IBI is present in gastroenterology, since the 1970s, with products for therapy related to abdominal pathology, such as dyspepsia, cholelithiasis, cholestasis and other chronic hepatopathies such as steatosis and Non-Alcoholic Liver Disease (NAFLD), to the treatment of gastrointestinal symptoms with products for the improvement of peristalsis, meteorism and constipation.


In 1993 IBI developed Ursilon Retard, a formulation patent for slow-release ursodeoxycholic acid (UDCA). Slow release along the whole gastrointestinal tract improves UDCA bioavailability and absorption, while the single daily dose enhances patient compliance.
The formulation has been investigated in several studies, of which the most significant are the papers by Simoni et al. (2002) and Alvisi et al. (1996), who compared various slow-release products and highlighted “…the good pharmacokinetics of Ursilon Retard, which can guarantee gradual and constant release into the blood with levels that can still be measured in the blood 12 hours after administration…”.
Furthermore, the R&D labs have developed an UDCA formulation in sachets for oral suspension, to meet the requirements of patients with problems in swallowing and with specific needs.
Since the 1980s, IBI has been collaborating with university and hospital centers to deepen chronic hepatopathy of metabolic origin and to find solutions to slow down this silent pathology, which in its natural history may evolve towards cirrhosis and hepatocellular carcinoma or play an important role in metabolic syndrome and cardiovascular risk. The company has focused on the development of a plant-derived product, the silybin present in the Silybum marianum, with the aim of supporting the liver without damaging it, considering that the NAFLD develops in several years and, therefore, mainly requires a behavioural approach, and at the same time, we must consider the restoration of cellular hepatic function through the complex mechanisms involved in metabolic hepatopathy. In recent years many works have been published on the extracts of Silybum marianum and on silybin in particular, and the positive action of this plant derivative in the mechanisms involved in hepatic and systemic damage has been demonstrated.


Meteorism is a frequent disorder due to the presence of excessive amounts of gas in the stomach and bowel. It manifests itself with a symptomatology characterized initially by abdominal discomfort, sense of swelling and intestinal noises (rumbling), which, protracting over time, can be complicated in severe abdominal pain and cramps. The meteorism is triggered during the digestive process, when the sugars and the cellulose "ferment" in the intestine, with the consequent formation of nitrogen, methane and carbon dioxide.
One of the most common causes of this disorder is the malfunctioning of the colon, known as irritable bowel syndrome, but it can also derive from food intolerances or, more simply, from the consumption of some non-water-soluble fibers, which tend to ferment and, as a consequence, to increase the production of gas. Plants such as pulses (beans, dried peas and lentils), cruciferous vegetables (cabbage, broccoli and cauliflower), soy, radishes, onions, cucumbers and peppers are high in these components.
Even fatty foods (fried, sauces), those with a high content of lactose (milk, ice cream, creams) and artificial sweeteners (sorbitol, mannitol and products that contain them) can promote the accumulation of gas in the stomach and bowel, as well as the abuse of tea, coffee or carbonated drinks. In addition to the fermentation of sugars and carbohydrates due to poor digestion, meteorism may have another cause: aerophagia, i.e. the ingestion of air during the swallowing of food and drink, which causes the typical swelling in the stomach. This disorder, due to the formation of air bubbles in saliva, which are subsequently ingested, often depends on bad habits such as eating quickly, chewing gum for a long time or smoking.

In addition to changing your lifestyle and eating habits, Meteosim can be a valid solution to meteorism and aerophagia. This IBI’s product is a self-medication which promotes the elimination of gas in the gastrointestinal tract. The effectiveness of Meteosim is due to the action of simethicone (activated dimethicone), a mixture of silicon dioxide combined silicon dioxide, which acts locally in the gastrointestinal tract and is capable of lowering the surface tension by "sequestering" the gas in excess and favoring its elimination. The simethicone makes sure that the bubbles of gas present flow and then be eliminated more easily relieving the annoying symptoms associated with meteorism and aerophagia. Simethicone is not absorbed by the body and does not interfere with the absorption of nutrients, therefore acting only on the gases. The large sample of patients treated in over 40 years of use and the large number of studies available attest to its effectiveness in reducing the discomfort related to excessive gas in the gastrointestinal tract, an indication confirmed by the Food and Drug Administration as early as 1973 Meteosim - simethicone - can be used to treat mild and transient disorders, easily recognizable and resolvable: it can be bought without a prescription, but must be used correctly to ensure its effectiveness. The medicinal product does not present any contraindications, except for hypersensitivity to the active substance or to other components of the product. It is generally contraindicated in pregnant women. (more info at

  • Meteosim chewable tablets: the recommended dose for adults is 4 tablets a day after meals or according to the doctor’s prescription.
  • Simethicone IBI: oral drops for children, suspension, the recommended dose for children is 15 drops, 2-4 times a day after meals or according to the doctor’s prescription.


