Navigating the labyrinth of peritoneal and extraperitoneal anatomy: abdominal spread made easy with a case based review.

Essential to understanding disease spread in abdomen is to separate the peritoneum from the extraperitoneum. These areas have distinct anatomy with well-define separate pathways. The peritoneum is comprised of connected recesses that are potential spaces, normally not imaged except when containing excess fluid or air. Peritoneal recesses are formed by the opposing peritoneal surfaces and subdivided by the attachments of the ligaments and mesenteries to the parietal peritoneum. Disease flows within the recesses by changes in abdominal pressure. This forms a distinct spread pattern. The extraperitoneum is traditionally stratified by the renal fascia into the anterior and posterior pararenal spaces and the perirenal space. The fascia contains and directs spread from the contained organs with the compartments. Each space has a unique spread pattern defined by the containing fascia. The extraperitoneum is connected to the mesenteries and ligaments forming the subperitoneal space. This space interconnects the extraperitoneum with the mesenteries allowing for the normal continuum of blood vessels, lymphatics, and nerves but also forms the pathways for bidirectional spread of disease.

A head with two tales: demystifying early spread of disease from the pancreatic head.

The pancreas is a centrally located extraperitoneal organ within the anterior pararenal space. It is extensively connected to the extraperitoneal spaces by location and a network of mesenteries and ligaments. This provides interconnected avenues for vessels, lymphatics, and nerves to course through-as well as avenues for the spread of disease. The head of the pancreas results from the fusion of its ventral analog (anterior head) with its dorsal analog (posterior head). This differentiation provides two distinct pathways of spread of disease from the head of the pancreas. This communication will discuss the embryology, anatomy, and pathways of disease spread from the anterior and posterior pancreatic head. While any disease process can use these pathways, proven cases of adenocarcinoma of the pancreas are used for illustrations.

Opportunistic CT Assessment of Parathyroid Glands: Utility of Radiologist-Recommended Biochemical Evaluation for Diagnosing Primary Hyperparathyroidism.

BACKGROUND. Existing gaps in primary hyperparathyroidism (PHPT) diagnosis and treatment have prompted calls for systemic change in the approach to this disease. One proposed change is opportunistic assessment for enlarged parathyroid glands on routine CT examinations, to target biochemical testing to individuals most likely to have un-diagnosed PHPT. OBJECTIVE. The purpose of our study was to assess the utility of a radiologist recommendation for biochemical testing in patients with a suspected enlarged parathyroid gland on routine CT for identifying previously undiagnosed PHPT. METHODS. This retrospective study included patients without known or suspected PHPT who underwent routine CT (i.e., performed for reasons other than known or suspected parathyroid disease) between August 2019 and September 2021 in which the clinical CT report included a radiologist recommendation for biochemical testing to evaluate for possible PHPT because of a suspected enlarged parathyroid gland. Neuroradiologists at the study institution included this recommendation on the basis of individual judgment without formal criteria. The EHR was reviewed to identify patients who underwent subsequent laboratory evaluation for PHPT. An endocrine surgeon used available laboratory results and clinical data to classify patients as having PHPT, secondary hyper-parathyroidism, or no parathyroid disorder independent of the CT findings. RESULTS. The sample comprised 39 patients (median age, 68 years; 20 women, 19 men) who received the radiologist recommendation for biochemical evaluation. Of these patients, 13 (33.3%) received the recommended biochemical evaluation. Of the 13 tested patients, three (23.1%) were classified as having PHPT, four (30.8%) as having secondary hyperparathyroidism, and six (46.2%) as having no parathyroid disorder. Thus, the number of patients needing to receive a radiologist recommendation for biochemical testing per correct PHPT diagnosis was 13.0, and the number of patients needing to undergo laboratory testing per correct PHPT diagnosis was 4.3. One of the three patients classified as having PHPT underwent surgical resection of the lesion identified by CT, which was shown on histopathologic evaluation to represent hypercellular parathyroid tissue. CONCLUSION. Radiologist recommendations for biochemical testing in patients with suspected enlarged parathyroid glands on routine CT helped to identify individuals with undiagnosed PHPT. CLINICAL IMPACT. Opportunistic assessment for enlarged parathyroid glands on routine CT may facilitate PHPT diagnosis.

Sex-Dependent Role of Adipose Tissue HDAC9 in Diet-Induced Obesity and Metabolic Dysfunction.

Obesity is a major risk factor for both metabolic and cardiovascular disease. We reported that, in obese male mice, histone deacetylase 9 (HDAC9) is upregulated in adipose tissues, and global deletion of HDAC9 protected against high fat diet (HFD)-induced obesity and metabolic disease. Here, we investigated the impact of adipocyte-specific HDAC9 gene deletion on diet-induced obesity in male and female mice. The HDAC9 gene expression was increased in adipose tissues of obese male and female mice and HDAC9 expression correlated positively with body mass index in humans. Interestingly, female, but not male, adipocyte-specific HDAC9 KO mice on HFD exhibited reduced body weight and visceral adipose tissue mass, adipocyte hypertrophy, and improved insulin sensitivity, glucose tolerance and adipogenic differentiation gene expression. Furthermore, adipocyte-specific HDAC9 gene deletion in female mice improved metabolic health as assessed by whole body energy expenditure, oxygen consumption, and adaptive thermogenesis. Mechanistically, compared to female mice, HFD-fed male mice exhibited preferential HDAC9 expression in the stromovascular fraction, which may have offset the impact of adipocyte-specific HDAC9 gene deletion in male mice. These results suggest that HDAC9 expressed in adipocytes is detrimental to obesity in female mice and provides novel evidence of sex-related differences in HDAC9 cellular expression and contribution to obesity-related metabolic disease.