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

A patient with primary herpes simplex virus (HSV) type 2 genital infection had dissemination in the 37th week of her first pregnancy. This was manifested by severe hepatitis, pancreatitis, and genital lesions. Temporary improvement followed the delivery of a healthy infant by cesarean section. Encephalitis became evident on the third postpartum day, and recovery was complicated by profound bradycardia, possibly due to viral myocarditis. Vidarabine was administered for seven days, and the patient survived with only mild neurologic sequellae. To our knowledge, this the fourth reported case of disseminated herpesvirus infection in pregnancy and the first due to HSV type 2. Pregnancy must be considered as a possible predisposing factor in dissemination of primary HSV infection.
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PMID:Disseminated herpesvirus infection. Association with primary genital herpes in pregnancy. 17 38

A 43-year-old homosexual man was hospitalized in April 1988 because of acute epigastric pain. It was known that he had had a HIV infection for a year, and in April 1988 it was defined as stage Walter Reed I. Acute, exudative, nonspecific pancreatitis was diagnosed. Three weeks later cerebral symptoms (disturbances of consciousness), hypoacusis, and impaired vision developed. The ocular fundus displayed areas of edema and whitish clouding in the retina, first in the left eye and later also in the right. These were initially assumed to be anemic infarctions until the differential diagnosis of acute retinal necrosis with possible herpesvirus infection was made. On the basis of ophthalmoscopic findings cytomegalovirus retinitis appeared improbable. Serologic examinations showed increased levels of IgG antibody titers of cytomegalovirus and herpes simplex virus (both 1:20,000). Therapy with intravenous infusions of Acyclovir was instituted (1500 mg/d). After a few days the patient regained consciousness as well as his hearing and vision. There was complete resolution of the retinal exudates. This excellent therapeutic result of Acyclovir therapy confirmed the diagnosis of acute retinal necrosis syndrome, identified the cerebral symptoms as herpes encephalitis, and explained the entire disease process as the first opportunistic infection in HIV infection, i.e., by that time the patient had developed stage Walter Reed 6 (AIDS). Problems of differential diagnosis and the therapeutic schedule with Acyclovir are discussed.
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PMID:[Acute retinal necrosis and herpes encephalitis. The key role of the ophthalmologist in diagnosing opportunistic infections in AIDS, successful therapy with acyclovir (Zovirax)]. 234 17

From 1974 through 1982, fulminant hepatitis was diagnosed in 34 patients at our institution. Of these patients, only two survived (survival rate, 6%). This syndrome was caused by viruses (B and non-B hepatitis and herpes simplex) in 23 patients, hepatotoxic drug in 6, Wilson's disease (hepatolenticular degeneration) in 3, and industrial poisons in 2. Most of the patients died within 10 days after the onset of encephalopathy. The poor prognosis in our group of patients was probably related to the preponderance of older patients and cases caused by non-B hepatitis virus. In our patients, the clinical course was complicated by renal failure, ascites, bleeding, sepsis, pancreatitis, and seizures. The major cause of death was hepatic failure.
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PMID:Fulminant hepatitis: Mayo Clinic experience with 34 cases. 392 80

Herpes simplex virus type 1 (HSV-1) was isolated from the gastric contents of a young man with acute idiopathic pancreatitis. Although the patient had a marked (eightfold) rise in serum complement fixing antibody titer to HSV-1, there was no evidence of primary infection. The source of the HSV-1 may have been reactivation in the oral or pharyngeal mucous membranes, with swallowing of the virus. HSV-1 is normally quite labile in acid media (less than five minutes at pH less than or equal to 3), but because the patient was receiving cimetidine, lack of gastric acid may have allowed prolonged survival of the virus.
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PMID:Isolation of herpes simplex virus type 1 from gastric contents of a patient with acute pancreatitis. 626 5

