Superior mesenteric artery (SMA) syndrome is an unusual cause of proximal intestinal obstruction. The syndrome is characterized by compression of the third portion of the duodenum due to narrowing of the space between the SMA and aorta and is primarily attributed to loss of intervening mesenteric fat pad. A 9-year-old girl presented with acute vomiting and abdominal pain. The patient was diagnosed with SMA syndrome based on imaging findings, and improved after conservative treatment. In general, risk factors for SMA syndrome in children include congenital anatomic abnormalities, rapid weight loss, severely handicapped children, and scoliosis. At the time of onset, there was no risk factor for SMA syndrome. After 6 months, she had menarche at 9 years and 7 months and was diagnosed with precocious puberty. She had a height spurt from around the age of 8, suggesting that it may have been a risk factor for SMA syndrome.
SMA syndrome is also one of the differentials in acute abdomen in children. However, it may not be accompanied by weight loss, and attention should be paid especially if there is an adolescent height spurt. In addition, it is important to keep in mind the complication of precocious puberty when SMA syndrome develops earlier than the standard pubertal age.

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A 70-year-old woman was admitted to our hospital because of anemia with headache and nausea. As a result of anemia workup, she was diagnosed with ascending colon cancer with a para-aortic lymph node metastasis. Ileocecal resection and excision of an enlarged para-aortic lymph node were performed. Histopathological diagnosis of the resected specimen was poorly differentiated adenocarcinoma (solid type) with some mucinous carcinoma, and the metastatic lymph nodes showed differentiation into mucinous carcinoma. Immunohistologically, CD8^＋T cell infiltration was observed in the cancer tissue, but mucinous carcinoma in the metastatic lymph nodes showed sparse CD8^＋T cell infiltration. During chemotherapy for liver metastases after surgery, lymph node metastases appeared near the hepatic hilum. The histology of lymph node metastases was diagnosed as mucinous carcinoma based on CT findings, and pembrolizumab was administered due to microsatellite instability-high.Twenty-two months after the start of treatment with pembrolizumab, the metastatic lymph nodes were judged to be in partial response and have maintained the reduction. The disappearance of liver metastases was confirmed 25 months after the start of pembrolizumab treatment. In our case, the time to partial response in the metastatic lymph nodes was longer than the reported median time to objective response to pembrolizumab. It is possible that the differentiation into mucinous carcinoma at the metastatic site caused the suppression of the infiltration of CD8-positive T cells into cancer cell clusters. The difference in time to response between mucinous and non-mucinous carcinoma in patients treated with immune checkpoint inhibitor is a matter for further study.

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Diagnosis of chronic pulmonary aspergillosis in patients with nonfibrotic hypersensitivity pneumonitis is difficult, especially after treatment with systemic corticosteroids has been initiated. Therefore, treatment for chronic progressive pulmonary aspergillosis (CPPA) is often delayed. Although the chief complaint of non-fibrotic hypersensitivity pneumonitis complicated by pulmonary aspergillosis is often fever, the fungus cannot be identified, even after repeated sputum culture tests. Herein, we report a case of pulmonary aspergillosis that developed after initiating treatment with systemic corticosteroids and was difficult to diagnose. The patient had a fever that continued after the introduction of steroids. CPPA was eventually diagnosed based on histopathological examination of a bronchoscopy sample. When CPPA is suspected in patients with hypersensitivity pneumonitis, bronchoscopy may improve their prognosis.

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