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Pancreatic calcifications are particularly frequent in patients with severe pancreatic insufficiency and long-lasting chronic pancreatitis. To clarify whether calcifications point to a more severe form of the disease, irrespective of its duration, we have retrospectively analyzed patients with chronic pancreatitis submitted to the secretin-cerulein test in our center over a six-year period. Out of 120 patients, calcifications were found in 55. Higher alcohol intake and longer duration of the disease were found in patients with calcifications, compared with patients without calcifications (p less than 0.001). In both groups, lipase and chymotrypsin were more severely impaired than bicarbonate; a greater reduction of pancreatic exocrine function was found in patients with calcifications, compared to those without (p less than 0.001, Mann-Whitney U-test). When the patients were classified according to the duration of the disease or the severity of exocrine function impairment, higher percentages of patients with calcifications were found in the classes with more advanced disease. A log-linear analysis showed that the prevalence of calcifications was associated with pancreatic function impairment, even within the same class of duration of the disease. It is likely that calcifications mark more severe forms of chronic pancreatitis, even in the early phases of the disease.

In this study we compared the effects of a low-fat, high-carbohydrate (LFHC) diet at two levels of polyunsaturated fatty acids on plasma lipids of 20 patients affected by familial endogenous hypertriglyceridemia. During the intervention period the proportion of dietary energy derived from fat was reduced from about 45% to 20% in all the subjects. Ten patients (group I) consumed a LFHC diet with a polyunsaturated to saturated fat (P/S) ratio of 0.4, while the other 10 patients (group II) had a diet with a P/S ratio of 1–7. During the intervention period we observed a significant decrease of total plasma triglycerides and cholesterol in both groups. In spite of the different P/S ratio, the decrease of total triglycerides and cholesterol was superimposable in the two groups. The fall in plasma triglycerides and cholesterol was due only to the decrease in very low density lipoproteins (VLDL). On the contrary, low density lipoproteins (LDL) cholesterol was unchanged in both groups. Finally, during the interven...

Thirty-four patients with chronic calcified pancreatitis were evaluated clinically and biochemically (at a time when painful relapses were not present) every 9 mo for 3 yr; 25 of them were also studied at 4 and 9 yr. Serum elastase-1, trypsin, lipase, and amylase in the same sera were measured at each visit; levels on entry and variations during the study were compared with the clinical and functional data of the patients. On entry, low levels of elastase-1 were found in 11.7% of the patients, high levels in 41.1%; in contrast, high levels of trypsin and lipase were found in only a small number of patients (5.8 and 11.7%, respectively), whereas low levels were present in a substantial number (47.8 and 32.3% for trypsin and lipase, respectively). Over time, we found a significant (p = 0.000002) reduction in elastase-1 levels. Such reduction was not found for trypsin, lipase, or amylase. The reduction of serum elastase-1 was significantly (p< 0.003) more frequent in patients presenting a reduction in painful relapses than in patients with a stable or increased attack rate; this association was weaker (p

Twenty adult patients affected by atopic dermatitis (AD) were submitted to the p-aminobenzoic acid (PABA) test in order to evaluate the proteolytic pancreatic function. All but one showed a normal PABA test. These results seem to exclude a proteolytic maldigestion as a pathogenetic factor in AD.

Levels of a new carbohydrate antigen, CA 19-9, which is a monosialoganglioside identified by a monoclonal antibody raised against colorectal carcinoma cells, were compared to conventional CEA assays in 615 sera from healthy controls, patients with benign gastrointestinal disorders, and patients with cancers of gastrointestinal or extragastrointestinal origin. Whereas CEA levels were higher in smokers, CA 19-9 values were independent of the smoking history. CA 19-9 was undetectable in lymphoma and myeloma patients, but some patients with extraintestinal epithelial cancers expressed this antigen in serum. For benign and malignant gastrointestinal diseases, CA 19-9 displayed higher sensitivity, specificity, and predictive values than CEA. CA 19-9 was elevated as frequently as CEA in patients with metastatic pancreatic cancer, but in patients with localized disease, CA 19-9 was elevated more often than was CEA. In colorectal cancer, patients with and without metastases were detected at similar rates by both assays. It is concluded that CA 19-9 is a marker of epithelial cancers, does not vary with the smoking status, and is superior to CEA in detecting gastrointestinal malignancies, especially those arising from the pancreatic gland.

