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The pancreas lies crosswise behind the stomach and has two jobs: it produces digestive enzymes for fat, protein and carbohydrate (the exocrine part) and the hormones insulin and glucagon for blood sugar (the endocrine part). If the organ fails, both are lost.¹,²
Normally the enzymes are released as inactive precursors and only switched on in the small bowel. In pancreatitis they become active while still inside the organ and digest its own tissue — from mild swelling through to areas of dead tissue.
The two forms sound similar but behave completely differently — in how they run, how they are treated and what they mean day to day.¹
| Feature | Acute pancreatitis | Chronic pancreatitis |
|---|---|---|
| Onset & setting | Sudden, within hours; usually in hospital | Creeping over years, often in flare-ups; managed as an outpatient |
| Leading complaint | Very severe upper abdominal pain | Recurring pain, easing off only late on |
| Trigger | Gallstones, alcohol | Alcohol, smoking, genetics |
| Consequences | Usually full recovery; severe courses are possible | Permanent loss of digestion and of insulin production |
Repeated acute episodes — above all where alcohol or smoking continue — can turn into chronic pancreatitis. Looking for the cause after the first episode is therefore not a formality.¹
In the acute form pain is the leading symptom: severe, persistent, starting in the upper abdomen and typically radiating round into the back like a belt. Leaning forward often eases it, lying flat makes it worse. Nausea, vomiting and fever frequently come with it.⁴
In the chronic form the picture shifts from pain towards loss of function:
The exocrine weakness only shows itself once a large part of enzyme production has been lost — fatty stools are therefore not an early sign, but they are a very treatable one.¹,³
Medicine-induced pancreatitis is rare but easily missed. A connection has been described for diuretics (thiazides, furosemide), azathioprine, mesalazine, valproate and oestrogen preparations — the evidence often rests on individual case reports.¹,³
The acute form is recognised from typical symptoms, a raised enzyme level and imaging; with the chronic form, measuring the loss of function is added.¹,²
What has to be ruled out includes biliary colic, a perforated stomach ulcer, a heart attack and other causes of abdominal pain. The liver is often examined at the same time, for example for fatty liver.
Acute pancreatitis is as a rule treated in hospital — because it is in the first few days that it is decided whether the course stays mild or turns severe. Most cases heal; severe courses with dead tissue are less common but serious.¹
Antibiotics are not given routinely, only where an infection has been demonstrated. Digestive enzymes are not standard in the acute phase — they only come into play once the body permanently produces too few of its own.
On current understanding the chronic form cannot be reversed. Three things are treated: pain, loss of function and progression. Treatment decisions always rest with the treating practice.¹,³
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If the pancreas delivers too few digestive enzymes, they are replaced from outside. The preparation is called pancreatin and contains lipase, amylase and proteases in gastro-resistant micropellets, so that stomach acid does not destroy them. The dose is set medically in lipase units — according to the fat content of the meal and according to how weight and stools develop.¹,³ The sticking point is rarely the substance itself but the way it is used: an enzyme taken at the wrong moment no longer meets the food.
| What you notice | Common explanation | What gets discussed |
|---|---|---|
| Fatty stools persist, weight falls | Dose too low, or too few calories | Adjusting the lipase units, dietary advice |
| The enzymes only partly work | Wrong timing — all of them before or after the meal | Splitting them between the start and the course of the meal |
| Hardly any effect despite correct use | Too much stomach acid inactivates the enzymes | An acid blocker such as pantoprazole can be considered |
If the inflammation destroys the insulin-producing cells as well, a form of diabetes develops that is neither type 1 nor type 2: pancreatogenic diabetes, often called “type 3c”. The decisive point is that it is not only insulin that is missing but also glucagon, the hormone that raises blood sugar.¹,³ The consequence: blood sugar swings more widely and slips more easily into a hypo, because the emergency mechanism is gone. Many people need insulin early — the basics are in the article Diabetes.
If fat is not digested, the fat-soluble vitamins A, D, E and K are missing as well. This goes unnoticed for a long time and then shows up as tiredness, difficulty seeing at night, a tendency to bleed or falling bone density. A lack of vitamin D together with being underweight, alcohol and smoking is a risky mixture for osteoporosis.
No tablet influences the course of chronic pancreatitis the way these two decisions do.¹
And a word about the mind: chronic pain and a daily life that revolves around food leave nobody untouched. Exhaustion and low mood deserve the same attention as the fatty stools.
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