Objective Orthostatic hypotension is caused by autonomic nerve dysfunction, mainly by severe sympathetic nerve dysfunction in diabetic patients. Diabetes affects the peripheral nerves in a length-dependent manner.Quantitative sudomotor axon reflex test (QSART)is one of the sensitive tests for detecting sympathetic nerve function. Weexamined the relation between orthostatic hypotension and QSARTat the foot and hand in type 2 diabetic patients.Methods Thirty-eight type 2 diabetic patients (age, 48.9±11.9 years; duration of diabetes, 13.4±8.6 years) and 13 age-matched non-diabetic controls were evaluated. All subjects aged under 65 years old were recruited. All subjects underwent Schellong tests and quantitative sudomotor axon reflex tests (QSART)at the back of the hand and dorsum of the foot. Results The sweating volume at the foot dorsum, but not the back of the hand, during the first 10 minutes of QSART was significantly related to the orthostatic hypotension on the Schellong test. In patients with normal, borderline and abnormal blood pressure response to standing, 6 out of 17 (35.3%), 9 out of 12 (75.0%) and 9 out of 9 (100%) had decreased sweating volume of the foot dorsum, respectively. Conclusions Our results suggest that orthostatic hypotension may be detected early by QSART at the dorsum of the foot in type 2 diabetic patients. (Internal Medicine 42: 560-564, 2003)

This study investigated the time-course of the nociceptive neuropeptide substance P and nerve growth factor (NGF), which facilitates substance P production, in lumbar and cervical dorsal root ganglia (DRG) of streptozotocin-induced diabetic rats. Levels of substance P and NGF were measured by radioimmunoassay and sandwich enzyme-linked immunosorbent assay, respectively, 2 months, 4 months and 8 months after induction of diabetes, and compared with age-matched non-diabetic control rats. At 2 months and 4 months, substance P and NGF levels were lower in the lumbar DRG of the diabetic rats than in controls. At 8 months, substance P and NGF were lower in both the lumbar and cervical DRG of the diabetic rats than in controls. These data demonstrate that a decrease in substance P levels in primary sensory neurons with NGF depletion occurs in an axonal length-dependent manner in diabetic rats, and that this decrease may be correlated with the duration of diabetes.

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We describe a patient with an eating disorder and hyperamylasemia originating from the salivary glands, who developed pancreatitis with a huge pancreatic pseudocyst. A 40-year-old woman was referred for the treatment of an eating disorder that had persisted for 9 years. She was admitted with abdominal pain, diarrhea, and nausea. She had bilateral parotid enlargement with marked elevation of total serum amylase level (3288 IU/l; normal range, 60-220) and an isolated increase of salivary isoamylase activity. After her symptoms resolved, oral intake of food was commenced. She subsequently complained of abdominal pain; this was associated with a slight elevation of serum pancreatic isoamylase and lipase levels, and a huge pancreatic pseudocyst was detected. Percutaneous drainage of the pseudocyst was successful. Endoscopic retrograde cholangiopancreatography demonstrated irregularity of the pancreatic duct. Based on these findings, the final diagnosis was parotid enlargement and acute exacerbation of chronic pancreatitis associated with a pancreatic pseudocyst in a patient with an eating disorder.

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