Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
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.
 ...
PMID:Pancreatic disease in AIDS--a review. 822 89

One hundred and fifty-one patients intolerant to zidovudine (AZT) received didanosine (ddI) to a maximum dose of 12.5 mg/kg/day. Patient response was assessed using changes in CD4+ lymphocyte subset count, HIV p24 antigen, weight, and quality of life. Seventy patients developed major opportunistic infections whilst on therapy; this was the first AIDS diagnosis in 17. Only minor changes in CD4+ lymphocyte subset count were observed in AIDS patients, although a more significant rise occurred in those with earlier stages of disease. Of those positive for p24 antigen at the commencement of the study 67% showed a positive response, and this was most likely in those with CD4+ lymphocyte subset counts above 100 mm3. A positive weight response was seen in 16% of patients. Most patients showed improvement in individual parameters and global score of quality of life. Adverse reactions possibly attributable to didanosine were common. The most common side-effect was diarrhoea, which resulted in cessation of therapy in 19 individuals. Peripheral neuropathy occurred in 12 patients and pancreatitis in six. Thirteen patients developed a raised serum amylase without abdominal pain. Seven patients developed glucose tolerance curves characteristic of diabetes but these were mild, did not require treatment and returned to normal on ceasing didanosine.
 ...
PMID:The use and toxicity of didanosine (ddI) in HIV antibody-positive individuals intolerant to zidovudine (AZT) 832 44

This phase 1 trial was conducted to evaluate the safety and tolerance of didanosine (ddI) in subjects with AIDS or AIDS-related complex (ARC) who previously had demonstrated hematologic intolerance of zidovudine. Thirty subjects, 21 with AIDS and nine with ARC, were enrolled. Initially, didanosine was administered orally twice daily for a total daily dose of either 750 mg or 1,500 mg. Subsequently, the dosage for those receiving 1,500 mg/d was reduced to a maximum of 750 mg/d (375 mg twice daily) when data from this and other phase 1 studies showed that the dosage of 1,500 mg/d (750 mg twice daily) was associated with an unacceptable risk of developing neuropathy. The subjects were studied for 46 weeks (mean time; range, 7-122 weeks). The dose-limiting toxic effect observed was peripheral neuropathy, which occurred in eight patients. Other significant toxic effects included pancreatitis in three patients and xerostomia in eleven. In general, didanosine was well tolerated from a hematologic standpoint by the majority of patients during prolonged administration.
 ...
PMID:Long-term follow-up of didanosine administered orally twice daily to patients with advanced human immunodeficiency virus infection and hematologic intolerance of zidovudine. 842 19

Didanosine (ddI) is a purine analogue that demonstrates in vitro anti-human immunodeficiency virus (HIV) activity, effects on the surrogate markers CD4+ T-lymphocytes and p24 antigen, and has adequate oral bio-availability. Recently, 500 mg/day of ddI in sachet form demonstrated clinical effectiveness compared with zidovudine (ZDV) for delaying HIV disease progression in patients with AIDS or AIDS related complex (ARC) and less than 300 CD4+ T-lymphocytes, or asymptomatic individuals with less than 200 CD4+ T-lymphocytes. All patients tolerated a minimum of 16 weeks of prior ZDV treatment. ddI treatment was associated with an increase in serum amylase and pancreatitis, however, there was no significant difference in the incidence of pancreatitis between the 500 mg ddI and ZDV groups. There was significantly more hematologic toxicity associated with ZDV and no difference between ddI and ZDV groups with respect to peripheral neuropathy. ddI is presently available in tablet form with 125% the bioavailability of the sachet form of ddI; therefore, the 500-mg sachet formulation corresponds to a 400-mg daily tablet dose of ddI. Future studies of ddI will involve ddI's effects on antiretroviral naive patients and the potential of combining ddI with other agents.
 ...
PMID:New developments in the clinical use of didanosine. 842 1

Extraneural manifestations of toxoplasmosis often are not recognized antemortem in patients with AIDS. We describe a patient who was seropositive for human immunodeficiency virus and presented with lethargy, abdominal tenderness, rapidly progressive ventilatory failure, rhabdomyolysis, myoglobinuria, and disseminated intravascular coagulation. Although the diagnosis of pancreatitis was not considered while the patient was alive, an autopsy demonstrated pancreatic necrosis associated with toxoplasmal cysts. No other infection was evident. This case suggests that Toxoplasma gondii can cause severe pancreatitis in patients with AIDS.
 ...
PMID:Necrotizing pancreatitis and multisystem organ failure associated with toxoplasmosis in a patient with AIDS. 845 54

Acute pancreatitis in HIV-infected patients with or without AIDS has been reported with increasing frequency over the past several years. Drugs used to treat HIV-infected patients are often the cause. We report a case of a 46-year-old HIV-infected man who presented to the emergency department with abdominal pain and was diagnosed with acute pancreatitis. The patient had recently begun taking 2',3'-dideoxyinosine (ddI). He died shortly after admission to the hospital; CT scan and autopsy confirmed the cause of death as hemorrhagic pancreatitis. We briefly review the literature on the incidence and severity of pancreatitis in association with ddI and pentamidine therapy.
 ...
PMID:Fatal pancreatitis as a complication of therapy for HIV infection. 853 Jul 81

