal endoscopy showed a mass arising from the gastric antrum. Due to the imaging findings, pancreatic cancer (PC), gastric lesion, cholecystitis, and cholecystic polypus were our primary consideration. Radical pancreatectomy, splenectomy, and cholecystectomy were performed successfully, and the gastric tumor was locally resected. Postoperative paraffin specimens confirmed the diagnosis of caudal PC, GA, and heterotopic pancreas (HP). Unfortunately, the patient died 13 mo later due to PC metastases to the liver, lung, and adrenal glands. CONCLUSION: GA is a rare benign disease, especially when occurring with HP. It may stem from the same origin as HP. This is the first case report to date of a patient suffering from the simultaneous occurrence of GA, HP, and PC. GA is a lesion that can mimic other benign or malignant gastrointestinal diseases; thus, a definitive diagnosis depends on postoperative pathological biopsy. Although GA and HP are both benign lesions, they should be resected because there is a chance of malignancy. Additional research should be conducted to better understand these submucosal lesions.

Synchronous hepatocellular carcinoma and gallbladder adenocarcinoma with neuroendocrine differentiation: a case report and literature review.

BACKGROUND: Double primary cancers have a low incidence rate, and synchronous hepatocellular carcinoma and gallbladder adenocarcinoma are rarely reported. Here, we report such a case- the 12th case of synchronous double primary cancers featuring HCC and GC, but the first case of neuroendocrine differentiation in the gallbladder. CASE PRESENTATION: A 77-year-old female was admitted to the hospital complaining of weakness and inappetence for six months. Contrast-enhanced computed tomography (CT) of the abdomen indicated an 11 cm space-occupying lesion in the right lobe of the liver. Later, magnetic resonance imaging showed a high possibility of a massive hepatoma, and multiple gallstones were also seen. After transhepatic arterial chemoembolization, a repeat abdominal CT showed obvious local nodular thickening in the gallbladder wall. Finally, resection of the right lobe of the liver and cholecystectomy were performed. During an approximately 2-year follow-up, the patient recovered uneventfully without recurrence or metastasis. CONCLUSION: The disease in this case is rare and lacked typical radiological features. More precise and advanced diagnostic techniques are needed to obtain a clear diagnosis and refine treatment strategies. The management strategy should always be curative, even in the presence of multiple malignancies.

Value of early diagnosis of sepsis complicated with acute kidney injury by renal contrast-enhanced ultrasound.

BACKGROUND: The incidence of acute kidney injury (AKI) in patients with sepsis is high, and the prognosis of patients with septic AKI is poor. The early diagnosis and treatment of septic AKI is of great significance in improving the prognosis of patients with sepsis. AIM: To explore the value of contrast-enhanced ultrasound (CEUS), serum creatinine (Scr), and other indicators in the early diagnosis of septic AKI. METHODS: Ninety patients with sepsis during hospitalization at Tongji Hospital of Tongji University were recruited as subjects. Each patient was recorded with relevant basic data, clinical indicators, and CEUS results. The patients were divided into AKI group and non-AKI group according to the results of renal function diagnosis after 48 h. On the 7th day, the renal function of the non-AKI group was re-evaluated and the patients were further divided into AKI subgroup and non-AKI subgroup. The differences of the indicators in different groups were compared, and the diagnostic value of each indicator and their combination for septic AKI was analyzed. RESULTS: Systemic inflammatory response score (2.58 ± 0.75), blood lactic acid (3.01 ± 1.33 mmol/L), Scr (141.82 ± 27.19 µmol/L), blood urea nitrogen (4.41 ± 0.81mmol/L), and rise time (10.23 ± 2.63 s) in the AKI group were higher than those in the non-AKI group. Peak intensity (PI) (10.78 ± 3.98 dB) and wash in slope (WIS) (1.07 ± 0.53 dB/s) were lower than those in the non-AKI group. The differences were statistically significant (P < 0.05). The PI (12.83 ± 3.77 dB) and WIS (1.22 ± 0.68 dB/s) in the AKI subgroup were lower than those in the non-AKI subgroup, and the differences were statistically significant (P < 0.05). The area under curve (AUC) of Scr for the diagnosis of septic AKI was 0.825 with a sensitivity of 56.76% and a specificity of 100%. The AUCs of WIS and PI (0.928 and 0.912) were higher than those of Scr. Their sensitivities were 100%, but the specificities were 71.70% and 75.47%. The AUC of the combination of three indicators for the diagnosis of septic AKI was 0.943, which was significantly higher than the AUC diagnosed by each single indicator. The sensitivity was 94.59%, and the specificity was 81.13%. CONCLUSION: The combination of Scr, PI, and WIS can improve the diagnostic accuracy of septic AKI. PI and WIS are expected to predict the occurrence of early septic AKI.

