Hepatic perfusion disorders: Etiopathogenesis and related diseases

In this article, we have reviewed the hepatic perfusion disorder （HPD）, etiopathogenesis of HPD and corresponding diseases. Review of the literature was based on computer searches （PubMed, Index Medicus） and personal experiences. We considered HPD reflects perfusion differences due to redistribution of arterial blood flow among segments, subsegments and lobes of the liver. The plain CT scan findings of HPD manifests as triangular or wedge-shaped areas of low attenuation. On contrast-enhanced CT scan, HPD manifests multiple （or single） transient wedge-shaped, rotundloid or irregular appearance, homogeneous hyperattenuation （in less cases, hypoattenuation） during the hepatic arterial phase （HAP） and isoattenuated or slightly hyperattenuated areas during the portal arterial phase. Dynamic enhanced magnetic resonance （MR） features are similar to enhanced CT scan. Angiographic findings include non-opacification of portal vein on portograms or wedge-shaped segmental staining in arterial and parenchymal phases on hepatic angiograms. The causes of HPD are arterioportal shunts （APS）, intrahepatic vascular compressions and portal vein occlusion, steal phenomenon by hypervascular tumors, vascular variations and any other unknown reasons. It is very important for radiologists to be familiar with the various appearances of HPD to avoid false-positive diagnosis of pseudolesions and not to overestimate the extent of the disease.

Highlights in pathogenesis of vitiligo

Vitiligo is a common pigmentary disorder. Many studies across decades and all over the world have attempted to illustrate the pathogenesis behind it; however, the pathogenesis of vitiligo remains elusive. This review article, we present the findings behind the most and updated theories behind this psychologically debilitating and disfiguring disease. The discussion begun with the role of genetic predisposition followed by neural theory first proposed in the 1950 s. Wehighlight the autoimmune hypothesis, followed by the reactive oxygen species model, zinc-α2-glycoprotein deficiency hypothesis, viral theory, intrinsic theory and biochemical, molecular and cellular alterations accounting for loss of functioning melanocytes in vitiligo. Many theories were elaborated to clarify vitiligo pathogenesis. It is a multifactorial disease involving the interplay of several factors. Future research is needed to clarify the interaction of these factors for better understanding of vitiligo pathogenesis and subsequent successful treatment.

Hepatitis B virus infection and intrahepatic cholangiocarcinoma

Intrahepatic cholangiocarcinoma(ICC)is a devastating malignant tumor arising from the peripheral intrahepatic bile duct epithelium.The incidence and mortality of ICC is markedly increasing over the past two decades worldwide,though the cause for this rise in incidence is unclear,thus intensifying the search for alternative etiological agents and pathogenetic mechanisms.Hepatolithiasis,primary sclerosing cholangitis,parasitic infection(Opisthorchis viverrini or Clonorchis sinensis),fibropolycystic liver disease,and chemical carcinogen exposure are thought to be the risk factors for ICC.Nevertheless,the majority of ICC patients do not have any of these risk factors,and none of the established risk factors can explain the recent increasing trend of ICC.Therefore,identifying other risk factors may lead to the prevention and early detection of ICC.Chronic hepatitis B virus(HBV)infection is the predominant cause of hepatocellular carcinoma in HBVendemic areas.This review discusses the evidence implicating chronic HBV infection as a likely etiology of ICC and the pathogenetic mechanisms that might be involved.

Upper aerodigestive tract disorders and gastro-oesophageal reflux disease

A wide variety of symptoms and diseases of the upper aerodigestive tract are associated to gastro-oesophageal reflux disease(GORD). These disorders comprise a large variety of conditions such as asthma, chronic otitis media and sinusitis, chronic cough, and laryngeal disorders including paroxysmal laryngospasm. Laryngopharyngeal reflux disease is an extraoesophageal variant of GORD that can affect the larynx and pharynx. Despite numerous research efforts, the diagnosis of laryngopharyngeal reflux often remains elusive,unproven and controversial, and its treatment is then still empiric. Aim of this paper is to review the current literature on upper aerodigestive tract disorders in relation to pathologic gastro-oesophageal reflux, focusing in particular on the pathophysiology base and results of the surgical treatment of GORD.

