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Query: UMLS:C0030305 (pancreatitis)
 16,014 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Patients with the acquired immunodeficiency syndrome (AIDS) can develop pancreatic disease from causes unrelated to AIDS as well as AIDS-specific lesions. AIDS-specific causes include opportunistic infection, AIDS-associated neoplasia, and medications used to treat complications of AIDS. Reported pancreatic opportunistic pathogens include Mycobacterium tuberculosis, Mycobacterium avium intracellulare, Cryptococcus neoformans, Candida, Aspergillus, Toxoplasma gondii, Pneumocystis carinii, cytomegalovirus, herpes simplex, cryptosporidium, and microsporidium. Although cytomegaloviral pancreatic infection can occur without clinically evident pancreatic disease, cytomegalovirus can cause pancreatitis. Other opportunistic infections that can cause pancreatitis include Toxoplasma gondii, Cryptococcus neoformans, and Candida. Mycobacterial infection can produce a pancreatic abscess. Hepatobiliary or pancreatic duct infection by cytomegalovirus, cryptosporidium, and microsporidium causes irregular ductular narrowing and dilatation. This cholangiographic abnormality resembles the pattern found in idiopathic sclerosing cholangitis. Reported AIDS-associated pancreatic neoplasms include Kaposi's sarcoma and lymphoma. Pancreatic involvement is usually part of widely disseminated tumor and rarely produces clinical symptoms. Pentamidine, trimethoprim-sulfamethoxazole, and 2', 3'dideoxyinosine are medications commonly used in AIDS patients which can cause pancreatitis. Pentamidine also causes hypoglycemia or hyperglycemia.
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PMID:Pancreatic disease in AIDS--a review. 822 89

The examination of 170 patients with chronic alcohol pancreatitis revealed diabetes mellitus (DM) in 21% of them. It manifested with polydipsia, polyuria and weight loss along with pancreatitis symptoms. DM complications were rare. Exercise tests were indicative of reduced insulin and glycagon reserves in the majority of the examinees. This condition depended on pancreatitis severity. DM in pancreatitis presents a high risk of hypoglycemia which should be taken into consideration when designing schemes of relevant treatment.
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PMID:[Diabetes mellitus in patients with chronic alcoholic pancreatitis]. 829 28

In order to analyse further the pathophysiology of pentamidine effects on blood glucose regulation, the following experimental models were established in rats: impairment of the renal function, bile duct ligation, inhibition of the P450 cytochrome enzyme system. In otherwise intact rats, 7.5 mg/day pentamidine was well tolerated whereas doses of 15 mg/day induced severe, relapsing and eventually lethal hypoglycaemia within a few days. Induction of a renal insufficiency of graded severity by treatment with gentamycin, subtotal nephrectomy and total bilateral nephrectomy resulted in repetitive, severe (sometimes lethal) hypoglycaemia, alternating with hyperglycaemia, glucosuria and ketonuria in pentamidine-treated rats (7.5 mg/d). No long-standing insulin-dependent diabetes was observed. In the dysglycemic animals, plasma insulin levels were inappropriate to the concomitant glycaemia; no stimulation was obtained by i.v. glucose. Glucagon levels were higher than normal, suppressible by i.v. glucose, responsive to IV arginine and to hypoglycaemia. Dysglycemic events were more frequent and marked in the rats with the most severe renal functional derangement. They were more frequent in the rats treated with pentamidine mesylate than in those treated with the isethionate salt. Control uremic rats (free of pentamidine) remained euglycaemic. The islets of Langerhans displayed severe vascular congestion and degranulation and necrosis of the B cells, while the non B cells (and particularly the A cells) were intact. Exocrine pancreatitis was occasionally observed in the most severely uremic rats. In contrast with uremic rats, neither surgical ligation of choledocus, nor treatment by P450 cytochrome inhibitors (particularly ketoconazole) precipitated dysglycaemia in the pentamidine-treated rats. These experimental data: 1) strengthen the concept of inappropriate insulin release from pentamidine-lesioned islet B cells due to pentamidine accumulation; 2) indicate a predominant role for renal insufficiency in determining the accumulation of this drug; 3) emphasize the clinical importance of renal insufficiency as a risk factor for pentamidine-induced dysglycaemia. Association with ketoconazole does not appear to be a risk factor.
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PMID:Pentamidine-induced dysglycaemia: experimental models in the rat. 833 59