Chronic constipation
The colon plays a fundamental role in constipation. In fact, during the digestive process it is precisely at the level of the colon that absorption takes place through its walls of water and salts. This activity is physiologically in constant equilibrium. If for various reasons there is an increase in the reabsorption of water between the walls of the colon, the faeces within the lumen will be drier and harder and the risk is to develop constipation. Otherwise if the reabsorption of water in the colon decreases there is a stagnation of liquids in the intestinal lumen and its result is diarrhea.
Getting precise data on how many people suffer from chronic constipation is not easy. In Italy , the figure is thought to be around 20% of the population. The Rome III diagnostic criteria have been developed to help doctor-patient communication on the pathology. Accordingly, a patient has chronic constipation if at least two of the following criteria are present in at least 25% of defecations:

  • Straining to have bowel movements
  • Hard or lumpy stools
  • Feeling of incomplete evacuation
  • Sensation of obstruction or blocking of the rectum
  • Manual manoeuvres to facilitate evacuation
  • Less than three intestinal evacuation per week

Chronic constipation is diagnosed if the disorder has lasted for at least three of the previous six months.
What are the main causes of constipation? The causes can be divided into primary and secondary.

The primary causes are:

  • Normal transit constipation
  • Slow transit constipation <0
  • Pelvic floor dysfunction

These problems are linked to dysfunction of the pelvic floor muscles or to their poor coordination with the anal sphincters.
Constipation can also be related to lifestyle conditions, a concomitant disorder or medications.

The main secondary causes include:

  • Endocrine or metabolic causes (diabetes, hypothyroidism, hypercalcaemia)
  • Structural causes (cancer, anal fissures, haemorrhoids)
  • Diet and lifestyle (drinking few liquids, eating few fibres, little physical movement)
  • Drugs (above all those acting on the central nervous system, opioids, levodopa)
  • Pregnancy (hormonal changes)
  • Poor toilet habits (ignoring the urge to defecate)
  • Psychological problems (depression, eating disorders)
  • Neurological disorders (Parkinson’s disease, multiple sclerosis).

If chronic constipation is not adequately treated, complications can arise, such as:

  • Haemorrhoids
  • Faecaloma
  • Bowel obstruction
  • Urinary and faecal incontinence
  • Psychological stress
  • Systemic effects in elderly patients
  • Possible consequences of untreated constipation

Chronic constipation is mainly managed by changes in lifestyle. The doctor will prescribe a fibre-rich diet, increased fluid intake and physical exercise. If the problem persists, the doctor will recommend an osmotic laxative to facilitate evacuation.

Laxatives can be divided into four main categories:

  1. Mass-formers – natural or synthetic polysaccharides that bind water in the lumen, thereby increasing the faecal volume and reducing stool consistency
  2. Stool softeners – anionic surfactants (docusate sodium, liquid paraffin) which increase the amount of water and lipids absorbed by the stool, making it softer and easing transit
  3. Osmotic laxatives – like Laxido, lactulose, sorbitol, magnesium hydroxide and magnesium sulphate, which by osmotic action draw water into the bowel, accelerating faecal transit
  4. Stimulant laxatives - derivatives of diphenylmethane or anthraquinone, act by stimulating motility, probably inducing local reflexes and reducing water absorption in the colon.

IBI has on the market a laxative based on polyethylene glycol (also known as macrogol), which has an essentially mechanical and osmotic action.
Oral administration generates a macrogol-water structure which prevents the reabsorption of water and goes through the whole intestinal tract. As a result, the stool is more hydrated and softer, it goes through the large intestine more quickly and is evacuated with less difficulty.
Combining macrogol with electrolytes makes the solution isotonic: maintenance of the electrolyte balance enables long-term use.
The product is authorized to treat chronic constipation and faecaloma.


Acute pancreatitis (AP) is a condition whose incidence varies both among countries and among regions. This is probably due to the wide range of its causes and to their different geographical distribution. In Italy, gallstone disease accounts for over 50% of AP diagnoses, whereas in the United States most cases appear to be alcohol-related. Disease onset is commonly around 45 years of age, but younger and older individuals are also affected. Its incidence does not appear to be related to gender or ethnicity.
AP is an acute inflammatory process affecting the pancreas, which can also involving peripancreatic tissues, and which manifests itself with variable anatomical and pathological pictures, but which share the same physiopathological basis. It can present as:

  • Interstitial oedematous pancreatitis
  • Oedematous pancreatitis with outbreaks of steatonecrosis, haemorrhage and necrosis
  • Focal or diffuse acute necrotic-haemorrhagic pancreatitis.

