Stercoral ulcer-related lower rectal perforation is an uncommon but potentially under-recognized condition. We report three cases of elderly women with localized lower rectal perforation associated with persistent rectal fecal impaction. All patients presented with hematochezia without generalized peritonitis despite the continued passage of loose or muddy stools. Serial computed tomography revealed persistent fecal impaction in the lower rectum during the clinical course. Continued bowel movement does not necessarily indicate effective rectal evacuation. Recognition of persistent rectal fecal impaction may facilitate an earlier diagnosis and appropriate management.

Methotrexate (MTX) and Janus kinase (JAK) inhibitors are effective treatments for rheumatoid arthritis (RA); however, they may increase the risk of opportunistic infections. We herein report a case of a patient with RA receiving MTX and upadacitinib who developed an active cytomegalovirus (CMV) infection and Epstein-Barr virus (EBV) reactivation, complicated by CMV meningitis and virus-associated hemophagocytic lymphohistiocytosis (HLH). This case highlights that clinicians should consider not only herpes zoster, but also infection or reactivation involving non-VZV herpesviruses, including CMV and EBV, particularly in patients receiving JAK inhibitors in combination with other immunosuppressive agents.

Renal complications resulting from persistent, uncontrolled hypertension include renovascular hypertension (RVH) and hypertensive emergency (crisis)-related nephropathy (HEN), both of which are characterized by hyperreninemia and are involved in the progression of nephropathy. In RVH, renal artery stenosis leads to increased renin secretion from the affected kidney, which induces focal segmental glomerulosclerosis (FSGS) lesions in the contralateral kidney, resulting in proteinuria. In HEN, severe hypertension (>200/120 mmHg) induces endothelial cell proliferation in renal arterioles, resulting in edematous thickening of the intima and narrowing of the lumen. This process increases renin secretion from the juxtaglomerular apparatus (JGA), further worsening hypertension and resulting in glomerular collapse and rapidly progressive renal impairment. Angiotensin-converting enzyme inhibitors (ACEIs) and angiotensin receptor blockers (ARBs) suppress aldosterone activity and promote renin activity, respectively. Prolonged administration has been suggested to lead to JGA hyperplasia and smooth muscle cell proliferation in the renal arterioles.

Lorlatinib, a central nervous system (CNS)-penetrant anaplastic lymphoma kinase (ALK) tyrosine kinase inhibitor, is effective in treating leptomeningeal carcinomatosis. A woman in her 30s with ALK-positive lung adenocarcinoma and leptomeningeal carcinomatosis developed an asymptomatic subdural hematoma (SDH) 7 weeks after starting lorlatinib, coinciding with the regression of leptomeningeal lesions. The posterior extent of the SDH appeared to be partially contiguous with the focal dural enhancement observed before treatment. Lorlatinib was continued under multidisciplinary supervision. The hematoma resolved without surgery and did not recur during the 6 years of treatment. SDH may occur during the rapid regression of leptomeningeal disease with suspected dural involvement under CNS-penetrant ALK inhibitor therapy.

A 52-year-old man presented with severe hyponatremia and Rathke's cleft cyst (RCC)-associated hypophysitis with enlargement of the pituitary stalk. Hyponatremia persisted despite treatment with high-dose hydrocortisone, hypertonic saline, and loop diuretics, ultimately requiring low-dose tolvaptan. Hyponatremia associated with RCC is usually attributed to secondary adrenal insufficiency (SAI), in which glucocorticoid replacement generally restores free water excretion but may unmask arginine vasopressin deficiency (AVP-D). In the present case, however, persistent AVP-mediated water retention beyond SAI appeared to predominate, suggesting AVP dysregulation associated with inflammatory pituitary involvement. This case highlights the therapeutic dilemma of balancing masked AVP-D against persistent AVP excess in hyponatremia associated with RCC.

A 56-year-old woman presented with an acute cerebral embolism. Mechanical thrombectomy retrieved a white embolus, and a pathological examination revealed a tumor fragment consistent with colorectal carcinoma. Imaging revealed no liver or lung metastases, but it identified a patent foramen ovale and pulmonary embolism, suggesting a paradoxical embolic pathway. Given the size of the tumor fragment, passage through the hepatic or pulmonary microcirculation would be difficult to explain given the size of the tumor fragment. These findings suggest venous invasion with direct entry of tumor material into the circulation, followed by right-to-left shunting, which resulted in a cerebral embolism.

