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Banti's Syndrome

Banti's syndrome (also known as Banti's disease), named for Guido Banti,[1] is a chronic congestive enlargement of the spleen[2] resulting in premature destruction of the red blood cells by the spleen.

banti's syndrome

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Banti syndrome is a disorder of the spleen, the large, gland-like organ in the upper left side of the abdomen that produces red blood cells before birth and, in newborns, removes and destroys aged red blood cells, and plays a role in fighting infection. In the case of Banti syndrome, the spleen rapidly but prematurely destroys blood cells.

This syndrome is characterized by abnormal enlargement of the spleen (splenomegaly) due to obstruction of blood flow in some veins and abnormally increased blood pressure (hypertension) within the veins of the liver (e.g., hepatic or portal veins), or the spleen (splenic veins). The disorder may be due to any number of different factors causing obstruction of portal, hepatic, or splenic veins including abnormalities present at birth (congenital) of such veins, blood clots, or various underlying disorders causing inflammation and obstruction of veins (vascular obstruction) of the liver.

In early stages, symptoms of Banti syndrome include weakness, fatigue, anemia , and abnormal enlargement of the spleen. As the disorder progresses, the anemia becomes more severe. The anemia may be aggravated by a bleeding esophagus that may cause vomiting of blood and the passage of dark stools composed of decomposing blood. Ultimately, in some cases, the liver itself becomes enlarged and subdivided by fibrous tissue (cirrhosis). However, the spleen enlargement in Banti syndrome is the primary symptom.

Banti syndrome may occur due to a number of different factors causing obstruction of, and abnormally increased blood pressure (hypertension) within, certain veins of the spleen (splenic veins) or the liver (e.g., hepatic or portal veins). These may include abnormalities present at birth (congenital) of such veins, blood clots, or various underlying disorders causing inflammation and obstruction of veins (vascular obstruction) of the liver, such as cirrhosis. Increased arsenic intake has also been implicated in some cases. Also, cases have occurred in patients taking long-term azathioprine, particularly after kidney transplantation.

Banti syndrome affects males and females equally. It is relatively common in parts of India and Japan, but rare in Western countries. Increased arsenic levels are present in drinking water in some countries and may contribute to regional differences in incidence.

The diagnosis of Banti syndrome my be confirmed by a thorough clinical evaluation and a variety of specialized tests, particularly advanced imaging techniques such as a splenic venography and magnetic resonance imaging (MRI). During MRI, a magnetic field and radio waves are used to create cross-sectional images of targeted parts of the body.

There is some evidence to support immunologic abnormalities in this syndrome [9]. Nayyar et al. found that total T cells and cytotoxic T cells were diminished. Since tumor necrosis factor (TNF) is involved in fibrosis, there is evidence that increased soluble TNF receptors I and II, which are found in this syndrome [10], explain the fibrosis around the portal vein. Furthermore, since TNF causes upregulation of vascular cell adhesion molecule-1 (VCAM-1), increased VCAM-1 is also observed in such patients [11,12].

Banti's syndrome, a disorder of the spleen is characterized by the spleen prematurely destroying red blood cells. This syndrome is defined by abnormal spleen enlargement (splenomegaly) caused by blood flow obstruction in some veins and abnormally high blood pressure (hypertension) in the hepatic, portal veins of the liver and the splenic veins of the spleen.

Banti's syndrome can be caused by a variety of conditions that cause obstruction and excessively high blood pressure (hypertension) within particular veins of the spleen (splenic veins) or the liver (liver veins) (e.g., hepatic or portal veins). These include congenital anomalies of such veins, blood clots, and other underlying illnesses causing inflammation and obstruction of veins in the liver (vascular obstruction), such as cirrhosis. In certain cases, increased arsenic intake has been responsible. Patients on long-term azathioprine, particularly following kidney transplantation, have also developed cases.

The symptoms of Banti's syndrome in the initial stages include weakness, anemia, fatigue, and abnormal enlargement of the spleen. With the progress of the syndrome, anemia tends to become more severe. This can be intensified by a bleeding esophagus, which can result in blood vomiting and the passing of dark feces containing decaying blood. In certain situations, the liver itself enlarges and becomes subdivided by fibrous tissue (cirrhosis).

In Banti's syndrome, however, spleen enlargement is the major symptom. The patients with Banti's syndrome bruise easily. They are more susceptible to bacterial infections and suffer from fever for longer durations.