Potential etiopathogenesis of seventh day syndrome following living donor liver transplantation:ischemia of the graft?

BACKGROUND: Seventh-day syndrome (7DS) is an early serious complication following liver transplantation with a high mortality because of its unknown etiopathogenesis. This study aimed to analyze the potential etiopathogenesis of 7DS. METHODS: A retrospective analysis of 98 consecutive living donor liver transplants performed from 2001 to 2007 at our center revealed that 5 patients had suffered from 7DS; their age, MELD score, portal vein inflow and other parameters were compared with those of the other recipients. RESULTS: The 5 patients showed common features: (a) initial uneventful recovery, and a dramatic rise of serum liver enzyme levels I to 2 weeks later; (b) decreased inflow in the portal vein accompanied by augmentation of serum creatinine and urea nitrogen level; and (c) serial liver biopsy findings of apoptosis and ischemic necrosis of hepatocytes. Four of the 5 patients died. Age, waiting time to transplantation, MELD score, operation time, cold ischemic time, portal interceptive time and diameter of the portal vein were not significantly different between the 2 groups, but a difference was found in the flow rate of the portal vein (t=3.234, P<0.001). CONCLUSIONS: The 5 patients suffered from a decreased portal vein inflow, ischemic liver necrosis, and renal failure. Hence, hypoperfusion of the liver graft was considered to be the etiopathogenesis of 7DS, for which, however sufficient evidence is lacking. More studies of 7DS are needed.

Müller-Weiss disease:Four case reports

BACKGROUND Müller-Weiss disease(MWD)is an idiopathic foot condition characterized by spontaneous tarsal“scaphoiditis”in adults.Frequently bilateral and affecting females during the 4th-6th decades of life,the pathogenesis of MWD remains unclear:It has been traditionally considered a spontaneous osteonecrosis of the navicular.The typical presentation of MWD is a long period of subtle discomfort followed by prolonged standing,atraumatic,disabling pain.Currently,there is no gold standard for the treatment of patients with MWD.Most support initial conservative therapy.Operative treatment should be considered for failure of conservative therapies longer than 6 months.The indication for surgery is severity of symptoms rather than severity of deformities.Operative treatment options include core decompression,internal fixation of the tarsal navicular,open or arthroscopic triple fusion,talo-navicular or talo-navicular-cuneiform arthrodesis,and navicular excision with reconstruction of the medial column.CASE SUMMARY In this study,we report four patients affected by MWD.Clinical and radiographic assessment,follow-up and treatment are reported.CONCLUSION As it is frequently misdiagnosed,MWD is challenging for orthopedic surgeons.Early diagnosis and effective treatment are mandatory to avoid sequelae.

Juvenile idiopathic arthritis

Juvenile idiopathic arthritis(JIA) is the most common chronic rheumatologic disease in childhood, which represents a nonhomogeneous group of disorders that share the clinical manifestation of arthritis lasting at least 6 wk under the age of 16. The exact diagnosis requires exclusion of other diseases that cause arthritis. The exact etiopathogenesis of JIA is still unknown. The interactions between genetic factors, environmental exposures and immune mechanisms are thought to contribute to pathogenesis of the disease. The "International League Against Rheumatism" classification divides JIA into 7 subtypes: oligoarticular JIA, rheumatoid factor(RF) positive polyarticular JIA, RF negative polyarticular JIA, systemic-onset JIA, enthesitis-related arthritis, juvenile psoriatic arthritis and undifferentiated JIA. Each subgroup of JIA is characterized by a different mode of presentation, disease course and outcome. The improvements in treatment of JIA in the last 2decades, such as the early introduction of intraarticular corticosteroids, methotrexate and biologic agents, have dramatically upgraded the prognosis of the disease. If untreated, JIA may cause devastating results, such as disability from joint destruction, growth retardation, blindness from chronic iridocyclitis, and even multiple organ failure and death in systemic-onset JIA. The aim of treatment is the induction of remission and control the disease activity to minimize the pain and loss of function, and to maximize quality of life. JIA is a disease having a chronic course, which involves active and inactive cycles over the course of years. Recent studies showed that nearly half of the patients with JIA enter adulthood with their ongoing active disease. This review elucidates how recent advances have impacted diagnosis, pathogenesis and current treatment.

