Severe hyperkalemia following ileostomy not colostomy in a patient undergoing chronic hemodialysis

In patients with end-stage renal disease (ESRD), the intestinal tract may assume an accessory potassium (K+) excretory role in the face of declining renal excretory function. Here, we report the case of a patient with ESRD who developed severe hyperkalemia following ileostomy not colostomy. A 6△-year-old woman undergoing hemodialysis began developing severe hyperkalemia after ileostomy. Previously, she had successfully undergone resection and colostomy of the transverse colon. The pre-dialysis serum K+ level was normal. Our present case demonstrates the importance of intestinal K+ secretion, especially in the colon, for maintaining hemostasis in patients with ESRD

ミゾリビンによる急性尿酸性腎症とメソトレキサートによる骨髄抑制を併発した1例

症例は83歳,男性.近医で関節リウマチの診断で加療(プレドニゾロン2mg,メソトレキサート(MTX)4mg),他に高尿酸血症,高血圧で加療中であった.当院へ入院13日前にミゾリビン(MZ)150mg追加投与された.入院2日前に食欲不振と全身倦怠感で近医を受診,尿素窒素99.5mg/dl,クレアチニン7.8mg/dlと急性腎不全を認めたため当院へ紹介入院した.入院時の検査所見で尿酸26.5mg/dLと著明な高尿酸血症を認めMZによる急性尿酸性腎症と診断した.そのためMZ及び尿酸の除去を目的に緊急血液透析を施行した.尿酸値及び腎機能は速やかに改善した.しかし,入院後より血小板及び白血球数の減少を認めた.骨髄検査では骨髄異形成症候群様であり,MZに加えMTXの関与を推測された.その後汎血球減少も改善している.本症例はMZの血中濃度も高くMZの排泄遅延による高尿酸血症のため急性腎不全を合併し更に腎機能の増悪がMTXによる無効造血を発症した可能性が考えられた.MZと尿酸も血液透析により体外への除去が可能でありMZによる急性尿酸性腎症の場合は早急な血液透析が有効である.An 83-year-old man was diagnosed with rheumatoid arthritis at a nearby hospital for which he was administered methotrexate (MTX) and prednisolone. Thirteen days before admission, he had started mizoribine (MZ) 150mg. Two days before admission to our hospital, he was admitted to a nearby hospital for appetite loss and general fatigue. Laboratory tests showed renal dysfunction at nearby hospital, and he was consequently admitted to our hospital for further examination. On admission, we reasoned that renal dysfunction had resulted from hyperuricemia during MZ administration because the serum concentration of uric acid (26.5mg/dL) and MZ (trough level, 5.14μg/mL) were markedly elevated. Accordingly, MZ treatment was terminated, and hemodialysis was initiated. The patient subsequently showed an improvement in his condition and renal function recovered. However, pancytopenia developed soon after admission, and bone marrow aspiration showed myelodysplastic syndrome-like lesions. We suspected MTX and MZ to be the main cause of pancytopenia. Because the onset of acute renal failure had been attributed to MZ, it was conjectured that the dose of MTX was too high. Therefore, MTX administration was cancelled, and pancytopenia ameliorated. In cases of transient renal dysfunction with MZ, it is necessary to consider discontinuation of MZ and initiation of hemodialysis

Multihormonal pituitary adenoma concomitant with Pit-1 and Tpit lineage cells causing acromegaly associated with subclinical Cushing’s disease: a case report

Abstract Background A functional pituitary adenoma can produce multiple anterior-pituitary hormones, such as growth hormone (GH) -producing adenomas (GHoma) with prolactin or thyrotropin stimulating hormone production in the same lineage. However, it is very rare that acromegaly shows subclinical Cushing’s disease (SCD) beyond the lineage. Here we describe the involvement of intratumoral coexistence with 2 types of hormone-producing cells associated with different lineage in acromegaly concomitant with SCD. Case presentation In our study, we performed clinical evaluation of the patient showing acromegaly with SCD. To elucidate the mechanisms of this pathology, we analyzed immunohistochemistry and gene expression of anterior-pituitary hormones and transcriptional factors in the resected pituitary tumor. On immunohistochemical staining, most of the tumor cells were strongly stained for GH antibody, while some cells were strongly positive for adrenocorticotropic hormone (ACTH). Gene expression analysis of a transsphenoidal surgery sample of the pituitary gland revealed that ACTH-related genes, such as POMC, Tpit, and NeuroD1 mRNA, had higher expression in the tumor tissue than the nonfunctional adenoma but lower expression compared to an adenoma of typical Cushing’s disease. Further, double-labeling detection methods with a fluorescent stain for ACTH and GH demonstrated the coexistence of ACTH-positive cells (GH-negative) among the GH-positive cells in the tumor. Additionally, Pit-1 expression was reduced in the ACTH-positive cells from tumor tissue primary culture. Conclusion Here we described a case of a pituitary tumor diagnosed with acromegaly associated with SCD. We performed quantitative-expression analyses of transcriptional factors of the tumor tissue and immunohistochemistry analysis of tumor-derived primary culture cells, which suggested that the multihormonal pituitary adenoma concomitant with Pit-1 and Tpit lineage cells caused acromegaly associated with SCD