Males and females are both in equal numbers affected by Banti syndrome. It is frequent in regions of India, Pakistan, and Japan, but it is uncommon in Western countries. Arsenic levels in drinking water have increased in several nations, which may contribute to regional disparities in the occurrence of the syndrome.

A thorough clinical evaluation and a variety of specialist testing, notably advanced imaging techniques such as splenic venography and magnetic resonance imaging, may be used to confirm the diagnosis of Banti's syndrome (MRI). A magnetic field and radio waves are utilized in MRI to obtain cross-sectional images of certain body areas.

The cause of Banti's syndrome affects the course of treatment. If a contributory component like arsenic or azathioprine is discovered, the exposure should be terminated. The main clinical issue is bleeding from enlarged blood vessels in the esophagus or stomach (varices).

The treatment of gastrointestinal bleeding caused by portal hypertension and the therapy of hypersplenism are the mainstays of the management of Banti's syndrome. Variceal ligation and endoscopic sclerotherapy were shown to be equally effective in 95 percent of patients with acute gastrointestinal bleeding, with a recurrence rate of roughly 20% and 3% recurrent bleeding, respectively. Some patients may also require shunt procedures as a last resort.

Banti's syndrome has a favorable prognosis, with a 5-year survival rate of 100% after successful varices ligation. A case report published in the International Journal of Case Reports in Surgery demonstrated that the post-operative recovery was excellent in the patient. Due to severe anemia requiring repeated transfusions and large splenomegaly posing a risk of traumatic rupture, the patient had a splenectomy. During the follow-up period, the post-operative recovery was excellent, with a rapid increase in platelet level and a steady rise in hemoglobin level.

There hasn't been any evidence of COVID producing Banti's syndrome in the literature. A case of a 32-year-old male who presented with hematemesis was reported in a recent research publication. Subsequent follow-up revealed that the patient was suffering from ascites, splenomegaly, and bleeding varices, eventually completing the signs and symptoms of Banti's syndrome.

Banti's syndrome should be considered in a patient with hematemesis and splenomegaly, although it is a rare illness. The patient suffered from flu-like symptoms for three weeks. He did not seek any medical attention, ultimately developing Banti's syndrome. His COVID-19 serology was positive.

COVID-19 is recognized to cause hypercoagulability, but the exact mechanism by which it causes Banti's syndrome is unknown. It could be caused by thrombosis of the portal arteries or embolization of the portal circulation. There is still a lot of research to be done to figure out what causes Banti's syndrome in COVID-19 positive patients.

Banti's disease is a condition where congestive splenomegaly can be observed in the absence of intrahepatic or extrahepatic obstruction. The diagnosis is established by splenectomy, but it is necessary to exclude liver diseases or portal vein obstruction before surgery. The advanced stage of Banti's disease may be complicated by upper gastrointestinal haemorrhages; so splenectomy has both diagnostical and therapeutical benefits. Primary lesions of the small splenic arterioles are one of the offered explanations. A patient with no intrahepatic or extrahepatic obstruction, is described. We also excluded diseases which might be complicated by splenomegaly, part of them after splenectomy. Cytogenetics showed normal female pattern. The histologic examination revealed no liver disease, but the spleen was congestive with reduced lymphoid tissue. Immunohistologically, the reduced spleen white-pulp nodules were composed of polyclonal B-cells and T-cells in a normal distribution, discarding indolent lymphoprolipherative disorder. Over one year after splenectomy the patient had no trouble. In conclusion, we believe that Banti's disease is a condition clearly separated from Banti's syndrome. We also believe that splenectomy is the treatment of choice.

COVID causing Banti's syndrome has not been reported in literature yet. Banti's syndrome is a rare disorder characterized by splenomegaly, ascites, and portal hypertension without coexisting cirrhosis of the liver. Here we report a case of a 32-year-old man who presented with hematemesis, and further workup revealed that the patient had bleeding varices, ascites, and splenomegaly, thus completing the picture of Banti's syndrome. Although this is a rare disorder, Banti's syndrome must be taken into account in a patient presenting with hematemesis and splenomegaly. The patient had flu-like symptoms for three weeks but did not seek any medical help and eventually presented with Banti's syndrome. His serology was positive for COVID-19. The coronavirus (COVID-19), discovered in 2019, has been creating havoc since it first emerged in China and is now spreading worldwide. Its presentation is somewhat similar to influenza. 041b061a72

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