Type 2 diabetes short term effects cs4,type 1 diabetes teenage years symptoms,type 2 diabetes doctor uk hypertension,jdrf walk to cure type 1 diabetes life - PDF 2016

Long-term use of liraglutide, a substance that helps to lower blood sugar levels in patients with type 2 diabetes, can have a deteriorating effect on insulin-producing beta cells, leading to an increase in blood sugar levels. Blood-sugar suppressors in the form of analogues of the incretin hormone GLP-1 are commonly used in the treatment of type 2 diabetes, since they stimulate the glucose response of the pancreatic beta cells to make them secrete more insulin.
To study the long-term effects of incretin therapy, which has never previously been assayed, researchers at Karolinska Institutet and the University of Miami worked with humanised mice, generated by transplanting human insulin-producing cells into the anterior chamber of the eye.
Tiny extensions on cells, cilia, play an important role in insulin release, according to a new study, which is published in Nature Communications. Starting from human skin cells, researchers at the University of Iowa have created human insulin-producing cells that respond to glucose and correct blood-sugar levels in diabetic mice. Insensitivity to insulin, also called insulin resistance, is associated with type 2 diabetes and affects several cell types and organs in the body.
Researchers at the University of Massachusetts Medical School have discovered a new pathway that triggers regeneration of beta cells in the pancreas, a key development that may aid in the development of diabetes treatments. The significant role of beta cell 'hubs' in the pancreas has been demonstrated for the first time, suggesting that diabetes may due to the failure of a privileged few cells, rather than the behaviour of all cells. Slideshare uses cookies to improve functionality and performance, and to provide you with relevant advertising. Clipping is a handy way to collect and organize the most important slides from a presentation.
Top of page780 An Atypical Presentation of Alpha 1-Antitrypsin Deficiency and HemochromatosisKathleen Raynor, MD, Adnan Khdair, MD, Kirk Zachary, MD, FACG, Irwin Grosman, MD, FACG. This according to a study on mice implanted with human insulin-producing cells conducted by a team of scientists from Karolinska Institutet, Sweden, and the University of Miami, USA. There is now compelling evidence that liraglutide therapy is efficacious at least in the short term, since it produces an initial reduction in blood sugar. The mice were given daily doses of liraglutide for more than 250 days, during which time the researchers were able to monitor how the pancreatic beta cells were affected. Abdulreda, Rayner Rodriguez-Diaz, Alejandro Caicedo, Per-Olof Berggren, 'Cell Metabolism', online 11 February 2016.
The researchers flag the possible consequences of this popular form of therapy in the next issue of the journal Cell Metabolism. However, many patients do not respond to the treatment and some even display adverse reactions such as nausea, vomiting and diarrhoea. The results showed an initial improvement in the insulin-producing cells, followed by a gradual exhaustion, with reduced secretion of insulin as a response to glucose.
A pulmonology consult was obtained and CT scan and PFTs showed no evidence of pulmonary disease. Based on biopsy and serum phenotype of homozygous ZZ a diagnosis of alpha 1-Antitrypsin deficiency was made. An additional diagnosis of hemochromatosis was also considered given the elevated ferritin and biopsy with heavy iron staining seen on Prussian blue stain.
Few case reports have cited the association between hemochromatosis and alpha 1-Antitrypsin deficiency, but most of these have involved middle-aged, Caucasian males. It Makes You Easily Irritable: When you miss your morning breakfast, you very soon begin to feel tired and cranky.
It has been hypothesized that the abnormal folding of the protein allows for excess accumulation of iron.
Therefore, this case is atypical based on the patient's age, gender, ethnicity, and presentation suggestive of metastatic cancer as the cause of her liver disease.
Those who eat a proper breakfast tend to stay more active and positive than those who don't.
A Polymorphism of the Alpha 1- Antitrypsin Gene Represents a Risk Factor for Liver Disease. Studies have shown that women who choose not to have a healthy breakfast in the morning have a 54% more chance of suffering from type 2 diabetes than those who do. The next day he became drowsier and at the same time we received a call from the blood bank informing that patient's blood was viscous and was turning into a gel upon withdrawal. Can Cause You To Suffer From Migraine: Skipping your breakfast means eating after 12 long hours. This would in turn get you to suffer from low blood sugar level, triggering hormones, which increase blood pressure ultimately leading to headaches and migraines.
