Background Hawaiʻi has the highest nontuberculous mycobacterial (NTM) lung infection prevalence in the United States. Limited data regarding skin and soft tissue infections (SSTI) due to NTM in Hawaiʻi exists. This study describes patient demographics, clinical courses of infection, treatment patterns, and clinical outcomes of NTM SSTIs in Hawaiʻi. Methods A retrospective chart review (n = 50) of patients diagnosed and treated at Hawaiʻi Pacific Health facilities for NTM SSTIs between January 2010 and July 2021 was conducted. Patient demographics, clinical course, and treatment data were collected from electronic medical records. Results Half of the patient population consisted of females, and the average age of patients during infection was 49 years (SD = 25.6). The majority of cases (80%) were caused by rapidly growing mycobacteria (RGM), most commonly Mycobacterium abscessus. NTM SSTI by race were Asian (48%), White (28%), and Native Hawaiian and Other Pacific Islanders (16%). Almost all Asian patients with NTM SSTI were Filipino or Japanese. Diagnosis was frequently delayed. The average time to diagnosis was 116 days. Most patients achieved complete resolution (72%) following a prolonged course of antimicrobial treatment (mean = 196 days) with surgical debridement. Conclusion Increased awareness among physicians and the community of non-mycobacterial skin infections is essential in Hawaiʻi due to the high prevalence of NTM and the high percentage of predisposed populations. Increased awareness of NTM could reduce delayed diagnosis and improve patient care. Further studies are required to inform optimal treatment and diagnostic strategies, improve patient outcomes, and aid public health surveillance efforts.

The presence of rheumatic heart disease (RHD) and systemic lupus erythematosus (SLE) has rarely been described in one patient. This report describes an adolescent Polynesian male with RHD who developed SLE years later. Initially, he fulfilled modified Jones criteria for rheumatic fever with aortic insufficiency, transient arthritis, elevated streptococcal titers, and a high erythrocyte sedimentation rate with a negative antinuclear antibody (ANA). He responded well to nonsteroidal anti-inflammatory and penicillin prophylaxis, which supported the diagnosis of rheumatic fever. Five years after his RHD diagnosis, he developed pancreatitis with glomerulonephritis, nephrosis, and pancytopenia. In addition, laboratory results revealed that he had multiple autoantibodies: anti-Sm and extremely elevated anti-dsDNA and ANA, fulfilling diagnostic criteria for SLE. The patient was treated, and he responded to pulse steroids followed by oral steroid therapy. To our knowledge, there are no known reported cases of a patient who was diagnosed with both RHD and SLE and met the clinical criteria for both diseases. The rarity of this concurrent disease process in one patient suggests a possible overlap in humoral immunity toward self-antigens as well as ethnic variability that increases predisposition to rheumatologic diseases.

In obesity, chronic membrane-localization of CD36 free fatty acid (FFA) translocase, but not other FFA transporters, enhances FFA uptake and intracellular lipid accumulation. This ectopic lipid accumulation promotes insulin resistance by inhibiting insulin-induced GLUT4 glucose transporter trafficking and glucose uptake. GLUT4 and CD36 cell surface delivery is triggered by insulin- and contraction-induced signaling, which share conserved downstream effectors. While we have gathered detailed knowledge on GLUT4 trafficking, the mechanisms regulating CD36 membrane delivery and subsequent FFA uptake in skeletal muscle are not fully understood. The exocyst trafficking complex facilitates the docking of membrane-bound vesicles, a process underlying the controlled surface delivery of fuel transporters. The exocyst regulates insulin-induced glucose uptake via GLUT4 membrane trafficking in adipocytes and skeletal muscle cells and plays a role in lipid uptake in adipocytes. Based on the high degree of conservation of the GLUT4 and CD36 trafficking mechanisms in adipose and skeletal muscle tissue, we hypothesized that the exocyst also contributes to lipid uptake in skeletal muscle and acts through the targeted plasma membrane delivery of CD36 in response to insulin and contraction. Here, we show that the exocyst complex is necessary for insulin- and contraction-induced CD36 membrane trafficking and FFA uptake in muscle cells.