Study on the value of serum miR-106b for the early diagnosis of hepatocellular carcinoma.

AIM: To analyze the incidence of hepatocellular carcinoma (HCC) in a population that underwent health checkups and had high serum miR-106b levels. METHODS: A total of 335 subjects who underwent checkups in the Digestive and Liver Disease Department of our hospital were randomly selected. RT-PCR was used to detect the level of miR-106b in serum samples. Laboratory and imaging examinations were carried out to confirm the HCC diagnosis in patients who had a > 2-fold change in miR-106b levels. Ultrasound-guided biopsy was also used for HCC diagnosis when necessary. On this basis, the clinical data of these subjects, including history of hepatitis virus infection, obesity, long-term history of alcohol use and stage of HCC, were collected. Then, the impact of these factors on the level of miR-106b in serum was analyzed. Furthermore, receiver operating characteristic (ROC) curve was drawn to evaluate the diagnostic efficacy of miR-106b for HCC. RESULTS: A total of 35 subjects had abnormal serum miR-106b levels, of which 20 subjects were diagnosed with HCC. t-test revealed that the difference in serum miR-106b level in terms of sex, age, history of hepatitis virus infection, obesity and long-term history of alcohol use was not statistically significant. However, serum miR-106b levels in patients with advanced HCC (stage III/IV) was higher than in patients with early HCC (stage I/II), and the difference was statistically significant (P = 0.000). Moreover, the ROC curve revealed that the area under the curve value for miR-106b was 0.885, which shows that serum miR-106b level has a certain clinical value for HCC diagnosis. CONCLUSION: The random sampling survey shows that serum miR-106b level is a valuable diagnostic marker for HCC. However, the diagnostic threshold value needs to be further researched.

Serum Calcium and Risk of Nonmedullary Thyroid Cancer in Patients with Primary Hyperparathyroidism.

BACKGROUND Clinical cases of nonmedullary thyroid carcinoma (NMTC) in combination with primary hyperparathyroidism (PHPT) have been reported occasionally. However, the clinical characteristics and risk factors of concomitant NMTC in PHPT patients remain unclear. This study aimed to assess the association between PHPT and NMTC, and evaluate the clinical characteristics and risk factors of NMTC in Chinese patients with PHPT. MATERIAL AND METHODS This was a retrospective cohort analysis. We reviewed the medical records of 155 patients who underwent surgery for PHPT in two large medical centers in China between 2009 and 2014. The clinical manifestations, biochemical abnormalities, and histological characteristics of PHPT patients were analyzed. RESULTS Of the 155 patients with PHPT, 58 patients (37.4%) had thyroid nodules and 12 patients (7.7%) were ill with concomitant NMTC. PHPT patients with NMTC demonstrated significantly lower preoperative serum calcium levels compared to PHPT patients with benign thyroid nodules (p<0.05). A significantly negative association between preoperative serum calcium levels and the presence of NMTC was found in PHPT patients (p<0.05). Furthermore, ROC analysis revealed that albumin-corrected serum calcium levels <2.67 mmol/L had good capacity to differentiate the PHPT patients with NMTC from those with benign thyroid nodules. CONCLUSIONS Compared with the reported much lower prevalence of thyroid carcinoma in the general population, our results suggest that PHPT might be a risk factor for the malignancy of thyroid nodules; a lower level of serum calcium may predict the existence of NMTC in PHPT patients with thyroid nodules.

Vascular endothelial growth factor attenuates hepatic sinusoidal capillarization in thioacetamide-induced cirrhotic rats.

