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Biomedical subjects

H Sarles

Publications and source records attributed to H Sarles.

At least 19 recordsLinked to original sources
PubMed1992

Inhibition of nucleation and crystal growth of calcium carbonate by human lithostathine.

Pancreatic juice is naturally supersaturated in calcium and bicarbonate ions. A mechanism controlling CaCO3 crystal formation and growth is therefore necessary to prevent duct clogging. The present study shows that lithostathine, a glycoprotein present in human pancreatic juice at a concentration in the range of 10 mumol/L, could be involved in such a control. Lithostathine in concentrations greater than 1.5 mumol/L significantly delayed crystal nucleation and inhibited growth of preformed CaCO3 crystals from supersaturated solutions. Adsorption of lithostathine on crystals was shown by immunodetection. Albumin also adsorbed on CaCO3 crystals, but neither albumin nor other pancreatic secretory proteins inhibited crystal nucleation or growth. Lithostathine adsorbed to sites specifically inhibiting crystal growth with a dissociation constant (Kd) = 0.9 x 10(-6) mol/L. The glycosylated amino-terminal undecapeptide generated by limited trypsin hydrolysis inhibited CaCO3 crystal growth with a Kd = 3.0 x 10(-6) mol/L, similar to that of lithostathine. On the contrary, the carboxy-terminal polypeptide was inactive. A synthetic undecapeptide identical to the N-terminal end but not glycosylated was equally active. The activity disappeared upon digestion of the undecapeptide with V8 protease. The N-terminal undecapeptide of lithostathine is therefore essential to the inhibitory activity of the protein on CaCO3 crystal growth.

Adsorption↗
PubMed1992

Chronic pancreatitis and diabetes.

Chronic pancreatitis is defined by a persistent destruction of the pancreatic parenchyma replaced by fibrosis. The lesions generally start in the exocrine gland, islets being attacked later in the fibrosis. The two most frequent forms are: 1. Chronic calcifying pancreatitis which is a pancreatic lithiasis responsible for more than 95% of chronic pancreatitis. In its most frequent form, calculi are built up of more than 98% calcium salts together with fibres of a degraded residue of lithostathine, a secretory protein. This disease is related (i) in most countries to alcohol, protein, fat and tobacco and (ii) in certain tropical countries to malnutrition (low-fat, low-protein diet) for some generations. A causative role for cassava and kwashiorkor is improbable. The mechanism of calcium precipitation is partly explained by the calcium-saturation of pancreatic juice and the decreased biosynthesis of lithostathine S, the secretory protein preventing crystallization. As a rule, diabetes (and steatorrhoea) appear after a clinical evolution characterized by recurrent attacks of upper abdominal pain, generally lasting some days with transiently increased concentrations of pancreatic enzymes in serum. When diabetes appears, pain frequently disappears. Complications are mostly observed in the first 10 years of clinical evolution. 2. Obstructive pancreatitis is due to an obstacle (tumours, scars) in the pancreatic duct. It is rarely a cause of diabetes. Diabetes due to chronic pancreatitis is characterized by the low incidence of ketosis and the high incidence of insulin-induced hypoglycaemia. Patients are generally thin. Serum insulin levels, either basal or stimulated, are decreased. Glucagon is less affected. Angiopathies and retinopathies are less frequent than in non-insulin-dependent diabetes. Neural complications are fairly frequent. The diagnosis is generally easy because diabetes appears at a late stage of the disease. The treatment generally requires insulin.

Chronic Disease↗
PubMed1992

A case of primary non-Hodgkin lymphoma of the pancreas.

Non-Hodgkin pancreatic lymphoma is a rare disease. Its diagnosis is difficult without histological examination. Ultrasonographic, computed tomodensitometric, and endoscopic retrograde cholangio-pancreatographic findings are not pathognomonic. The better prognosis of these tumors, compared to adenocarcinoma, and their sensitivity to chemotherapy, implies the need for pathologic examination of every pancreatic tumor.