Cryoglobulins testing was positive.Plasma viscosity was found to be elevated at 8 times the normal.
Subsequently an ophthalmology consult was obtained and he was found to have a central retinal vein occlusion(CRVO).
Bone marrow exam revealed B cells within the lymphoid aggregates staining positive for BCL2. Discussion: Cryoglobulinemia arises from chronic stimulation of the immune system by HCV binding to B lymphocytes via CD81.
The clinical triad of palpable purpura, arthralgias, and weakness is the result of deposition of circulating immune complexes. CNS involvement can manifest as confusion, encephalopathy with or with out focal neurological deficits. In conclusion cryoglobulinemia is a rare cause of encephalopathy in HCV infected patients.Top of page782 An Unusual Cause of Painless JaundiceDarryn Potosky, MD, William Twaddell, MD. Her symptoms did not improve and she subsequently developed jaundice, prompting further evaluation.
She denied any significant alcohol use or known liver disease in herself or family members. Physical exam was notable only for jaundice and the lack of any stigmata of chronic liver disease. Viral studies revealed immunity to hepatitis A and B and absence of infection with hepatitis C.
Liver histology revealed atypical portal infiltrates with monotonous appearing lymphocytes expanding outside sinusoidal tracts (Figure A). Immunostains were positive for of CD 10, CD 20, and TdT (Figure B), a DNA polymerase expressed solely in premature lymphocytes. This phenotype matched the bone marrow biopsy and established the diagnosis of acute precursor B-lymphoblastic leukemia. The patient was treated with intravenous steroids resulting in a dramatic improvement in her bilirubin and normalization of her transaminases. She was subsequently given standard induction chemotherapy, achieving a complete marrow remission. Hepatic pseudotumors mimic malignancy and not infrequently pose a considerable diagnostic challenge. Case report: A 19 yr old male with mental retardation presented with vague abdominal discomfort, decreased appetite, and low grade fevers. He had a history of a yet uncharacterized immune deficiency syndrome with possible chemotactic neutrophil defect and polyclonal hypergammaglobulinemia with multiple recurring infections like mastoiditis, periorbital cellulitis, and prostate abscess. Abdominal CT demonstrated 3 heterogeneous liver lesions with central hyperintensity and surrounding hypodensity, the largest measuring 4 cm. Biopsy of liver lesion revealed a focal myxoid spindle cell proliferation with large stellate cells, abundant lymphoplasmacytic infiltrate, eosinophils, and occasional neutrophils consistent with IPT. Vancomycin and cefepime were started empirically given the worsening leukocytosis and persisting fevers.
Anecdotal reports of regression after antibiotics, NSAIDs and corticosteroids are not uncommon. He had previously undergone multiple chemotherapy regimens, and most recently, placement of selective internal radiation spheres in the right hepatic lobe 2 months prior to presentation. Physical exam was significant for cachexia and tenderness to palpation in the epigastrium without peritoneal signs. Esophagogastroduodenoscopy revealed diffuse, nearly circumferential antral and duodenal bulb ulcerations (Figure A). Biopsies of the antral region showed granulation tissue with spherical "calcifications" and surrounding benign superficial gastric foveolar mucosa (Figure B). Pretreatment consists of selective occlusion of the gastroduodenal artery and any collateral vessels using endovascular coils. Technetium99 macroaggregates of albumin are then injected to determine any residual shunting to untargeted areas. If no further selective occlusion is necessary, the spheres are injected at a later session. The patients are usually given 4 weeks of corticosteroids and proton pump inhibitor for prophylaxis.
Initial studies of radiation sphere treatments have shown an incidence of gastric ulceration with biopsy proven presence of spheres in 3-10% of patients. One series of 4 patients with biopsy proven presence of spheres showed resolution of symptoms on proton pump inhibitor in 2 patients, however, the other 2 patients did not have resolution of symptoms in the follow-up period.Top of page785 Macrophage Activation Syndrome Associated Acute Liver FailureAdam Peyton, DO, Kiran Rao, MD. This showed a hypercellular marrow with increased erythroid precursor showing megaloblastic change and dyserythroises.