Helicobacter pylori and inflammatory skin diseases

Throughout the history of mankind, infections have been the major cause of diseases. Over the last decades, not only the incidence of emerging infectious diseases have increased, but also tremendous strides have been made in understanding the biology of several pathogenic microorganisms. Helicobacter pylori(H. pylori) is a spiral-shaped, gram-negative bacterium, which infects over the half of the world's population. H. pylori has been implicated in the pathogenesis of a number of gastrointestinal disorders. However, new researches have demonstrated that H. pylori is also involved in the pathogenesis of various extragastric diseases. The difference in the clinical outcome of H. pylori infection may be explained, at least in part, by host response to the infection and H. pylori virulence factors. It is obvious that as developments in the research on H. pylori spring up, an understanding of the pathophysiology of H. pylori infection will continue to be identified. Here in this review, we summarize the current knowledge about H. pylori and its association with inflammatory skin diseases.

THERAPY FOR CANCER—METHODS AND SUGGESTIONS

On the basis of the theory of Traditional Chinese Medicine,authors put forwathe etiopathogenesis and pathogenetic mechanism of solid tumors,and formulated a scheme for tre^ment of cancer with acupuncture therapy.

Mucosa-associated lymphoid tissue lymphoma with unusual 18F-FDG hypermetabolism arising at the colorectal anastomosis

Mucosa-associated lymphoid tissue (MALT) lymphoma usually originates from the stomach and presents with low ^(18)F-fluorodeoxyglucose (FDG) avidity with average maximum standard uptake value of 3.6. Colorectal MALT lymphoma is a rare entity that contributes to 1.6% of all MALT lymphomas and < 0.2% of large intestinal malignancies. The case reported herein firstly revealed stage Ⅱ MALT lymphoma with unexpected higher ^(18)F-FDG avidity of 18.9 arising at the colorectal anastomosis in a patient with a surgical history for sigmoid adenocarcinoma, which was strongly suspected as local recurrence before histopathological and immunohistochemical examinations. After accurate diagnosis, the patient received four cycles of standard R-CVP regimen (rituximab, cyclophosphamide, vincristine and prednisone), combined target therapy and chemotherapy, instead of radiotherapy recommended by National Comprehensive Cancer Network guidelines. He tolerated the treatment well and reached complete remission.

Etiopathogenesis of reproductive tract infections and the emerging role of bitter taste receptors:A scoping review

Reproductive tract infections pose an immense public health concern worldwide as over 600 million new cases are recorded annually along with several complications,including infertility,ectopic pregnancy,preterm delivery,and neonatal death.Despite improved understanding of the mechanisms of pathogenic invasion,the etiopathogenesis of reproductive tract infections is yet to be completely understood.Recent data has suggested a critical role of bitter taste receptors of the reproductive tract in etiopathogenesis of reproductive tract infections.Here,we review the literature on current etiopathogenesis of reproductive tract infections and the role of bitter taste receptors of the reproductive tract in etiopathogenesis of reproductive tract infections.Emerging evidence suggests a critical role of microbiota disorder of the reproductive tract in reproductive tract infections.Several bacterial,protozoan parasitic,helminthic parasitic and viral pathogens have been identified as causative agents of reproductive tract infections.These pathogens subvert host defenses and activate specific architectural units of the uroepithelium such as Toll-like receptors,which recognize conserved motifs on the pathogens.The activated Toll-like receptors mediate downstream signaling,stimulating nuclear factor-κB,which in turn activates the production of proinflammatory cytokines.This pathway is also associated with recruitment of immunocytes to the site of aggression and release of proteinases,which drive tissue damage in the reproductive tract.Defects in detection of pathogenic components by the bitter taste receptors of the reproductive tract may play a critical role in the etiopathogenesis of reproductive tract infections.This review provides important information for identification of novel frontiers for the treatment of reproductive tract infections.