AIM: To investigate the effect of vascular endothelial growth factor (VEGF) transfection on hepatic sinusoidal capillarization. METHODS: Enhanced green fluorescent protein (EGFP)/VEGF transfection was confirmed by immunofluorescence microscopy and immunohistochemistry both in primary hepatocytes and in normal liver. Cirrhotic rats were generated by thioacetamide (TAA) administration and then divided into a treatment group, which received injections of 400 microg of plasmid DNA encoding an EGFP-VEGF fusion protein, and a blank group, which received an equal amount of normal saline through the portal vein. The portal vein pressure was measured in the normal and cirrhotic state, in treated and blank groups. The average number of fenestrae per hepatic sinusoid was determined using transmission electron microscopy (TEM), while the relative abundance of VEGF transcripts was examined by Gene array. RESULTS: Green fluorescent protein was observed in the cytoplasms of liver cells under immunofluorescence microscopy 24 h after transfection with EGFP/VEGF plasmid in vitro. Staining with polyclonal antibodies against VEGF illustrated that hepatocytes expressed immunodetectable VEGF both in vitro and in vitro. There were significant differences in the number of fenestrae and portal vein pressures between normal and cirrhotic rats (7.40 +/- 1.71 vs 2.30 +/- 1.16 and 9.32 +/- 0.85 cmH2O vs 17.92 +/- 0.90 cmH2O, P < 0.01), between cirrhotic and treated rats (2.30 +/- 1.16 cmH2O vs 4.60 +/- 1.65 and 17.92 +/- 0.90 cmH2O vs 15.52 +/- 0.93 cmH2O, P < 0.05) and between the treatment group and the blank group (4.60 +/- 1.65 cmH2O vs 2.10 +/- 1.10 cmH2O and 15.52 +/- 0.93 cmH2O vs 17.26 +/- 1.80 cmH2O, P < 0.05). Gene-array analysis revealed that the relative abundance of transcripts of VEGF family members decreased in the cirrhotic state and increased after transfection. CONCLUSION: Injection of a plasmid encoding VEGF through the portal vein is an effective method to induce the formation of fenestrae and decrease portal vein pressure in cirrhotic rats. Therefore, it may be a good choice for treating hepatic cirrhosis and portal hypertension.

Value of portal hemodynamics and hypersplenism in cirrhosis staging.

AIM: To determine the correlation between portal hemodynamics and spleen function among different grades of cirrhosis and verify its significance in cirrhosis staging. METHODS: The portal and splenic vein hemodynamics and spleen size were investigated by ultrasonography in consecutive 38 cirrhotic patients with cirrhosis (Child's grades A to C) and 20 normal controls. The differences were compared in portal vein diameter and flow velocity between patients with and without ascites and between patients with mild and severe esophageal varices. The correlation between peripheral blood cell counts and Child's grades was also determined. RESULTS: The portal flow velocity and volume were significantly lower in patients with Child's C (12.25+/-1.67 cm/s vs 788.59+/-234 mm/min, respectively) cirrhosis compared to controls (19.55+/-3.28 cm/s vs 1254.03+/-410 mm/min, respectively) and those with Child's A (18.5+/-3.02 cm/s vs 1358.48+/-384 mm/min, respectively) and Child's B (16.0+/-3.89 cm/s vs 1142.23+/-390 mm/min, respectively) cirrhosis. Patients with ascites had much lower portal flow velocity and volume (13.0+/-1.72 cm/s vs 1078+/-533 mm/min) than those without ascites (18.6+/-2.60 cm/s vs 1394+/-354 mm/min). There was no statistical difference between patients with mild and severe esophageal varices. The portal vein diameter was not significantly different among the above groups. There were significant differences in splenic vein diameter, flow velocity and white blood cell count, but not in spleen size, red blood cell and platelet counts among the various grades of cirrhosis. The spleen size was negatively correlated with red blood cell and platelet counts (r = -0.620 and r = -0.8.34, respectively). CONCLUSION: An optimal system that includes parameters representing the portal hemodynamics and spleen function should be proposed for cirrhosis staging.

Expression of local renin and angiotensinogen mRNA in cirrhotic portal hypertensive patient.