Adult↗
PubMed1992

Radiolucent and calcified pancreatic lithiasis: two different diseases. Role of alcohol and heredity.

One hundred and eighteen consecutive patients presenting with pancreatic calculi have been studied by means of plain films of the abdomen and endoscopic retrograde cholangiopancreatography. Patients were divided into the following groups: 1) Evenly calcified calculi, 74 patients, 66 men, aged at onset (M +/- SM) 40 +/- 10 years; daily consumption of alcohol, 157 +/- 121 g, and of tobacco, 26 +/- 15 cigarettes. Two patients presented with another case in the same family. Composition of calculi--at least 95% calcium salts and a degraded form of lithostathine S (formerly called PSP S2-5)--was similar in the Occidental alcoholic and in the tropical form: calcified calculi are probably related to alcohol and nutritional disorders. 2) Radiolucent stones, 17 patients, 12 men and 5 women, aged at onset 38 +/- 18 years. These patients had a low alcohol and tobacco consumption. There were four familial cases. 3) Radiolucent core with a calcified shell (target calculi), 27 cases, 23 men; age at onset, 38 +/- 15 years; daily ethanol consumption, 111 +/- 93, and tobacco, 19 +/- 15 cigarettes. There were two familial cases. It has been shown that these calculi originated from transparent calculi that later calcified. The frequency of women and of familial cases was significantly greater in groups 2 + 3 than in group 1. The consumption of alcohol and tobacco and the proportion of men were significantly lower in group 2 than in groups 1 and 3. We discuss the role of heredity in lithostathine precipitation and of alcohol in calcium precipitation.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1992

[Description of a new disease: pancreatic lithiasis with radiolucent calculi].

118 patients presenting with pancreatic lithiasis were consecutively observed in our service. They underwent both an endoscopic pancreatography and god plain films of the abdomen. Calculi were classified in 3 groups: 1) Radiolucent calculi (17 cases, 5 females; 4 hereditary cases) are build up of amorphous residues of lithostathine S. They are not related to either alcohol, diet or tobacco. 2) Target calculi (27 cases, 4 females; 3 hereditary cases) have a radiolucent core as in 1 and a peripheral calcification. They are a late evolutionary stage of radiolucent lithiasis. The frequency of females and of hereditary cases is significantly greater in form 1 + 2 than in form 3. These two forms are a newly described disease without relationship with nutrition, alcohol or tobacco but the peripheral calcification of radiolucent calculi is favoured by alcohol and tobacco. This disease could be hereditary. 3) Calcic lithiasis (74 cases, 8 females, 2 hereditary cases) is the most frequent form of pancreatic lithiasis. Its cause is nutritional.

Alcohol Drinking↗
PubMed1992

[Description of a new disease, pancreatic lithiasis with radiotransparent calculi].

118 patients presenting with pancreatic lithiasis were consecutively observed in our service. They underwent both an endoscopic pancreatography and good plain films of the abdomen. Calculi were classified in 3 groups: 1) Radiolucent calculi (17 cases, 5 females; 4 hereditary cases) are build up of amorphous residues of lithostathine S. This disease is not related to either alcohol, diet or tobacco. 2) Taget calculi (27 cases, 4 females; 3 hereditary cases) have a radiolucent core as in 1 and a peripheral calcification. They are a late evolutionary stage of radiolucent lithiasis. The frequency of females and of hereditary cases is significantly greater in form 1 + 2 than in form 3. These two forms are a newly described disease without relationship with nutrition, alcohol or tobacco but the peripheral calcification of radiolucent calculi is favoured by alcohol and tobacco. This disease could be hereditary. 3) Calcic lithiasis (74 cases, 8 females, 2 hereditary cases) is the most frequent form of pancreatic lithiasis. Its cause is nutritional.

Adult↗
PubMed1991

Mucinous ductal ectasia of the pancreas: a premalignant disease and a cause of obstructive pancreatitis.