Microsporidia are ubiquitous, obligate intracellular protozoan parasites increasingly detected as opportunistic pathogens in AIDS patients. These parasites have been associated with chronic diarrhoea, hepatitis, cholangitis, pancreatitis, enteritis, keratoconjunctivitis, and peritonitis in either homosexuals or heterosexuals. Optimum diagnostic and therapeutic measures of these pathogens still elude both clinicians and researchers. Further study is required to elucidate the exact prevalence and clinical characteristics of microsporidia.
 ...
PMID:Microsporidium in AIDS patients: a perspective. 862 69

This study evaluated the efficacy of switching to didanosine in patients who were clinically or immunologically progressing despite zidovudine therapy. This multicenter, open-label study involved 400 patients with the acquired immunodeficiency syndrome (AIDS) or AIDS-related complex (ARC), who had tolerated zidovudine for at least 12 weeks and had signs of clinical or immunological disease progression. They were randomly assigned to receive 600 mg/d of zidovudine (n=133), 500 mg/d of didanosine (n=131), or 200 mg/d of didanosine (n=136). The primary end point was a new AIDS-defining event or death. The study was prematurely terminated, after the first interim analysis, mainly owing to results of two controlled studies demonstrating that a change to didanosine was associated with an improved outcome in patients with advanced HIV-1 disease. The median duration of follow-up was 53 weeks. The primary end point rates were 41, 58, and 59 (per 100 person-years) in the didanosine 500 mg, didanosine 200 mg, and zidovudine groups (zidovudine vs. didanosine 500 mg, relative risk 1.28, 95% confidence interval, 0.88-1.86, p = 0.19; didanosine 200 vs. 500 mg, relative risk 1.24, 95% confidence interval, 0.85-1.79, p = 0.26). In subjects with a baseline CD4 count of 100/mm3 or more, the primary end point rates were 8, 29, and 25 (per 100 person-years) in the didanosine 500 mg, didanosine 200 mg, and zidovudine groups, respectively (zidovudine vs. didanosine 500 mg, relative risk 2.96, 95% confidence interval 0.91-9.62, p = 0.07). No difference was seen in survival. In the didanosine 500 mg group, more patients had a 50% increase in CD4 cells (10% vs. 1% in zidovudine group, p = 0.01) and an increase of > or = 2.5 kg in body weight (2% versus 3%). Fatal pancreatitis developed in one patient assigned to didanosine 500 mg and in one to zidovudine. Our data suggest that switching from zidovudine to currently recommended doses of didanosine in subjects with ARC or AIDS who show evidence of clinical and laboratory disease progression can be associated with improvements in clinical outcome as well as in surrogate markers of HIV disease progression. This effect tended to be greater among individuals with higher CD4 counts (>100/mm3).
 ...
PMID:Switching from zidovudine to didanosine in patients with symptomatic HIV infection and disease progression. ddI Iberian Study Group. 867 28

Although the efficacy of switching from zidovudine (AZT) to didanosine (ddI) has already been evaluated in controlled studies, prior investigations were not specifically designed to evaluate this issue in patients with acquired immune deficiency syndrome (AIDS). This open, randomized, multicenter study (ISS 901) was designed to evaluate the clinical benefit in patients with AIDS of switching to ddI after 6-18 months of AZT and no major intolerance. Patients were randomized to continue AZT, maintaining the current dosage at randomization (n = 79), or to receive ddI (n = 80) at the dosage of 375 mg and 250 mg b.i.d. for body weight > 60 and < or = 60 kg, respectively. Primary efficacy measures were survival and time to new AIDS-defining events, analyzed by the intent-to-treat approach. The two groups were comparable for baseline characteristics, follow-up (15 months), and time spent on allocated treatment. At the end of the study, 104 patients (48 AZT, 56 ddI) had died and 90 had at least one new AIDS-defining event (44 AZT, 46 ddI). Kaplan-Meier estimates of survival and of time to first new AIDS-defining event showed no differences between the treatment groups. No differences were detected in other efficacy measurements (p24 antigenemia, CD4+ count, Karnofsky score, and body weight), occurrence of severe toxicities, and treatment modifications. Pancreatitis occurred only in ddI-treated patients (6%). In our population of patients with advanced disease, switching from AZT to ddI did not produce apparent benefits, suggesting that application of this strategy earlier in the course of human immunodeficiency virus disease should be considered.
 ...
PMID:A randomized trial (ISS 901) of switching to didanosine versus continued zidovudine after the diagnosis of AIDS. 875 22

In the past, numerous reports on drugs probably causing acute pancreatitis have been published. However, most of these case reports were anecdotal with a lack of obvious evidence and did not present a comprehensive summary. Although drug-associated pancreatitis is rare, it is gaining increasing importance with the introduction of several potent new agents, i.e., anti-acquired immunodeficiency syndrome drugs. The following comprehensive review scrutinizes the evidence present in the world literature on drugs associated with acute or chronic pancreatitis and, based on this, categorizes in a definite, probable, or possible causality. In addition, explanations for the pathophysiological mechanisms are discussed.
 ...
PMID:Drug-associated pancreatitis: facts and fiction. 926 Feb 10


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>