Testing for ANA, AMA, ASMA, alpha 1 antitrypsin and ceruloplasmin were all normal and serology for EBV, HSV, CMV, and HIV were all negative.
Ultrasound showed hepatomegaly, no CBD dilatation, no pancreatic mass, and no liver masses.
The bone marrow slides were obtained for review and transjugular liver biopsy was performed. Re-review of bone marrow biopsy showed florid erythrocytic hyperplasia with mild dysplasia, numerous macrophages and histiocytes throughout with prominent phagocytosis. Immunohistochemical stains reveal positive staining of macrophages in sinusoids for CD68, a macrophage marker. Discussion: Macrophage Activation Syndrome (MAS) or Hemophagocytic Lymphohistiocytosis, is characterized by fever, lymphadenopathy, hepatosplenomegaly, pancytopenia, liver dysfunction, hypertriglyceridemia, hyperferritinemia, and hemophagocytosis. The pathogenesis of MAS is unknown; however, it is thought to be caused by activation and uncontrolled proliferation of T lymphocytes and macrophages leading to cytokine overproduction. Hyperferritinemia is a laboratory hallmark of MAS as phagocytic macrophages are an important source of ferritin.
MAS is typically secondary to an underlying medical condition, such as a viral, bacterial, fungal, and parasitic infections, as well as collagen-vascular diseases and malignancies, particularly T-cell lymphomas. Typical immunohistochemical staining reveals hemophagocytosis with infiltration of portal and sinusoidal tracts by activated macrophages (CD68+) and activated T cells (CD8+). Wide varieties of treatment have been attempted including IVIG, corticosteroids, etoposide, and liver transplantation. Reported in 0.3-2% of pregnancies, it occurs in the first trimester of pregnancy, between 4-10 weeks' gestation. HG can be associated with maternal morbidity and rare mortality and may recur in subsequent pregnancies. A 32-year-old black female G6P0050 presented 11 weeks pregnant with 1-week of intractable nausea, vomiting, and epigastric pain in the setting of elevated transaminases.
Detailed obstetrical history was significant for five prior pregnancies over the past six years, all associated with severe HG complications that led to two spontaneous abortions and two elective abortions. The correlation of her HCG levels with transaminases in relation to each HG admission had a most impressive pattern over the six-year course (Figure).
Many serum results are abnormal according to non-pregnant population standards (increased plasma volumes lowering serum albumin, placental leak of alkaline phosphatase causing elevation).
Alanine aminotransferase, aspartate aminotransferase are normally unchanged in pregnancy and increases in these may reflect hepatobiliary pathology.
This case illustrates that B-HCG levels correlate with aminotransferase elevation in the setting of HG and can result in significant maternal morbidity.Top of page787 Overlap of Hepatopulmonary Syndrome and Portopulmonary HypertensionAndres Yarur, MD,1 Tom Brown, MD,2 Chakradhar Reddy, MD,1 Eugene Schiff, MD, MACG1. Division of Gastroenterology and Hepatology, University of Miami, Miller School of Medicine, Miami, FL; 2. Overlap of these syndromes was confirmed by both right heart catheterization meeting criteria for POPH and a transthoracic echocardiogram with bubble contrast showing evidence of right to left intrapulmonary shunting.
Nevertheless, on repeat right heart catheterization 11 months after initial presentation, her mean pulmonary pressures had increased from 40 mmHg to 43 mmHg while on treatment.

Intriguingly, over the same period of time she no longer experienced oxygen desaturation on 6 minute walk test. Hypothetically, HPS and POPH are separate and somewhat contradictory entities and should not coexist at the same time in a cirrhotic patient. Review of the literature reveals 9 other reported cases of overlap of HPS and POPH, some of which were similar to our case in that the HPS tends to resolve while the POPH progresses. Does the development of POPH in the setting of preexisting HPS result in a resolution of HPS? Further studies are needed.Top of page788 Biliary Obstruction After Orthotopic Liver Retransplantation Secondary to Bile Duct Traumatic NeuromaCraig Lammert, MSc, MD, Samir Parekh, MD, Steven Keilen, MD. To our knowledge, there have been only a few cases of traumatic neuromas causing biliary obstruction described after OLT. We report the first case of biliary obstruction secondary to a bile duct traumatic neuroma after liver retransplantation for hepatitis C virus (HCV) related graft failure. His postoperative course was complicated by recurrent HCV infection resulting in graft failure within 3 years, despite attempts at treatment with pegylated interferon and ribavirin.
