Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0030305 (pancreatitis)
 16,014 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Most antiviral drugs are nucleoside analogues with potential teratogenic, embryotoxic, carcinogenic and antiproliferative activities. They must be administered with caution during pregnancy, because some are known teratogens (e.g. amantadine) and a similar propensity cannot be entirely excluded for others (e.g. aciclovir). Their adverse effects mostly involve bone marrow depression (e.g. granulocytopenia with ganciclovir, anaemia with zidovudine) or neurotoxicity (e.g. seizures with interferon-alpha, peripheral neuropathy with zalcitabine), although gastrointestinal effects are also seen. Idiosyncratic reactions include didanosine-induced acute pancreatitis. Only inosine pranobex is largely free from toxicity. Idoxuridine must be administered topically, given the severity of its systemic adverse effects. Drug interactions involving antiviral agents mostly reflect shared toxicity with other agents (e.g. neutropenia with ganciclovir and zidovudine, pancreatitis with didanosine and alcohol), although renal excretion or hepatic metabolism may be implicated. Given the possibility of severe adverse reactions and drug interactions, antiviral chemotherapy should only be used for potentially serious virus infections. Topical administration avoids systemic adverse effects but not mutagenic risks, and may result in exposure of individuals other than the patient (e.g. aerosolised ribavirin).
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PMID:Adverse effects and drug interactions of clinical importance with antiviral drugs. 801

We reported a case of acute pancreatitis occurring during administration of valproic acid for epilepsy. About four years prior to the first onset of acute pancreatitis, treatment with valproic acid for his seizures was started. The first pancreatitis improved by conservative therapy within a week. He continued valproic acid after the first episode. Two months later, the second acute pancreatitis occurred. The second episode was complicated with disseminated intravascular coagulation, but responded to conservative therapy. After the second episode, the valproic acid was discontinued and pancreatitis has not recurred. Pancreatitis associated with valproic acid may be severe, and therefore valproic acid should be used with caution.
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PMID:[A case of acute pancreatitis during administration of valproic acid]. 839 36

A 5-year-old mentally retarded child developed laboratory evidence of pancreatitis during accidental acute carbamazepine (CBZ) intoxication. He had been seizure-free with CBZ for 4 years for a seizure disorder with no obvious toxicity. CBZ had been discontinued 5 months before he was admitted to the hospital. After he accidentally ingested a CBZ overdose, he was found vomiting and lethargic. Serum amylase and lipase levels were increased for several days. With supportive treatment and no CBZ, he recovered and serum amylase and lipase levels returned to normal. No other causes of pancreatitis were identified. Therefore, most likely the chemical pancreatitis was associated with the acute CBZ intoxication.
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PMID:Acute chemical pancreatitis associated with carbamazepine intoxication. 842 54

Alpers' syndrome is a progressive neurodegenerative disorder with liver disease that usually presents in the first few years of life. Only rarely have patients presented later in life with delayed onset of Alpers' syndrome. Herein we present a case of a 17-year-old male with a progressive 8-month course of severe headaches, multiple stroke-like episodes with visual deficits, and seizures that concluded with acute hemorrhagic pancreatitis. Neuropathological findings were characteristic for Alpers' syndrome: neurodegeneration and astrogliosis of the occipital cortices including the striate cortices, similar but less advanced changes in the parietal cortices, right Ammons horn sclerosis, degeneration of the posterior columns, and mild cerebellar Purkinje cell loss. Examination of the liver revealed extensive centrilobular hepatocyte necrosis. Skeletal muscle did not contain ragged red fibers, nor were there mitochondrial DNA point mutations characteristic for mitochondrial encephalomyopathy, lactic acidosis, and stroke-like episodes (MELAS).
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PMID:Alpers' syndrome presenting with seizures and multiple stroke-like episodes in a 17-year-old male. 860 37

We present a case of acute lethal poisoning by oil of "epazote" (oil of chenopodium), in a 2 y 9 m female. The volatile oil was administered according to the advice of a "curandera" (female healer), in a total quantity of 40 ml. Clinical features of the poisoning were: vomiting, deep coma, seizures, mydriasis, apnea, metabolic acidosis, neurogenic shock and death. The EEG suggested a diffuse encephalopathy, the CT scan with an image of severe brain edema and ventricular collapse. Relevant postmortem findings were brain edema and neuronal necrosis, pneumonia, enteritis, pericholangitis, mild pancreatitis and tubular necrosis. The phytochemical analysis of volatile oil identified ascaridol, the main active compound of the chenopodium herbs, in a quantity of 39 mg/ml (1,560 mg in the dose administered), and Chenopodium graveolens as the plant employed to prepare it. According to the age of the patient, 60 mg of ascaridol would be the recommended dose formerly used in the treatment of parasitic disease. Thus 1,560 mg was 26 times higher than the recommended dose, and exceeded by 56% the dose of 1,000 mg reported as lethal in humans.
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PMID:[Fatal poisoning caused by oil of epazote, Chenopodium graveolens]. 896 84

