Non-traumatic rupture of the superior thyroid artery with concomitant parathyroid adenoma and multinodular goiter.
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ABSTRACT:
SUBMITTER: Hanashiro N
PROVIDER: S-EPMC5536369 | biostudies-other | 2017 Jul
REPOSITORIES: biostudies-other
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Project description:Traumatic subarachnoid hemorrhage (SAH), a common finding following head trauma, is usually a benign condition with a favorable outcome, seldom requiring surgical intervention. Unlike nontraumatic aneurysmal SAH, most cases of traumatic SAH occur in the sulci of the cerebral convexities, and only rarely arise at the base of the brain. Basal traumatic SAH can be life-threatening and is primarily associated with rupture of vertebrobasilar arteries. We herein present a rare case of basal traumatic SAH resulting from rupture of the posterior communicating artery (PCoA). A 77-year-old male was taken to the emergency department in a semicomatose state. Upon arrival at emergency room, the patient had a Glasgow coma scale (GCS) score of 6 (E1M3V2), and the neurologic examination demonstrated no focal neurologic deficit. Although the trauma history was evident from abrasions and bruising on the face and chest, brain computed tomography (CT) demonstrated basal SAH, which is typical for nontraumatic aneurysmal SAH. Subsequent digital subtraction angiography (DSA) disclosed a traumatic rupture at the mid-portion of right PCoA and ongoing extravasation of contrast media. Despite emergent trapping of the right PCoA by endovascular surgery, the patient's clinical condition only minimally improved. The patient remained bed-ridden with stuporous mentality and persistent hydrocephalus. To the best of our knowledge, this is the first reported case of basal traumatic SAH originating from rupture of the PCoA. This case demonstrates that a meticulous vascular workup is mandatory for every patient with basal SAH, even though a trauma history is clear.
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Project description:Primary benign tumors of the trachea are uncommon. These tumors may cause tracheal occlusion and lead to a misdiagnosis of asthma. Ectopic parathyroid adenoma (EPA) can be seen anywhere between the mandibular angle and the mediastinum. The distal part of the trachea is a rare location for EPA, and EPA obstructing the endotracheal lumen has not been reported in the literature. We herein describe a 52-year-old female with a several-year history of asthma treatment who presented with progressive dyspnea. Computed tomography revealed a mass that was obstructing the tracheal lumen. Total mass excision was performed via endobronchial treatment, and pathologic examination revealed EPA.
| S-EPMC4246358 | biostudies-literature
Project description:Parathyroid adenoma is the main cause of primary hyperparathyroidism, which is characterized by enlarged parathyroid glands and excessive parathyroid hormone secretion. Here, we performed transcriptome analysis, comparing parathyroid adenomas with normal parathyroid gland tissue. RNA extracted from ten parathyroid adenoma and five normal parathyroid samples was sequenced, and differentially expressed genes (DEGs) were identified using strict cut-off criteria. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analyses were performed using DEGs as the input, and protein-protein interaction (PPI) networks were constructed using Search Tool for the Retrieval of Interacting Genes/Proteins (STRING) and visualized in Cytoscape. Among DEGs identified in parathyroid adenomas (n = 247; 45 up-regulated, 202 down-regulated), the top five GO terms for up-regulated genes were nucleoplasm, nucleus, transcription DNA-template, regulation of mRNA processing, and nucleic acid binding, while those for down-regulated genes were extracellular exosome, membrane endoplasmic reticulum (ER), membrane, ER, and melanosome. KEGG enrichment analysis revealed significant enrichment of five pathways: protein processing in ER, protein export, RNA transport, glycosylphosphatidylinositol-anchor biosynthesis, and pyrimidine metabolism. Further, PPI network analysis identified a densely connected sub-module, comprising eight hub molecules: SPCS2, RPL23, RPL26, RPN1, SEC11C, SEC11A, RPS25, and SEC61G. These findings may be helpful in further analysis of the mechanisms underlying parathyroid adenoma development.