The surgery and postoperative course were uneventful, and he was discharged 15 days after surgery with improving laboratory values.
Within one month post-OLT, the patient was placed on pegylated interferon and ribavirin to prevent HCV recurrence. MRI demonstrated intra and extrahepatic biliary ductal dilation with abrupt narrowing of the common hepatic duct at the porta hepatis. Endoscopic retrograde cholangiography (ERC) was performed demonstrating abrupt cutoff at the level of the bile duct anastomosis. Attempts at passing a guidewire beyond the obstruction by ERCP and by a percutaneous transhepatic approach were both unsuccessful. An external biliary drain was placed, and then the patient underwent successful Rou-en-Y bile duct revision. Liver biopsy at the time of surgery showed moderate portal and lobular inflammation and periportal fibrosis most consistent with HCV recurrence. After surgery, the patients liver enzymes and bilirubin normalized and he was restarted on HCV antiviral therapy. This case illustrates the potential for biliary obstruction as a result of traumatic neuroma in liver transplant patients. Although the development of biliary obstruction from traumatic neuromas after OLT is rare, it is a foreseeable outcome after damage of conducting nerve fibers, and therefore, should be considered as a potential etiology of biliary obstruction in the post-OLT patient.Top of page789 Simultaneous Expression of Both Surface Antigen and Surface Antibody at High Titers in a Young Asian Girl with Chronic Hepatitis BArun Srivatsa, MD, Jason Gutman, MD, Benedict Maliakkal, MD.
Yet she continues to have high titers of both hepatitis B surface antigen and antibody in her blood at this time. The other explanation is that the virus may have developed a variant epitope of the Hep B surface antigen. This would explain the fact that she had presence of viral DNA and HBsAg in her blood at the same time as having detectable Hep B surface antibody. The fact that she has high titers of hepatitis B surface antibody indicates that a mutation in the viral genome may have occurred after she developed immunity to the original non mutant strainConclusion: Simultaneous occurrence of both Hepatitis B surface antigen and antibody in high titers indicates surface mutant strains or variation in Hepatitis B surface antigen epitopes. She was successfully treated with Interferon-beta 1b(Betaseron®) which is currently not FDA approved for treatment of Hepatitis C. This agent is traditionally used in the management of multiple sclerosis in the USAMethods: A 58 year old lady contracted hepatitis C through a needle stick injury while working as a phlebotomist. She was treated with Pegylated interferon (Pegasys®) but stopped therapy because of side effects related to facial swelling and flushing thought to be anaphylactic in nature. She was then followed with regular monitoring of blood work and viral load and continued to be viremic, but otherwise asymptomatic.
Subsequently around five years later, she developed tingling and numbness of her left leg associated with a foot drop. She was seen by a neurologist and was diagnosed with demyelinating disease thought to be either Multiple sclerosis or post infectious demyelination related to hepatitis C. At this point, after extensive discussion with her neurologist, it was decided that Interferon-beta 1b (Betaseron®) would be a better choice compared to conventional pegylated Interferon because of the theoretical benefit of the former on demyelinating disease.
The most common tumor resulting in pseudomesotheliomatous carcinoma of the pleura is primary adenocarcinoma of the lung.
In the previous 2 months, he had developed recurrent ascites requiring multiple paracenteses. After extensive investigations of the pleural effusions and ascites, no definitive diagnosis could be made. Subsequently, due to the high suspicion for malignancy a PET CT scan was done, which showed extensive tumor throughout the right hemithorax outlining the pleura with marked pleural thickening and diffuse lymphadenopathy. The tumor extended into the chest wall with extensive peritoneal involvement and multiple sites of metastases. Although we presumed the patient had metastatic disease, the primary location remained unknown.
Only 4-5% of primary melanomas present with extracutaneous manifestations, and whether the malignancy is primary or metastatic, the prognosis remains grave. Therefore, every attempt should be made for an accurate diagnosis.Top of page792 Median Arcuate Ligament Syndrome with Early Collateralization in a Liver TransplantAmanda Woodworth, MD, Jorge Ortiz, MD, Radi Zaki, MD, Kamran Khanmoradi, MD, Mindy Horrow, MD, Victor Araya, MD.