25 patients with chronic urticaria suspected to be of ‘alimentary origin’, were studied for a quantitative or qualitative deficiency of pancreatic enzyme secretion. All showed a normal fecal chymotrypsin excretion and 23/25 a normal bentiromide (PABA) and pancreolauryl test. In 2 females the urinary PABA and pancreolauryl tests were borderline pathological. This does not support the hypothesis that a pancreatic deficiency (of the kind which could be identified with the methods used) is associated with chronic urticaria in patients in whom improvement of urticaria occurs under a hydric or low antigenic diet.

Serum levels of elastase-1 were measured in 174 patients with pancreatic diseases and in 131 controls and were compared with the circulating levels of trypsin, lipase and amylase and with clinical data. In 48 patients with chronic pancreatitis serum enzyme levels were also compared with the pancreatic exocrine capacity. About 50% of the patients with chronic pancreatic disease showed increased levels of serum elastase, sometimes even in the face of long lasting pain-free periods, and/or of severe pancreatic impairment. On the contrary, serum trypsin and lipase were almost always either normal or below the normal range in the absence of painful relapses and/or in the presence of an impairment of the exocrine pancreatic function. A strict correlation was found between elastase-1 and trypsin (r = 0.778) and lipase (r = 0.834). However, controls and patients with chronic pancreatic diseases behaved differently, an increase in trypsin and in lipase levels being associated in the patients with chronic pancreatitis with an increase in elastase-1 values significantly larger than that observed in controls. These findings raise the hypothesis, at present unproven, that trypsin and lipase serum assays are more reliable indices of pancreatic exocrine function, whereas serum elastase-1 levels may indicate the presence of acute pancreatic episodes, even if subclinical, the importance of which, in the natural history of the disease, remains unknown.

Plasma levels of lactoferrin (LF) have been found to be increased in a few patients with cystic fibrosis (CF). This study was aimed at investigating plasma LF levels in children with CF (26 cases) and in controls (C) (19 cases). Plasma LF was measured by a radioimmunoassay method. Plasma LF levels were not significantly different in CF and in C, even though 10 CF patients showed LF levels above the mean + 2 SD value of the controls. Neither the duration of the disease nor the age of the controls was correlated with LF or with the exocrine pancreatic capacity. A significant relationship between the presence of an acute lung inflammation and LF levels was found. This study shows that LF is increased in CF only in the presence of an acute inflammatory state. Further studies are necessary to establish the usefulness of an LF assay as an index of the presence of an acute inflammatory process.

Eleven patients with Paget's disease of bone, treated intermittently for 2-4 years with porcine calcitonin (pCT) and clinically resistant to pCT [no modifications of serum alkaline phosphatase (ALP) and urinary hydroxyproline ( uHOP ) during pCT administration] were treated with 0.5-0.25 mg/day of human calcitonin (hCT) for 3-6 months. Nine of our patients showed biochemical improvement during the first 2 months of treatment, with reduction in ALP and uHOP . In one patient with slightly increased ALP and uHOP , and in another one during the second treatment course, hCT treatment did not modify the biochemical indices of bone disease. However all patients, including those with biochemical resistance, experienced a remarkable diminution of bone pain, which had not been observed during previous pCT treatment courses. Therefore, hCT appears to be indicated for therapeutic use in patients who are resistant to foreign calcitonins.

