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Chronic pancreatic alterations in AIDS
patients.Pancreas.
1999 Nov;19(4) : 335-8.
Patients
with acquired immunodeficiency syndrome (AIDS) can develop
biliary and pancreatic disorders, like sclerosing cholangitis
and acute pancreatitis. Chronic pancreatic changes are rare and
only poorly described. In this study, we report our endoscopic
retrograde cholangiopancreatography (ERCP) findings in 20
patients with AIDS, focusing on pancreatographic changes. ERCP
findings from 20 patients with advanced disease were analyzed.
Patients with history of chronic alcoholism were ruled out. ERCP
findings were correlated to the coexistence of an opportunistic
infection and the taking of antiviral therapies. Bile duct and
pancreatic duct abnormalities were observed in 11 (55%) of 20
and seven (37%) of 19 patients, respectively. Bile duct lesions
were mainly sclerosing cholangitis, and chronic pancreatic
alterations consisted of side-branch involvement (n = 4),
multiple and diffuse strictures of the main duct (n = 1), and
diffuse dilatation of the main pancreatic duct (n = 2). The
presence of an opportunistic infection was correlated with
sclerosing cholangitis but not with chronic pancreatic changes.
Similarly, there was no association between the finding of an
abnormal cholangiogram and the presence of pancreatic
alterations. This population of patients with AIDS had a
significant proportion (37%) of chronic pancreatic ductal
changes, which do not seem to be related to morphologic
alterations and/or opportunistic infections of the biliary
tract.
The
pancreas in AIDS.
Gastroenterol Clin North Am. 1997
Jun;26(2):337-65.
Although
autopsy studies reveal significant pancreatic lesions in about
10% of AIDS patients, pancreatic lesions infrequently produce
symptoms and are rarely recognized premortem. Patients with AIDS
can develop pancreatic disease from causes not related to AIDS
or AIDS-specific lesions. AIDS-specific causes include
opportunistic infection, AIDS-associated neoplasia, and
medications used to treat complications of AIDS. Pancreatic
involvement is usually part of a widely disseminated tumor and
rarely produces clinical symptoms.
Study of
prevalence, severity, and etiological factors associated with
acute pancreatitis in patients infected with human
immunodeficiency virus.
Am J Gastroenterol. 1997 Nov;92
(11):2044-8.
OBJECTIVES: Patients with the human immunodeficiency virus (HIV)
disease can develop pancreatic gland inflammation from HIV
infection and related causes, or from factors totally
independent of it. The incidence and severity acute pancreatitis
in patients with HIV diseases and the frequency of associated
etiological factors have not been examined in any detail. The
purpose of this study was to (a) determine the prevalence of
acute pancreatitis, (b) evaluate severity of pancreatic gland
inflammation, (c) identify commonly associated etiological
factors with acute pancreatitis, and (d) examine the
relationship between CD4 lymphocyte counts and serum pancreatic
enzyme levels (amylase and lipase) in patients with HIV disease.
METHODS: We examined the medical records of 321 patients with
HIV disease seen at Sinai Hospital of Baltimore between July of
1993 to June of 1994. Data collected from these records included
clinical, laboratory, and radiologic features of pancreatitis,
staging of HIV disease, risk factors, CD4 lymphocyte counts,
medications associated with the presence of opportunistic
infections, Kaposi's sarcoma, and lymphoma. RESULTS: From 321
patients with HIV disease, 45 patients developed at least one
episode of acute pancreatitis as defined by clinical and
laboratory criteria during the 1-yr period. A statistically
significant negative correlation was found between serum
pancreatic enzyme level and the number of CD4 lymphocytes (r =
-0.15, p < 0.05 for serum amylase; r = -0.2, p < 0.05 for serum
lipase). Furthermore, patients with asymptomatic HIV infection
or CD4 lymphocyte count >500 mm3 did not develop asymptomatic
hyperamylasemia or acute pancreatitis. Furthermore, the presence
of gallstones, active injection drug use, pentamidine therapy,
Pneumocystis carinii, Mycobacterium avium intracellulare
correlated significantly (p < 0.001) with the diagnosis of acute
pancreatitis. CONCLUSIONS: A detailed review of medical records
of patients with HIV disease seen in a community hospital in 1
yr (1993-1994) suggests a high incidence (14%) of mild to
moderately severe acute pancreatitis. In this group of patients,
pancreatic gland inflammation is commonly associated with
gallstones, intravenous drug abuse, pentamidine intake, and
Pneumocystis carinii and Mycobacterium avium intracellulare
infections. In addition, marked reduction in CD4 lymphocyte
count is associated with increase in serum pancreatic enzyme
levels (amylase, lipase activity) suggesting pancreatic gland
inflammation or altered pancreatic enzyme turnover.
Pancreatic disorders in pediatric acquired immune deficiency
syndrome.
Hum Pathol. 1995
Jul;26(7):765-70.
Acute
pancreatitis, reported in 17% of pediatric patients with
acquired immune deficiency syndrome (AIDS), is said to have a
poor prognosis. We describe the pancreatic changes observed at
autopsy from 71 children with human immunodeficiency virus (HIV)
infection and document their nature, extent, and clinical
relevance. The median age at autopsy of the children was 17
months (range, 2 months to 19 years); 38 were boys and 33 were
girls. Parental intravenous drug use was the most frequent risk
factor for AIDS, followed by blood transfusions. Respiratory
failure and sepsis constituted the predominant causes of death.
Nonspecific changes, such as edema, inflammation, fibrosis,
inspissated material in acini and ducts, and enlarged Langerhans'
islet predominated. Acute and chronic pancreatitis were mild
except in one instance of a fatal acute probably dideoxyinosine-associated
pancreatitis. Pancreatic involvement by opportunistic
infections, such as cytomegalovirus (CMV), Mycobacterium avium
intracellulare (MAI), and Candida, was focal and rare despite
the high prevalence of these infections at autopsy. Focal
lymphoplasmacytic infiltration and vascular calcifications were
also observed. We conclude that pancreatic changes were
frequently noted at autopsy in children with AIDS. They were
usually mild, reflected systemic disease states, and were
usually not life threatening. The incidence of opportunistic
infections of the pancreas was low.
Pancreatic disease in AIDS--a review.
J Clin Gastroenterol. 1993
Oct;17(3): 254-63.
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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