During liver transplantation, the median arcuate ligament can cause a decrease in celiac artery blood flow leading to hepatic artery thrombosis in liver transplant recipients. In the setting of hepatic artery thrombosis, collateralization may allow for graft survival but until recently had only been seen later in the post-operative period. In the case below, we describe a patient with median arcuate ligament syndrome, subsequent hepatic artery thrombosis and the early development of lifesaving collaterals.
The patient is a 67-year-old male with end stage liver disease secondary to alcoholic cirrhosis. After orthotopic liver transplantation, the initial post-operative ultrasound revealed an area of infarct in the periphery of the right lobe but otherwise good flow throughout all vessels with a hepatic artery resistive index average of 0.68. Subsequent ultrasounds obtained revealed declining hepatic artery resistive indices and a hepatic artery stenosis was visualized at the anastamosis.
On post-operative day nine, the patient returned to the operating room for an exploratory laparotomy, lysis of adhesions around the hepatic artery and ligation of the gastroduodenal artery. Intraoperative ultrasound was performed at that time revealing improvement in hepatic artery flow. Post-operatively the patient's liver function tests rose and subsequent ultrasounds revealed persistent parvus-tardus waveforms with low resistant indices throughout the entire hepatic artery felt to be related to celiac axis compression. A CT angiogram of the abdomen with 3D reconstruction was then obtained revealing stenosis of the proximal celiac artery secondary to median arcuate ligament syndrome. After review of pre-operative and post-operative imaging, stenosis was visualized at the proximal celiac axis on numerous imaging modalities. The patient returned to the operating room for an attempted release of the arcuate ligament.
Due to excessive bleeding in a friable artery, the vessel was ligated and an aortohepatic bypass with bovine jump graft was performed. Post-operatively the patient demonstrated good flow through the graft but subsequently it thrombosed. The patient continued on a fairly routine post-operative course with elevated but stable liver function tests.
The patient also noted that his stools were lighter in color and that he had an increased frequency of bowel movements. On physical exam, the patient's liver was palpable three centimeters below the right costal margin. An EGD revealed a small hiatal hernia, five pigmented, smooth nodules in the body and fundus of the stomach and one pigmented nodule in the duodenal bulb.
Biopsy specimens from the gastric fundus nodules and the duodenal bulb nodule were consistent with metastatic melanoma. A repeat scan done at the time of the patient's presenting symptoms, only four months after the patient's last serial CT scan, showed a new mass lesion in the right lobe of the liver. However, the patient's alpha-fetoprotein, carcinoembryonic antigen, and cancer antigen 19-9 levels were all normal. Liver biopsy confirmed metastatic melanoma and the patient enrolled in experimental protocol. Presenting symptoms are similar to those caused by any gastrointestinal tumor, such as abdominal pain, dysphagia, constipation, small bowel obstruction, hematemesis, and melena. Diagnosis is made by CT scan, ultrasonography, barium studies, and endoscopic evaluation, such as EGD, endoscopic retrograde cholangiopancreatography, and colonoscopy. Treatment options may include surgical resection, chemotherapy, immunotherapy, and chemoembolization.
The prognosis in these patients is extremely poor because metastatic lesions are often found in the liver and other visceral organs.
Laboratory tests showed pancytopenia, acute renal insufficiency, hyperbilirubinemia and positive stool Clostridium difficile (C.
He continued to clinically deteriorate and have high stool output despite aggressive treatment of C. Flexible sigmoidoscopy showed pseudomembranous colitis but colon biopsies were non-diagnostic. His course was further complicated by pneumonia, bacteremia, coagulopathy, dialysis-dependent renal failure and upper gastrointestinal bleed.
Esophagogastroduodenoscopy (EGD) showed gastric erythema and friability consistent with possible stress gastritis and normal duodenum. Repeat upper endoscopy to establish the diagnosis showed severely denuded mucosa in the stomach and duodenum.
He was treated with high-dose corticosteroids and extracorporeal plasmapheresis, complicated by line-related sepsis. The risk is significantly increased when the recipient and donor share a major histocompatibility antigen haplotype.
The diagnosis is often delayed because other common OLT complications, such as infection, can present with a similar clinical picture.
