Chapter 197: The Chicken or the Egg? (September 28, 1/1 more subscription)

Although the cause of type 2 diabetes is caused by the body's resistance to insulin, Sun Lien has never seen it to such a serious extent.

"This patient is the most likely to have type 2 diabetes, but there are other factors to consider. Director Wu of the Department of Intensive Care Medicine was not relieved because Professor Zhang happily agreed to take the patient, but he reminded with some anxiety, "He stayed in our ICU for three days, and yesterday he pushed down for a CT examination of the abdomen - the results of the imaging department said that the patient had pancreatic atrophy, and there was a large amount of fat infiltration in the pancreas." ”

That's kind of interesting. Sun Lien's eyes widened, and at the same time, he still had some thoughts of complaining about Director Wu in his heart. That's the most important thing! What do you mean by that?

The pancreas is one of the main organs in the human body that deals with fat and sugar metabolism, and there are two parts: endocrine and exocrine. The exocrine pancreas itself works primarily by secreting pancreatic juice rich in sodium bicarbonate, trypsinogen, lipase, and amylase. Pancreatic juice then passes through the pancreatic duct into the duodenum, where it mixes with the food that has been initially digested to help digest proteins, fats, and sugars.

The islets are the main components of the endocrine glands. A cells, B cells, D cells, and PP cells together make up the islets. A cells secrete glucagon and B cells secrete insulin. These two cells are the main means of regulating blood sugar fluctuations in the body. D cells, on the other hand, control the secretion of A and B cells by secreting somatostatin. PP cells secrete pancreatic polypeptides, whose main functions are to inhibit gastrointestinal motility, pancreatic juice secretion, and gallbladder contraction, which mainly interact with the exocrine part of the pancreas.

Both exocrine and endocrine departments are organic components of the pancreas. Pancreatic atrophy means that the secretion units of the endocrine or exocrine department are reduced, and the total amount of secretion is bound to decrease.

Pancreatic fat infiltration is another more troublesome problem. In essence, pancreatic fatty infiltration, like fatty liver, is an organic lesion of an organ caused by abnormal fat metabolism. Fat infiltration can seriously affect the endocrine function of the pancreas, which can seriously affect blood glucose and protein metabolism.

Sun Lien finally understood why this patient was so valued by the intensive care department.

Shrinkage and fatty infiltration of the pancreas can lead to severe diabetes and even hyperosmolar coma in patients. Severe type 2 diabetes can in turn lead to pancreatic atrophy and pancreatic fatty infiltration.

The real headache for the critical care department is who first appears in these two symptoms – is it the primary pancreatic atrophy and fatty infiltration that causes diabetes, or is it diabetes that causes pancreatic atrophy and fatty infiltration? If it is primary pancreatic atrophy, what is the cause of pancreatic atrophy? If diabetes is causing pancreatic atrophy, what is causing such severe insulin resistance?

Severe insulin resistance can be summarized clinically as "patients need more than 200 units of insulin per day to maintain normal blood glucose". The patient in the ICU had taken more than 170 units of insulin in the emergency room and his blood sugar level was still as high as 22.8 mmol/L. It is almost certain that he has severe symptoms of insulin resistance.

Sun Lien followed Professor Zhang and walked towards the Comprehensive Diagnostic Center. The intensive care department has promised Zhang Zhifu that the patient will be transferred to the diagnostic center as soon as possible. Professor Zhang happily agreed, and at the same time decided to go back first to communicate with his team members about the patient's condition.

On the way back, Sun Lien was still frowning and thinking about the cause of the symptoms of insulin resistance, and he didn't even answer the words that Professor Zhang had planned to chat a few times - Professor Zhang glanced back at Sun Lien, and then looked at his frowning and thoughtful expression, and laughed softly. Never talking about chatting again, but slowing down the pace of progress a little while keeping quiet.

It's a great thing that young doctors are willing to ponder the patient's condition. As he walked forward with his legs hunched, Professor Zhang smiled and recalled his youth, when decades ago, he was often criticized by his mentor as "easily distracted" and "improper". In fact, it was just that Zhang Zhifu was too focused on pondering the problem.

At that time...... If the mentor didn't criticize himself...... Maybe he won't be angry and continue to work in the clinic, right? Professor Zhang Zhifu had a smile on his face, and his two crooked legs seemed to be a little stronger. Later, when I was rated as a professor, my supervisor, who had been an associate professor for almost my whole life, was actually the same group of people who were promoted to full professors...... Professor Zhang Zhifu felt ashamed of his mentor.

"I see you've been thinking all the way. Although he planned to leave enough time and space for Sun Lien to think, the distance from the ICU to the comprehensive diagnosis center was always limited. When he walked to the door of the comprehensive diagnosis center, Professor Zhang Zhifu stopped, turned his head to look at Sun Lien and asked, "How is it?

"I still don't understand why he has such severe insulin resistance. Sun Lien stopped and replied honestly, "Generally speaking, patients with type 2 diabetes have insulin resistance, but they need to use more than 200 units of severe resistance every day...... It's so rare that I don't even remember a few patients like this. The only person I came into contact with was an elderly man in his 80s who had been ill for more than 20 years. ”

The patient Sun Lien was talking about was the patient he had seen when he had previously participated in the endocrinology department's request for consultation. After the old man was diagnosed with type 2 diabetes, he took glipizide for 18 years. However, there has been no follow-up test, and no blood sugar has been tested. Until two years ago, the elderly man was readmitted to the hospital for examination because the wound was difficult to heal after it was broken. The glucose control regimen was also adjusted to a mixed human insulin regimen of 16 units in the morning and 18 units in the evening for subcutaneous injection.

"People with type 2 diabetes have a long course of illness and are still elderly...... Resistance is not unexpected. Professor Zhang nodded and motioned for Sun Lien to continue.

"Later, I was admitted to the hospital for ketoacidosis, but my consciousness was quite clear. Sun continued, "The endocrinology department checked his IAA (insulin autoantibody) and confirmed that it was positive. For the first five days, more than 280 units of insulin were injected each day. Even so, his blood sugar level still couldn't be controlled, and his blood sugar was as low as 13mmol/L before meals. ”

About 3%~6% of patients with type 2 diabetes will be positive for IAA antibody. In patients with type 1 diabetes, the detection rate of this indicator is about 90%. It can be said that almost all patients with positive IAA antibodies have type 1 diabetes. In patients with type 2 diabetes, if they have positive IAA antibodies, it means that the pancreas has been mistakenly attacked by the autoimmune system. On the one hand, this attack will lead to a further decrease in the number of pancreatic B cells and a sharp decrease in the amount of insulin secreted by the patient.

Such patients soon develop symptoms of insulin dependence – metformin, the most commonly used oral glucose-control drug, is an insulin-acting sensitizer. However, under insulin dependence, this "miracle drug" is completely ineffective - after all, no matter how good an insulin sensitizer is, it must have its own insulin for sensitization to work.

At the same time, insulin secretagogues and hypoglycemic drugs have failed. Even DPP-4 inhibitors that are considered new drugs - sitagliptin, vildagliptin, saxagliptin and the like will be greatly reduced. They also have an insulin-sensitizing component in their mechanism of action.

Diabetic patients at this stage must take insulin subcutaneously for life. Combined with the original insulin resistance, the daily dosage can be hopelessly high. For example, this old man...... During the hospitalization, the maximum amount of insulin injected per day was 426U.