Coexistence of ulcerative colitis and Sjögren's syndrome in a patient with Takayasu's arteritis and Hashimoto's thyroiditis

A 31-year-old woman with a 15-year history of Takayasu's arteritis (TA) and a 13-year history of Hashimoto's thyroiditis presented with hematochezia. She received a diagnosis of Sjögren's syndrome at 1 month before her visit to Kyungpook National University Medical Center. Her colonoscopic findings were compatible with a diagnosis of ulcerative colitis (UC). She was treated with oral mesalazine, and her hematochezia symptoms subsequently disappeared. The coexistence of UC and TA has been reported; however, reports on the coexistence of UC and Sjögren's syndrome, or of UC and Hashimoto's thyroiditis are rare. Although the precise etiologies of these diseases are unknown, their presence together suggests that they may have a common pathophysiologic background. Furthermore, in patients with autoimmune or vascular diseases, including TA, systemic manifestations should be assessed with consideration of inflammatory bowel diseases including UC in the presence of gastrointestinal symptoms such as diarrhea and hematochezia.

A Case of Mediastinal Tuberculous Lymphadenitis Mimicking a Submucosal Tumor of the Esophagus / 대한내과학회지

Esophageal involvement in tuberculosis is rare, and the clinical presentation may mimic an esophageal submucosal tumor. A 30-year-old woman presented with dysphagia for 1 month. At esophagoscopy, a 3-cm subepithelial mass with normal covering mucosa was found 28~25 cm from the upper incisors. We diagnosed the lesion as a submucosal tumor of the esophagus and performed endoscopic ultrasonography 1 week after the first examination. The second endoscopy showed a large, linear ulceration on the same subepithelial mass. The histologic examination obtained following an endoscopic biopsy revealed chronic granulomatous inflammation, and a molecular nested PCR study for Mycobacterium tuberculosis was positive. The final diagnosis was mediastinal tuberculous lymphadenitis with invasion into the esophagus. We suggest the use of molecular biology techniques when there is a strong clinical suspicion of tuberculosis and difficulty in arriving at a definite diagnosis.

The expression of corticotropin-releasing factor and its receptors in the spinal cord and dorsal root ganglion in a rat model of neuropathic pain / 대한해부학회지

Corticotropin-releasing factor (CRF) is a peptide involved in the activation of the hypothalamic-pituitary-adrenal (HPA) axis. CRF is distributed not only along the HPA axis but also throughout pain-relevant anatomical sites. CRF elicits potent antinociception at the three main levels of pain transmissions: namely, the brain, spinal cord, and peripheral sensory neurons. The widespread distribution of CRF receptors 1 and 2 in the brain offers several targets wherein CRF could alter pain, some of which may be independent of the HPA axis. In this study, we assessed the expression of CRF and its receptors, CRF receptor type (CRFR)1 and CRFR2, in the spinal dorsal horn and dorsal root ganglion (DRG) in a rat model of neuropathic pain induced by spinal nerve injury (SNI). CRF was expressed in a few DRG neurons and primary afferent fibers in the dorsal horns of nasmall yi, Ukrainianve rats, and the CRF-positive neurons in DRG and fibers in the spinal dorsal horn were found to have increased after SNI. CRFR1 was not expressed in DRG or the dorsal horn and CRFR2 was expressed weakly in the small neurons in DRG in the nasmall yi, Ukrainianve rats. After SNI, CRFR1 was expressed in the activated microglia in the ipsilateral dorsal horn, and immunoreaction for CRFR2 was increased in the contralateral DRG following SNI. Consequently, it has been suggested that the increased expression of CRF and CRFR2 in DRG neurons and primary afferent fibers in dorsal horn, and CRFR1 in the activated microglia, may be involved in the mediation of stress responses as well as in microglial activation in the neuropathic pain state following SNI.

A Case of Pasteurella Multocida Prosthetic Valve Endocarditis with Multiple Peripheral Arterial Embolism

Infective endocarditis caused by Pasteurella multocida is a rare disease with a high mortality rate. Most patients have a previous history of animal contact. The most common comorbid condition is a chronic liver disease, which is attributable to the high mortality rate. Over half of the patients who survived the disease had required valve replacement surgery. We report the case of a 70-year-old man diagnosed with prosthetic valve endocarditis caused by Pasteurella multocida and complicated with multiple peripheral arterial embolism. He had neither any underlying immunocompromising diseases nor previous history of animal contact. He was successfully cured after antibiotic therapy for 6 weeks without valve replacement surgery.

The Expression of Corticotropin-Releasing Factor in the Central Nucleus of the Amygdala, Induced by Colorectal Distension, is Attenuated by General Anesthesia

Corticotrophin-releasing factor (CRF), a key regulator of the hypothalamic-pituitary axis, is expressed in the central nucleus of the amygdala (CeA) and its expression is upregulated in stress-related disorders. We investigated here the effect of noxious colorectal distension (CRD) on the expression of CRF in the CeA of conscious and unconscious rats. Adult male rats with or without general anesthesia were exposed to visceral pain induced by CRD for 5 min; this procedure was repeated 3 times with 1 min resting after each distension. The rats were sacrificed and sections of the CeA were immunostained for CRF as an indicator for anxiety response, and for phosphorylated extracellular signal-regulated kinase (p-ERK) as a marker for pain-specific activation of neurons; sections of lumbosacral spinal cord were immunostained for c-Fos as a marker for activation of spinal neurons. CRD elicited a significant increase in the expression of CRF and p-ERK in the CeA and of c-Fos in the spinal cord. General anesthesia attenuated the increase in CRF and p-ERK in the CeA, but did not affect the expression of spinal c-Fos. These results suggest that conscious recognition of pain at higher brain centers is an important determinant of CRF expression in the CeA.