scholarly journals Banti’s Syndrome Presenting as Hematemesis - A Case Report

2021 ◽  
Vol 10 (10) ◽  
pp. 749-751
Author(s):  
Aishwarya Ghule ◽  
Sourya Acharya ◽  
Samarth Shukla ◽  
Sunil Kumar ◽  
Parth Godhiwala
Keyword(s):  
Portal Hypertension ◽  
Portal Pressure ◽  
Normal Liver ◽  
Liver Function Tests ◽  
Massive Bleeding ◽  
Idiopathic Portal Hypertension ◽  
Hepatic Veins ◽  
Massive Splenomegaly ◽  
History Of ◽  
Banti's Syndrome

Massive splenomegaly presenting with hypersplenism, pancytopenia and portal hypertension, without any underlying known cause is known as Banti’s syndrome. There are various causes of splenomegaly. When all the known causes of portal hypertension are ruled out, it is termed as Banti’s syndrome. This syndrome was discovered by Guido Banti in 1882 and is named after him. Banti’s syndrome is also known as idiopathic portal hypertension or non-cirrhotic portal fibrosis.1 Banti’s syndrome is commonly found in India and Japan than in the West. 2 There is absence of any haematologic cause, primary hepatic cause or any tumour or mass lesion involving the spleen. Banti had stated that the primary organ involved was spleen and not the liver leading to secondary splenomegaly. Other features include normal liver function tests, varices seen in endoscopy, cytopenia of one or more cell lines, absence of cirrhosis, patent hepatic veins and elevated portal pressure with multiple collaterals. The complications include rupture of varices and massive bleeding. 3 We report a case of a 20-year-old male who presented to us with a history of fever for 7 days and one-episode of hematemesis on the day of admission. All known causes of hypersplenism were ruled out and he was diagnosed to have idiopathic massive splenomegaly with portal hypertension and hypersplenism.

Persistently raised aspartate aminotransferase (AST) due to macro-AST in a rheumatology clinic

Diagnosis ◽  
2015 ◽  
Vol 2 (2) ◽  
pp. 137-140 ◽  
Author(s):  
Wycliffe Mbagaya ◽  
Joanne Foo ◽  
Ahai Luvai ◽  
Claire King ◽  
Sarah Mapplebeck ◽  
...  
Keyword(s):  
Liver Function ◽  
Aspartate Aminotransferase ◽  
Normal Liver ◽  
Abdominal Ultrasound ◽  
Liver Function Tests ◽  
Analytical Investigation ◽  
Normal Liver Function ◽  
Rheumatology Clinic ◽  
History Of ◽  
Liver Biopsies

AbstractMacrocomplexes between immunoglobins and aspartate aminotransferase (macro-AST) may result in persistently increased AST concentration. The presence of macro-AST in patients has been implicated in unnecessary investigations of abnormal liver function tests. We report the case of a 44-year-old female who presented to the rheumatology clinic with a 12-months’ history of constant widespread pain affecting her limbs and was found to have an elevated AST concentration. Further information from her GP revealed a 14-years’ history of elevated AST with otherwise normal liver function. Previous abdominal ultrasound and two liver biopsies carried out 2 years apart were normal. This prompted further analytical investigation by the biochemistry department which identified macro-AST as the cause. This case illustrates that persistently raised isolated AST concentration with no other abnormal indices may warrant macroenzyme analysis potentially avoiding unnecessary invasive investigations.

scholarly journals AN EXPERIMENTAL STUDY INTO THE CAUSE OF THE INCREASED PORTAL PRESSURE IN PORTAL CIRRHOSIS

1907 ◽  
Vol 9 (1) ◽  
pp. 93-104 ◽  
Author(s):  
Frederick C. Herrick
Keyword(s):  
Arterial Pressure ◽  
Portal Pressure ◽  
Normal Liver ◽  
Volume Flow ◽  
Cirrhotic Liver ◽  
Return Flow ◽  
Hepatic Veins ◽  
Portal Cirrhosis ◽  
Arterial Inflow ◽  
Flow Through