By critically evaluating the test employed in the diagnosis of chronic pancreatitis a number of considerations can be done. First of all the best discrimination between subjects with normal pancreatic function and patients with pancreatic insufficiency is given by direct hormonal stimulation tests using secretin and/or pancreozymin. Caerulein too, in a next future, could become a good tool in the functional diagnosis of the chronic pancreatitis. A more adequate statistical evaluation of the results seems also to improve the accuracy of the diagnostic classification. Without such an adequate statistical approach all the exopancreatic functional parameters (volume, HCO 3 − output, enzyme output) still merit full consideration since all these ‘variables’ improve the quality of the diagnostic information. Tests based on indirect functional stimulation of the pancreas, such as the Lundh test meal and other tests using intraduodenal perfusion with basic food elements, give less valid diagnostic information in comparison with direct stimulation tests. However, for therapeutic purposes, the indirect tests are sometimes more suitable, since they give information on the true post-prandial digestive capacity of the examined patient, whether the duodenal or the pancreatic area is responsible for the functional defect. Particularly interesting is the assay of radioactivity in the duodenal aspirate after the Lundh test meal and, above all, after the administration of secretin and pancreozymin. The latter procedure, in fact, ignores endogenous production of secretin and pancreozymin and enables easy measurement of volume and, therefore, accurate determination of the % of75Se-seleniomethionine. This test may be supplemented by the simultaneous calculation of volume, HCO 3 − and enzymes, as well as by sequential scintiphotography. This radioselenium test represents, therefore, an useful alternative of the classical secretin-pancreozymin test. A large number of ‘older’ diagnostic tests (serum provocative tests, tolerance tests, scintigraphy or scintiphotography alone) should instead be forgotten. These, in fact, dot not give reliable information or, even worse, they often suggest an incorrect diagnosis of chronic pancreatitis.

Fecal chymotrypsin (FCT) has been measured by a new photometric method (Monotest Chymotrypsin; Boehringer, Mannheim) in 78 patients: 44 with chronic pancreatitis and 34 not affected by any pancreatic disease. The results were compared with those from other tests of pancreatic secretory (secretin-cerulein test) and digestive [serum and urinary p-aminobenzoic acid (PABA) and pancreolauryl] capacity. When FCT values were severely reduced (below 6.7 U/g), from 90 to 100% of the patients also presented abnormal pancreatic secretory and digestive capacity. On the other hand, 87% of the patients with normal FCT (above 20 U/g) presented normal secretory and digestive capacity. Patients with intermediate FCT values (between 6.7 and 20 U/g) showed normal or abnormal pancreatic secretory and digestive capacity with the same probability. Therefore, FCT, carried out as a first test, seems to identify subjects that need no further pancreatic function tests (normal and severely impaired FCT) and patients who need other more complex functional investigations (intermediate FCT values).

SUMMARY The response of serum calcium, PTH, CT and gastrin to an infusion of secretin (3 CU/kg/h) over a period of 90 min was studied in ten healthy males and two female patients with hypoparathyroidism. In the healthy males serum calcium, after a transient fall, significantly increased at 45 min after the onset of the infusion (P < 0·001). Serum iPTH rose significantly within 5 min whereas serum CT and gastrin concentrations did not change. The two hypoparathyroid patients did not show any variations in either serum iPTH or calcium. These findings suggest that infusion of pharmacological doses of secretin into normal subjects modifies serum calcium, and that this change is due to PTH release.

Thirty-eight patients (13 men and 25 women) with impaired glucose tolerance, aged 33–70 yr, underwent a dietary program adding 20 g of raw bran to their usual diet without changing their dietary habits. After 1 mo of treatment, the areas under the curves for glucose and insulin were reduced from 26,214 ± 5618 to 24,529 ± 5207 g/min (P < 0.001) and from 15,893 ± 9714 to 12,440 ± 7377 mU/min (P < 0.001), respectively, cholesterol was reduced from 234 ± 40 to 212 ± 29 mg/dl (P < 0.001), and triglycerides were reduced from 108 ± 56 to 97 ± 50 mg/dl (P < 0.05). Body weight (initially 128.44% relative body weight) decrease 0.8% (P < 0.02). After the first month, 14 subjects were studied for a further 2 mo. Six patients continued bran feeding, and eight, who stopped bran, were used as controls. Patients who took bran maintained metabolic improvement over the 3-mo treatment period, while those who stopped bran did not.

A 14C-triolein breath test was carried out on 49 subjects suffering from chronic pancreatitis or from other digestive diseases, and its results were compared with the daily fecal fat excret

This long-term follow-up of 27 patients treated with conservative surgery for necrohemorrhagic pancreatitis (NHP) showed that an almost complete recovery of the exocrine function is achieved within 4 years after discharge, while about half of the patients presented still abnormal endocrine function. The morphological sequelae, pointed out by endoscopic retrograde pancreatography in almost 50% of the cases, remained unchanged during the follow-up period. Therefore, these data seem to exclude an evolution of NHP towards chronic pancreatitis.

