The dose-limiting salivary gland toxicity of ²²⁵Ac-labelled PSMA for treatment of metastatic, castration-resistant prostate cancer remains unresolved. Suppressing the metabolism of the gland by intraparenchymal injections of botulinum toxin appears to be a promising method to reduce off-target uptake. A ⁶⁸Ga-PSMA PET/CT scan performed 45 days after injection of 80 units of botulinum toxin A into the right parotid gland in a 63-year-old patient showed a decrease in the SUVmean in the right parotid gland of up to 64% as compared with baseline. This approach could be a significant breakthrough for radioprotection of the salivary glands during PSMA radioligand therapy.
Botulinum Toxins ; Humans ; Metabolism ; Methods ; Middle Aged ; Parotid Gland ; Positron-Emission Tomography and Computed Tomography ; Prostatic Neoplasms ; Salivary Glands ; Xerostomia

We report the case of a patient who presented with cystic lymphoid hyperplasia of the right parotid gland as the index diagnosis of HIV infection. Histological examination of the excised parotid gland revealed a solid-cystic lymphoepithelial lesion with a non-keratinous squamous epithelium, which grew into the lymphoid component via anastomosing cords and islands. These anastomosing cords and islands contained variably abundant B cells, several subepithelial multinucleated histiocytes, salivary ducts infiltrated by small lymphocytes, and a dense lymphoid infiltrate containing lymphoid follicles with enlarged, irregular germinal centres.
Adult ; B-Lymphocytes ; cytology ; Biopsy ; Epithelial Cells ; cytology ; Epithelium ; metabolism ; HIV Infections ; diagnosis ; Humans ; Hyperplasia ; pathology ; virology ; Immunohistochemistry ; Lymphocytes ; cytology ; Male ; Parotid Gland ; pathology ; virology ; Salivary Glands ; pathology ; Tomography, X-Ray Computed

Although renal calcium crystal deposits (nephrocalcinosis) may occur in acute phosphate poisoning as well as type 1 renal tubular acidosis (RTA), hyperphosphatemic hypocalcemia is common in the former while normocalcemic hypokalemia is typical in the latter. Here, as a unique coexistence of these two seperated clinical entities, we report a 30-yr-old woman presenting with carpal spasm related to hypocalcemia (ionized calcium of 1.90 mM/L) due to acute phosphate poisoning after oral sodium phosphate bowel preparation, which resolved rapidly after calcium gluconate intravenously. Subsequently, type 1 RTA due to Sjogren's syndrome was unveiled by sustained hypokalemia (3.3 to 3.4 mEq/L), persistent alkaline urine pH (> 6.0) despite metabolic acidosis, and medullary nephrocalcinosis. Through this case report, the differential points of nephrocalcinosis and electrolyte imbalances between them are discussed, and focused more on diagnostic tests and managements of type 1 RTA.
Acidosis, Renal Tubular/*diagnosis/etiology ; Acute Disease ; Adult ; Antibodies, Antinuclear/blood ; Calcium Gluconate/therapeutic use ; Chronic Disease ; Female ; Humans ; Hydrogen-Ion Concentration ; Hypocalcemia/*chemically induced/complications/drug therapy ; Nephrocalcinosis/complications/*diagnosis/ultrasonography ; Parotid Gland/ultrasonography ; Phosphates/*adverse effects ; Salivary Glands/radionuclide imaging ; Sjogren's Syndrome/complications/*diagnosis/metabolism ; Submandibular Gland/ultrasonography

OBJECTIVETo investigate the clinical and laboratory characteristics of tumor like Sjögren's syndrome (TLSS) patients and non-tumor like Sjögren's syndrome (NTLSS) and the incidence of lymphoma in patients of Sjögren's syndrome (SS).

METHODSA retrospective analysis was carried out in 199 primary SS (including TLSS) patients who were recruited in Peking University School and Hospital of Stomatology from 1998 to 2010. Clinical and laboratory information were collected. The patients were divided into two groups: TLSS (n = 25) and NTLSS (n = 174). Clinical and laboratory characteristics were compared between these two groups by a statistical analysis.

RESULTSOf the 25 TLSS patients, 23 had enlargements of parotid glands and 2 had enlargements of submandibular glands. There were significant differences of salivary scintigraphy appearance (P = 0.018), hypergammaglobulinemia (P = 0.014), rheumatoid factor positive rate (P = 0.001), formation of the ectopic germinal centers (P = 0.014), double positive rate of anti-SSA antibody and anti-SSB antibody (P < 0.001) between the TLSS and NTLSS patients. Among the 25 TLSS patients, 3 developed lymphomas, accounting for 1.5% (3/199) of the total 199 patients and 12% (3/25) of the TLSS patients. Lymphoma subtypes included one diffused large B-cell lymphoma and two mucosa-associated lymphoid tissue lymphoma. There was no lymphoma detected in NTLSS patients.

