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M V Singer

Publications and source records attributed to M V Singer.

At least 91 records · Page 5Linked to original sources
PubMed1994

[Non-surgical therapy of pancreatitis complications (pseudocyst, abscesses, stenoses)].

Acute and chronic pseudocysts differ. Chronic pseudocysts develop during the evolution of chronic pancreatitis unrelated to a specific bout of clinically recognizable acute pancreatitis. Acute pseudocysts arise in conjunction with an episode of acute pancreatitis. Whereas until recently surgical therapy has been the standard treatment for acute (or chronic) pancreatic pseudocysts, a range of nonsurgical options has been developed. The most important nonsurgical treatment of all is to watch and wait. Pseudocysts following acute pancreatitis should be observed when they are truly asymptomatic and less than or equal to 6 cm in diameter and left alone if not increasing in size. Only if after a six-week observation period pancreatic pseudocysts increase in diameter and become symptomatic, percutaneous needle aspiration, catheter drainage or an endoscopic drainage procedure (cystogastrostomy/cystoduodenostomy) or ultimately operative drainage procedure should be considered. Antibiotic therapy should be considered for all patients presenting with pancreatic necrosis. They should be treated with drugs administered intravenously at the maximum recommended dose as early as possible after onset of symptoms, continued throughout at least the first two weeks of the disease. Moreover, they should be treated alone and/or in combination with antibiotics that are active against gram-negative organisms of intestinal origin, commonly isolated in necrotic tissue, pseudocysts and infected pancreatic abscesses, and that are capable of penetrating into the pancreatic juice and necrotic tissue (e.g. mezlocillin, cephalosporin, metronidazole). Removal of pancreatic stones and pancreatic stenosis by endoscopic procedures in the treatment of pain in patients with chronic pancreatitis is still not an established and generally accepted treatment. Controlled trials to validate stenting and ESWL in chronic pancreatitis are needed.

Abscess↗
PubMed1994

[Acute cholecystitis--conservative therapy].

In about 95% of patients with acute cholecystitis the cystic duct is obstructed by a gall stone. The imprisoned bile salts have a toxic action on the gall bladder wall. Acute cholecystitis is liable to be confused with other causes of sudden pain and tenderness in the right hypochondrium. Below the diaphragm, acute retrocecal appendicitis, intestinal obstruction, a perforated peptic ulcer or acute pancreatitis may be confusing factors; however, the gall bladder remains shrunken, fibrotic, full of stones and nonfunctioning. Recurrent acute cholecystitis may follow, but there may be surprisingly long clinically silent periods. The treatment of choice is elective cholecystectomy. General measures include bed rest, intravenous fluids, a light diet and relief of pain with pethidine and buscopan. Antibiotics are given to treat septicemia and prevent peritonitis and empyema. During the first 24 h., 30% of the gall bladder cultures are positive. This rises to 80% after 72 h. Common infecting organisms are Escherichia coli, Streptococcus faecalis and Klebsiella, often in combination. Anaerobes are present, if sought, and are usually found with aerobes. They include Bacteroides and Clostridia. Antibiotic(s) should have a spectrum to cover the colonic type micro-organisms which are usually found with infection of the biliary tree. The choice depends upon the clinical picture. A broad-spectrum penicillin or a cephalosporin is usually adequate for the stable patient with pain and mild fever. The severely septicemic patient is better treated with a combination of ureidopenicillin (mezlocillin or piperacillin) and metronidazole.

Acute Disease↗
PubMed1994

The problem of classification and staging of chronic pancreatitis. Proposals based on current knowledge of its natural history.

BACKGROUND: Even though the four international meetings held so far on classification of pancreatitis have helped considerably to further our understanding of the disease, all have serious drawbacks that limit their clinical utility. The main problem with the Marseille classifications is the need for histologic proof, and the Cambridge classification relies on imaging modalities that are not sensitive or specific enough. RESULTS: Chronic pancreatic inflammation (CP) has been observed in association with several systemic diseases (such as autoimmune diseases), and since the natural history of the pancreatic affliction in these conditions is clearly distinct from that seen in other forms of CP, these need to be classified separately. Furthermore, many clinical/aetiologic forms of chronic calcifying pancreatitis (CCP) exist which differ sufficiently in their clinical features and management to deserve individual recognition. PROPOSAL: A subclassification of CCP into alcoholic, tropical, hereditary, hypercalcaemic, hyperlipoproteinaemic, drug-induced, and idiopathic is proposed. The staging of chronic alcoholic pancreatitis has been a controversial issue, mainly because of the apparent unpredictability of the course of pain. However, several large follow-up studies in the past decade suggest that recurrent acute exacerbations dominate the clinical picture in the first few years after onset of symptoms, and progressive pancreatic insufficiency is the predominant feature in the late stages of the disease. On the basis of the results of these studies it is proposed that alcoholic chronic pancreatitis be divided into four stages: I) latent or subclinical, II) early, or stage of inflammatory complications, III) late, or stage of severe pancreatic insufficiency, and IV) advanced, or stage of secondary painless pancreatitis.

Alcohol Drinking↗
PubMed1994

Effect of a 28-day therapy with famotidine on blood levels of alcohol and gastrin and intragastric pH in healthy human subjects.