Background　Evidence comparing infections across advanced therapies (ADTs) for ulcerative colitis (UC) remains inconsistent, and infection category profiles are poorly characterized, particularly in real-world Japanese settings. We compared the risk of hospitalized infections and descriptively characterized the distribution of infection categories among hospitalized infection events across ADTs.Methods　We conducted a retrospective cohort study using the Medical Data Vision Database. Patients with UC who initiated treatment with a tumor necrosis factor (TNF) antagonist, ustekinumab, tofacitinib, or vedolizumab between April 2008 and May 2022 were followed. Adjusted hazard ratios (aHRs) were estimated using Cox models (TNF antagonists as the reference), and hospitalized infections were classified according to the organ system.Results　We included 9,012 patients receiving ADTs (TNF antagonists, 3,990; ustekinumab, 1,380; tofacitinib, 1,183; and vedolizumab, 2,459). Hospitalized infections occurred in 90, 16, 21, and 52 patients prescribed TNF antagonists, ustekinumab, tofacitinib, and vedolizumab, respectively; the incidence rates per 1,000 person-years were 19.09, 9.64, 14.53, and 17.24, respectively. In the multivariable analysis, ustekinumab was associated with a lower risk of hospitalized infection than TNF antagonists (aHR 0.46, 95% confidence interval [CI] 0.25-0.82), whereas tofacitinib (aHR 0.73, 95% CI 0.43-1.22) and vedolizumab (aHR 0.76, 95% CI 0.53-1.10) were not significantly different. Among the first hospitalized infection events, the distribution of infection categories was comparable across ADTs, with respiratory infections being the most common.Conclusions　Ustekinumab was associated with a lower risk of infection-related hospitalization than TNF antagonists. The distribution of infection categories among the first hospitalized infection events was comparable across the ADTs. These findings provide the first large-scale, real-world, comparative evidence from Japan.

A 36-year-old man developed acute progressive ataxia, an impaired consciousness, and ophthalmoplegia after an upper respiratory tract infection. A cerebrospinal fluid analysis revealed pleocytosis in the patient. Initial plain brain magnetic resonance imaging (MRI) showed no remarkable findings, whereas initial brain perfusion single-photon emission computed tomography demonstrated hyperperfusion in the brainstem. Follow-up contrast-enhanced MRI revealed diffuse dural thickening, and a histopathological examination supported the diagnosis of hypertrophic pachymeningitis. Anti-GQ1b antibodies were detected, leading to a diagnosis of Bickerstaff brainstem encephalitis (BBE). This case suggests that hypertrophic pachymeningitis may be a rare complication of BBE.

We present the case of a 73-year-old man diagnosed with insulin autoimmune syndrome (IAS) during an investigation of hypoglycemia. This disease is a rare cause of hypoglycemia induced by autoantibodies against insulin. The patient was diagnosed with IgG4-related disease (IgG4-RD). Moreover, the patient had myelodysplastic syndrome (MDS). We hypothesized that immunological dysregulation driven by MDS may have contributed to the coexistence of these two rare conditions in our patient. Treatment with prednisolone promptly resolved hypoglycemia and improved the disease activity of IgG4-RD. We present this case as, to the best of our knowledge, it is the first peer-reviewed case report of coexisting IAS and IgG4-RD.

Background Gastroesophageal reflux disease (GERD) commonly occurs or worsens after laparoscopic sleeve gastrectomy (LSG); however, evidence regarding optimal medical management remains limited. This prospective study evaluated the endoscopic and symptomatic outcomes of Vonoprazan (VPZ), a potassium-competitive acid blocker, in erosive esophagitis (EE) following LSG.Methods Among 54 consecutive patients who underwent LSG, 19 who developed GERD symptoms within one year were included in the analysis. At symptom onset, esophagogastroduodenoscopy (EGD) was promptly performed to assess EE according to the Los Angeles (LA) classification, and the Frequency Scale for the Symptoms of GERD (FSSG) questionnaire was administered. All symptomatic patients were treated with VPZ (20 mg once daily for 4 weeks), after which EGD and FSSG assessments were repeated to evaluate therapeutic efficacy.Results Of the 19 patients, 16 (84.2%) had EE (LA grades A/B/C: 4/7/5), and 3 had non-erosive reflux disease (NERD). Among the patients with EE, 11 had de novo cases, and no grade C esophagitis was present preoperatively. The median interval to symptom onset was 40 days (range, 2-196 days). After 4 weeks of VPZ, complete mucosal healing was confirmed in all patients with EE (100% healing rate). The median FSSG scores in the EE group significantly improved from 28 (14-45) to 7 (1-31) (p<0.001).Conclusion Short-term improvements in the endoscopic findings and symptoms were observed after 4 weeks of VPZ treatment in patients with EE, which represented the majority of postoperative GERD cases in this cohort. Larger controlled studies are required to confirm these findings.

A prompt and accurate diagnosis is essential because the management of thrombotic microangiopathy (TMA) depends on its underlying etiology. We report a case of diffuse cutaneous systemic sclerosis (dcSSc) in which scleroderma renal crisis-associated TMA preceded the development of overt skin sclerosis. A 53-year-old woman presented with TMA and severe renal dysfunction. She tested positive for anti-RNA polymerase III antibodies and subsequently developed skin sclerosis, leading to a diagnosis of dcSSc. Angiotensin-converting enzyme inhibitor therapy resulted in a clinical improvement in the patient. Therefore, systemic sclerosis should be considered in the differential diagnosis of TMA, even in the absence of skin manifestations at presentation.