High clinical suspicion and obtaining biopsies for histopathologic diagnosis augments the diagnostic yield of endoscopy, particularly in challenging cases that defy usual diagnosis.Top of page796 Ischemia, Hemorrhage and Obstruction of the Duodenum and Common Bile Duct After Transarterial Chemoembolization for Hepatocellular CarcinomaKavita Singh, MD, David Van Thiel, MD, Joseph Ahn, MD, Stanley Cohen, MD, Nikunj Shah, MD.
TACE provides a local delivery of chemotherapy followed by embolization of the vessel that supplies blood to the tumor. TACE can be used to treat hepatocellular carcinoma (HCC) and several other metastatic liver cancers. He was found to have HCC in the caudate lobe of the allograft and underwent TACE without any complications. One month later, he presented for a 2nd chemoembolization as the previous lesion was increasing in size.
An EGD showed edematous, thickened folds in the second portion of the duodenum with narrowing of the duodenal lumen by an extrinsic lesion. A CT scan of the abdomen showed dilatation in the 4th portion of the duodenum and hyperdense material consistent with hemorrhage. Seven months earlier she was diagnosed with sigmoid diverticulitis and was treated with oral antibiotics.
Past medical history includes hypertension and coronary artery disease status post angioplasty 9 years ago and a 30 pack year smoking history. In the ER she was afebrile and the abdomen was soft, non tender, non distended with good bowel sounds. The CT scan showed portal vein thrombosis, low attenuation liver lesions and extensive sigmoid diverticulitis with a 4 1.8 cm abscess. Exploratory laparotomy with sigmoid colectomy and loop transverse colostomy were performed. The patient had uneventful post operative course and was discharged home on ertapenem one gram daily to finish 4 weeks of intravenous antibiotic treatment. Pylephlebitis, a suppurative thrombophlebitis of the portal vein, is usually secondary to infection either in the region drained by the portal system or in the structures contiguous to the portal vein. Management of pylephlebitis is by treating the primary source using broad spectrum intravenous antibiotics and surgical intervention (appendectomy or colectomy with abscess drainage).

We present a case of HCC presenting as extensive peritoneal involvement as the presenting site of the disease. 52yr old female with past medical history of hepatitis and chronic alcoholism presented with progressive distension of the abdomen of one month duration. CT of the abdomen and pelvic area with contrast revealed enhanced thickened omentum typical for omentum cake with ascitis with multiple omental masses implanted along with splenomegaly and ascitis.
A CT guided diagnostic paracentesis showed exudative effusion with cytology negative for malignant cells.
An MRI abdomen was consistent with marked seeding of the peritoneum and thickening of the omental mantle consistent with carcinomatosis.
Findings were also suggestive of carcinomatosis involving the spleen and the liver with ascitis. An exploratory laparotomy, total abdominal hysterectomy and bilateral salpingo-oopherectomy with omentectomy, appendectomy, and a liver biopsy were performed. Liver biopsy showed portal fibrosis with dense lymphocytic infiltration and lymphoid nodules with bile duct proliferation and focal bile duct degeneration suggestive of chronic hepatitis with HCV. Peritoneal nodules showed moderate to poorly differentiated grade 3 hepatocellular carcinoma. Sixteen patients presenting with recurrent peritoneal implants after follow-up in the postoperative period of resection of hepatocellular carcinoma was studied by Chun-Nan Yeh. Limited data available show that resection of peritoneal metastasis arising from HCC may be of value in improving patient survival. Our case had markedly increased AFP with extensive peritoneal spread and in retrospect with single lesion in the liver it might be taken a case of peritoneal disease. In conclusion, this case presents exclusively as primary peritoneal carcinomatosis as a presentation of HCC. Ctr.)Top of page799 Angiosarcoma of the Liver Presenting as Congestive Heart FailureEkta Gupta, MD, Murat Gokden, MD, Kevin Olden, MD, FACG, James Rose, MD. She was afebrile, tachycardic (pulse rate 136) and had jugular venous distension, systolic ejection murmur, hepatomegaly and lower extremity edema. Computed tomography confirmed presence of mass which appeared hypodense with mild peripheral enhancement.