CONCLUSIONSThere are clinical and laboratory differences between TLSS and NTLSS patients, with a more tendency to develop lymphomas in TLSS patients.

Adult ; Antibodies, Antinuclear ; metabolism ; Female ; Humans ; Hypergammaglobulinemia ; metabolism ; Lymphoma, B-Cell, Marginal Zone ; diagnostic imaging ; etiology ; metabolism ; pathology ; Lymphoma, Large B-Cell, Diffuse ; diagnostic imaging ; etiology ; metabolism ; pathology ; Male ; Middle Aged ; Parotid Gland ; pathology ; Radionuclide Imaging ; Retrospective Studies ; Rheumatoid Factor ; metabolism ; Salivary Glands ; diagnostic imaging ; Sjogren's Syndrome ; complications ; diagnostic imaging ; metabolism ; pathology ; Submandibular Gland ; pathology

OBJECTIVETo investigate the expression and relationship of programmed cell death 5 (PDCD5) and cell apoptosis in the parotid gland after leading duct ligation in rat and elucidate the role of PDCD5 on the atophy of parotid gland.

METHODSThe Wistar rat model of leading duct ligation was established, and the samples of parotid gland were obtained from different time point (0, 1, 3, 5, 7, 14, 21, 30, 60, 90 and 120 d). The expression of PDCD5 protein was examined by immunohistochemistry. Cell apoptosis was detected by terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end labeling (TUNEL).

RESULTSThe distribution of PDCD5 protein in normal parotid was in cytoplasm with uniformity. The expression of PDCD5 protein was significantly increased and reached the peak at 3 d (1.261 ± 0.048) following main duct ligation. PDCD5 was located both in cytoplasm and nuclear of parotid gland cells. The PDCD5 density in acinar cells was higher than that in duct cells at day 1 and 3 after duct ligation (P < 0.01). The apoptotic cells were obviously upregulated at 3 d after duct ligation. The apoptosis index observed in acinar cells [(21.750 ± 0.119)%] was more than that in duct cells [(5.720 ± 0.205)%]. The difference of apoptosis index between acinar cells and duct cells was statistically significant (P < 0.01). The increased PDCD5 levels were positively correlated with cell apoptosis induced by duct ligation.

CONCLUSIONSThe expression of PDCD5 is associated with the atophy of the parotid gland after rat parotid duct ligation, indicating that PDCD5 might play an important role in apoptotic pathways after parotid duct ligation.

Acinar Cells ; metabolism ; Animals ; Apoptosis ; Apoptosis Regulatory Proteins ; metabolism ; Atrophy ; Cell Nucleus ; metabolism ; Cytoplasm ; metabolism ; Ligation ; Male ; Parotid Gland ; cytology ; metabolism ; pathology ; Rats ; Rats, Wistar ; Salivary Ducts

Adenocarcinoma ; metabolism ; pathology ; Adenocarcinoma, Clear Cell ; metabolism ; pathology ; Biomarkers ; metabolism ; Carcinoma ; metabolism ; pathology ; surgery ; Diagnosis, Differential ; Female ; Humans ; Keratins ; metabolism ; Membrane Proteins ; metabolism ; Middle Aged ; Mucin-1 ; metabolism ; Myoepithelioma ; metabolism ; pathology ; surgery ; Neoplasm Recurrence, Local ; Parotid Gland ; surgery ; Parotid Neoplasms ; metabolism ; pathology ; surgery ; S100 Proteins ; metabolism

OBJECTIVETo investigate the effect of Sarcandra glabra in scavenging reactive oxygen species (ROS) produced by γ-ray irradiation in the parotid gland of miniature pigs.

METHODSForty-five male miniature pigs were randomly divided into control group, radiation group and radiation plus medication group, and each group contained 3 parallel groups (subgroups a, b and c). From 1 week before exposure of the parotid gland region to 15 Gy γ-ray irradiation (which was not administered in the control group), the miniature pigs in radiation plus medication group were given Sarcandra glabra powder, while those in the other groups received an equal amount of saline. Bilateral parotid glands were taken and weighed on the days 10, 40 and 90 following the exposure in subgroups a, b, and c, respectively, and ROS content in the parotid glands were determined by enzyme-linked immunosorbent assay.

RESULTSThe content of ROS was significantly lower in radiation plus medication group than in the radiation group (P<0.01). In the radiation plus medication group, the ROS content showed no significant difference between subgroups a and b or between subgroups a and c (P>0.01), but differed significantly between subgroups b and c (P<0.01). Sarcandra glabra showed a strong ROS-scavenging effect 10 days after the irradiation, and the ROS content was similar with that in the control group (P>0.01); at 40 and 90 days, the ROS-scavenging effect of Sarcandra glabra was still observable, but the ROS content was significantly higher in the irradiation plus medication group than in the control group (P<0.01).