Gli AA. riferiscono i risultati di alcune indagini morfologiche intorno alla micro-angiopatia diabetica, condotte con l'ausilio della microscopia ottica e di quella elettronica su 92 frammenti bioptici (58 di rene, 25 di muscolo e 9 di gengiva). Essi confermano il carattere ubiquitario delle lesioni capillari, ma riferiscono di aver rilevato alcune differenze circa la sede dell'apposizione di sostanze elettrondense sulla membrana basale dei capillari (versante interno nei capillari glomerulari; versante esterno nei capillari del muscolo e della gengiva). Gli AA. ritengono che l'evoluzione delle lesioni iniziali della nefroangiopatia diabetica proceda secondo le seguenti tappe: proliferazioni delle cellule mesangiali con produzione di sostanza simil-membrana od apposizione sul suo versante endoteliale di sostanze elettrondense; comparsa di fibrille collagene.

Cytoplasmic `saccules', bordered by monolayer membranes, containing round, virus-like particles, with a diameter of about 200 Å, are described in liver cells of 11 patients suffering from viral hepatitis. The differences between this pattern, glycogenic clumps of granules, polysomes, and cytoplasmic autolysis processes are discussed.

In four patients with organic hyperinsulinism (two with surgically proven beta-cell adenomas of the body of the pancreas) a standard tolbutamide test during continuous somatostatin infusion (5 microgram/min) was carried out. Tolbutamide induced insulin release was completely inhibited by somatostatin as in normal subjects. These results suggest that the inhibition test with somatostatin does not seem to be a better or safer way of diagnosing insulin producing tumours.

Secretin (1 CU/Kg) plus Caerulein (100 ng/Kg) or Cholecystokinin (1 or 2 IvyU/Kg) were given by rapid intravenous injection (Schedule 1) or by continuous infusion (Schedule 2) to 63 control subjects (C) and 69 patients affected by chronic pancreatitis (CP). Duodenal juice was collected for two and four 30-minute periods in schedule 1 and schedule 2, respectively. Volume, bicarbonate, and enzyme content were measured. Secretin-Daerulein, by rapid intravenous injection, showed a strong overlapping between C and CP values and led to some side-effects. Secretin-Caerulein by continuous intravenous infusion gave almost identical results as the Secretin-Cholecystokinin.

In examining a group of 90 hypercalcaemic patients (37 with primary hyperparathyroidism), a comparison was made of the diagnostic reliability of: 1) tests commonly used for diagnosis of primary hyperparathyroidism; 2) radioimmunoassay of plasma parathormone; 3) a recently introduced model of multivariate statistical analysis. The results indicate that, at present, the model of multivariate statistical analysis used is of higher diagnostic reliability in the diagnosis of primary hyperparathyroidism than renal phosphate excretion tests and the radioimmunoassay of PTH itself.

Lactoferrin is present in pancreatic juice, and greatly increased concentrations are found in the pancreatic juice of patients with chronic pancreatitis. It is not known whether these high levels of lactoferrin represent a genetically determined defect predisposing to the later development of chronic pancreatitis or are simply a consequence of the disease. In view of the morphological and functional similarities between the pancreatic and parotid glands, we have measured the immunoreactive lactoferrin concentration in pure parotid saliva of 30 patients with chronic calcific pancreatitis, 26 controls, 5 patients with proven pancreatic cancer, 2 patients with Sjogren's disease and 2 patients with chronic recurrent parotitis. No difference in the lactoferrin concentration was detected between control subjects and patients with chronic pancreatitis or pancreatic cancer. Raised levels were found in the 4 patients with parotid gland disease. These findings suggest that increased lactoferrin secretion is confined to the exocrine pancreas in patients with chronic pancreatitis and is thus probably a phenomenon secondary to the disease.

Urinary excretion of kallikrein has been studied in a patient with hypokalemic alkalosis, hyperplasia of the renal juxtaglomerular apparatus and hyperreninemia, secondary aldosteronism and resistance to the pressor effect of angiotensin II (Bartter's syndrome). Urinary kallikrein was found exceedingly high in several determination, whereas it was low in patients with essential hypertension and high in patients with primary aldosteronism. Urinary kallikrein decreased after spironolactone therapy. The rise of kallikrein excretion (which is not related to plasma renin) in this case is probably caused by a direct action of the chronic excess of plasma aldosterone; it could not be accounted for as secondary to natriuresis.

