Purposes: Fluorine-18 fluorodeoxyglucose positron emission tomography (FDG-PET) has been widely used for the diagnosis of pancreatic cancer. Because autoimmune pancreatitis is easily misdiagnosed as pancreatic cancer and can be tested for by FDG-PET analysis based on the presence of suspected pancreatic cancer, we attempted to clarify the differences in FDG-PET findings between the two conditions. Methods: We compared the FDG-PET findings between 15 patients with autoimmune pancreatitis and 26 patients with pancreatic cancer. The findings were evaluated visually or semiquantitatively using the maximum standardized uptake value and the accumulation pattern of FDG. Results: FDG uptake was found in all 15 patients with autoimmune pancreatitis, whereas it was found in 19 of 26 patients (73.1%) with pancreatic cancer. The accumulation pattern of nodular shape was frequently seen in pancreatic cancer with significance, whereas a longitudinal shape indicated the existence of autoimmune pancreatitis. Heterogeneous accumulation was found in almost all cases of autoimmune pancreatitis, whereas homogeneous accumulation was found in pancreatic cancer. Most cases of pancreatic cancer showed solitary localization with significant difference, whereas multiple localizations in the pancreas favored the existence of autoimmune pancreatitis. FDG uptakes in the hilar lymph node were more frequently seen in autoimmune pancreatitis than in pancreatic cancer with significance, and those in the lachrymal gland, salivary gland, biliary duct, retroperitoneal space, and prostate were only seen in autoimmune pancreatitis. Conclusions: FDG-PET provides a useful tool for differentiating autoimmune pancreatitis from suspected pancreatic cancer, if its accumulation pattern and extra-pancreatic involvements are considered. IgG4 measurement and other current image tests will confirm further diagnosis.

In order to clarify the reasons why hyperthyroidism due to Graves' disease is mild in aged patients compared to young patients, we examined the degree of hyperthyroidism and immune abnormalities in 371 untreated patients. The patients were divided into nine groups based on their age; groups A to I consisted of patients aged 0-9, 10-19, 20-29, 30-39, 40-49, 50-59, 60-69, 70-79, and 80-89 years, respectively. Serum thyroxine (T4), triiodo-thyronine (T3), and thyroglobulin levels were highest in group B (patients aged 10-19 years) and decreased progressively with advancing age. T3/T4 ratio was also highest in group B and decreased progressively with age. These data reconfirmed that the degree of hyperthyroidism is milder in older patients. The prevalence of positive microsomal and thyroglobulin antibodies was highest in group B (patients aged 10-19 years) and progressively lower in older groups, suggesting that an association with Hashimoto's thyroiditis is less prevalent in aged patients. We suggest that hyperthyroidism due to Graves' disease is mild in aged patients because responsiveness of the thyrocyte to the abnormal stimulator, thyrotropin-receptor antibody, may be reduced. Such reduced responsiveness may not be due to Hashimoto's thyroiditis, since the prevalence of antithyroid antibodies is lower in aged than in younger patients with hyperthyroidism due to Graves' disease.

A 60-year-old uremic patient treated with hemodialysis for 13 years developed acute hypotension during hemodialysis and overt heart failure subsequently in a period of relatively mild hypocalcemia after parathyroidectomy. Blood pressure during hemodialysis was maintained by continuous calcium infusion alone. Cardiomegaly was improved by normalization of serum calcium. The cardiac complication is considered to be exacerbation of the underlying myocardial dysfunction by the acute decline of serum calcium which might be a feature of the ‘hungry bone’ syndrome. Latent myocardial dysfunction might be exacerbated by only mild hypocalcemia after parathyroidectomy in long-term hemodialysis patients.

Blood urea nitrogen (BUN/creatinine ratio was abnormally high (24.8 +/- 0.6) in untreated hyperthyroid patients due to both increase in BUN and decrease in creatinine concentration. BUN, creatinine and BUN/creatinine ratio were all completely normalized after restoration of euthyroid status. On the other hand, BUN/creatinine ratio was slightly suppressed in hypothyroidism before treatment and it was reversed by thyroxine treatment (12.6 +/- 4.0 and 16.3 +/- 3.3, before and after treatment, respectively). An age-related increase in BUN/creatinine ratio, which was primarily due to an age-related increase in BUN, was also found in hyperthyroid subjects (21.9 +/- 2.8 vs 27.7 +/- 9.0; first vs fifth decade) and in normal controls (13.7 +/- 2.8 vs 16.0 +/- 2.9; first vs fifth decade). To elucidate reasons for abnormal increase in BUN/creatinine ratio in hyperthyroidism, measurement of cardiac output and kinetic analysis on urea nitrogen (UN) and creatinine were performed. The results indicated a marked increase in cardiac output. Serum creatine concentration was clearly increased in hyperthyroid patients. Thus, serum creatinine concentration was suppressed due to a decrease in creatinine synthesis and an increase in renal creatinine excretion. BUN was high, primarily due to an increase in UN production secondary to excessive protein catabolism together with insufficient excretion of UN.

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