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G Uomo

Publications and source records attributed to G Uomo.

66 records · Page 4Linked to original sources

Antioxidant treatment in hereditary pancreatitis. A pilot study on three young patients.

BACKGROUND: Abdominal pain is the most challenging symptom of hereditary pancreatitis. No specific and proven therapy is yet available; analgesics, often in large doses, are required also in children and young patients. PATIENTS AND METHODS: We performed an open-label, pilot study on three young patients, coming from the same kindred, with hereditary pancreatitis. The study period lasted two years (July 1997-July 1999) and was divided into four sub-periods of six months each. In the first and third period the patients took only oral analgesics, if necessary; in the second and fourth period, an antioxidant regimen per os was added. This treatment consisted of sulphadenosyl-methionine (800 mg per day), Vitamin C (180 mg per day), Vitamin E (30 mg per day), Vitamin A (2,400 microg per day), and selenium (75 microg per day). RESULTS: Compliance of patients to the treatment schedule was satisfactory and no important side-effects were observed. Antioxidant treatment led to a significant reduction (p<0.05) in the number of days with abdominal pain experienced by the three patients and this was verified for both periods of treatment. Albeit, consumption of analgesics was lower in the antioxidant treatment periods. CONCLUSIONS: Oxidative stress may be one of the principle contributors to pain in hereditary pancreatitis and orally administered antioxidant treatment appears to be effective for control of the condition, in young patients, suffering from this rare disease.

Abdominal Pain↗

Chronic pancreatitis: relation to acute pancreatitis and pancreatic cancer.

The relationship between chronic pancreatitis (CP) and other pancreatic diseases, such as acute pancreatitis (AP) and pancreatic cancer (PK), remains a fairly debated question. The progression from alcoholic AP to CP is controversial, and some long-term epidemiological studies suggest that alcoholic CP might be the result of recurrent alcoholic AP (necrosis-fibrosis sequence) and a subgroup of alcoholics may present recurrent AP without progression to CP. Other predisposing factors (genetic, nutritional, environmental) seems to be important in inducing different outcomes of pancreatic damage due to alcohol. However, recurrent episodes of AP are clearly involved in pathophysiology of CP in patients with hereditary pancreatitis. A relationship between CP and subsequent PK development has long been suspected, but we actually don't know whether this association is direct or is the result of confounding factors, such as alcohol intake or cigarette smoking. Many issues should be considered as indicators of a causal association, and several of them are not fulfilled. Nonetheless, epidemiological studies (case-control or cohort studies) showed that the risk of PK is increased in patients with CP; the risk is significantly higher in tropical calcifying CP and hereditary pancreatitis. Studies on growth factors, oncogenes, tumor-suppressor genes, and angiogenesis suggest that the sequence PC-KP is plausible from the biological standpoint.

Acute Disease↗

[Pain in chronic pancreatitis: recent pathogenetic findings].

Pain is the major symptom in chronic pancreatitis. Its intensity frequently necessitates partial or complete pancreatectomy. The mechanisms of pain are not yet fully understood and, thereby, the therapeutic management is still controversial. Possible causes of pain include outflow obstruction with increased ductal and parenchymal pressure within the pancreas, and inflammatory involvement of intrapancreatic nerve fibres. Possible extrapancreatic causes are common bile duct and duodenal stenosis. The first theory has recently been substantiated by the demonstration of a definite relationship between intrapancreatic pressure, as measured intraoperatively, and intensity of pain. Infiltration of inflammatory cells around the nerves together with an increase in the number of nerve fibres in the fibrotic pancreatic tissue has been proposed as a possible cause of pain in chronic pancreatitis. Moreover, immunohistological studies have shown that the amount of neurotransmitters, such as substance P, is increased in afferent pancreatic nerves. Stenosis of the common bile duct and duodenum has been reported to be associated with severe abdominal pain. Common bile duct and duodenal stenosis in chronic pancreatitis may be caused by extension of fibrosis and active inflammation of the pancreas within the wall of duodenum and bile duct. This article updates the different pathogenetic mechanisms in pancreatic pain and the current therapeutic possibilities with their advantages and shortcomings.

Chronic Disease↗

[Hemorrhage in the Wirsung's duct caused by aneurysm of the splenic artery in chronic pancreatitis].

Two cases of haemorrhage from rupture of a splenic artery aneurysm into the pancreatic duct are reported. Both patients suffered from chronic pancreatitis; when haemorrhage appeared both patients experienced abdominal pain. In one patient the melaena was repetitive, in the other one--with a single episode of melaena - the endoscopy showed fresh blood near the papilla. In both patients ultrasonography and computerized tomography (CT) revealed a cystic mass in the pancreatic tail; CT scan also showed a clear contrast enhancement of these lesions after iodinated medium intravenous bolus. Coeliac arteriography confirmed the presence of two large saccular aneurysmal dilatation of the splenic artery. Both patients underwent a laparotomy: distal pancreatectomy with aneurysm resection and splenectomy were successfully performed.

Aortic Dissection↗

Gabexate mesilate in the treatment of acute pancreatitis.

Despite controversial experimental and clinical findings, the use of Aprotinin (A) in the treatment of acute pancreatitis (AP) is still widespread in our country. Compared to A, Gabexate Mesilate (FOY) should have the following advantages: lack of antigenicity, low molecular weight with better cellular penetrance, wide inhibitory spectrum (against phospholipase A2 too) and good tolerability. In order to verify the efficacy of FOY versus, we decided to carry out a prospective multicenter (34 centers) randomized double blind trial in moderate-severe AP with FOY 3g/day versus A 1,500,000 U.I.K./day infused for 7 days with central venous line. Based on standard clinical, biochemical and radiological data, 199 patients suffering from AP were enrolled to the study from January 1989 to December 1990. The main admission criteria were: onset of the disease from no more than 72 hours, at least 2 Ranson positive criteria and C.T. evidence of acute pancreatic damage. Seventeen no protocol patients were excluded. The Etiology in the 182 analyzed patients (106 male, 76 female; mean age 57.6 years, range 21-91) were: biliary 102 (56%), alcohol 47 (25.8%), post-operative 13 (7.1%), unknown causes 13 (7.1%) and others 7 (3.8%). Median Ranson's Score was 3. CT examination showed 66 AP with edema, while 116 cases (63.7%) were recognized as severe forms with pancreatic necrotic involvement of 30% of the gland in 71 (61.2%), 50% in 31 (26.7%), and more than 50% in 14 (12.1%). Out of 182 patients, 91 were treated with A and 91 with FOY. The two groups were comparable regarding the main prognostic factors.(ABSTRACT TRUNCATED AT 250 WORDS)

Acute Disease↗