The irreversible pancreatic insufficiency manifests itself mainly following chronic pancreatitis, a clinical condition characterized by an inflammatory process of the pancreas, which progressively causes the destruction of the glandular parenchyma. Pain is the main symptom; there are also other clinical signs, such as weight loss, steatorrhea and typical malabsorption symptoms. Loss of body weight, malnutrition and lack of specific nutrients increase in relation to the severity of the IPE. In these patients the energy intake is noticeably reduced not only due to poor digestion, but also due to an insufficient intake of food due to postoperative pain, nausea and alcohol abuse. These nutritional deficits can then be associated with various complications, such as diabetes mellitus and chronic inflammation. Overall, the malnutrition observed in patients with chronic pancreatitis produces an unfavorable energy balance and increases the risk of a deficit of micro- and macronutrients, in particular vitamins and mineral salts, the deficiency of which can cause multiple clinical consequences. In particular, chronic pancreatitis is associated with the malabsorption of vitamin D3, which plays an important role in bone metabolism. Subjects with chronic pancreatitis are more susceptible to changes in bone metabolism, which may reduce bone mineral density, increasing the risk of fracture. These subjects show a bone fragility, with a prevalence of fractures especially at the hip comparable or greater than that observed in patients with other gastrointestinal diseases, including Crohn's disease, for which the guidelines of the American Gastroenterological Association are available. for the screening of diseases related to bone metabolism, first of all osteoporosis. The study by Tignor and coll, showed for the first time that chronic pancreatitis may represent a risk factor for fractures and therefore requires the definition of guidelines related to the management and prevention of metabolic alterations, similar to what is already available for other high-risk patients with gastrointestinal diseases.
CT abdomen, chronic pancreatitis, fibrous
and
calcified appearance of the pancreas, arrow
Over 40% of patients with PPE secondary to chronic pancreatitis have a high
intestinal bacterial growth, resulting from an alteration of gastrointestinal
motility and biliopancreatic secretion, as well as a reduced secretion of
pancreatic enzymes. From a clinical point of view there are two phases: an early
phase, in which abdominal pain and recurrent episodes of acute inflammation
prevail with complications; an advanced phase, whose symptoms are related to the
onset of exocrine and / or endocrine pancreatic insufficiency. Advanced chronic
pancreatitis is a risk factor for pancreatic cancer. Numerous risk factors have
been described for the onset of chronic pancreatitis, although in most cases the
etiology is idiopathic. The most common cause of chronic pancreatitis is the
abuse of alcohol, which is toxic to pancreatic acinar cells because it
determines the cytoplasmic accumulation of lipids, responsible for the fibrotic
process and therefore pancreatic insufficiency. Alcohol also causes a greater
lithogenicity of pancreatic secretions, which can produce the formation of
stones and the obstruction of the pancreatic duct, thus increasing the risk of
ulcerations, stasis, atrophy and fibrosis. The abuse of alcohol and the
consumption of a diet rich in lipids can finally increase the products of
oxidative metabolism, which in turn cause a biliary reflux inside the pancreatic
duct, favoring the obstruction.
A study conducted between 2000 and 2005 in Italy, however, seems to impose a review on the association between alcohol abuse and development of chronic pancreatitis. The PanCrolnf study, conducted in 893 patients newly diagnosed with chronic pancreatitis recruited in 21 Italian centers, in fact showed an unexpectedly lower correlation compared to previous data between alcohol abuse and chronic pancreatitis (44%), although it is difficult to distinguish if this result is the consequence of a reduction in the consumption of alcohol or is attributable to a previous overestimation. The study also found that in Italy 10% of cases of chronic pancreatitis are autoimmune pancreatitis and cystic dystrophy of the duodenal wall, the latter closely related to daily alcohol abuse. This demographic and clinical analysis, extended to the entire national territory, proposes for the first time a classification of chronic pancreatitis based on risk factors rather than etiologic factors, highlighting a previously underestimated pathogenetic complexity. The elimination of alcohol and the reduction of fats introduced with the diet remain however some of the recommendations indicated by the guidelines of the Italian Association for the Study of Pancreas (AISP), recently developed for the diagnosis and treatment of chronic pancreatitis. The guidelines were constructed according to levels of evidence and degrees of recommendation and developed using a rigorous methodology based on molecular analysis and imaging diagnostics. From a diagnostic point of view, the AISP guidelines indicate as an elective technique for the diagnosis of early stages of chronic pancreatitis, cholangiopancreatography (MRCP), reduction of pancreatic secretion by CCK, caused by intestinal resection; rapid gastric emptying, followed by the passage of large particles responsible for digestive difficulties; reduction of pancreatic secretion secondary to pancreas resection; absence of coordination between gastric emptying and biliopancreatic secretion due to surgical reconstruction.