A hemodialysed patient with abdominal pain, severe lactic acidosis and prolonged hypoglycemia is described. The diagnosis of acute necrotizing pancreatitis was delayed and the patient died from both systemic and peripancreatic complications of the acute pancreatitis. The article deals with the problem of diagnosing acute pancreatitis in an end-stage renal failure (ESRF) patient; on the possible surgical options open to the physician in the management of acute pancreatitis and on a pathophysiological explanation behind both the lactic acidosis and hypoglycemia in this patient.
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PMID:Acute necrotizing pancreatitis, lactic acidosis and prolonged hypoglycemia in a hemodialysed patient--a logical but unfortunately fatal combination. 879 36

We describe a two-year-old girl who presented with coma following an upper respiratory tract infection. Nonketotic hypoglycemia, metabolic acidosis and mild hyperammonemia were detected. The urinary organic acid profile was consistent with glutaric aciduria type II. Pancreatitis was diagnosed at autopsy. Although pancreatitis has been described in a number of inborn errors of metabolism including organic acidemias, to the best of our knowledge this is the first report of acute pancreatitis occurring in glutaric acidemia type II. It was stressed, therefore, that this complication should be searched for in organic aciduria patients, and the measurement of plasma amylase and lipase levels should be added to the battery of laboratory investigations in such cases.
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PMID:Acute pancreatitis in a patient with glutaric acidemia type II. 933 18

Necrolytic migratory erythema is characterized by waves of irregular erythema in which a central bulla develops, and subsequently erodes and becomes crusted. It usually occurs in patients with an alpha-islet cell tumor of the pancreas. However, necrolytic migratory erythema has also been observed in patients without an associated glucagonoma. We describe a woman with iatrogenic necrolytic migratory erythema. She received intravenous glucagon for hypoglycemia associated with an insulin-like growth factor II-secreting hemangiopericytoma. After chemotherapy, she developed necrolytic migratory erythema. The characteristics of the previously reported patients with nonglucagonoma-associated necrolytic migratory erythema are reviewed. In patients with nonglucagonoma-associated necrolytic migratory erythema, the dermatosis-related conditions most commonly observed were celiac disease or malabsorption, cirrhosis, malignancy, and pancreatitis; less common conditions included hepatitis, inflammatory bowel disease, heroin abuse, and odontogenic abscess. Although the pathogenesis of necrolytic migratory erythema remains unknown, hyperglucagonemia appears to have had a causative role in the development of this dermatosis in our patient. Patients who develop necrolytic migratory erythema should be evaluated for the presence of a glucagonoma; if a glucagonoma is ruled out, evaluation for other conditions known to occur with necrolytic migratory erythema, such as liver disease, malabsorptive disorders, and nonislet-cell tumors is warranted.
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PMID:Iatrogenic necrolytic migratory erythema: a case report and review of nonglucagonoma-associated necrolytic migratory erythema. 959 6

