巨大リンパ管奇形（頚部顔面病変）

Sarcopenic obesity (SO) is characterized by excess adiposity together with reduced skeletal muscle mass and impaired muscle function, and primarily affects older adults. Its pathogenesis involves chronic low-grade inflammation, insulin resistance, ectopic lipid accumulation, mitochondrial dysfunction, and disrupted skeletal muscle homeostasis. Current models mainly explain how inflammatory and metabolic signals are generated through adipose-muscle crosstalk, but less clearly address why these signals persist within the local interstitial environment. The lymphatic system maintains interstitial homeostasis by regulating tissue drainage, mediator clearance, immune trafficking, lipid transport, and microenvironmental renewal. In SO, ageing and obesity may jointly impair lymphatic function: obesity increases inflammatory, lipid, and metabolic lymphatic stress, whereas ageing lowers baseline lymphatic reserve. These abnormalities may sustain a pro-inflammatory, pro-lipotoxic, and repair-unfavorable interstitial milieu. In this review, we summarize ageing- and obesity-associated lymphatic abnormalities and propose a clearance-centered framework in which impaired lymphatic clearance amplifies local inflammation, lipid stress, insulin resistance, gut-muscle axis disturbance, and defective skeletal muscle repair in SO. Skeletal muscle deterioration may further weaken contraction-assisted lymphatic return, potentially reinforcing impaired clearance and local inflammatory-metabolic stress. This framework complements the adipose-muscle crosstalk model and highlights testable directions for future SO-specific studies.

Passive immunotherapy targeting amyloid-β (Aβ) has emerged as a major therapeutic strategy for Alzheimer's disease (AD), yet its clinical benefits remain modest and are frequently accompanied by vascular adverse events such as amyloid-related imaging abnormalities (ARIA). While the removal of extracellular Aβ plaques is associated with therapeutic efficacy, accumulating evidence suggests that additional cellular and vascular mechanisms may also contribute to complementary therapeutic outcomes alongside plaque removal. Recent studies show that Aβ antibodies are broadly distributed within the brain and interact with multiple neural and immune cell populations, rather than being limited to Aβ plaques. These observations support an expanded view of passive Aβ immunotherapy as a multicellular coordinated clearance process. Aβ antibodies engage diverse cellular and anatomical compartments, including neurons, glial cells, perivascular macrophages, peripheral immune cells, and meningeal lymphatic pathways, thereby influencing Aβ dynamics across intracellular and extracellular pools. Within this framework, therapeutic outcomes are influenced not only by plaque clearance but also by interactions between Aβ antibodies and cellular and anatomical compartments that regulate Aβ clearance and treatment-associated vascular response. This perspective may help explain variability in clinical efficacy and the emergence of vascular side effects, while also providing additional considerations for optimizing Aβ antibody design and therapeutic strategies.

BACKGROUND: Kaposiform hemangioendothelioma and kaposiform lymphangiomatosis (KHE/KLA) are rare, non-malignant lymphovascular anomalies often complicated by Kasabach-Merritt phenomenon (KMP). Morbidity and mortality are high. There are no prior reports of the dietary management in these disorders. CASE REPORT: A 2-month-old female presented with hemorrhagic ascites, abdominal compartment syndrome, and severe KMP secondary to extensive retroperitoneal and intestinal KHE/KLA. Following emergent surgical management for abdominal decompression and diverting ileostomy, medical and nutritional therapy with steroids, vincristine, sirolimus, and parenteral nutrition were employed for management. After maintaining a near fat-free enteral diet supplemented with intravenous lipid therapy in the outpatient setting, she underwent successful ileostomy takedown 18 months after initial diagnosis without the need for intestinal resection and maintenance of adequate growth. CONCLUSION: This case underscores the value of clinical and pathology-guided diagnosis, coordinated medical therapy, and dietary fat restriction for achieving intestinal autonomy and preserving bowel length in intra-abdominal KHE/KLA.

Staphylococcus aureus, particularly methicillin-resistant S. aureus (MRSA), remains a leading cause of skin and soft tissue infections (SSTIs) worldwide. Patients with renal edema, including those with nephrotic syndrome and chronic kidney disease (CKD), and critical illness, are particularly susceptible because of barrier dysfunction, immune impairment, and altered antimicrobial pharmacokinetics. This narrative review examines the mechanisms linking renal edema to increased susceptibility to cutaneous S. aureus infection and discusses their diagnostic and therapeutic implications. Three interconnected pathophysiological pathways appear central to this susceptibility: disruption of the cutaneous barrier, nephrotic and uremic immune dysfunction, and impaired lymphatic immune surveillance. These abnormalities facilitate bacterial colonization, and invasion, while S. aureus further exploits the renal host through adhesins, toxins, biofilm formation, and immune-evasion mechanisms. The review also highlights the challenges of managing severe staphylococcal infections in patients with kidney disease and critical illness, where augmented renal clearance, expanded volume of distribution, extracorporeal renal support, and fluctuating renal function may substantially influence antimicrobial exposure. Current management requires early recognition, source control, individualized antimicrobial selection, renal-adapted dosing, therapeutic drug monitoring, and antimicrobial stewardship. Although emerging anti-virulence and immunomodulatory strategies show promise, most remain at the preclinical or early translational stage. Overall, renal edema should be regarded as a biologically active modifier of host-pathogen interactions that contributes to increased susceptibility to cutaneous S. aureus infection across the spectrum of kidney disease.