The rare cause of hematemesis was originally related to this medicine!

Case introduction: A 55-year-old female patient presented with a history of colon adenocarcinoma after sigmoid colectomy.
She came to the hospital due to hematemesis.

The patient feels unwell when he wakes up, he suddenly vomits a lot of blood, without abdominal pain, fever or chills.

The patient denied a history of heartburn or peptic ulcer, and denied the use of any non-steroidal anti-inflammatory drugs or anticoagulants.

After completing 12 cycles of 5-fluorouracil, leucovorin, and oxaliplatin (FOLFOX) chemotherapy 5 years ago, the patient developed stage 3a colon adenocarcinoma.

The patient's surgical history was significant.
He underwent sigmoid colectomy in 2014, cholecystectomy in 2013, and partial hysterectomy in 2011.

The patient has no history of smoking or illegal drug use.

The father of the patient has alcohol-related cirrhosis.

The patient has no family history of other gastrointestinal or liver diseases.

The patient did not receive medication and denied using any supplements or over-the-counter medications.

When he arrived in the emergency department, the patient was afebrile, his heart rate was 101 beats/min, blood pressure was 98/52 mmHg, and the blood oxygen saturation in indoor air was 95%.

The patient can speak complete sentences.

It is worth noting that on physical examination, the patient has oropharyngeal bleeding.

The patient has no signs of scleral jaundice, jaundice, palm erythema, spider hemangioma, organ enlargement, abdominal ascites, or flapping tremor.

The admission laboratory examination showed that the hemoglobin level was 11.
3 g/dL, the platelet count was 177 cells/L, and the white blood cell count and basal metabolism test were within the normal range.

Biochemical examination of the liver showed that aspartate aminotransferase was 22 IU/L, alanine aminotransferase was 28 IU/L, alkaline phosphatase was 86 IU/L, and total bilirubin was 1.
0 mg/dL.The patient's coagulation test was unremarkable.

The patient started intravenous infusion of pantoprazole and urgently received upper gastrointestinal endoscopy.
The results showed that small esophageal varices and gastroesophageal varices (GOV) extended along the greater curvature of the stomach, accompanied by high-risk lesions of recent bleeding.

Hemostatic spray was used in the case of transjugular intrahepatic portosystemic shunt (TIPS), and the patient began to receive octreotide instillation.

Ultrasound and Doppler imaging of the liver showed mild nodules on the liver surface, which were related to cirrhosis, the hepatic blood vessels were unobstructed, and the portal vein blood flow was normal.

CT of the abdomen and pelvis showed that the liver was normal in size without cirrhosis.

The branch of the portal vein is unobstructed.

There are partial GOV and small paraumbilical veins that are re-patched.

A transhepatic liver biopsy including portal vein pressure was performed.
The results showed that the right atrial pressure (RAP) was 5 mmHg and the hepatic venous wedge pressure (WHVP) was 10 mmHg.

Liver biopsy showed mild bullous fat and no fibrosis.

There is no abnormality in the portal area.

Case diagnosis Although the hepatic venous pressure gradient (HVPG) is normal, there is a high degree of clinical suspicion that the patient has portal hypertension.
Therefore, the portal pressure is directly measured.
The results show that the patient’s portal pressure is 17 mmHg and the portal pressure gradient is 12 mmHg.

The patient then underwent TIPS and gastro-renal shunt embolization to reduce the portal pressure gradient from 12 mmHg to 1 mmHg.

This patient was diagnosed with non-cirrhotic portal hypertension (NCPH) associated with the administration of oxaliplatin.

Knowledge Class: What is NCPH? Portal hypertension refers to a group of clinical syndromes caused by increased pressure in the portal venous system due to various reasons.
The most common cause is liver cirrhosis, but 10%-20% of portal hypertension are still secondary to various non- Cirrhosis of the liver is collectively referred to as NCPH.

NCPH is a group of heterogeneous portal venous diseases, mainly due to the effect of primary liver disease or systemic disease on the liver, which leads to increased portal pressure without the formation of cirrhosis.

NCPH is a rare disease with lack of specific clinical features.
It has manifestations of portal hypertension, such as esophageal and gastric varices, splenomegaly, and ascites, but the liver function is basically normal, and it is easy to be misdiagnosed as cryptogenic cirrhosis.

The etiology includes idiopathic portal hypertension, portal vein thrombosis, Budd-Chiari syndrome, hepatic schistosomiasis, congenital liver fibrosis, myeloproliferative diseases, as well as some autoimmune, immunodeficiency syndromes and other diseases.

NCPH is divided into pre-hepatic, hepatic, and posterior according to the location of blood flow obstruction, and hepatic can be divided into pre-sinusoidal, sinusoidal, and posterior sinus.

There is currently no uniform diagnostic standard for NCPH.
Exclusionary diagnosis is often used in clinical practice.
The liver pathological changes of this group of diseases are mostly relatively specific and cannot be completely diagnosed by pathological changes alone.
The diagnosis needs to be combined with clinical manifestations, laboratory tests, and imaging .

NCPH oxaliplatin, which is related to the administration of oxaliplatin, is a third-generation platinum derivative and has become the basis of chemotherapy regimens for the treatment of colorectal cancer.

Compared with 5-fluorouracil single agent, oxaliplatin is associated with a significant improvement in clinical outcome.

But oxaliplatin is also associated with significant toxicity.

Common toxicities include peripheral neuropathy, splenomegaly, thrombocytosis, liver steatosis, and portal vein-sinusoidal vascular disease (which can lead to NCPH).

For patients with signs of portal hypertension after receiving oxaliplatin treatment, if there is no underlying chronic liver disease, and portal or hepatic vein thrombosis and other related diseases that can cause NCPH are excluded, they should be suspected of oxaliplatin-related portal hypertension .

This patient was diagnosed with oxaliplatin-related NCPH 5 years after chemotherapy.

The patient performed well for more than a year after TIPS, without any complications.

References: [1] Bertha M, VanWagner LB.
An Uncommon Cause of Hematemesis[J].
Clin Liver Dis (Hoboken).
2021 Apr 13;17(3):174-179.
[2] Xiaoke Li, Shuwen Xue, Xinle Yang, Research status of non-cirrhotic portal hypertension[J].
Journal of Clinical Hepatobiliary Diseases, 2020, 36(11):2565-2568.
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