Evaluation of unexplained acute and acute recurrent pancreatitis using endoscopic retrograde cholangiopancreatography, sphincter of Oddi manometry and endoscopic ultrasound.

BACKGROUND AND STUDY AIMS: Unexplained pancreatitis represents a diagnostic challenge. The aim of this study was to determine the diagnostic utility of endoscopic retrograde cholangiopancreatography (ERCP) with sphincter of Oddi manometry (SOM), bile analysis, and endoscopic ultrasound (EUS) in evaluating such patients. PATIENTS AND METHODS: Of 162 patients referred for evaluation of pancreatitis, 72 with a known cause were excluded. The remainder ( n=90) was classified as having prior acute ( n=24) or recurrent acute pancreatitis ( n=66). Bile sampling and SOM were performed at the time of ERCP. EUS was used to assess for tumors and for chronic pancreatitis. Clinical outcomes were evaluated by questionnaire. RESULTS: ERCP was successful in 88/89 patients (99 %). Manometry was successful in 63/67 patients (94 %), and 56 patients underwent EUS. Findings were categorized into five distinct etiologies: sphincter of Oddi dysfunction (SOD) ( n=28; 31 %), pancreas divisum ( n=18; 20 %), biliary ( n=18; 20 %), idiopathic ( n=18; 20 %) and tumor-related ( n=8; 9 %). Features of moderate or severe chronic pancreatitis by EUS and ERCP criteria were found in 18 patients (21 %); an additional nine patients had chronic pancreatitis by EUS criteria alone. EUS identified all the tumors. The condition was improved in 96 % of all patients undergoing endoscopic therapy. CONCLUSION: An etiology was identified in the majority of patients with unexplained pancreatitis. SOD represented the most common finding. Moderate to severe chronic pancreatitis was found in over one-fifth of these patients. Bile analysis, SOM, and EUS are useful tools in the evaluation of unexplained acute pancreatitis.

Cholecystokinin-Stimulated mebrofenin (99mTc-Choletec) hepatobiliary scintigraphy in asymptomatic postcholecystectomy individuals: assessment of specificity, interobserver reliability, and reproducibility.

OBJECTIVES: Cholecystokinin-stimulated hepatobiliary scintigraphy (CCK-HBS) is a noninvasive method reported to be highly accurate in the diagnosis of sphincter of Oddi dysfunction. Our primary aim was to assess the specificity of CCK-HBS by evaluating its ability to exclude disease in 20 asymptomatic postcholecystectomy individuals. Secondary aims were to assess the interobserver reliability in scoring the CCK-HBS examinations between three blinded observers and to assess reproducibility of CCK-HBS repeated in the same individuals. METHODS: Twenty asymptomatic postcholecystectomy individuals with normal liver serum chemistries underwent CCK-HBS on two separate occasions. Three nuclear medicine specialists read each CCK-HBS study in a blinded fashion. RESULTS: There was good agreement between the three observers reading the same scans for both the first scan (kappa = 0.554) and the second scan (kappa = 0.507). There was poor agreement between the first and second scans on the same patient, read by the same nuclear medicine specialist (kappa = 0.062-0.385). The overall specificity of the CCK-HBS score was 77.5%; however, the specificity was only 60% when a true negative was defined as two negative CCK-HBS examinations. CONCLUSIONS: Quantitative CCK-HBS is of poor specificity in asymptomatic postcholecystectomy individuals. Hence, it is of questionable value in excluding sphincter of Oddi dysfunction in patients suspected to suffer from this disorder.

Sphincter of Oddi dysfunction is associated with chronic pancreatitis.

OBJECTIVES: Chronic pancreatitis can be caused by ductal obstruction resulting from cicatricial papillary stenosis, but sphincter of Oddi motility studies have been inconclusive in patients with established chronic pancreatitis. We sought to determine whether there is an association between papillary sphincter dysfunction and changes of early chronic pancreatitis. METHODS: Consecutive patients who underwent sphincter of Oddi manometry to investigate unexplained upper abdominal pain (n = 104) were assessed for evidence of chronic pancreatitis by pancreatic ductography, endoscopic ultrasound, and pancreatic fluid bicarbonate concentration. RESULTS: Sphincter of Oddi dysfunction patients were four times more likely (odds ratio = 4.6) to have evidence of chronic pancreatitis than were those without sphincter dysfunction (p = 0.01). Of 68 patients with sphincter of Oddi dysfunction, 20 (29%) had structural evidence of chronic pancreatitis. Twenty of 23 (87%) patients with chronic pancreatitis had sphincter of Oddi dysfunction. CONCLUSIONS: Sphincter of Oddi dysfunction is associated with changes of chronic pancreatitis in patients with unexplained pancreaticobiliary pain. Longitudinal follow-up is required to confirm these preliminary findings.

Phenotype differences of resistance to thyroid hormone in two unrelated families with an identical mutation in the thyroid hormone receptor beta gene (R320C).

A new family with resistance to thyroid hormone (RTH) harboring a mutation in the thyroid hormone receptor (TR) beta gene (R320C) is reported. The phenotype of affected members is compared to that of affected members of an unrelated family with an identical mutation in the TR beta gene that occurred independently. In one of the two families higher concentrations of free T4 were required to maintain a normal TSH level in affected subjects and unaffected first degree relatives but not in relatives by marriage. While this finding suggests that genetic background modulated the relative insensitivity to thyroid hormone caused by the mutant TR beta, it is uncertain whether the higher thyroid hormone levels prevented the occurrence of hyperactivity and attention deficit.