Toll-Like Receptor Gene Expression in Nasal Polyp

Objective: To investigate the expression of Toll-like receptors (TLRs) and the correlation between TLR expression and mucosal changes in chronic sinusitis-related nasal polyposis. Methods: Patients with nasal polyps were enrolled in this study as the study group. The control group consisted of individuals undergoing surgery due to nasal obstruction caused by concha hypertrophy who were not diagnosed with chronic sinusitis-related nasal polyposis (NP). There were 30 patients in the study group (individuals with NP) and 20 patients in the control group. Sterile tissue samples were taken from the patients and were kept at -80°C. A piece of tissue sample was put into the eppendorf tube. Expression of TLR2 and TLR4 gene was investigated in the tissue samples. The samples were taken after the surgery;they were carried into the liquid nitrogen and were kept at -80° C before study. Results: TLR2 and TLR4 expression was measured in both groups and then analyzed using Student’s t-test. In the experimental group, the level of TLR2 expression was significantly higher than in the control group (P < 0.001);however, TLR4 expression was not significantly different between the two groups (P = 0.656). Conclusion: TLRs are thought to play a role in the etiopathogenesis of NP. In addition, the authors consider that a possible treatment for NP could be a TLR-specific treatment. Thus, in the future it will be essential to determine the extent to which TLRs function in NP formation and to apply this knowledge to design a specific therapeutic regimen for the enhanced treatment of NP.

Matrix Metalloproteinase-9 in the Etiopathogenesis of Placenta Accreta Spectrum:A Literature Review

The recent increase in placenta accreta spectrum has been correlated with a rise in the rate of cesarean sections.A recent study provides evidence that hampered wound healing results in cesarean scar defects that lead to a failure in the normal process of decidualization and deeper adherence of trophoblasts.Matrix metalloproteinase(MMP)is crucial in every step of wound healing as it alters the wound matrix,facilitating cell migration,as well as tissue remodeling.MMP-9 expression is higher in placental and decidual tissue in cases of placenta accreta.Based on these findings,assessment of MMP-9 expression can shed new light on the etiopathology of placenta accreta spectrum disorder and can be a potential diagnostic marker.

Pathomolecular characterization of HCC in non-cirrhotic livers

Hepatocellular carcinoma(HCC)is the most common primary liver cancer and usually arises in cirrhotic livers.Increasingly,it is diagnosed in non-cirrhotic livers.A variety of risk factors and etiologies can trigger the development of HCC in non-fibrotic and non-cirrhotic backgrounds.The most important causes are metabolic syndrome and hepatitis B virus infection.Postulated pathogenetic mechanisms are direct carcinogenesis,chronic liver injury and repair cycles,and genetic/epigenetic aberrations.Histopathology has a very important role in the diagnosis of non-cirrhotic HCC.Gross features of non-cirrhotic HCC are quite different from HCC originating in a cirrhotic background.Microscopic characteristics are similar to a classical HCC.However,certain histological variants show a predilection to occur in non-cirrhotic livers.These encompass fibrolamellar,scirrhous,steatohepatitic and mixed hepato-cholangiocarcinoma subtypes.Due to the non-cirrhotic background,adenoma,metastasis and most of the other non-neoplastic and neoplastic conditions enter the differential diagnosis.Genomic studies and morpho-molecular classifications of HCC provide further understanding of the molecular pathogenesis of non-cirrhotic HCC.This group however,has rarely been exclusively studied.This review offers an update of etiology,patho-molecular characteristics and differential diagnosis of HCC arising in non-cirrhotic backgrounds.