CONCLUSIONSarcandra glabra displays a ROS-scavenging effect in the parotid gland of miniature pigs against irradiation, especially at 10 days following the exposure, which may serve as the main mechanism for the protective effect of Sarcandra glabra against radiation injury in the parotid gland.

Animals ; Drugs, Chinese Herbal ; pharmacology ; Free Radical Scavengers ; pharmacology ; Magnoliopsida ; chemistry ; Male ; Parotid Gland ; metabolism ; radiation effects ; Radiation Injuries ; prevention & control ; Radiation-Protective Agents ; pharmacology ; Reactive Oxygen Species ; metabolism ; Swine ; Swine, Miniature

Carcinosarcoma ; metabolism ; pathology ; radiotherapy ; surgery ; Follow-Up Studies ; Humans ; Keratins ; metabolism ; Ki-67 Antigen ; metabolism ; Male ; Middle Aged ; Mucin-1 ; metabolism ; Parotid Gland ; pathology ; surgery ; Parotid Neoplasms ; metabolism ; pathology ; radiotherapy ; surgery ; Radiotherapy, Adjuvant ; Vimentin ; metabolism

PURPOSE: The sarco/endoplasmic reticulum Ca(2+)-ATPase (SERCA), encoded by ATP2A2, is an essential component for G-protein coupled receptor (GPCR)-dependent Ca(2+) signaling. However, whether the changes in Ca(2+) signaling and Ca(2+) signaling proteins in parotid acinar cells are affected by a partial loss of SERCA2 are not known. MATERIALS AND METHODS: In SERCA2(+/-) mouse parotid gland acinar cells, Ca(2+) signaling, expression levels of Ca(2+) signaling proteins, and amylase secretion were investigated. RESULTS: SERCA2(+/-) mice showed decreased SERCA2 expression and an upregulation of the plasma membrane Ca(2+) ATPase. A partial loss of SERCA2 changed the expression level of 1, 4, 5-tris-inositolphosphate receptors (IP(3)Rs), but the localization and activities of IP3Rs were not altered. In SERCA2(+/-) mice, muscarinic stimulation resulted in greater amylase release, and the expression of synaptotagmin was increased compared to wild type mice. CONCLUSION: These results suggest that a partial loss of SERCA2 affects the expression and activity of Ca(2+) signaling proteins in the parotid gland acini, however, overall Ca(2+) signaling is unchanged.
Amylases/metabolism ; Animals ; Blotting, Western ; Calcium/metabolism ; Calcium Signaling/drug effects/genetics/*physiology ; Carbachol/pharmacology ; Immunohistochemistry ; Inositol 1,4,5-Trisphosphate Receptors/metabolism ; Mice ; Mice, Knockout ; Parotid Gland/*metabolism ; Sarcoplasmic Reticulum Calcium-Transporting ATPases/genetics/*metabolism ; Signal Transduction/drug effects/genetics/physiology

PURPOSE: In non-excitable cells, which include parotid and pancreatic acinar cells, Ca(2+) entry is triggered via a mechanism known as capacitative Ca(2+) entry, or store-operated Ca(2+) entry. This process is initiated by the perception of the filling state of endoplasmic reticulum (ER) and the depletion of internal Ca(2+) stores, which acts as an important factor triggering Ca(2+) entry. However, both the mechanism of store-mediated Ca(2+) entry and the molecular identity of store-operated Ca(2+) channel (SOCC) remain uncertain. MATERIALS AND METHODS: In the present study we investigated the Ca(2+) entry initiation site evoked by depletion of ER to identify the localization of SOCC in mouse parotid and pancreatic acinar cells with microfluorometeric imaging system. RESULTS: Treatment with thapsigargin (Tg), an inhibitor of sarco/endoplasmic reticulum Ca(2+)-ATPase, in an extracellular Ca(2+) free state, and subsequent exposure to a high external calcium state evoked Ca(2+) entry, while treatment with lanthanum, a non-specific blocker of plasma Ca(2+) channel, completely blocked Tg-induced Ca(2+) entry. Microfluorometric imaging showed that Tg-induced Ca(2+) entry started at a basal membrane, not a apical membrane. CONCLUSION: These results suggest that Ca2+ entry by depletion of the ER initiates at the basal pole in polarized exocrine cells and may help to characterize the nature of SOCC.
Animals ; Calcium/*metabolism ; Calcium Channels/drug effects/metabolism ; Cells, Cultured ; Endoplasmic Reticulum/drug effects/*metabolism ; Mice ; Mice, Inbred ICR ; Microscopy, Fluorescence ; Pancreas/cytology/drug effects/*metabolism ; Parotid Gland/cytology/drug effects/*metabolism ; Thapsigargin/pharmacology