Five cases of localized ectasiae of pancreatic ducts associated with epithelial mucinous metaplasia have been previously reported by Itai et al. (Radiology 1986; 161:697-700). During a 1-year period, we collected four new observations of patients presenting with recurrent attacks of pancreatic pain due to similar clusters of cystlike dilated ducts communicating with the main pancreatic duct and lined by a columnar epithelium interspersed with numerous goblet cells. Duct lumina were filled with mucous. Carcinoembryonic antigen levels were high in the pure pancreatic juice, but normal in the blood. Sonography and CT scan showed cystlike, intrapancreatic defects localized three times in the head of the pancreas and once in the body. Endoscopic retrograde cholangiopancreatography (ERCP) showed a huge dilation of some collateral ducts filled by radiolucent defects. The main pancreatic duct was dilated proximally to pathological ducts in three cases. Neither pancreatic stones nor exocrine insufficiency could be demonstrated 7 years after the clinical onset; one case presented with an in situ carcinoma. Since mucinous ductal ectasia is a precancerous state, surgery is mandatory. ERCP is probably the best method of diagnosis.

Adult↗
PubMed1991

Immunoreactive forms of pancreatic stone protein in six mammalian species.

Secretory forms of the pancreatic stone protein (PSP S, Mr 17, 500-22,000) have been purified from human pancreatic juice. PSP S are inhibitors of CaCO3 crystal growth. The presence of similar proteins in bovine, canine, monkey, porcine, and rat pancreatic secretion was investigated in terms of biological role and immunological relationship. Pancreatic proteins were analyzed by electrophoretic separation and by subsequent immunoblotting with a rabbit polyclonal antibody against human PSP. A single immunoreactive form was detected in dog, pig, and rat (Mr 17,000), and two distinct immunoreactive forms were observed in cow and monkey (Mr 15,000 and 17,000). Inhibition of CaCO3 crystal growth was demonstrated in dog and rat. Further kinetic studies of the inhibition process in the rat showed that PSP S binds to the crystal surface according to a Langmuir adsorption isotherm with a dissociation constant (Kd) of 1.5 x 10(-6) M. These results suggest that proteins homologous to human PSP S are present in other mammalian species and may act as stabilizers of Ca(2+)-supersaturated pancreatic juice.

Animals↗
PubMed1991

The cephalogastric phase of the pancreatic response to food in the dog.

We studied post-meal pancreatic secretion and gastrin release in conscious dogs with duodenal Thomas cannulas. Normal dogs were tested in physiological conditions and with an i.v. infusion of atropine 20 micrograms/kg/h or secretin 0.5 CU/kg/h. The responses were also studied after antral and truncal vagotomy. In the early phase (0-20 min) of the response, before gastric emptying started, antral vagotomy reduced fluid and protein outputs, and truncal vagotomy reduced them still more. Atropine reduced only the protein response. Gastrin release reached a peak after 20-25 min. After antral and truncal vagotomy, gastrin release was reduced within 10 min after the meal. Late-phase (greater than 20 min) pancreatic secretion depended on the presence of chyme in the duodenum. The effects of atropine and antral vagotomy in the cephalogastric phase could be explained by antropancreatic reflexes stimulating fluid secretion (atropine-resistant pathway) and protein output (atropine-sensitive pathway).

Animals↗
PubMed1991

Involvement of tubular complexes in pancreatic regeneration after acute necrohemorrhagic pancreatitis.

