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)

In a review of pediatric autopsies from 1951 to 1985, we identified 40 cases in which pancreatitis was diagnosed pathologically. Twenty-six of these patients were under 4 years of age, and the male-to-female ratio was 1.5. Six groups of patients were identified: 10 with hepatobiliary disease, including 9 with biliary atresia; 7 with immunosuppressive therapy for tumors (n = 2), leukemia (n = 4) and aplastic anemia (n = 1); 6 with viral infections; 8 with congenital anomalies, including congenital heart disease (n = 3); and 9 with miscellaneous problems. Several patients had surgery and various intercurrent complications. Clinical features attributable to the pancreatitis included vomiting or excessive nasogastric drainage (60%), pleural effusions (40%), and abdominal pain (25%). However, the diagnosis was suspected clinically in only 5 of 40 patients. Our findings suggest several pathogenic mechanisms exist for childhood pancreatitis: biliary obstruction, infections, drug toxicity, immunosuppression (acting in synergy with drug toxicity, trauma, and low-flow states resulting from shock, heart failure, and vasculopathy.
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PMID:Clinicopathologic studies in childhood pancreatitis. 334 10

Excluding the most frequent kinds of problems seen with the nonsteroidal antiinflammatory drugs (NSAID)--gastritis, peptic ulceration and renal effects--published reports indicate that these drugs may cause a wide variety of rare adverse reactions. The most serious of these are hypersensitivity reactions: blood dyscrasias (aplastic anemia, thrombocytopenia, agranulocytosis, hemolytic anemia), erythema multiforme and hepatitis. Aseptic meningitis and anaphylactoid reactions may strike patients with underlying immunologic abnormalities; urticaria, bronchospasm and proctocolitis may affect aspirin-sensitive patients. Other unusual reactions include several kinds of bullous dermatitis, febrile reactions, pneumonitis, esophageal ulceration, parotitis, pancreatitis and neurological or psychological effects.
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PMID:Rare adverse reactions to nonsteroidal antiinflammatory drugs. 398 96

Fanconi's anaemia (FA) is a hereditary disease transmitted in a recessive manner, characterized by congenital malformations and bone marrow aplasia. A high rate of chromosome breakage is observed in mitoses of cultured blood cells, but the caryotypes are normal. Forty-four patients (27 boys and 17 girls) were followed in the same department between 1962 and 1976. Most were treated with androgens, sometimes combined with corticosteroids. Nine patients died of acute granuloblastic leukaemia, with more than 25% bone marrow blasts; in three of these, cytogenetic examination showed clonal anomalies. Five patients were in preleukaemic state with non-blastic bone marrow; 4 showed clonal anomalies and 2 of these died of aplasia; the 5th patient had gross liver and spleen enlargement and died of haemorrhage. Among the 30 remaining patients 12 are still alive and 18 died of cerebral haemorrhage (7), hepatic failure (3), cardiac failure (1), pancreatitis (1), septicaemia (2) or graft-versus-host reaction after bone marrow transplantation. One patient transplanted 4 years ago has complete chimerism and is still alive without treatment. The incidence of leukaemic or preleukaemic state in this series was 30%, while no case of leukaemia was observed in 200 patients with acquired aplastic anaemia. Neither parents norsibship had leukaemia. Androgen treatment apparently did not increase the risk of leukaemia which developed within 1 to 13 years (mean = 5 years) of the diagnosis, was preceded by a 2 1/2 year long preleukaemic state with clonal chromosomal anamolies and invariably was of the granulocytic type. None of the patients developed cancer. The median survival in this series was 4 1/2 years.
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PMID:[Fanconi's anemia. Incidence of its development into leukemia]. 622 98

The study was conducted on 75 multitransfused children aged between 2 and 13 years who attended the Department of Paediatrics, LNJPN Hospital, New Delhi from July 1990 to July 1991. These included 64 cases of thalassaemia major, 4 cases of haemophilia, 3 patients of acute lymphatic leukaemia and one each of acute myeloid leukaemia, aplastic anemia, chronic idiopathic thrombocytopenic purpura and acute haemorrhagic pancreatitis. HBsAg was tested in all, Anti-HBc was tested in 44 patients and Anti-HCV in 43 patients. Anti HDV was tested in HBsAg positive patients and IgM anti-HAV was tested in patients suffering from hepatitis. Liver function tests were evaluated in all patients. HBsAg was positive in 31% of patients; 40% of males and 15% of females were HBsAg positive, the difference being statistically significant. 84% of patients were Anti-HBc positive, 21% were anti HCV positive, 4% were Anti HDV positive. 15% of the patients had post transfusion hepatitis. Anti HCV was present in 57% of the hepatitis patients; none had anti-HAV IgM.
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PMID:Hepatitis B and hepatitis C in multitransfused children. 964 Oct 34

