Liver cyst

Often in routine imaging examinations of the abdomen, either an ultrasound or CAT scan of the abdomen, a cyst is found in the liver. The vast majority of these correspond to simple hepatic cysts.

The term cyst refers to any lesion that is filled with liquid content. Simple hepatic cysts have imperceptible walls and that do not communicate with the bile duct. They range in size from millimeters to giant lesions. They are more common in women, particularly large symptomatic cysts.

Symptoms

Most simple hepatic cysts cause no symptoms. When a cyst is large (greater than 4 cm), it may have nonspecific symptoms such as abdominal pain, early satiety or nausea. However, the evaluation of these symptoms should always be careful as these complaints may arise from other causes such as irritable bowel syndrome, lumbago, or cholelithiasis (gallbladder stones). Much less often a large cyst may be complicated by bleeding, torsion, infection or rupture.

Evaluation

A typical simple cystic liver lesion found on ultrasound may not require additional studies when small to moderate. On ultrasound, the cyst is seen as an anechogenic lesion without septa, with imperceptible wall and posterior reinforcement.

CT and MRI show a water density lesion density of water that is not enhanced with intravenous contrast.

Differential diagnosis

The differential diagnosis of simple liver cyst includes the following conditions:

  • Abscess: Usually the presence of symptoms such as pain and fever, laboratory abnormalities such as elevated C-reactive protein, associated with imaging features (peripheral enhancement) are easy to distinguish in most cases.
  • Hydatid cyst: Hydatid cysts often have calcifications in the cyst wall and “complex” adjacent smaller or multiloculated cysts with thick walls and internal echoes corresponding to parasitic structures can be distinguished. Hydatid serology is frequently positive.
  • Polycystic disease: The presence of multiple cysts in the liver suggest the diagnosis of polycystic liver disease, most often associated with renal cysts (autosomal dominant polycystic kidney disease, ADPKD). However, in other cases, the cysts are found only in the liver (autosomal dominant polycystic liver disease).
  • Cystadenoma: This is a rare benign tumor. It has thickened walls and is often multiloculated. Treatment is resection.
  • Cystadenocarcinoma: An uncommon malignant tumor, probably derived from the malignant transformation of a cystadenoma. Treatment also is surgical.
  • Necrotic tumor: Some malignant tumors metastatic and primary liver occasionally may have a liquefied necrotic component that may seem like a simple cyst, however, clinical symptoms usually allow differentiation.

Treatment

The vast majority of simple hepatic cysts require no treatment. When a cyst is large (greater than 4 cm), it is usually recommended controlling images, for which an ultrasound is usually sufficient. If the cyst does not grow after 2 or 3 years, there is no need for more controls.

In those cases when the cyst is large and symptomatic, treatment is surgery. While there are several surgical options, the most widely used is the unroofing of the cyst, either by open surgery or laparoscopy. The drainage of the cyst by aspiration is not a satisfactory option since the cyst usually recurs.

12 questions about fatty liver

  1. What is fatty liver?

Fatty liver is a disease in which the liver increases its content of fat (triglycerides and cholesterol). The liver may increase its size and becomes yellowish. It is frequently associated with bad eating habits and lack of physical activity. Alcohol consumption is a common cause of fatty liver.

  1. What are the symptoms of fatty liver?

A fatty liver does not cause any symptoms in the majority of affected people. Some patients may feel slight tenderness or pain in the right upper quadrant of the abdomen, where the liver is. Some physical changes can be seen in people with fatty liver, such as a black coloration of the skin in the neck or armpits (a sign known as acanthosis nigricans).

  1. How frequent is fatty liver?

Fatty liver is one of the most frequent metabolic conditions, affecting approximately 20% of the adult population. Up to 70% of obese persons have fatty liver.

  1. What is the cause of fatty liver?

The cause of fatty liver is unknown. Frequently it is associated with the so-called metabolic syndrome or insulin resistance. This metabolic derangement is linked to unhealthy eating and physical activity habits. One of the common causes of fatty liver is alcohol consumption.

  1. Is fatty liver a genetic condition?

Fatty liver is not a hereditary condition, but there is some familiar association determined by some genetic predisposition and also because it is common that eating habits are shared in the same family, which may predispose to fatty liver development.

  1. What is the treatment of fatty liver?

The treatment of fatty liver is basically the modification of eating habits with a diet restricted in carbohydrates (sugar, pasta, rice, bread, corn, potatoes) and fats. Together with diet, increasing physical activity is key.

Medications are not part of the usual management of fatty liver, but in certain circumstances, vitamin E and pioglitazone may be treatment options.

  1. Is physical activity beneficial if I have fatty liver?

Physical activity is one of the most effective ways to reverse the liver injury caused by this condition. Physical activity must be gradual, ideally aerobic and regular (3 to 4 times per week). A medical checkup by a doctor evaluating cardiovascular risk before an exercise program is always a good idea.

