Your browser doesn't support javascript.
loading
Show: 20 | 50 | 100
Results 1 - 2 de 2
Filter
1.
PLoS One ; 13(10): e0204979, 2018.
Article in English | MEDLINE | ID: mdl-30379828

ABSTRACT

Type 3C Diabetes, or diseases of the exocrine pancreas has been reported to occur in approximately 30% of adult patient with pancreatitis. The incidence of glucose abnormalities or risk factors that may predict the development of abnormal glucose in the pediatric pancreatitis population is not known. We performed a retrospective chart review from 1998-2016 for patients who carry the diagnosis of acute pancreatitis (AP), acute recurrent pancreatitis (ARP), and chronic pancreatitis (CP). We extracted glucose values, HbA1c%, and data from oral glucose tolerance and mixed meal testing with timing in relation to pancreatic exacerbations. Patient characteristic data such as age, gender, body proportions, family history of pancreatitis, exocrine function and genetic mutations were also assessed. Abnormal glucose was based on definitions put forth by the American Diabetes Society for pre-diabetes and diabetes. Fifty-two patients had AP and met criteria. Of those, 15 (29%) had glucose testing on or after the first attack, 21 (40%) were tested on or after the second attack (in ARP patients) and 16 (31%) were tested after a diagnosis of CP. Of the patients tested for glucose abnormalities, 25% (13/52) had abnormal glucose testing (testing indicating pre-DM or DM as defined by ADA guidelines. A significantly higher proportion of the abnormal glucose testing was seen in patients (85%, 11/13) with a BMI at or greater than the 85th percentile compared to the normal glucose patients (28%, 11/39) (p = 0.0007). A significantly higher proportion of the abnormal glucose patients (77%, 10/13) had SAP during the prior AP episode to testing compared to the 10% (4/39) of the normal glucose patients (p<0.0001). Older age at DM testing was associated with a higher prevalence of abnormal glucose testing (p = 0.04). In our patient population, a higher proportion of glucose abnormalities were after the second episode of pancreatitis, however 62% (8/13) with abnormalities was their first time tested. We identified obesity and having severe acute pancreatitis (SAP) during the prior AP episode to testing could be associated with abnormal glucose. We propose that systematic screening for abnormal glucose after the first episode of acute pancreatitis in order to better establish the timing of diabetes progression.


Subject(s)
Glucose/metabolism , Pancreatitis/pathology , Acute Disease , Blood Glucose/analysis , Child , Chronic Disease , Chymotrypsin/genetics , Female , Genetic Predisposition to Disease , Glucose Tolerance Test , Glycated Hemoglobin/analysis , Humans , Male , Pancreatitis/epidemiology , Pancreatitis/metabolism , Polymorphism, Genetic , Prevalence , Recurrence , Retrospective Studies , Risk Factors , Trypsin/genetics , Trypsin Inhibitor, Kazal Pancreatic/genetics
2.
Laryngoscope ; 123(6): 1537-46, 2013 Jun.
Article in English | MEDLINE | ID: mdl-23401162

ABSTRACT

OBJECTIVES/HYPOTHESIS: To describe the clinical phenotype of pediatric patients with unilateral enlarged vestibular aqueduct (EVA) and then to compare the findings to two clinically related phenotypes: bilateral EVA and unilateral hearing loss without EVA. In view of clinical observations and previously published data, we hypothesized that patients with unilateral EVA would have a much higher rate of contralateral hearing loss than patients with unilateral hearing loss without EVA. STUDY DESIGN: Retrospective cohort study. METHODS: Patients with unilateral or bilateral EVA were identified from a database of children with sensorineural hearing loss who were seen at a tertiary care institution between 1998 and 2010. Those with imaging findings consistent with well-established EVA criteria were identified. A comparative group of patients with unilateral hearing loss without EVA was also identified. The following specific outcome measurements were analyzed: 1) hearing loss phenotype, 2) laterality of EVA and hearing loss, 3) midpoint and operculum vestibular aqueduct measurements, and 4) genetic test results. RESULTS: Of the 144 patients who met our inclusion criteria, 74 (51.4%) had unilateral EVA. There was a strong correlation between the presence of hearing loss and ears with EVA. Fifty-five percent of patients with unilateral EVA had hearing loss in the contralateral ear; in most of these patients, the hearing loss was bilateral. Contralateral hearing loss occurred in only 6% of patients with unilateral hearing loss without EVA. No significant differences were found in temporal bone measurements between the ears of patients with unilateral EVA and ipsilateral hearing loss and all ears with EVA and normal hearing (P = .4). There was no difference in the rate of hearing loss progression in patients with unilateral EVA between ears with or without EVA (16 of 48 [33.3%] vs. 9 of 27 [33.3%], respectively; P = 1.0). There was no difference in the rate of hearing loss progression in patients with bilateral and unilateral EVA (41 of 89 ears [46.1%] vs. 25 of 75 ears [33.3%], respectively; P = .1); however, both EVA groups had higher rates of progression compared to patients with unilateral hearing loss without EVA. There was a strong correlation between the presence of hearing loss at 250 Hz and the risk of more severe hearing loss and progressive hearing loss. Patients with bilateral EVA and SLC26A4 mutations had a higher rate of progression than patients who had no mutations (P = .02). No patients with unilateral EVA had Pendred syndrome. CONCLUSIONS: Children with unilateral EVA have a significant risk of hearing loss progression. Hearing loss in the ear contralateral to the EVA is common, suggesting that unilateral EVA is a bilateral process despite an initial unilateral imaging finding. In contrast to bilateral EVA, unilateral EVA is not associated with Pendred syndrome and may have a different etiology. Temporal bone measurements, hearing loss severity, and hearing loss at 250 Hz were all correlated with the risk of progressive hearing loss. Clinicians should become knowledgeable regarding the implications of this disease process so that families can be counseled appropriately.


Subject(s)
DNA/genetics , Hearing Loss, Sensorineural/etiology , Membrane Transport Proteins/genetics , Mutation , Audiometry, Pure-Tone , Child , Child, Preschool , Disease Progression , Female , Follow-Up Studies , Genetic Testing , Hearing Loss, Sensorineural/complications , Hearing Loss, Sensorineural/diagnosis , Hearing Loss, Sensorineural/genetics , Humans , Infant , Infant, Newborn , Male , Phenotype , Polymerase Chain Reaction , Prognosis , Retrospective Studies , Severity of Illness Index , Sulfate Transporters , Time Factors , Tomography, X-Ray Computed , Vestibular Aqueduct/abnormalities
SELECTION OF CITATIONS
SEARCH DETAIL