There are increasing challenges for the practising gastroenterologist in treating AIDS-related gastrointestinal diseases. The differential diagnoses of dysphagia and odynophagia include cytomegalovirus (CMV) and herpes simplex virus (HSV) infection, non-specific aphthous ulceration and non-AIDS oesophageal diseases, especially reflux oesophagitis. Chronic subacute abdominal pain with nausea, vomiting, early satiety and weight loss is suggestive of an obstructive lesion caused by lymphoma or Kaposi's sarcoma. Severe acute abdominal pain can indicate pancreatitis or intestinal perforation due to cytomegalovirus. Right upper quadrant pain (with or without fever, vomiting or abnormal liver function tests with a cholestatic profile) is suggestive of hepatobiliary pathology including cholecystitis, cholangitis, acalculous cholecystitis and AIDS cholangiopathy. Diarrhoea is the most common gastrointestinal symptom of AIDS, affecting 50-90% of patients. Causes of AIDS diarrhoea include protozoa (Cryptosporidium parvum, Isospora belli, Enterocytozoon bieneusi, Septata intestinalis, Cyclospora spp, Entamoeba histolytica and Giardia lamblia), bacteria (Mycobacterium avium-intracellulare, Clostridium difficile, Salmonella, Shigella and Campylobacter jejuni), and viruses (CMV, HSV and possibly HIV). Chronic diarrhoea, malnutrition and weight loss can shorten the life-span of patients with AIDS. Elemental diets, isotonic formulas, medium chain triglycerides and total parenteral nutrition have been tried with little success in AIDS patients with severe diarrhoea and wasting.
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PMID:AIDS and the gut. 805 32

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

A wide variety of infectious agents has been associated with acute pancreatitis. Strict diagnostic criteria were developed to assess with relationship between individual microorganisms and acute pancreatitis. Pathologic or radiologic evidence of pancreatitis associated with well-documented infection was noted with viruses (mumps, coxsackie, hepatitis B, cytomegalovirus, varicella-zoster virus, herpes simplex virus), bacteria (Mycoplasma, Legionella, Leptospira, Salmonella), fungi (Aspergillus), and parasites (Toxoplasma, Cryptosporidium, Ascaris). Clues to the infectious nature of pancreatitis lay in the characteristic signs and symptoms associated with the particular infectious agent. How often these agents are responsible for idiopathic pancreatitis is unclear.
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PMID:Infectious causes of acute pancreatitis. 889 96

Controlled clinical trials in renal transplantation have demonstrated that mycophenolate mofetil is well tolerated and has lower renal transplant rejection rates than azathioprine regimens. This study reports on the clinical experiences at two institutions with mycophenolate mofetil (MMF) for severe lupus nephritis. Twelve patients with relapsing or resistant nephritis previously treated with cyclophosphamide therapy and one patient who refused cyclophosphamide as initial therapy for diffuse proliferative nephritis but accepted MMF were included. During combined MMF/prednisone therapy, serum creatinine values remained normal or declined from elevated values: mean change in serum creatinine was -0.26+/-0.46 microM/L, P = 0.039. Proteinuria significantly decreased: mean change in urine protein-to-creatinine ratios was -2.53+/-3.76, P = 0.039. Decreased serum complement component C3 and elevated anti-double-stranded DNA antibody levels at baseline improved in some, but not all, patients. The mean initial dose of MMF was 0.92 g/d (range, 0.5 to 2 g/d). The mean duration of therapy was 12.9 mo (range, 3 to 24 mo). Adverse events included herpes simplex stomatitis associated with severe leukopenia (n = 1), asymptomatic leukopenia (n = 2), nausea/ diarrhea (n = 2), thinning of scalp hair (n = 1), pancreatitis (n = 1), and pneumonia without leukopenia (n = 1). Recurrence of the pancreatitis led to discontinuation of MMF in this patient; all other adverse events resolved with dose reduction. It is concluded that MMF is well tolerated and has possible efficacy in controlling major renal manifestations of systemic lupus erythematosus. Controlled clinical trials are needed to define the role of MMF in the management of lupus nephritis.
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PMID:Mycophenolate mofetil therapy in lupus nephritis: clinical observations. 1020 68