Although heavy alcohol intake is known to be one of the most common causative factors of liver disease, pancreatitis, upper gastrointestinal and neurological disorders, the influence of the drinking pattern is largely unknown. The study investigated the relationship of alcohol-related medical disorders in alcoholics and their drinking pattern. Two hundred and forty-one chronic alcoholics were referred consecutively for detoxification and their drinking pattern was sufficient for them to be included in this study. History of alcohol abuse as well as drinking behaviour in the last 6 months were assessed by a semi-structured interview. Findings included intensive clinical examination with abdominal ultrasound in most subjects. Heavy drinking with frequent inebriation was most often found in our sample (44.4%), whereas continuous heavy alcohol consumption without intoxication (33.6%), and an episodic drinking style (22.0%) were less frequent. The heavy drinkers suffered more often from pancreatitis, oesophageal varices, polyneuropathy or erectile dysfunction than episodic drinkers. They also showed more upper gastrointestinal disorders, although the estimated life-time alcohol intake was comparable to continuous drinkers. No difference relating to withdrawal delirium or seizures could be found between the groups of alcoholics. Frequent heavy drinkers showed a trend to more alcohol-related medical disorders than alcoholics with a different drinking pattern, although they were younger and their estimated life-time alcohol intake was comparable to that of continuous drinkers. Thus, the drinking pattern, particularly frequent inebriation, has an influence on the occurrence of alcohol-related disorders.
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PMID:Drinking pattern and alcohol-related medical disorders. 1041 7

We present a rare case of acute pancreatitis associated with temporal lobectomy due to intractable seizure in a 23-year-old man. The patient underwent elective right temporal lobectomy and hippocampectomy. Severe upper abdominal pain occurred just 10 hours after surgery. The diagnosis of acute pancreatitis was based on the elevation of serum amylase and lipase levels, and the findings of abdominal computerized tomography. Other possible causative factors of acute pancreatitis including alcohol, biliary tract stone, hypertriglyceridemia, hypercalcemia, hyperparathyroidism, biliary dysmotility and autoimmune disease were excluded by a series of examinations. The possibility of drug-induced pancreatitis was very low in this patient. The patient was discharged after supportive treatment. No recurrence of seizure or abdominal pain was noted in the three months after discharge. Acute abdominal pain after brain surgery deserves clinical evaluation for acute pancreatitis.
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PMID:Acute pancreatitis associated with temporal lobectomy and intractable seizure. 1074 19

Despite limited understanding of therapeutic aetiopathogenesis of ulcerative colitis and Crohn's disease, there is a strong evidence base for the efficacy of pharmacological and biological therapies. It is equally important to recognise toxicity of the medical armamentarium for inflammatory bowel disease (IBD). Sulfasalazine consists of sulfapyridine linked to 5-aminosalicylic acid (5-ASA) via an azo bond. Common adverse effects related to sulfapyridine 'intolerance' include headache, nausea, anorexia, and malaise. Other allergic or toxic adverse effects include fever, rash, haemolytic anaemia, hepatitis, pancreatitis, paradoxical worsening of colitis, and reversible sperm abnormalities. The newer 5-ASA agents were developed to deliver the active ingredient of sulfasalazine while minimising adverse effects. Adverse effects are infrequent but may include nausea, dyspepsia and headache. Olsalazine may cause a secretory diarrhoea. Uncommon hypersensitivity reactions, including worsening of colitis, pancreatitis, pericarditis and nephritis, have also been reported. Corticosteroids are commonly prescribed for treatment of moderate to severe IBD. Despite short term efficacy, corticosteroids have numerous adverse effects that preclude their long term use. Adverse effects include acne, fluid retention, fat redistribution, hypertension, hyperglycaemia, psycho-neurological disturbances, cataracts, adrenal suppression, growth failure in children, and osteonecrosis. Newer corticosteroid preparations offer potential for targeted therapy and less corticosteroid-related adverse effects. Azathioprine and mercaptopurine are associated with pancreatitis in 3 to 15% of patients that resolves upon drug cessation. Bone marrow suppression is dose related and may be delayed. The adverse effects of methotrexate include nausea, leucopenia and, rarely, hypersensitivity pneumonia or hepatic fibrosis. Common adverse effects of cyclosporin include nephrotoxicity, hypertension, headache, gingival hyperplasia, hyperkalaemia, paresthesias, and tremors. These adverse effects usually abate with dose reduction or cessation of therapy. Seizures and opportunistic infections have also been reported. Antibacterials are commonly employed as primary therapy for Crohn's disease. Common adverse effects of metronidazole include nausea and a metallic taste. Peripheral neuropathy can occur with prolonged administration. Ciprofloxacin and other antibacterials may be beneficial in those intolerant to metronidazole. Newer immunosuppressive agents previously reserved for transplant recipients are under investigation for IBD. Tacrolimus has an adverse effect profile similar to cyclosporin, and may cause renal insufficiency. Mycophenolate mofetil, a purine synthesis inhibitor, has primarily gastrointestinal adverse effects. Biological agents targeting specific sites in the immunoinflammatory cascade are now available to treat IBD. Infliximab, a chimeric antibody targeting tumour necrosis factor-or has been well tolerated in clinical trials and early postmarketing experience. Additional trials are needed to assess long term adverse effects.
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PMID:Comparative tolerability of treatments for inflammatory bowel disease. 1108 48