  1. What diet should I follow if I have fatty liver?

A healthy diet is one of the two pillars of fatty liver treatment. The diet consists in the drastic reduction of sugar, decreasing carbohydrates such as bread, pasta, potato, rice and corn, avoiding animal fat. In addition, it is recommended to increase the consumption of vegetables, fish, nuts, avocado, and yogurt. A Mediterranean diet is probably one of the most healthy diets to avoid fatty liver and to decrease cardiovascular risk.

  1. Can I drink alcoholic beverages if I have fatty liver?

Alcohol, even in small amounts, may aggravate the liver injury in people with fatty liver. For this reason, it is recommended completely avoiding alcohol in people affected with this disease. This has the additional benefit of decreasing the intake of calories, helping losing weight, given that alcoholic drinks are a considerable caloric source.

  1. Can fatty liver be cured?

One of the features of fatty liver is its reversibility. People succeeding in changing their habits, losing weight and exercising may completely cure fatty liver.

  1. How is it evaluated the severity of fatty liver?

Nonalcoholic fatty liver may be classified as simple fatty liver when there is fat accumulation without inflammation and in nonalcoholic steatohepatitis when it is accompanied by inflammation and injury. Blood tests such as aminotransferases and sometimes a liver biopsy may help in differentiating both conditions.

  1. What are the risks of fatty liver?

Fatty liver progresses without symptoms for many years, even decades. Some people may develop most severe consequences of the disease if they get progressive liver injury (fibrosis), leading to liver cirrhosis or liver cancer (hepatocellular carcinoma). When these complications occur, one of the options is liver transplantation. Aside from these complications, people with fatty liver have increased risk for developing cardiovascular disease such as heart attacks or stroke, and diabetes mellitus.

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Antileishmanial efficacy of Boerhaavia diffusa L. and Ocimum sanctum L. against experimental visceral leishmaniasis.

 

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Antileishmanial efficacy of Boerhaavia diffusa L. and Ocimum sanctum L. against experimental visceral leishmaniasis.

Indian J Exp Biol. 2015 Aug;53(8):522-9

Authors: Kaur S, Bhardwaj K, Sachdeva H

Abstract
The chemotherapy of visceral leishmaniasis (VL) has several limitations including resistance and toxicity of the existing drugs. Down regulation of immune system further aggravates the problems. To combat this situation we evaluated the leishmanicidal efficacy of Boerhaavia diffusa and Ocimum sanctum through oral route in L. donovani infection in BALB/c mice. Results have demonstrated maximum clearance of the parasites from infected animals treated with combination of B. diffusa and O. sanctum (@ 100 and 400 mg/kg body wt., respectively 5 days) as depicted through Leishman Donovan Units in liver. Up-regulation of cell-mediated immunity was also observed in animals of this group as heightened delayed type hypersensitivity responses and increased IgG2a levels were observed. Moreover, increased levels of SGOT, SGPT, serum urea, blood urea nitrogen and serum creatinine were brought down to normal levels. Since VL is associated immunosuppression, the above treatment is a good option as it helps in the up-regulation of Th1 responses and reduction in parasite load in L. donovani infected mice. These findings suggest a new option for antileishmanial chemotherapy at lower cost and nil toxicity.

PMID: 26349315 [PubMed – in process]

http://www.ncbi.nlm.nih.gov/pubmed/26349315?dopt=Abstract

Evaluation of Acute toxicity of Lambda Cyhalothrin in Mus musculus L.

 

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Evaluation of Acute toxicity of Lambda Cyhalothrin in Mus musculus L.

Indian J Exp Biol. 2015 Aug;53(8):551-5

Authors: Tomar M, Kumar A, Kataria SK

Abstract
Lambda Cyhalothrin (LCT) is a type II synthetic pyrethroid widely used in agriculture, home pest control and protection of food stuff. Here, we evaluated its toxicity on biochemical parameters (Total protein, Acetyl cholinesterase, RNA and DNA) and liver histological alteration in mice after 24 h of oral administration @ 25, 50 and 75% of LD50 i.e.; 26.49 mg/kg/body wt. Distilled water (DW) and Cyclophosphamide (CP @ 40 mg/kg/body wt.) were used as negative and positive control; respectively. LCT treated mice showed significant decrease in total protein (P < 0.01), acetyl cholinesterase (P < 0.001) and DNA (P < 0.001) in a dose dependent manner. On the contrary, RNA content showed significant increase (P < 0.01) at 50% of LD50 of LCT. Histological observations of the mice liver showed vascular congestion and hepatocyte degeneration with 6.63 mg/kg/body wt. of LCT; and accumulation of RBCs with sinusoid degeneration and wide necrotic area with pyknosis with 13.25 and 19.88 mg/kg/body wt., respectively. The results demonstrated LCT induced biochemical changes and hepatotoxicity in female mice.