1A), consisting of variable-sized vascular channels, solid and myxoid areas and necrosis (Fig. Presence of HF in these patients is very rare with only 2 case reports describing presence of high output HF thought to be secondary to arteriovenous shunting. It should be considered in a patient with unexplained high output HF.Top of page800 Acquired Hepatocerebral DegenerationVishal Ghevariya, MD, MS,1 Fred Fallick, MD,2 Manpreet Singh, MD,1 Sury Anand, MD1.
This phenomenon leads to development of characteristic neuro-psychiatric manifestations that varies according to the involvement of the part of the brain. A 42-year old male with cirrhosis presented with tremors, ataxic gait, apathy and memory impairment.
Physical examination was remarkable for muscle wasting, spider nevi, and tremors of the limbs. Laboratory studies revealed thrombocytopenia, macrocytic anemia, normal TSH, high ALT, negative urine toxicology, HIV test and hepatitis profile.
MRI of the brain showed symmetrical signal enhancement on T1 weighed images in the globus pallidus and lenticular nucleus. Differential diagnosis of above MRI findings include acquired hepatocerebral degeneration (AHD), total parenteral nutrition (TPN) related chronic manganese poisoning, Leigh's disease, and Tay-Sach disease.
Deposition of copper in basal ganglia can occur in Wilson disease and signal enhancement is seen on T2 weighed images. Deposition of manganese in the brain is responsible for both the MRI findings and the clinical manifestations due to basal ganglia dysfunction.
Chelation therapy improves both the clinical syndrome and high intensity signal enhancement. Successful liver transplantation improves both neurological and radiological abnormalities.Top of page801 Spur Cell Anemia as a Cause of Unconjugated Hyperbilirubinemia and Its Resolution After Liver TransplantationAdriana Prada Ruiz, MD, Naim Alkhouri, MD, Vera Hupertz, MD, Bijan Eghtesad, MD, Kdadakkal Radhakrishnan, MD.
Her previous medical history was significant for a Kasai procedure at 2.5 months of age and a liver transplantion at 2 years of age.
She did very well for 15 years after OLT and was receiving immunosuppression with tacrolimus.
At 18 years of age she presented with abdominal pain localized in the RUQ with radiation to her back, dry cough and shortness of breath. Chest X ray and CT scan identified massive right side pleural effusion with almost complete collapse of the right lung and moderate left effusion.
Liver Biopsy showed no rejection, moderate pericellular sinusoidal fibrosis and mild chronic hepatitis. Hepatic venogram with indirect pressure measurements showed a normal portosystemic gradient of 7 mmHg.
The peripheral blood smear showed multiple spur cells (>20%) consistent with a diagnosis of spur cell anemia.
Because of her poor quality of life and anemia refractory to multiple transfusions of packed red blood cells, she underwent cadaveric OLT. To our knowledge, this is the first pediatric case of reversal of spur cell anemia after OLT.
Liver transplantation should be considered in patients with chronic liver disease and spur cell anemia unresponsive to medical treatment.Top of page802 Hepatoid Carcinomatosis Without Primary Liver LesionHoussam kharrat, MD,1 Omar Shoukfeh, Medical Student2. Medication: pravastatin, estropipate, irbesartan, L-methylfolate, propranolol, Iron, sumatriptan.
Patient had CT abdomen and pelvis which showed dilated small bowel, mild ascites, and mesenteric stranding suspicious of infiltrative disease.
An NG was placed and abdominal paracentesis was done, albumin gradient was less than 1.1 with high protein. Patient underwent exploration for possible small bowel obstruction and debulking of the tumor.
During surgery patient was noted to have diffuse peritoneal implants that covered small bowel omentum, and liver capsule without invasion.
Biopsy showed poorly differentiated carcinoma with hepatocellular differentiation, immuno stain was strongly positive AFP. This phenomenon has been identified as a hepatoid variant form of yolk sac tumor, also known as H-YST. Since then, multiple case reports of similar malignancies arising from stomach, colon, renal pelvis, pancreas, gallbladder have been described. The abnormal physical findings include tachycardia, scleral icterus, hepatomegaly, splenomegaly and 2+ bilateral leg edema.