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| S-EPMC2942929 | biostudies-literature
Project description:Background Parathyroid adenoma (PA) is a common but relatively poorly understood endocrine tumor. A significant number of PA patients also have papillary thyroid carcinoma (PTC). The clinicopathological characteristics of PA and its relationship with PTC need further study. Methods The clinical data of 99 PA patients were reviewed and the clinicopathologic features of PA were analyzed. PTC occurred in 22 PA patients. The clinicopathologic features of 22 patients with PA + PTC and 77 patients with PA alone were compared. According to age, gender and thyroid surgery methods, 22 PA + PTC patients were matched with 1,123 patients with PTC alone during the same period. The pathological characteristics of the two groups of patients were compared. All data analysis was performed using SPSS23.0, variables were compared by t-test, chi square test or Mann Whitney U-test as appropriate. Results Ninety-nine PA patients (21 males, 78 females) with a median age of 51 [10–80] years were included. The preoperative parathyroid hormone (PTH) (P=0.007) and preoperative blood calcium (P=0.036) of male patients were higher than those of female patients, and the proportion of asymptomatic patients (P=0.008) and postoperative PTH level (P=0.013) were lower. The preoperative PTH level (P=0.002), preoperative blood calcium level (P=0.004), preoperative alkaline phosphatase (ALP) level (P=0.018) and postoperative PTH levels (P=0.023) in PA + PTC group were lower than those in PA group. The asymptomatic rate was higher in PTC + PA group than that in PA group (P<0.001). There was no statistical difference between PA + PTC group and PTC group in multifocal tumor, capsule invasion, lymph node metastasis (P>0.05). The lymph node metastasis rate in PA + PTC group (9/215) was significantly lower than that in PTC group (37/337) (P=0.005). Conclusions PA exhibited the following characteristics: occurred in all age groups; more common in women but more severe in men; more located in the lower pole. The coexistence of PTC and PA did not promote the progression of PA, nor did it increase the aggressiveness of PTC. Conversely, their co-existence may lead to early diagnosis of the disease. PA patients (22.2%) also have PTC, so surgeons should pay attention to thyroid disease to prevent the need for reoperation.
| S-EPMC10240434 | biostudies-literature
Project description:Transcriptional profiling of genes expressed in normal parathyroid glands (Normal) and adenomatous parathyroid glands from patients with primary hyperparathyroidism (PHPT). Stratagen Human Refernece RNA, pooled from 10 human cell lines, was used to identify genes, which are specifically expressed or suppressed in parathyroid tissue. Comparison between normal and tumor parathyroids shows genes that might be involved in hyperproliferation and PTH hypersecretion in tumors.
2016-12-01 | GSE83421 | GEO
Project description:IntroductionVascular complications like superior mesenteric artery (SMA) thrombosis and pancreaticoduodenal artery (PDA) pseudoaneurysm carry high morbidity and mortality. SMA provides the primary arterial supply to the small intestine and ascending colon. PDA aneurysms are extremely rare, accounting for only 2 % of all visceral artery aneurysms. We present a rare case of SMA thrombosis with concomitant PDA pseudoaneurysm.Case presentationHerein is the case of a 60-year-old male who presented with rectorrhagia, persistent generalized abdominal pain. After being diagnosed with colitis and mesenteric artery thrombosis based on a computed tomography (CT) scan, he was discharged from the hospital with rivaroxaban and mesalazin. However, he had to return to the hospital due to worsening of the symptoms. After a proper workout, SMA artery thrombosis with a concomitant PDA pseudoaneurysm was diagnosed for him. Therefore, he underwent surgery to stent the thrombosis and coil the pseudoaneurysm. His symptoms dramatically improved after the treatment.DiscussionAngiography is the diagnostic and, with embolization, therapeutic procedure of choice, with surgery as a backup if embolization fails. However, even with these procedures, the mortality rate is high if the pseudoaneurysm ruptures.ConclusionIn order to carry out the proper choice of surgical treatment before further complications occur, SMA thrombosis and PDA pseudoaneurysms must be investigated in each patient presenting with nonspecific abdominal pain, regardless of the risk factors.