PMID: 26349319 [PubMed – in process]

http://www.ncbi.nlm.nih.gov/pubmed/26349319?dopt=Abstract

Biocompatible Low-Retention Superparamagnetic Iron Oxide Nanoclusters as Contrast Agents for Magnetic Resonance Imaging of Liver Tumor.

 

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Biocompatible Low-Retention Superparamagnetic Iron Oxide Nanoclusters as Contrast Agents for Magnetic Resonance Imaging of Liver Tumor.

J Biomed Nanotechnol. 2015 May;11(5):854-64

Authors: Wei Y, Liao R, Liu H, Li H, Xu H, Zhou Q

Abstract
Although superparamagnetic iron oxide (SPIO) nanoparticles have been developed as a contrast agent for magnetic resonance imaging (MRI), acute iron overload due to the persistently high retention of SPIOs in the liver and spleen that are slowly converted to ferroproteins is a serious safety concern. Here, we report that the addition of poly-L-lysine polymers to an SPIO hydroxyethyl starch solution produced tightly controlled, monodispersed nanoparticles in a size-dependent manner as effective contrast agents for the MRI of liver tumors. High MRI contrast was demonstrated with an orthotopic liver tumor model at a low injection dose. Simultaneously, rapid bioclearance of excess iron in the lung and spleen and in blood serum was observed within 24 h post-injection. The full excretion of excess iron was confirmed in urine post-intravenous injection, suggesting that the effective clearance of SPIOs could be achieved with our SPIO nanoclusters as a liver imaging contrast agent to resolve acute iron overload in the clinical usage of SPIOs as a contrast agent.

PMID: 26349397 [PubMed – in process]

http://www.ncbi.nlm.nih.gov/pubmed/26349397?dopt=Abstract

Hypoglycemic and Hypolipidemic Effects of the Cracked-Cap Medicinal Mushroom Phellinus rimosus (Higher Basidiomycetes) in Streptozotocin-Induced Diabetic Rats.

 

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Hypoglycemic and Hypolipidemic Effects of the Cracked-Cap Medicinal Mushroom Phellinus rimosus (Higher Basidiomycetes) in Streptozotocin-Induced Diabetic Rats.

Int J Med Mushrooms. 2015;17(6):521-31

Authors: Rony KA, Ajith TA, Janardhanan KK

Abstract
Phellinus rimosus is a parasitic host specific polypore mushroom with profound antioxidant, antihepatotoxic, anti-inflammatory, antitumor, and antimutagenic activities. This study investigated the hypoglycemic and hypolipidemic activities of the wood-inhabiting polypore mushroom Ph. Rimosus in streptozotocin (STZ)-induced diabetic rats. Diabetes was induced by single intraperitoneal injection of STZ (45 mg/kg) to Wistar rats. The effects of 30 days treatment with Ph. Rimosus (50 and 250 mg/ kg) and glibenclamide (0.65 mg/kg) on blood glucose level, serum insulin, serum lipid profile, liver glycogen, liver function enzymes, and non-enzymic and enzymic antioxidants activities in pancreas, liver, and kidney were evaluated in STZ-induced diabetic rats. Oral administration of Ph. Rimosus extract exhibited a significant reduction in blood glucose, triacylglycerol, total cholesterol, LDL-cholesterol, and liver function enzymes, and increased serum insulin, liver glycogen, and HDL-cholesterol levels in STZ-induced diabetic rats. Furthermore, Ph. Rimosus treatment increased antioxidant status in pancreas, liver, and kidney tissues with concomitant decreases in levels of thiobarbituric acid- reactive substances. Results of this study indicated that Ph. Rimosus possessed significant hypoglycemic and hypolipidemic activities and this effect may be related to its insulinogenic and antioxidant effect.

PMID: 26349510 [PubMed – in process]

http://www.ncbi.nlm.nih.gov/pubmed/26349510?dopt=Abstract

CytoSorb, a novel therapeutic approach for patients with septic shock: a case report.

 

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CytoSorb, a novel therapeutic approach for patients with septic shock: a case report.

