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🏥 | Actor Katsuhiko Watabiki died of pancreatic cancer ... Early detection by CT and MRI

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Actor Katsuhiko Watabiki died of pancreatic cancer ... Early detection by CT and MRI

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In addition, chronic pancreatitis and obesity with a BMI (weight <kg> divided twice by height <meter>) of 2 or more are also at risk.

[Dr. Nakagawa Cancer Survivor's Wisdom] "Tell me that you will end" An actor who died of pancreatic cancer on the XNUMXth of last month ... → Continue reading

 Daily Gendai Healthcare

We will deliver the medical and health articles of the evening paper "Daily Gendai". From everyday health laws to the latest medical information, all articles are based on interviews with doctors and specialists.

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Chronic pancreatitis

Chronic pancreatitis(Mansei Suien,English: Chronic pancreatitis) Is chronicpancreasCaused by inflammationPancreatitisThat thing.Causes permanent trait disorders with pancreatic fibrosis and pancreatic duct stenosis, resulting in diminished hormone secretory function[1]..The initial symptom is repeated upper abdominal pain attacks.Pain disappears with advanced and irreversible pancreatic insufficiencyPancreatic diabetesWeight loss due to impaired absorption of nutrientsSteatorrheaSymptoms such as[2]..In addition, impaired glucose tolerance due to decreased insulin secretion may appear at all stages. According to a 2002 survey, the sex ratio was 2.8 for males and 1 for females and males.[3].


Drinking and smoking are the biggest factors.Others include the following.In Europe and the United States, factor classification by the "TIGAR-O Classification System (TIGAR-O classification)" is widely used.

Clinical picture

It is classified into alcoholic chronic pancreatitis and non-alcoholic chronic pancreatitis (idiopathic, hereditary, familial, etc.) according to the cause.In addition, the stage is divided into three stages: compensatory stage, transition stage, and decompensated stage.[2].

The initial symptoms of the compensatory phase are intermittent dull pain in the upper abdomen, epigastrium and back due to repeated acute pancreatitis, or severe abdominal pain that repeats every few months.In the body, normal cells are destroyed and tissue fibrosis, pancreatic duct deformation, stenosis, and atrophy gradually progress.This abdominal pain gradually becomes less severe after about 7 to 8 years, and the transition period begins.The diminished pain that occurs from the transitional period to the decompensated period is due to the reduction of inflammation due to the deterioration of the condition due to tissue fibrosis and stones and the transition to an irreversible state of pancreatic function.[1]..In addition, asymptomatic chronic pancreatitis in which symptoms progress without characteristic abdominal pain attacks has also been reported.[5].

During the decompensated period, symptoms associated with pancreatic dysfunction such as decreased appetite, diarrhea, decreased nutrient absorption function, and weight loss due to diabetes (pancreatic diabetes) appear.[2]..Steatorrhea, which is characteristic of the decompensated period, is called steatorrhea, and is caused by poor digestion and malabsorption of fat and protein due to decreased secretion of digestive enzymes.[1]..Malabsorption of digestion is a decrease in nutrient absorption and directly causes weight loss.[5], Malabsorption of fat leads to deficiency of fat-soluble vitamins (A, D, E, K)[1][5].

Characteristics of patients with pancreatic diabetes

Characteristics of pancreatic diabetes associated with decreased pancreatitis[3]

  1. There is a lot of thinness.
  2. There are few complications of hyperlipidemia.
  3. Initially, insulin resistance exists, but it becomes more sensitive as glucagon secretion decreases as pancreatitis progresses.
  4. The frequency of diabetic microangiopathy in pancreatic diabetes is the same as in type 2 diabetes.
  5. There are many insulin treatment groups, but in severe chronic pancreatitis, hypoglycemia is likely to occur due to lack of glucagon secretion, and it can be controlled with a small amount.
  6. Glycemic control is apparently good due to digestive and absorption disorders due to chronic pancreatitis, and diabetic control may worsen as it improves.