Synthetic linear somatostatin infused in two patients with insulin producing tumors lowered slightly basal insulin and a little less basal glucose levels; above all it inhibited insulin release induced by glucose, glucagon, and tolbutamide.

5 healthy volunteers were submitted to i.v. infusion for 45 min of graded doses of commercial GIH secretin (0.01, 0.025, 0.05, 0.5, 1 and 2 CU/kg h-1). Parathormone serum levels were measured before and during the infusion. All the dosages of exogenous secretin were followed by a significant increase in serum PTH levels in a dose-dependent fashion. Commercial GIH secretin, even at low doses, seems to increase circulating parathyroid hormone levels significantly.

An endoscopically controlled clinical trial on maintenance Ranitidine treatment of scarred duodenal ulcer was carried out in 78 patients, randomly allocated to either 150 mg Ranitidine at night or low-dose antacid when necessary in a 1 -year follow-up study. The maintenance Ranitidine regime prevented ulcer relapse in 23 of 31 cases (74.2%), without any significant adverse reaction. In the control group, the relapse was prevented in 12 of 30 cases (40%); the difference was found to be statistically significant.

This investigation was aimed at comparing a new method for measuring faecal fat excretion, carried out with a semi-automated instrument by using near infrared analysis (NIRA), with the traditional titrimetric (Van de Kamer) and gravimetric (Sobel) methods. Near infrared analysis faecal fat was assayed on the three day stool collection from 118 patients (68 chronic pancreatitis, 19 organic diseases of the gastrointestinal tract, 19 alcoholic liver disease, 12 functional gastrointestinal disorders). A strict linear correlation was found between NIRA and both the titrimetric (r = 0.928, p less than 0.0001) and the gravimetric (r = 0.971, p less than 0.0001) methods. On homogenised faeces, a mean coefficient of variation of 2.1 (SD 1.71)% was found. Before homogenisation (where a mean coefficient of variation of 7% was found) accurate results were obtained when the mean of five measurements was considered. In conclusion, the assay of faecal fat excretion by the near infrared reflessometry appears a simple, rapid and reliable method for measuring steatorrhoea.

Using an immunoenzymatic method, we studied lipase in the serum and urine of 23 controls, 22 chronic pancreatitis patients in symptomatic remission, and in 9 patients with proven pancreatic cancer. Serum and urine lipase and its fractional urinary clearance were compared with those of amylase and immunoreactive trypsin. Lipase immunoreactivity was detectable in the urine of 81.5% of the studied subjects (controls: 82%, chronic pancreatitis: 86%, pancreatic cancer: 66%); its output was higher than the upper limit of controls in 31.8% of chronic pancreatitis and in only 1 of pancreatic cancer, and it was significantly correlated with the urinary output of trypsin (r = 0.487, P less than 0.001), but not with that of amylase. A significant correlation was found between urinary output and serum levels for lipase, but not for trypsin or amylase. Fractional clearance of lipase was of the same magnitude as that of trypsin but only 0.1% that of amylase. 19% of chronic pancreatitis and pancreatic cancer showed a fractional clearance of lipase above the upper limit of controls, compared with 45% for trypsin and 3.2% for amylase. No difference in urinary clearance of the three enzymes was found between chronic pancreatitis and pancreatic cancer. In conclusion, although of no diagnostic relevance in pain-free patients with chronic pancreatic disease, this measurement can provide information on the mechanisms of renal excretion of pancreatic enzymes.

An increase in fasting cholecystokinin (CCK) levels has been reported in patients with pancreatic insufficiency, but the relationship of these findings to the clinical conditions has not been established. We, therefore, measured fasting serum CCK-like immunoreactivity in 70 patients with chronic relapsing pancreatitis (CRP) (38 non-surgically treated and 32 previously surgically treated) and in 44 healthy subjects. The radioimmunoassay detected three circulating forms of CCK. The mean value of the CCK levels in CRP (260.3 +/- 300.8 pg/ml) was significantly higher than that of the controls (56.6 +/- 61.7 pg/ml) (p less than 0.001), but in 39 (56.7%) of the 70 CRP cases the CCK was in the normal range. A smaller overlap with the controls was observed in the non-surgically than in the surgically treated patients (45 vs. 71.8%). In the 38 non-surgically treated CRP cases no relationship was observed between the CCK levels and each of the following parameters: age, length of history, presence or absence of pancreatic calcification, nutritional and alcoholic habits, and the results of exocrine function tests. The absence of the last-mentioned correlation is somewhat unexpected if the high CCK levels are due to the interruption of a feedback loop for CCK secretion. However, previous pancreatic surgical drainage and/or treatment with pancreatic enzymes, present in almost all these patients, could have an effect on CCK behaviour.