AIM: To investigate the expression of local renin and angiotensinogen mRNA in cirrhotic portal hypertensive patients. METHODS: The expression of local renin and angiotensinogen mRNA in the liver, splenic artery and vein of PH patients was detected by RT-PCR analysis. RESULTS: Expression of local renin mRNA in the liver of control group was (0.19+/-0.11), significantly lower than that in splenic artery (0.45+/-0.17) or splenic vein(0.39+/-0.12) respectively, (P<0.05). Expression of local angiotensinogen mRNA in the liver was (0.64+/-0.21), significantly higher than that in splenic artery(0.41+/-0.15) or in splenic vein (0.35+/-0.18) respectively, (P<0.05). Expression of local renin mRNA in the liver, splenic artery and vein of PH group was (0.78+/-0.28), (0.86+/-0.35) and (0.81+/-0.22) respectively, significantly higher than that in the control group, (P<0.05). Expression of local angiotensinogen mRNA in the liver, splenic artery and vein of PH group was (0.96+/-0.25), (0.83+/-0.18) and (0.79+/-0.23) respectively, significantly higher than that in the control group, (P<0.05). There was no significant difference between the liver, splenic artery and vein in the expression of local renin or local angiotensinogen mRNA in PH group, (P<0.05). CONCLUSION: In normal subjects the expression of local renin and angiotensinogen mRNA was organ specific, but with increase of the expression of LRAS, the organ-specificity became lost in cirrhotic patients. LRAS may contribute to increased resistance of portal vein with liver and formation of splanchnic vasculopathy.

Angiogenesis effect on rat liver after administration of expression vector encoding vascular endothelial growth factor D.

AIM: To verify the expressing efficiency and angiogenesis effect after administration of expression vector encoding for vascular endothelial growth factor D in normal and ischemic rat liver. METHODS: Ten female S-D rats were administrated with liver tissue dot injection of naked PCHO/hVEGF-D, 50 microg/dot, three dots for each. The same amount of physiological saline was used as control in the neighboring lobe. Fourteen S-D rats, using inflow occlusion of left lateral lobe, were divided into two groups, seven rats in each group. One was ischemic plasmid group, which received naked plasmid PCHO/hVEGF-D injection of 150 microg. The other received the equal amount of natural saline injection and designed as control. The expressions of hVEGF-D in mRNA and protein levels were identified by in situ hybridization and immunohistochemistry, respectively. Endothelial cells were labeled by the factor VIII immunohistochemistrically. The average number of peri-sinusoidal capillaries of each group was calculated and compared statistically 8 days after injection. RESULTS: A large amount of hVEGF-D in mRNA level was found in both normal and ischemic plasmid groups and but none in their corresponding control groups. The protein of hVEGF was also highly expressed in both normal and ischemic plasmid groups than in the controls. The mean number of capillaries under microscopy (X200) of the plasmid group and control was 10.2+/-2.78 vs 7.1+/-2.02 (P<0.05), and those of ischemic plasmid group and ischemic control were 7.43+/-1.72 vs 4.71+/-1.11 with statistical difference (P<0.05). CONCLUSION: The naked PCHO/hVEGF-D dot injection to normal, ischemic rat liver can produce comparatively high expression of hVEGF in both protein and mRNA levels, and prominently increase the number of new capillaries around hepatic sinuses. Therefore, it could be another ideal choice for the treatment of ischemic liver diseases.

Expressions of vascular endothelial growth factor in cirrhotic tissues and their relations to proto-oncogene c-fos, c-myc.

OBJECTIVE: To investigate the significance of vascular endothelial growth factor (VEGF) in the pathogenesis of liver cirrhosis and the correlation between VEGF and proto-oncogene c-fos and c-myc in cirrhotic liver. METHODS: The proteins of VEGF, c-fos, and c-myc were identified immunohistochemically in each tissue section of 53 cases of liver cirrhosis. The correlations between VEGF, c-fos and c-myc were analyzed. The levels of VEGF protein in different Child gradings were also compared. RESULTS: The proteins of VEGF were more highly expressed in Child A and B patients than in Child C patients and controls. The expressions of both c-fos and c-myc were not statistically significant between VEGF positive and negative patients. CONCLUSIONS: The protein level of VEGF can reflect the compensation status of cirrhosis patients and may act as an anti-cirrhotic factor. The proto-oncogene c-fos, c-myc and VEGF may have different mechanisms in the course of cirrhosis or hepatic tumorigenesis.