Pathological classification

  • Chronic calcification pancreatitis[1]
  • Obstructive chronic pancreatitis[1]
  • Autoimmune chronic pancreatitis[1]


  • Pseudocyst formation[1]
  • Bile duct and duodenal obstruction[1]
  • Rupture of the pancreatic duct (one of the causes of ascites or pleural effusion)[1]
  • Splenic vein thrombosis (one of the causes of gastric varices)[1]
  • Pseudoaneurysm or pseudocyst of an artery near the pancreas[1]
  • Pancreatic adenocarcinomaIncreased risk of developing[1]


A definitive diagnosis is made by the following 6 items including interviews.[5][2].

  1. Characteristic image findings. By CT, MRCP (Magnetic Resonance Cholangiopancreatography), Abdominal Echo, Endoscopic Ultrasonography, ERCP (Endoscopic Retrograde Pancreatobiliography)
  2. Characteristic organizational findings
  3. Recurrent upper abdominal pain
  4. Abnormalities of pancreatic enzymes in blood or urine
  5. Exocrine pancreatic disorder
  6. Persistent drinking history of 1g or more (pure ethanol equivalent) per day

Differential disease

  • Pancreatic cancer, intraductal papillary mucinous tumor (IPMN)[5]


No severity and staging using blood and urine pancreas-related enzyme levels[5]..Glucose tolerance tests such as glucose tolerance tests are a powerful factor in staging.[5].

Blood test

Comprehensive judgment from multiple types of results[5].

  • Exocrine dysfunction
    • Pancreatic juice volume in secretin load testBicarbonate-amylaseDecreased secretion
    • Decreased urinary PABA in BT-PABA test
    • Fecal elastase 1 measurement
    • 13CBz-Tyr-Ala breath test
  • Decreased endocrine function
    • Concomitant diabetes
  • Tumor marker[1]
  • Genetic testing[5]
    • Chymotrypsinogen gene (PRSS1)
    • Insufficient evidence of usefulness (FTR gene, pancreatic secretory trypsin inhibitor gene (SPINK1) analysis)[5]

Image inspection

Confirmed by calcification of the pancreas on imaging[5].

Calcification of the pancreas
Stone image in the pancreatic duct


Includes symptomatic treatment and lifestyle improvement for each symptomdiet remedyIs done.In the case of obstructive chronic pancreatitis due to stones, stone crushing therapy using shock waves[6]And the pancreatic duct may be surgically treated[1].

Pancreatic enzyme supplementation
Insulin administration, digestive enzyme administration[3]
Treatment with drugs is mainly pain control.
  • Nutrition therapy is required according to the stage (pathological condition).Low-fat diet (fat content less than 25 g / day).However, there are negative views on the uniform application of a low-fat diet.[3]..In order to prevent malnutrition, it is possible to eat a diet with a fat content of more than 30 g / day in combination with drug therapy.[3]..In addition, do not limit diets to avoid hyperglycemia[3].
  • Prohibition-essential as it has a significant impact on life expectancy[5].

Related item


  1. ^ a b c d e f g h i j k l m n o Chronic pancreatitis MSD Manual Professional Edition
  2. ^ a b c d Chronic pancreatitis KOMPAS Keio University Hospital
  3. ^ a b c d e f Tetsuhide Ito, Mikihiko Yasuda, Akira Kawabe, Takama Ohno et al.Nutrition therapy for chronic pancreatitis"Journal of the Japanese Society of Gastroenterology" 2007 Vol. 104, No. 12, p.1722-1727, two:10.11405 / nisshoshi.104.1722, Japanese Society of Gastroenterology
  4. ^ Yuji Nakamura, Tomohiro Omori, Susumu Higuchi, Katsuya Maruyama, "Alcoholic Calcification in Japanese Men and Background Factors"Pancreas," 2006, Vol. 21, No. 4, p.374-377, two:10.2958 / suizo.21.374, Japan Pancreatic Society
  5. ^ a b c d e f g h i j k l Sexual Pancreatitis Clinical Practice Guidelines 2015 (Revised 2nd Edition) Japanese Society of Gastroenterology
  6. ^ Hirotaka Ohara, Kazuo Goto, Yoshiki Noguchi, Nobu Hoshino, "Basic and clinical study of extracorporeal shock wave lithotripsy (ESWL) for pancreatic stone disease"Journal of the Japanese Society of Gastroenterology" 1991 Vol. 88, No. 12, p.2861-2870, two:10.11405 / nisshoshi1964.88.2861, Japanese Society of Gastroenterology

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