Lesions of the pancreas induced by viral infection have drawn relatively little attention because of their low incidence, and the histopathologic features of viral pancreatitis have not been fully elucidated. We report the autopsy findings of 2 patients, a 59-year-old woman with allergic granulomatous angiitis and a 73-year-old man with invasive pulmonary aspergillosis who had a disseminated visceral herpes simplex virus (HSV) infection. In both cases, the liver was the organ most severely affected by the viral infection. The pancreas showed multiple small foci of hemorrhagic necrosis, which were not accompanied by fat necrosis of the surrounding adipose tissue. Histopathologically, Cowdry type A intranuclear inclusions and a ground-glass appearance of the nuclei were found in many degenerated acinar cells around the necrotic foci. The gross appearance and histopathologic features of HSV pancreatitis were characteristic and, in particular, distinct from those of the more common acute hemorrhagic pancreatitis. Immunohistochemistry using an anti-HSV antibody revealed immunoreactivity in the intranuclear inclusions and ground-glass nuclei, and polymerase chain reaction analysis disclosed that the causative virus in these 2 cases was HSV-1. Herpes simplex virus pancreatitis constitutes a rare, but distinct pathologic entity among a group of acute pancreatitis diseases with diverse etiopathogenesis.
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PMID:Herpes simplex pancreatitis. 1256 43

New immunosuppressive protocols and advanced surgical technique resulted in an improved outcome of pancreatic transplantation (PTx) with infection remaining the most common complication. Seventy-two enteric-drained whole PTxs performed at the Innsbruck University Hospital between September 2002 and October 2004 were retrospectively analyzed. Prophylactic immunosuppression consisted of either the standard protocol consisting of single bolus antithymocyteglobulin (ATG) (Thymoglobulin, Sangstat or ATG Fresenius) induction (9 mg/kg), tacrolimus (TAC), mycophenylate mofetil (MMF) and steroids (38 patients) or a 4-day course of ATG (4 mg/kg) tacrolimus and steroids with MMF (n = 19), or Sirolimus (n = 15). Perioperative antimicrobial prophylaxis consisted of Piperacillin/Tazobactam (4.5 g q 8 h) in combination with ciprofloxacin (200 mg q 12 h) and fluconazole (400 mg daily). Ganciclovir was used for cytomegalovirus (CMV) prophylaxis if donor was positive and recipient-negative. Patient, pancreas, and kidney graft survival at 1 year were 97.2%, 88.8%, and 93%, respectively, with no difference between the groups. All retransplants (n = 8) and single transplants (n = 8) as well as all type II diabetics and nine of 11 patients older 55 years received standard immunosuppression (IS). The rejection rate was 14% and infection rate 46% with no difference in terms of incidence or type according to the three groups. Severe infectious complications included intra-abdominal infection (n = 12), wound infection (n = 7), sepsis (n = 13), respiratory tract infection (n = 4), urinary tract infection (n = 12), herpes simplex/human herpes virus 6 infection (n = 5), CMV infection/disease (n = 7), post-transplant lymphoproliferative disorder (PTLD, n = 3), invasive filamentous fungal infection (n = 4), Clostridial/Rotavirus colitis (n = 1), and endocarditis (n = 1). All four patients in this series died of infectious complications (invasive aspergillosis n = 2) (one with Candida glabrata superinfection), invasive zygomycosis (n = 1), PTLD (n = 1). Five grafts were lost (vascular thrombosis n = 3, pancreatitis n = 1, noncompliance n = 1). Infection represented the most frequent complication in this series and all four deaths were of infectious origin. Better prophylaxis and management of infections now should be the primary target to be addressed in the field of pancreas transplantation.
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PMID:Infectious complications following 72 consecutive enteric-drained pancreas transplants. 1676 33


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