Nucleoside analogues represent the cornerstones of antiretroviral regimens. A range of drug- or tissue-specific toxicities, such as peripheral neuropathy, myopathy, pancreatitis and lactic acidosis with hepatic steatosis, has been documented with these agents. The fat atrophy seen on long term antiretroviral therapy may also be related to nucleoside analogues. The mechanisms by which nucleoside analogues cause toxicity are not clearly established. In vitro, the triphosphates of these agents are weak to modest substrates for human DNA polymerases, showing the greatest affinity for mitochondrial DNA polymerase gamma. Short term exposure in vitro to some nucleoside analogues has been demonstrated to cause increased lactate production or falls in mitochondrial DNA suggestive of mitochondrial toxicity. However, stavudine and to a lesser extent zidovudine are poor substrates for mitochondrial thymidine kinase type 2, the predominant form in cells that are not actively mitotic such as neurons, myocytes and adipocytes. These are the cell types where the proposed mitochondrial toxicities neuropathy, myopathy and lipoatrophy are observed. Thus, active concentrations of phosphorylated products of stavudine and zidovudine may not be present in mitochondria. The familial mitochondrial diseases do not have identical presentations to nucleoside analogue toxicities. These disorders most commonly involve the CNS, typically with seizures or dementia, and occasionally the kidneys. Although nucleoside analogues are known to penetrate the CNS and are commonly renally excreted unchanged, mitochondrial toxicities at these sites have not been documented. Furthermore, toxicity caused by nucleoside or nucleotide analogues does not always appear to arise through the mitochondrial route. Cidofovir appears to cause renal tubular dysfunction via a toxic intracellular metabolite, and zidovudine-related anaemia appears to be related to decreased globin RNA synthesis. In vitro or animal models suggest that zidovudine myopathy, stavudine-related (but not zalcitabine- or didanosine-related) neuropathy and didanosine-related pancreatitis may all be not related, or not exclusively related, to mitochondrial dysfunction. The integration of nucleoside analogues into nuclear DNA, best documented with zidovudine but likely to occur with other agents, represents an alternative but potentially delayed pathway to cytotoxicity and cell apoptosis. This is the mechanism of cell death during therapy with antineoplastic nucleoside analogues, and may have contributed to the multisystem toxicities observed with the anti-hepatitis B drug fialuridine. New research evaluating the effects of long term exposure of cell lines is required to address the possibility that nuclear genotoxicity plays a role in long term nucleoside analogue toxicity.
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PMID:Toxicity of antiretroviral nucleoside and nucleotide analogues: is mitochondrial toxicity the only mechanism? 1114 57

We report the first case to our knowledge of chronic pancreatitis associated with mitochondrial encephalopathy with the A8344G mitochondrial DNA (mtDNA) mutation. This 10-year-old-girl had suffered from recurrent abdominal pain with elevated serum amylase and lipase since the age of 6, and easy fatigability, tremor and astatic seizures since the age of 8. A biopsy of quadriceps muscle revealed ragged-red-fibers and cytochrome c oxidase deficiency. Analysis of mtDNA in peripheral blood identified an A8344G mutation in the mitochondrial tRNA(Lys) gene. Taken together with physical signs of myoclonic seizures and cerebellar dysfunction, we diagnosed her as myoclonic epilepsy with ragged-red fibers associated with chronic pancreatitis. Although no association between mitochondrial disease and pancreatitis has yet been established, this case suggests it is necessary to consider the participation of mitochondrial abnormality in the pathogenesis of recurrent pancreatitis.
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PMID:A case of MERRF associated with chronic pancreatitis. 1129 46


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