| S-EPMC10425394 | biostudies-literature
Project description:BackgroundPrimary hyperparathyroidism is characterized by enlarged parathyroid glands due to an adenoma (80-85 %) or multiglandular disease (~15 %) causing hypersecretion of parathyroid hormone (PTH) and generally hypercalcemia. Parathyroid cancer is rare (<1-5 %). The epigenetic mark 5-hydroxymethylcytosine (5hmC) is reduced in various cancers, and this may involve reduced expression of the ten-eleven translocation 1 (TET1) enzyme. Here, we have performed novel experiments to determine the 5hmC level and TET1 protein expression in 43 parathyroid adenomas (PAs) and 17 parathyroid carcinomas (PCs) from patients who had local invasion or metastases and to address a potential growth regulatory role of TET1.ResultsThe global 5hmC level was determined by a semi-quantitative DNA immune-dot blot assay in a smaller number of tumors. The global 5hmC level was reduced in nine PCs and 15 PAs compared to four normal tissue samples (p < 0.05), and it was most severely reduced in the PCs. By immunohistochemistry, all 17 PCs stained negatively for 5hmC and TET1 showed negative or variably heterogeneous staining for the majority. All 43 PAs displayed positive 5hmC staining, and a similar aberrant staining pattern of 5hmC and TET1 was seen in about half of the PAs. Western blotting analysis of two PCs and nine PAs showed variable TET1 protein expression levels. A significantly higher tumor weight was associated to PAs displaying a more severe aberrant staining pattern of 5hmC and TET1. Overexpression of TET1 in a colony forming assay inhibited parathyroid tumor cell growth.Conclusions5hmC can discriminate between PAs and PCs. Whether 5hmC represents a novel marker for malignancy warrants further analysis in additional parathyroid tumor cohorts. The results support a growth regulatory role of TET1 in parathyroid tissue.
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Project description:BackgroundThyroid stimulating hormone (TSH) secreting pituitary adenoma (TSHoma) with coexisting thyroid cancer is extremely rare, and proper treatment of both diseases may pose a unique clinical challenge. When TSHoma has plurihormonality, particularly involving the co-secretion of growth hormone (GH), management can be more complicated. Herein, we present a difficult-to-manage case of papillary thyroid cancer with an incurable TSH/GH-secreting pituitary adenoma.Case presentationA 59-year-old man was referred to our hospital due to memory impairment and inappropriate TSH level. Sella magnetic resonance imaging revealed a huge pituitary mass extending to the suprasellar area. Clinical diagnosis of TSH/GH co-secreting pituitary adenoma was made based on elevated free T4, total T3, serum α-subunit, insulin-like growth factor-1 levels and non-suppressible GH levels after oral glucose loading. Rectal cancer and multifocal papillary thyroid microcarcinoma (PTMC) were diagnosed during initial screening for internal malignancy; lower anterior resection was performed and close observation was planned for PTMC. Long-acting octreotide therapy was commenced, which resulted in a dramatic reduction in TSHoma size and facilitated control of hormonal excess. Total thyroidectomy and radioactive iodine (RAI) therapy were needed during follow up due to the growth of PTMC. After the surgery, the pituitary adenoma represented resistance to somatostatin analogue therapy and the tumor size gradually increased despite the addition of dopamine agonist therapy. Furthermore, TSH suppressive therapy with levothyroxine was impossible and an adequate TSH level for RAI therapy was unmountable. Late debulking pituitary surgery was ineffective, and the patient gradually deteriorated and lost to follow up.ConclusionWe report the first aggravated case of TSH/GH co-secreting pituitary tumor after total thyroidectomy for concomitant multifocal PTMC. Deferring of thyroid surgery until the TSHoma is well controlled may be the optimal therapeutic strategy in patients with TSHoma and coexistent thyroid cancer; ablative thyroid surgery may result in catastrophic pituitary tumor growth.
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