The gene mutation present in patients with cystic fibrosis alters the transport of sodium chloride through the cell membrane. In physiological conditions, the chlorine is exchanged with the bicarbonate so as to create a basic luminal environment, necessary to guarantee the solubility of the proteins. The gene mutation of the sodium / chloride transporter causes acidification of the intestinal lumen and increases the viscosity of the secretions, which can obstruct the pancreatic duct and progressively destroy the parenchyma through phenomena of proteolysis, fibrosis and cyst formation. The reduction of bicarbonate secretion prevents the neutralization of the chyme acid and is generally associated with pancreatic insufficiency, especially in the more advanced stages of the disease.
The reduction of duodenal pH to values between 3 and 5 causes inactivation of pancreatic enzymes and denaturing of bile salts, essential for the solubilization of lipids, whose digestion and absorption are therefore compromised. IPE is present in more than 80% of patients with cystic fibrosis; moreover, the probability of developing IPE depends on the nature of the gene mutation at the base of the defect (particularly high in patients with DF508 mutation). In general, patients presenting a genotype with two "severe" mutations have a high probability of developing IPE, while those with at least one "mild" genotypic mutation usually maintain a functioning pancreas of IPE in the elderly. The natural aging process may produce some changes in the structure of the pancreas, which include fibrosis, lipomatosis, ductal epithelial hyperplasia and intraluminal protein stores. At the same time, symptoms of poor digestion and malabsorption may appear or increase, which in the elderly are partly due to inadequate enzymatic secretion, caused by the degenerative processes of the pancreas. A study conducted in 159 healthy patients aged 60 to 92 years showed that faecal elastase-1 levels significantly decreased with age, reaching a concentration lower than the cut-off (200 mg / g) in the 21 , 7% of study participants, indicative values of an IPE resulting from atrophy and degeneration of the gland. The results of the study show that among elderly subjects, apparently healthy and free of important gastrointestinal diseases, a good percentage of individuals could benefit from pancreatic enzyme replacement therapy, although no correlation between faecal elastase-1 levels was found and the abdominal clinical symptomatology. Careful clinical surveillance by general practitioners is therefore important to this population.
Complications of chronic pancreatitis are characterized by:
Vitamin A deficiency: Blindness (vision problems especially at night), Skin
disorders, Low resistance to infections
Vitamin E deficiency symptoms (adults): Mild hemolytic anemia, Non-specific
neurological deficiencies, Reproductive and infertility disorders, Red blood
cell fragility, Age-related spots, Cataracts, Neurological damage, Decreased
sexual desire Changes in function muscular, liver, bone marrow and brain
Vitamin D deficiency: Hypocalcaemia, Tetany, paraesthesia and convulsions
Vitamin K deficiency: Coagulopathy.
Vitamin B12 deficiency: Pernicious anemia Funicular myelosis
Hypopotassiemia: Prolonged diarrhea can cause loss of potassium in the intestine
Weakness, muscle cramps Cardiac arrhythmia
The treatment is surgical in the most serious cases, when there is compression of the neighboring organs; in other cases a perendoscopic drainage can be created between the pseudocyst and the stomach. In other cases, percutaneous drainage can still be made. In the minor cases, one proceeds only by monitoring the patient, as the pseudocyst regresses spontaneously.