In a randomized, placebo-controlled study of 10 healthy human subjects blood alcohol levels after consumption of beer, 24-h intragastric pH, and serum gastrin concentrations were serially measured during a 28-day therapy with famotidine. The subjects consumed placebo or famotidine (40 mg at 1830 h) and beer (500 ml at 1900 h) every day for 28 days. On days 1, 7, and 28 of the study 24-h intragastric pH-metry and blood alcohol and gastrin estimations were performed. Famotidine did not significantly alter either the peak or the 2-h integrated blood alcohol response to beer. The median intragastric pH on days 1, 7, and 28 was significantly (p < 0.006) increased by famotidine. After 7 days of famotidine therapy, however, the pH was significantly (p < 0.03) lower than on day 1 (4.0 versus 2.4); this effect persisted on day 28 (2.3). Whereas basal plasma levels of gastrin were not significantly altered by famotidine, the 2-h integrated plasma gastrin response to beer was significantly (p < 0.05) higher with famotidine than with placebo. We conclude that 1) a 28-day therapy with famotidine does not alter blood alcohol levels in response to social consumption of beer; 2) after 7 days of therapy tolerance to its gastric acid-inhibitory effect is seen; and 3) an exaggerated postprandial release of gastrin may be involved in the development of this tolerance.

Adult↗
PubMed1993

Role of somatostatin in regulation of insular-acinar axis.

Cysteamine is known to deplete somatostatin from pancreatic D cells. In the isolated perfused rat pancreas we investigated its effects on somatostatin and glucagon release as well as exocrine pancreatic secretion in the presence of 1.8 mM glucose. Cysteamine, 10 mM, released somatostatin, but had no effect on CCK-stimulated amylase secretion. Arginine-stimulated glucagon release, however, was significantly inhibited by cysteamine. Concomitantly we still observed stimulation of somatostatin secretion, but also a potentiation of CCK-stimulated amylase secretion. Our results are consistent with a role of somatostatin in the regulation of exocrine pancreatic secretion via its effect on pancreatic A and B cells.

Amylases↗
PubMed1993

Alcohol and gastric acid secretion in humans.

The secretory response of gastric acid to pure ethanol and alcoholic beverages may be different because the action of the non-ethanolic contents of the beverage may overwhelm that of ethanol. Pure ethanol in low concentrations (< 5% vol/vol) is a mild stimulant of acid secretion whereas at higher concentrations it has either no effect or a mildly inhibitory one. Pure ethanol given by any route does not cause release of gastrin in humans. Alcoholic beverages with low ethanol content (beer and wine) are strong stimulants of gastric acid secretion and gastrin release, the effect of beer being equal to the maximal acid output. Beverages with a higher ethanol content (whisky, gin, cognac) do not stimulate gastric acid secretion or release of gastrin. The powerful stimulants of gastric acid secretion present in beer, which are yet to be identified, are thermostable and anionic polar substances. The effect of chronic alcohol abuse on gastric acid secretion is not as predictable. Chronic alcoholic patients may have normal, enhanced, or diminished acid secretory capacity; hypochlorhydria being associated histologically with atrophic gastritis. There are no studies on the acute effect of alcohol intake on gastric acid secretion in chronic alcoholic patients. The acid stimulatory component of beer and wine needs to be characterised and its possible role in the causation of alcohol induced gastrointestinal diseases needs to be investigated.

Alcohol Drinking↗
PubMed1992

Novel generation of hormone receptor specificity by amino terminal processing of peptide YY.

The physiological significance of multiple Y receptors has not been determined since until recently only one form of endogenous agonists was known, namely PYY1-36 and NPY1-36. Recently, a new molecular form of PYY was characterized as des(Tyr-Pro)PYY (PYY3-36 or PYY-II). Its ability to interact at various Y receptors was not characterized. Analytical chromatography of fresh canine colon extracts shows two peaks of immunoreactivity eluting in the positions of PYY-II and PYY1-36 (PYY). PYY-II was about 40% of the total PYY immunoreactivity indicating that it is one of the major forms of PYY expressing its biological activity. It is shown that PYY-II will not displace label from the Y1 receptors found on a human neuroblastoma cell line. It is further shown that PYY-II is as potent as PYY for the inhibition of pancreatic secretion, which must occur through Y2 receptors. The enzymatic removal of Tyr-Pro from PYY to form PYY-II must therefore regulate the relative expression of a non-selective agonist (PYY) to a highly selective Y2 agonist (PYY-II). Amino terminal processing of PYY represents a novel type of regulation of peptide hormone specificity. It has important biological implications for PYY and potential relevance for other peptide hormone receptor systems.

Animals↗
PubMed1992

[Neuroendocrine tumors of the gastrointestinal tract. 1: Clinical aspects].

Endocrine cells are characterized by common biochemical properties and specific cellular markers. Endocrine tumors, too, differ from other types of tumor in a number of ways. These have to do with the classification, the occurrence of functioning or nonfunctioning forms, benign and malignant courses, solitary or multiple presentation, as well as entopic and ectopic growth forms. The incidence of the gastrointestinal functioning tumors is about 0.5-1.0 per 100,000, the nonfunctioning tumors predominating many times over. The diagnosis of functioning endocrine tumors in the early phases of the disease is based on the biochemical demonstration of substances released into the blood, and the clinical picture is determined not primarily by the size or extent of the tumor, but by the biological effects of the tumor secretions. The clinical symptomatology associated with these tumors is often much more marked than the measurable tumor manifestation.

Carcinoid Tumor↗