The numerous attempts to classify obesity demonstrate the difficulty of grouping the obesity syndrome into a single schema. The criteria can be subdivided into 3 groups: the first based on etiology and pathogenesis; the second based on clinical observation, anthropomorphic measurements and adipose tissue histology; and the third based on psychological and nutritional behavior, and environmental elements. The etiological classification subdividing obesity into genetic, hypothalamic, nutritional, physical inactivity, and endocrine groups is important because it best approximates the clinical reality of obesity.

The lack of information on skin lesions in patients with chronic alcoholic pancreatitis prompted us to carry out an investigation on 54 patients with well-documented alcoholic chronic pancreatitis, on 54-pair-matched controls and on 30 patients with alcoholic liver cirrhosis. This study suggests that in chronic pancreatitis, but not in alcoholic liver cirrhosis and in controls, an increased frequency of skin lesions as seborrheic dermatitis, comedones and oily and scaling skin is present. These changes do not seem to be directly related to chronic alcoholism and/or diabetes. It is hypothesized that the folate deficiency induced by chronic consumption of pancreatic extracts, probably worsened by maldigestion and malabsorption, may be the main pathophysiological factor involved in these skin lesions.

Linear discriminant analysis, a multivariate statistical procedure, applied to serum calcium, phosphate, alkaline phosphatase, bicarbonate, chloride, creatinine and tubular reabsorption of phosphate, proved to be effective in distinguishing patients with Primary Hyperparathyroidism from other hypercalcaemic patients in eithy-four retrospective cases. The application of the model to thirty-four prospective cases enabled us to separate correctly, hyperparathyroid patients from non-parathyroid hypercalcaemic patients.

Frequency of duodenal ulcer in patients with chronic pancreatitis is still controversial. This study aims to prospectively investigate the frequency of duodenal ulcer in a group of 190 patients (162 males and 28 females) affected by chronic relapsing pancreatitis admitted to our department between 1970 and 1979. 41 cases (21.5%) were endoscopically observed (22% of the males and 17.9% of the females; male:female ratio 1.2:1). Drinking habits, cigarette consumption, presence of pancreatic calcifications and surgery did not affect the frequency of duodenal ulcer. Exocrine pancreatic insufficiency, as fecal fat excretion higher than 7 g/day, seems to be linked with an increased frequency of duodenal ulcer (exact Fisher's test: p = 0.0586). Moreover, duodenal ulcer was present in about one third of the patients who afterwards died, but it was the cause of death in only 1 case. Even if a prospective control population is lacking, the male:female ratio of duodenal ulcer in chronic pancreatitis seems to be different from that observed in a comparable hospitalized group (1.2:1 vs. 2.4:1) and from that reported in literature in the general adult population.

As some rosacea patients complain of gastrointestinal troubles and the administration of pancreatic extracts ameliorates both dyspepsia and skin lesions, the pancreatic exocrine function in 21 subjects affected with rosacea has been investigated by means of the secretin-cerulein infusion test. 21 healthy controls have been studied for comparison. No difference was found between rosacea and control subjects for flow rate, bicarbonate and chymotrypsin concentration and output, while lipase concentration and output was significantly lower in rosacea patients, with a decrease ranging from 18.5 to 66% of normal values. Therefore, a deficient lipase secretion could be responsible, at least partly, for the clinical manifestations of rosacea.

INTRODUCTION Many factors contribute to glucocorticoid-in deced osteopenia.Corticosteroid excess leads to in testinal malabsorption of calcium through a direct inhibition of the intestinal absorptive process(l, 2) or through an impaired vitamin D metabolism (3, 4). A direct action of the corticosteroid on bone tissue has also suggested (5). On the other hand an impaired calcitonin (CT) secretion has been suggested to be a factor in the pathogenesis of some forms of decreased bone mass (6,7) . To explore a possible relationship between CT secretion and steroid induced bone loss we studied the secretion of this hormone before and during long term treatment with eorticosteroids.