Coxsackievirus infection causes severe pancreatitis and myocarditis in humans, often leading to death in young or immunocompromised individuals. In susceptible strains of mice, coxsackievirus strain CB4 causes lethal hypoglycemia. To investigate the potential of gamma interferon (IFN-gamma) in protection and clearance of the viral infection, IFN-gamma knockout mice and transgenic (Tg) mice specifically expressing IFN-gamma in their pancreatic beta cells were infected with CB4. Lack of IFN-gamma in mice normally resistant to CB4-mediated disease resulted in hypoglycemia and rapid death. However, expression of IFN-gamma in the beta cells of Tg mice otherwise susceptible to lethal infection allowed for survival and protected them from developing the accompanying hypoglycemia. While all the mice had high levels of viral replication in their pancreata and comparable tissue pathology following viral infection, the Tg mice had significantly lower levels of virus at the peak of infection, significantly higher numbers of activated macrophages before and after infection, and less damage to their acinar tissue. Additionally, despite having increased levels of inducible nitric oxide synthetase (iNOS) expression, treatment of Tg mice with the iNOS inhibitor aminoguanidine did not alter the level of protection afforded by IFN-gamma expression. In conclusion, IFN-gamma protects from lethal coxsackievirus infection by activating macrophages in an iNOS-independent manner.
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PMID:Protection from lethal coxsackievirus-induced pancreatitis by expression of gamma interferon. 997 52

We report a case of nesidioblastosis in a 66-year-old man with chronic alcohol-induced pancreatitis manifested by attacks of hypoglycemia for several years. The state of the patient improved after subtotal pancreatectomy.
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PMID:Nesidioblastosis in an adult man--case report. 1041 74

In the majority of patients suffering from chronic pancreatitis an endocrine pancreatic insufficiency is correlated with exocrine dysfunction. The prevalence of impaired or diabetic glucose tolerance is 40-70%, half of these patients suffer from an insulin-dependent diabetes mellitus. In general the probability of endocrine insufficiency progressively increases within the ten years following diagnosis of chronic pancreatitis. Onset and severity of the endocrine dysfunction depend on parenchymal destruction of the pancreas but are also influenced by ongoing alcohol consumption. Pathological findings in the endocrine pancreas are a loss of B-cells with decrease in secretion of insulin but also a loss of B-cell responsiveness to glucose by impaired perisinusoidal diffusion. Disturbances of the enteroinsulinar axis with diminished levels of incretins due to an exocrine insufficiency are also discussed. In addition, an impaired A-cell function may be important, that is characterized by diminished levels of stimulated glucagon. Increased plasma levels of somatostatin were found, the source of which is unknown. The susceptibility to severe hypoglycemia in patients with diabetes mellitus secondary to chronic pancreatitis is higher than in Type I diabetics. This is mainly caused by the impaired glucagon secretion but also influenced by malnutrition and concomitant hepatic dysfunction due to the toxic affect of alcohol. Diagnostic procedures are the measurement of C-peptide-concentrations and profiles of blood glucose after fasting and stimulation with L-arginine or glucose. Especially in the beginning of the endocrine insufficiency the determination of basal levels of blood glucose or C-peptide are not useful. Unless treatment by diet is effective, the therapy of diabetes secondary to chronic pancreatitis should be done by insulin replacement. A certain degree of hyperglycemia may be tolerated due to the risk of hypoglycemia and the persistent alcohol consumption in these patients. Intensified insulin therapy should only be done in selected patients with good compliance. Long-term complications in patients with pancreatogenic diabetes are comparable to diabetes Type I and largely depend on the duration of the diabetes. Life expectancy is reduced, death in these patients is mainly due to persistent alcohol and nicotine abuse (cardiovascular disease, malignant tumors, etc.), in only a minority pancreatitis or diabetes (mainly hypoglycaemia) are relevant risk factors.
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PMID:[Secondary diabetes in chronic pancreatitis]. 1044 9

Many animals with diabetes mellitus are severely ill on clinical presentation. The spectrum of disease is quite variable and includes diabetic ketoacidosis (DKA), ketosis without acidosis, hyperosmolar nonketotic syndrome (HNKS), and other nonketotic variants (negative urine ketones, serum osmolality < 340 mOsm/kg with or without acidosis). These more severe forms of diabetes are often precipitated by concurrent diseases such as pyelonephritis, pancreatitis, pyometra, hyperadrenocorticism, renal failure, and heart failure. To make matters worse, in-hospital treatment of diabetic dogs and cats is commonly associated with serious complications, including hypoglycemia, hypokalemia, and hypophosphatemia.
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PMID:Complications and concurrent disease associated with diabetes mellitus. 1088 75


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