Citations

The elderly chronic kidney disease (CKD) population is growing. Both aging and CKD can disrupt calcium (Ca2+) homeostasis and cause alterations of multiple Ca2+-regulatory mechanisms, including parathyroid hormone, vitamin D, fibroblast growth factor-23/Klotho, calcium-sensing receptor and Ca2+-phosphate product. These alterations can be deleterious to bone mineral metabolism and soft tissue health, leading to metabolic bone disease and vascular calcification and aging, termed CKD-mineral and bone disorder (MBD). CKD-MBD is associated with morbid clinical outcomes, including fracture, cardiovascular events and all-cause mortality. In this paper, we comprehensively review Ca2+ regulation and bone mineral metabolism, with a special emphasis on elderly CKD patients. We also present the current treatment-guidelines and management options for CKD-MBD.

Although the ulnar nerve is closely associated with the triceps brachii muscle, the literature does not normally describe it as supplying this muscle. However, recent research has examined the ulnar nerve in the upper arm and identified branches supplying the medial head of the triceps brachii muscle. This study aims to expand upon this research by describing the course and incidence of these branches in a larger sample size. We examined 50 specimens in 25 cadavers. Ulnar innervation of the medial head of the triceps brachii was identified in 14 specimens (28%). The mean distance of the ulnar nerve branch midpoint was 26% along a line between the surgical neck and an epicondyle line, with a range of 11–39%. Innervation of the triceps brachii muscle by the ulnar nerve has important clinical and surgical implications. Clin. Anat. 26:1028–1030, 2013. © 2013 Wiley Periodicals, Inc.

A significant mimicker of malignancy in the esophagus is the presence of atypical/bizarre stromal cells (BSCs). Two patients, a 60-year-old woman and a 59-year-old man, with esophageal polyps at the gastroesophageal junction showed highly atypical/bizarre cells in the polyps’ stroma. BSCs were admixed with inflammatory cells and had large atypical nuclei, prominent nucleoli, and variably abundant amphophilic cytoplasm. Immunohistochemical studies showed that BSCs expressed vimentin whereas S-100, CD68, HMB45, CD45, Pan-cytokeratin, CK5/6, p63, CD10, EMA, MART-1, desmin, smooth muscle actin, CD31, CD34, and CMV were negative. Ki-67 showed low proliferative rate (less than 1% positivity). No evidence of intracellular mucin was found after histochemical stains (AB/PAS and mucicarmine). Follow-up endoscopic mucosal resection was available in both cases and showed benign esophageal mucosa and submucosa with disappearance, in one case, or marked decrease of BSCs. Esophageal BSCs reports in the literature invariably locate them in distal esophagus polyps or masses. Awareness of BSCs, of their location and associations, may help to prevent misdiagnosis of malignancy. The literature of esophageal BSCs is reviewed and the approach to this abnormality is discussed.

ObjectiveReview Mayo Clinic experience of localized tongue amyloidosis.Study DesignCase series with retrospective chart review.SettingAcademic medical center.Subjects and MethodsCases of localized tongue amyloidosis were identified from the dysproteinemia database at the Mayo Clinic in Rochester, Minnesota. Electronic records were reviewed with focus on presenting symptoms, laboratory results (ie, serum or urine immunoelectrophoresis, bone marrow biopsy, and fat aspirate analysis), treatment modality, and status of disease at follow‐up.ResultsSix cases of localized tongue amyloidosis presented to the Mayo Clinic between 1969 and 2011. Mean patient age was 69 years (range, 43‐90). Patients presented with asymptomatic tongue mass(es). Biopsy of the tongue mass in all patients showed amyloid on Congo red stains. Work‐up for systemic amyloidosis, including bone marrow biopsy, fat aspiration, and serum and urine protein immunoelectrophoresis, was negative for all 6 patients, nor was there other organ involvement. Two patients underwent resection of the lesions, and the remaining patients elected for observation. Recurrence requiring repeat excision occurred in 1 of the patients that underwent resection. Repeat evaluation for systemic involvement was performed in 3 patients 1 to 3 years after the initial diagnosis. None of these patients went on to develop systemic involvement.ConclusionsLocalized tongue amyloidosis remains a rare diagnosis and requires exclusion of systemic involvement. Localized lesions may be observed or resected; however, recurrence may occur with resection. Patients with localized tongue amyloidosis do not appear to be at increased risk of developing systemic involvement.

Abstract Inflammation elevates intracellular Ca2+ ([Ca2+]i) concentrations in airway smooth muscle (ASM). Store-operated Ca2+ entry (SOCE) is an important source of [Ca2+]i mediated by stromal interaction molecule–1 (STIM1), a sarcoplasmic reticulum (SR) protein. In transducing SR Ca2+ depletion, STIM1 aggregates to form puncta, thereby activating SOCE via interactions with a Ca2+ release-activated Ca2+ channel protein (Orai1) in the plasma membrane. We hypothesized that STIM1 aggregation is enhanced by inflammatory cytokines, thereby augmenting SOCE in human ASM cells. We used real-time fluorescence microscopic imaging to assess the dynamics of STIM1 aggregation and SOCE after exposure to TNF-α or IL-13 in ASM cells overexpressing yellow fluorescent protein–tagged wild-type STIM1 (WT-STIM1) and STIM1 mutants lacking the Ca2+-sensing EF-hand (STIM1-D76A), or lacking the cytoplasmic membrane binding site (STIM1ΔK). STIM1 aggregation was analyzed by monitoring puncta size during the SR Ca2+ depletion induced by cyclopiazonic acid (CPA). We found that puncta size was increased in cells expressing WT-STIM1 after CPA. However, STIM1-D76A constitutively formed puncta, whereas STIM1ΔK failed to form puncta. Furthermore, cytokines increased basal WT-STIM1 puncta size, and the SOCE triggered by SR Ca2+ depletion was increased in cells expressing WT-STIM1 or STIM1-D76A. Meanwhile, SOCE in cells expressing STIM1ΔK and STIM1 short, interfering RNA (siRNA) was decreased. Similarly, in cells overexpressing STIM1, the siRNA knockdown of Orai1 blunted SOCE. However, exposure to cytokines increased SOCE in all cells, increased basal [Ca2+]i, and decreased SR Ca2+ content. These data suggest that cytokines induce a constitutive increase in STIM1 aggregation that contributes to enhanced SOCE in human ASM after inflammation. Such effects of inflammation on STIM1 aggregations may contribute to airway hyperresponsiveness.

Prostatic stromal hyperplasia with atypia (PSHA) is a rare histologic finding diagnosed incidentally on prostate biopsies, transurethral resection specimens, and radical prostatectomy specimens. PSHA has a bizarre histologic appearance and these lesions often raise concern for sarcoma; however, their clinical course is indolent and does not include extraprostatic progression. We discuss a case of PHSA discovered on prostate biopsy performed for an abnormal digital rectal examination and review the literature on this rare pathologic finding.