1. In the liver of portal cirrhosis there is a far freer communication between the arterial and portal currents than in the normal liver. 2. Factors contributing to the increased portal pressure in portal cirrhosis are (1) the direct communication of the arterial pressure to the portal vessels through dilated capillaries, (2) the larger volume-flow of the hepatic artery in proportion to the portal flow in cirrhosis as compared to that in the normal liver. 3. A portal cirrhotic liver gives passage to an amount of portal fluid proportionate to .its weight. There is no obstruction to the portal vessels from fibrosis in the large portal cirrhotic liver. 4. From an arterial inflow there is a free return flow through the portal as well as through the hepatic veins in both normal and cirrhotic livers. 5. From a portal inflow the return is through the hepatic vein only. The Gad's theory of valves and the arterial capillary network account for this fact. 6. The portal pressure has a decided influence on the arterial volume-flow and vice versa. This influence is more marked in the cirrhotic than in the normal liver. 7. The communication of the arterial pressure to the portal pressure is an important factor in an explanation of the increased portal pressure in portal cirrhosis.

scholarly journals Fatal Nonhepatic Hyperammonemia in ICU Setting: A Rare but Serious Complication following Bariatric Surgery

2016 ◽  
Vol 2016 ◽  
pp. 1-6 ◽  
Author(s):  
Gyanendra Acharya ◽  
Sunil Mehra ◽  
Ronakkumar Patel ◽  
Simona Frunza-Stefan ◽  
Harmanjot Kaur
Keyword(s):  
Bariatric Surgery ◽  
Normal Liver ◽  
Liver Function Tests ◽  
Altered Mental Status ◽  
Ammonia Level ◽  
Gastric Bypass Procedure ◽  
History Of ◽  
Serum Ammonia Level ◽  
Pedal Edema ◽  
Serum Ammonia

Bariatric surgery is well established in reducing weight and improving the obesity-associated morbidity and mortality. Hyperammonemic encephalopathy following bariatric surgery is rare but highly fatal if not diagnosed in time and managed aggressively. Both macro- and micronutrients deficiencies play a role. A 42-year-old Hispanic female with a history of Roux-en-Y Gastric Bypass Procedure was brought to ED for progressive altered mental status. Physical exam was remarkable for drowsiness with Glasgow Coma Scale 11, ascites, and bilateral pedal edema. Labs showed elevated ammonia, low hemoglobin, low serum prealbumin, albumin, HDL, and positive toxicology. She remained obtunded despite the treatment with Narcan and flumazenil and the serum ammonia level fluctuated despite standard treatment with lactulose and rifaximin. Laboratory investigations helped to elucidate the etiology of the hyperammonemia most likely secondary to unmasking the functional deficiency of the urea cycle enzymes. Hyperammonemia in the context of normal liver function tests becomes diagnostically challenging for physicians. Severe hyperammonemia is highly fatal. Early diagnosis and aggressive treatment can alter the prognosis favorably.

Portal hemodynamics in idiopathic portal hypertension (Banti's syndrome)

1987 ◽  
Vol 92 (3) ◽  
pp. 751-758 ◽  
Author(s):  
Kunihiko Ohnishi ◽  
Masayuki Saito ◽  
Shinichi Sato ◽  
Hidetaka Terabayashi ◽  
Shinji Iida ◽  
...  
Keyword(s):  
Portal Hypertension ◽  
Idiopathic Portal Hypertension ◽  
Portal Hemodynamics ◽  
Banti's Syndrome

Hepatitis C infection and chemotherapy toxicity

2017 ◽  
Vol 25 (2) ◽  
pp. 474-480 ◽  
Author(s):  
Amy Ly ◽  
Heather H Cheng ◽  
Laura Alwan
Keyword(s):  
Hepatitis C ◽  
Viral Infection ◽  
Case Reports ◽  
Normal Liver ◽  
Liver Function Tests ◽  
Solid Organ ◽  
Hepatitis C Infection ◽  
Chemotherapy Toxicity ◽  
Palliative Intent ◽  
History Of