In childhood, aplastic anemia is a rare disease of unknown etiology. Besides toxic effects, also an infectious or an autoimmune origin are discussed. We report on an 8-year-old boy with very severe aplastic anemia (VSAA) who developed pancreatitis together with panniculitis. Initially, active cytomegalovirus (CMV) infection was thought to be possibly contributive. Ganciclovir was tried resulting in clearance of CMV, but VSAA persisted. Two months after the onset of VSAA, oligosymptomatic pancreatitis was observed together with the onset of severe febrile panniculitis, occurring with multiple painful enlarged subcutaneous infiltrates of up to 7 cm in diameter. Treatment according to the Severe Aplastic Anemia-94 (SAA-94) protocol consisting of glucocorticoids, cyclosporin A (CsA), anti-thymocyte globulin and granulocyte colony-stimulating factor was instituted. Since this treatment did not lead to remission after day 110, escalation of the CsA dose up to 8 mg/kg body weight was tried. This regimen resulted in complete recovery of panniculitis and symptoms of pancreatitis. Incomplete hematological remission was reached and, to date, the patient has not required transfusions for 6 months. Because this boy suffered simultaneously from three rare disorders, which all responded to intense immunosuppression, this observation may underline common autoimmune mechanisms of these distinct diseases.
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PMID:Panniculitis, pancreatitis and very severe aplastic anemia in childhood: a challenge to treat. 1113 23

The chief dangers reported with some common drugs are reviewed. Hazards of antibiotic therapy include: the increasing incidence of sensitization to penicillin with occasional anaphylactic reactions; aplastic anemia with chloramphenicol, and the poor tolerance of infants for chloramphenicol; staphylococcal enterocolitis; unnecessary "prophylactic" use of antibiotics. Thiazide diuretics may precipitate potassium depletion, skin reactions, pancreatitis, blood dyscrasias, gout, diabetes mellitus and hepatic coma. Reserpine can increase gastric acidity, induce mental depression, and when used with digitalis lead to ventricular premature beats. Hydralazine may aggravate angina pectoris, cause tachycardia, and bring about a syndrome resembling disseminated lupus erythematosus. Guanethidine may result in loose stools, impotence, and postural hypotension. Hazards of phenothiazines include jaundice, parkinsonian states and tremors, convulsions, hypotension, and blood dyscrasias. The butanediols have numerous side effects including gastrointestinal, cutaneous and hypotensive reactions. Prolonged corticosteroid therapy introduces a new danger in surgical treatment. The progesterone-like drugs may induce masculinization of the female fetus.
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PMID:Dangers in the use of some potent drugs. 1398 37

To identify risk factors associated with the development of diabetes mellitus and to describe the prevalence of diabetes in pediatric hematopoietic cell transplant (HCT) survivors. The follow-up records of 748 patients who survived for at least 2 years after pediatric HCT were retrospectively reviewed for diagnosis of diabetes. Risk factors for type 2 diabetes were analyzed using multivariate statistics. Among 748 patients with a median of 11 years of follow-up, 38 developed diabetes after HCT. Four patients (three leukemia and one neuroblastoma) developed type 1 diabetes 8 to 14 years after HCT, at between 10 and 19 years of age. Thirty-four patients (32 leukemia and 2 aplastic anemia) developed type 2 diabetes 1 to 24 years after HCT, at between 11 and 41 years of age. Of the 34 patients with type 2 diabetes, 23 were non-Hispanic white, 3 had experienced asparaginase toxicity (hyperglycemia and/or pancreatitis), and 26 had a family history of diabetes. Risk factors associated with type 2 diabetes were diagnosis of acute or chronic leukemia, race/ethnicity other than non-Hispanic white, family history of diabetes, and asparaginase toxicity. The prevalence of type 1 diabetes among all surviving patients was 0.52%, or three times higher than the general U.S. population. The prevalence of type 2 diabetes was 9% among leukemia survivors and 2% among aplastic anemia survivors, both higher than expected. Pediatric HCT survivors are more likely to develop diabetes than the general population.
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PMID:Diabetes mellitus in long-term survivors of pediatric hematopoietic cell transplantation. 1476 93