Localized acute necrohemorrhagic pancreatitis was induced in rats by multiple trypsin injections. Morphological alterations were monitored by light and electron microscopy until complete recovery. In the acute phase, typical pictures of focal acute necrohemorrhagic pancreatitis were observed. In the postacute phase, fibrosis and tubular complexes are characteristic of damaged areas. Tubular complexes appear from the dedifferentiation of acinar cells. They are characterized by duct-like cells bordering wide, empty luminae. In the recovery phase, cellular proliferation was accompanied by differentiation, with progressive acquisition of the morphological characteristics of acinar cells at the periphery of the tubular complexes. In that instance, cellular proliferation was concomitant with the development of collagen septa in tubular complexes. In these structures both duct-like and acinar-like cells presented mitoses. Cell division persisted in the dedifferentiated cells until tubular complexes disappeared. A very similar process was observed in the embryonic pancreas, where organized parenchyma originated from proliferation and differentiation of protodifferentiated cells. We concluded that pancreatic repair following necrohemorrhagic pancreatitis involves proliferation of cells from intact acini and from tubular complexes, at variance with edematous pancreatitis, where regeneration is exclusively due to acinar cell proliferation.

Acute Disease↗
PubMed1991

Definitions and classifications of pancreatitis.

The historical progress of medical knowledge has followed two primary courses. One course has been based mostly on pathology: the description of specific groups of features and of the corresponding causes and symptoms, i.e., the description of different diseases that are progressively distinguished one from another. At the present time, disorders of molecular biology as well as pathological lesions are increasingly playing a role in the definition of diseases. The second course is a preliminary step to the first: when pathological data have not been available, patients have been classified according to symptoms. This does not lead to the description of the diseases but rather of the syndromes. It is puzzling to see that this obsolete method is still commonly used in pancreatology.

Humans↗
PubMed1991

Is tobacco a risk factor for chronic pancreatitis and alcoholic cirrhosis?

In a case control study alcohol intake and tobacco use were assessed between 1975 and 1987 in 103 male patients suffering from alcoholic cirrhosis of the liver, in 145 patients with chronic pancreatitis, and in 264 control subjects. The patients with chronic pancreatitis were significantly younger than the patients with cirrhosis (mean (SD) age 41.92 (2.4) v 60.9 (11.6) years). Among the patients with chronic pancreatitis, 94% were both smokers and drinkers compared with 83% of patients with cirrhosis of the liver. The relative risks for each disease were calculated by conditional multiple logistic regression. Whereas daily intake of alcohol was a major risk factor for both cirrhosis of the liver and chronic pancreatitis, smoking was significantly related only to the risk of having chronic pancreatitis. Moreover, the mean age at onset of pancreatitis was lower among smokers.

Adult↗
PubMed1991

Liver cirrhosis and chronic calcifying pancreatitis are associated with different morphotypes.

The different morphotypes of patients have been determined by sonography of the upper abdomen and statistical calculation according to a previously published method. Patients have been classified into the following 3 groups: 'longilignes', 'normotypes' and 'brèvilignes' which fit with ancient anatomical descriptions. In 74 normal controls, there were 21.6% brévilignes and 44.5% longilignes, in alcoholic cirrhosis (n = 31) 77.4 and 6.4%, respectively, in postnecrotic viral cirrhosis (n = 28). 25.0 and 17.8% and in alcoholic chronic calcifying pancreatitis (n = 25) 12.0 and 76.0%. These differences which are significant between all groups show that the morphotype of the human body is different in cirrhotic and pancreatitis patients. As morphotypes preexist to cirrhosis and chronic pancreatitis, this is an argument for the assumed predisposition (possibly hereditary) to cirrhosis and chronic pancreatitis.

Chronic Disease↗
PubMed1991

Persistence of the X-ray-transparent matrix of vanishing pancreatic stones.

We present three observations of patients with chronic calcifying pancreatitis with multiple pancreatic calculi visible on X-ray films of the abdomen. These patients were studied with plain films and sonography. On X-ray films, visible calcifications disappeared. In contrast, sonography and computerized tomography showed that the X-ray-transparent material of stones persisted. It is known that these stones are composed of different insoluble residues of PSP-S2-5, the secretory calcium stabilizer of pancreatic juice. This shows that the spontaneous or drug-induced disappearance of pancreatic stones on radiologic films is not sufficient for healing chronic calcifying pancreatitis.

Adult↗