There exists little guidance on chemotherapy toxicity management in patients with a history of or active hepatitis C viral infection. We report four cases of patients with solid organ tumors and hepatitis C viral infection, who have experienced severe or unexpected toxicities with chemotherapy. Based on the four case reports, we recommend increased laboratory monitoring for toxicities, initial dose reductions for chemotherapy given with palliative intent, or pre-emptive use of growth factor support, even if the patient presents with normal liver function tests. In this patient population, we also recommend treating active hepatitis C viral infection prior to chemotherapy treatment when possible.

scholarly journals Outcomes of partial splenic embolization in patients with massive splenomegaly due to idiopathic portal hypertension

2016 ◽  
Vol 22 (43) ◽  
pp. 9623 ◽  
Author(s):  
Omer Ozturk ◽  
Gonca Eldem ◽  
Bora Peynircioglu ◽  
Taylan Kav ◽  
Aysegul Görmez ◽  
...  
Keyword(s):  
Portal Hypertension ◽  
Idiopathic Portal Hypertension ◽  
Partial Splenic Embolization ◽  
Massive Splenomegaly ◽  
Splenic Embolization

scholarly journals Portal hyperflow in patients with hepatosplenic mansonic schistosomiasis

2004 ◽  
Vol 59 (1) ◽  
pp. 10-14 ◽  
Author(s):  
Roberto de Cleva ◽  
William Abrão Saad ◽  
Paulo Herman ◽  
Vincenzo Pugliese ◽  
Bruno Zilberstein ◽  
...  
Keyword(s):  
Portal Hypertension ◽  
Esophageal Varices ◽  
Portal Pressure ◽  
Previous History ◽  
Portal Flow ◽  
Portal Hemodynamics ◽  
Significant Drop ◽  
Hemodynamic Assessment ◽  
History Of ◽  
Hepatosplenic Schistosomiasis

PURPOSE: The purpose of this study was to assess portal hemodynamics in patients with portal hypertension due to hepatosplenic schistosomiasis as well as to assess the contribution of splanchnic hyperflow to the pathophysiology of the portal hypertension. METHODS: Sixteen patients with schistosomal portal hypertension and previous history of upper digestive bleeding due to esophageal varices rupture underwent elective esophagogastric devascularization and splenectomy and were prospectively studied. All patients underwent intraoperative invasive hemodynamic portal monitoring with a 4F-thermodilution catheter. The intraoperative portal hemodynamic assessment was conducted after laparotomy (initial) and after esophagogastric devascularization (final). RESULTS: The initial portal pressure was elevated (mean 28.5 ± 4.5 mm Hg), and a significant drop of 25% was observed at the end of the surgery (21.9 ± 4.9 mm Hg). The initial portal flow was elevated (mean 1766.9 ± 686.6 mL/min). A significant fall (42%) occurred at the end of the surgical procedure (1025.62 ± 338.7 mL/min). Fourteen patients (87.5%) presented a portal flow of more than 1200 mL/min, and in 5 cases, values greater than 2000 mL/min were observed. CONCLUSIONS: Esophagogastric devascularization and splenectomy promote a significant reduction of the elevated portal pressure and flow in schistosomal portal hypertension. These data favor the hypothesis of portal hyperflow in the physiopathology of portal hypertension of schistosomiasis.

scholarly journals Portal hemodynamics in idiopathic portal hypertension (Banti's syndrome)

Kanzo ◽  
1986 ◽  
Vol 27 (5) ◽  
pp. 615-621
Author(s):  
Kunihiko OHNISHI ◽  
Masayuki SAITO ◽  
Kunio OKUDA
Keyword(s):  
Portal Hypertension ◽  
Idiopathic Portal Hypertension ◽  
Portal Hemodynamics ◽  
Banti's Syndrome
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