Int J Artif Organs. 2015 Aug 31;:0

Authors: Hinz B, Jauch O, Noky T, Friesecke S, Abel P, Kaiser R

Abstract
INTRODUCTION: Hemoadsorption using CytoSorb has gained attention as a potential immunotherapy to control systemic inflammation and sepsis. We report on a patient with septic shock, successfully treated with CytoSorb therapy.
METHODS: A 72-year-old male with periodically recurring infectious episodes was admitted with the suspicion of urosepsis. In the following hours his hemodynamic situation deteriorated markedly, exhibiting respiratory-metabolic acidosis, elevated inflammatory marker plasma levels, a severely disturbed coagulation, increased retention parameters, liver dysfunction, and confirmation of bacteria and leucocytes in urine. After admission to the ICU in a state of septic shock the patient received renal support with additional hemoadsorption using CytoSorb. Three CytoSorb sessions were run during the following days.
RESULTS: The first and consecutive second session resulted in a reduction of procalcitonin, C-reactive protein and bilirubin and a markedly reduced need for vasopressors while hemodynamics improved significantly (i.e., cardiac index, extravascular lung water). Due to a recurring inflammatory “second hit” episode, another session with CytoSorb was run, resulting in a marked decrease in leukocytosis and liver (dys)function parameters.
CONCLUSIONS: The rapid hemodynamic stabilization with reduction of vasopressor needs within hours and reduction of the capillary leakage as well as a quick reduction in infection markers were the main conclusions drawn from the use of CytoSorb in this patient. Additionally, treatment appeared to be safe and was well tolerated. Despite the promising results of CytoSorb application in this patient, further studies are necessary to elucidate to what extent these favorable consequences are attributable to the adsorber itself.

PMID: 26349530 [PubMed – as supplied by publisher]

http://www.ncbi.nlm.nih.gov/pubmed/26349530?dopt=Abstract

Shear Wave Elastography for Assessment of Steatohepatitis and Hepatic Fibrosis in Rat Models of Non-Alcoholic Fatty Liver Disease.

 

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Shear Wave Elastography for Assessment of Steatohepatitis and Hepatic Fibrosis in Rat Models of Non-Alcoholic Fatty Liver Disease.

Ultrasound Med Biol. 2015 Sep 5;

Authors: Kang BK, Lee SS, Cheong H, Hong SM, Jang K, Lee MG

Abstract
The purpose of this study was to evaluate shear wave elastography (SWE) as a method for determining the severity of non-alcoholic fatty liver disease (NAFLD) and the stage of hepatic fibrosis, as well as the major determinants of liver elasticity among the various histologic and biomolecular changes associated with NAFLD. Rat NAFLD models with various degrees of NAFLD severity were created and imaged using SWE. The explanted livers were subjected to histopathologic evaluation and RNA expression analysis. Among the histologic and biomolecular findings, the fibrosis stage and the collagen RNA level were significant independent factors associated with liver elasticity (p < 0.001). Liver elasticity was effective in detecting non-alcoholic steatohepatitis (NASH) and in determining fibrosis stage, and the corresponding areas under the receiver operating characteristic curves were 0.963 and 0.927-0.997, respectively. In conclusion, SWE is a potential non-invasive method for the detection of NASH and staging of hepatic fibrosis in patients with NAFLD.

PMID: 26349582 [PubMed – as supplied by publisher]

http://www.ncbi.nlm.nih.gov/pubmed/26349582?dopt=Abstract

Fourier Transform Infrared Spectroscopic Studies on Modulation of N-Nitrosodiethylamine-Induced Hepatocarcinogenesis by Azadirachta indica.

 

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Fourier Transform Infrared Spectroscopic Studies on Modulation of N-Nitrosodiethylamine-Induced Hepatocarcinogenesis by Azadirachta indica.

J Environ Pathol Toxicol Oncol. 2015;34(3):227-36

Authors: Bharati S, Rishi P, Koul A

Abstract
Fourier transform infrared spectroscopy was employed in the present study to obtain information about the molecular composition of hepatic tumor versus hepatic tissue. A hepatic cancer model was developed by administering N-nitrosodiethylamine (NDEA) to male Balb/c mice. The results revealed that NDEA-induced hepatic cancer tumor tissue had altered molecular composition compared with normal liver tissue. Compared with the normal tissue, the saturation level of membrane phospholipids was observed to be decreased in tumors along with an abnormal distribution of protein secondary structures. A significant decrease in glycogen and a significant increase in total nucleic acid content were also observed in tumor cells. The administration of aqueous Azadirachta indica leaf extract (AAILE) prior to NDEA treatment resulted in the normalization of saturation levels in phospholipids and total nucleic acid content and in the distribution of protein secondary structures in tumors. A significant increase in the amount of stored glycogen was observed in AAILE cotreated tumors compared with NDEA-induced tumors, which might indicate that AAILE cotreatment impeded the ability of tumor cells to consume glucose at a faster rate. The normalization of molecular composition upon AAILE cotreatment in hepatic tumors might indicate that AAILE hampered the process of evolution of tumors, which could be responsible for its observed chemopreventive action.

PMID: 26349605 [PubMed – in process]

http://www.ncbi.nlm.nih.gov/pubmed/26349605?dopt=Abstract