It can evolve from a mild to a severe form. Mild AP accounts for 80-90% of cases. It is associated with minimal organ dysfunction and often results in full recovery; morphologically, the gland is characterized by interstitial oedema. In contrast, severe AP is associated with local pancreatic complications and systemic impairment of the respiratory, cardiovascular and renal systems. Several different causes seem to induce AP onset.

The main AP types are:

  • Acute biliary pancreatitis, which can be divided into gallstone (due to gallbladder or bile duct stones) and non-gallstone disease (due to primary functional or morphological changes in the bile tract).
  • Non-biliary acute pancreatitis, which is most frequently alcohol-related. Alcohol acts on the pancreas directly, by inducing pancreatic cell injury, and indirectly by altering the balance between enzymes and their inhibitors and through the production of free radicals.

Postoperative pancreatitis is rare and can be due to procedures involving the pancreas or nearby or even distant organs, e.g. transplant and heart bypass surgery. Traumatic acute pancreatitis is favoured by the organ’s proximity to the spine.
Lastly, drug-induced pancreatitis, infectious pancreatitis and metabolic pancreatitis (due to hyperlipaemia, hyperparathyroidism and hypercalcaemia) are much less common.
Endoscopic retrograde cholangiopancreatography (ERCP) is a technique that enables visualization of the biliary and pancreatic duct system using a side-viewing duodenoscope after direct injection of a contrast agent. ERCP provides a valuable aid to the diagnosis and treatment of biliary and pancreatic duct disease. Despite its unquestionable advantages, it is however not risk-free, since pancreatitis, the most common and severe complication, develops in about 8% of patients. Although post-ERCP pancreatitis is seldom serious, some patients develop a severe form of the disease or secondary complications that require hospitalization and can lead to death.
Post-ERCP pancreatitis seems to account for 4% of all AP cases in Italy. Its clinical and humoral characteristics appear to be similar to those seen in patients with AP due to other causes.
Notably, all forms of AP are characterized by the same pathophysiological mechanism, namely autodigestion of the gland owing to premature activation in the pancreas of the digestive enzymes it secretes. In physiological conditions, autodigestion is prevented by the secretion of inactive proteolytic enzymes and by their activation by intestinal enterokinase solely in the duodenum. Additional protection is conferred by the presence of protease inhibitors – outside the intestinal lumen, in the circulation and in pancreatic tissue itself – which in physiological conditions inhibit protease activity when it is unnecessary or inappropriate.
AP is diagnosed by clinical examination and is confirmed by laboratory and instrumental tests. The ideal humoral marker seems to be C-reactive protein (CRP) – which is characteristic of the acute phase of inflammation – whose plasma level peaks 48-72 hours after disease onset. Although there is no universally acknowledged threshold, a value of ≤ 15 mg/dl at 48 hours is associated with a 94% negative prognostic value and is widely accepted. CRP has proven useful above all in identifying the progression from oedematous to necrotizing AP. Other important prognostic markers are the levels of amylase, lipase, calcaemia and haematocrit. Morphological studies are performed with radiological techniques, in particular ultrasound, CT and MRI.
AP is not usually diagnosed until 48-72 hours from symptom onset, when the process may have taken a definitive direction even though its pathogenic expression may still be limited. Therefore, in the early phase it is not always clear whether the condition will develop into a mild or a more severe form. To this end, multiple score systems are useful, as they enable an assessment of the pathophysiological changes and can be used to identify those patients who are at higher risk of mortality and to monitor disease evolution and treatment response.

The goals of AP treatment are to:

  • manage pain
  • eliminate inflammation
  • block enzymatic autodigestion
  • prevent and treat complications.

The mild forms can be managed by peripheral parenteral nutrition, pain control and clinical monitoring.
If the disease evolves towards a severe form the patient is started on two treatments, one that addresses the general symptoms and provides support, and a specific therapy.
The general and support treatment entails: fasting, pain management, fluid therapy, functional rest through nasogastric tube feeding or enteral (rather than parenteral) nutrition, H2 blockers, antibiotic prophylaxis, and measures to control respiratory and renal insufficiency, shock, and coagulation abnormalities.
The specific therapy targets the pathogenic mechanisms and therefore aims to block the activated enzymes, both local and circulating.
Two categories of medications can be used:

  • Secretion inhibitors: anticholinergics, calcitonin, glucagon, somatostatin and octreotide
  • Protease inhibitors: aprotinin and gabexate-mesilate

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