The EGD revealed portal hypertensive gastropathy but no signs of active or old bleeding were noticed. Therefore, the patient's anemia was consistent with the hemolytic process called Spur Cell Anemia seen secondary to End stage liver disease. Spur cell anemia is an unusual type of hemolytic anemia in patients with Liver Cirrhosis, particularly in those who abused alcohol. The mechanism of production of these cells has been attributed to the increased Cholesterol : Phospholipids ratio in RBC cell membranes with subsequent remodeling by the spleen because of rigid cell membranes.
The spur cell anemia should be suspected in any Cirrhotic patients presenting with hemolysis. We report the first case of granulomatous hepatitis induced by Sarapin®, a medication derived from the carnivorous plant Sarracenia purpurea (Pitcher Plant). An 85 year old woman with history of osteopenia, hypertension, hyperlipidemia, coronary artery disease and cerebral vascular accident was admitted for chest pain and hypertension. Home medication review showed a new substance recently added to her multiregimen medication, called Sarapin®, in the form of locally administered injections for chronic joints pain.
These injections have been administered in various locations in 6 consecutive sessions over the last 3 months. Core needle biopsy of the liver showed preserved hepatic architecture with mixed chronic inflammatory infiltrate disease. The diagnostic workup helped in ruling out sarcoidosis, mycobacterial and fungal infection or primary biliary cirrhosis as possible cause for her granulomatous hepatitis. After discontinuing Sarapin® injections the transaminases and alkaline phosphatase decreased slowly, the patient became asymptomatic and was discharged. This case illustrates the potential for liver toxicity with the use of Sarapin® and the difficulty for its identification as a single offending agent. The lack of any information in the literature regarding liver toxicity after the use of Sarapin® makes the confirmation of our diagnosis even harder. Further observations and studies are necessary to clarify the relation between the human liver and the Pitcher Plant.Top of page805ABSTRACT WITHDRAWNTop of page806 Left-Sided Portal Hypertension Caused by an Accessory SpleenOmar Sharif, MD, Ihab Hammoud, MD, Mostafa Ibrahim, MD, FACG. The incidence of LSPH has increased over the past three decades due to increased awareness of this entity. Case: A 55 year old female presented to the Emergency room with three days history of hematemsis, melena and weakness.
She has remote past history of alcohol abuse, however she denied any similar episodes in the past.
On presentation she was hypotensive and tachycardic, otherwise the physical examination was essentially unremarkable. The initial gastroscopy showed isolated gastric varices with stigmata of recent hemorrhage. An ultrasound of her abdomen with doppler showed no hepatic masses, patent hepatic vasculature and splenic vein. A computed tomography of her abdomen showed normal liver and pancreas, patent splenic, hepatic, portal veins without evidence of hepatic steatosis.
The hepatobiliary surgery team was consulted and the patient underwent laparoscopic resection of the accessory spleen with ligation of the short gastric veins.
A repeat gastroscopy in six months showed disappearance of the gastric varicesConclusion: Most cases of LSPH are related to splenic vein thrombosis in the context of chronic pancreatitis. The venous drainage of the accessory spleen into the short gastric veins is probably the reason for development of the varices. Review of literature showing less than 50 publications of CMV hepatitis in the immunocompetent patient.
The patient had been having fevers for two weeks prior to admission with complaints of generalized fatigue and myalgias. She drank only glass of wine per night and denied previous history of liver disease, blood transfusions, tattoos or IVDA. She was admitted to the hospital for further work-up of unexplained fever and had negative work-up to date including four sets of blood cultures, urine analysis, chest x-ray and ultrasound of the abdomen. Acute hepatitis panel, HIV, ceruloplasmin, HFE gene, alpha-1 anti-trypsin, iron studies, autoimmune markers and heterophile antibody were all negative.
LFTs were done every week after discharge, which showed persistent elevation of liver enzymes. It can have an asymptomatic course, present with a mononucleosis-like syndrome or have multi-organ involvement. Review of literature shows in the normal host, CMV hepatitis usually has a self-limited course but few case reports show a role for anti-viral therapy, although no consensus stands for when and who to treat.
CMV infection should be in the differential diagnosis of an immunocompetent patient who presents with unexplained prolonged fevers and abnormal liver enzymes.
In recent years, selenium supplementation has been touted by media as beneficial to health. On admission, she was in rapid atrial fibrillation, treated with diltiazem and atenolol, with resolution of dyspnea.

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