Impact Of body Mass Index on Cardiopulmonary Outcomes of COVID-19 Hospitalizations Complicated by Severe Sepsis.

Background: Body Mass Index (BMI) has a significant impact on Coronavirus disease (COVID-19) patient outcomes; however, major adverse cardiac and cerebrovascular outcomes in patients with severe sepsis have been poorly understood. Our study aims to explore and provide insight into its association. Methods: This is an observational study looking at the impact of BMI on COVID-19-severe sepsis hospitalizations. The primary outcomes are adjusted odds of all-cause in-hospital mortality, respiratory failure, and major adverse cardiac and cerebrovascular events (MACCE), which include acute myocardial infarction, cardiac arrest, and acute ischemic stroke. The secondary outcome was healthcare resource utilization. Coexisting comorbidities and patient features were adjusted with multivariable regression analyses. Results: Of 51,740 patients with severe COVID-19-sepsis admissions, 11.4% were overweight, 24.8% had Class I obesity (BMI 30-34.9), 19.8% had Class II obesity (BMI 35-39.9), and 43.9% had the categorization of Class III obesity (BMI >40) cohorts with age>18 years. The odds of MACCE in patients with class II obesity and class III obesity (OR 1.09 and 1.54; 95CI 0.93-1.29 and 1.33-1.79) were significantly higher than in overweight (p < 0.001). Class I, Class II, and Class III patients with obesity revealed lower odds of respiratory failure compared to overweight (OR 0.89, 0.82, and 0.82; 95CI 0.75-1.05, 0.69-0.97, and 0.70-0.97), but failed to achieve statistical significance (p = 0.079). On multivariable regression analysis, all-cause in-hospital mortality revealed significantly higher odds in patients with Class III obesity, Class II, and Class I (OR 1.56, 1.17, and 1.06; 95CI 1.34-1.81, 0.99-1.38, and 0.91-1.24) vs. overweight patients (p < 0.001). Conclusions: Patients with Class II and Class III obesity had significantly higher odds of MACCE and in-hospital mortality in COVID-19-severe sepsis admissions.

Retrograde venous invasion in renal cell carcinoma: a complication of sinus vein and main renal vein invasion.

Renal cell carcinoma, especially clear cell, gains access to the venous system as the initial route of extrarenal spread. Intravenous growth can involve extrarenal veins or renal veins in other portions of the kidney, referred to herein as retrograde venous invasion. This study investigates the incidence and defines the pathological features of retrograde venous invasion. Retrograde venous invasion is defined as rounded nodules of tumor separated from the primary tumor and in a location that conforms to the venous outflow. Nine cases of retrograde venous invasion were identified in a series of 115 renal cell carcinomas (8%). Two blocks from each case were stained with elastic van Gieson, Masson trichrome, CD31 and desmin to evaluate intravenous involvement. All cases were staged using the 2010 TNM staging schema. The tumors ranged in size from 4.2 to 17 cm. All cases showed sinus vein and main renal vein invasion (pT3a); three cases involved the vena cava (pT3b). Direct continuity between the primary tumor and tumor in the main renal vein was grossly evident in every case. Involved sinus veins could be followed retrograde to the cortex between renal pyramids with tumor nodules arrayed along the pyramid-cortex interface. Histologically, the involved parenchymal veins lacked a smooth muscle media and elastica. CD31 demonstrated an endothelial cell lining around many nodules. As intravenous nodules enlarged endothelium was lost, extra-venous invasion occurred and nodules coalesced and merged with the primary tumor. In conclusion, retrograde venous invasion occurred only with main renal vein involvement. Gross evaluation allowed detection in every case. Histological confirmation of intravenous nature is challenging due to the absence of smooth muscle in parenchymal veins. As retrograde growth becomes extensive nodules coalesce and merge with the primary tumor and may be included in measurement of primary tumor size if this process is unrecognized.

Diagnosis of IgG4-related tubulointerstitial nephritis.

IgG4-related systemic disease is an autoimmune disease that was first recognized in the pancreas but also affects other organs. This disease may manifest as tubulointerstitial nephritis (IgG4-TIN), but its clinicopathologic features in the kidney are not well described. Of the 35 patients with IgG4-TIN whose renal tissue specimens we examined, 27 (77%) had acute or progressive chronic renal failure, 29 (83%) had involvement of other organ systems, and 18 of 23 (78%) had radiographic abnormalities. Elevated total IgG or IgG4 serum levels were present in 79%. All pathologic specimens featured plasma cell-rich TIN, with most showing diffuse, expansile interstitial fibrosis. Immune complexes along the tubular basement membranes were present in 25 of 30 (83%). All specimens had a moderate to marked increase in IgG4+ plasma cells by immunohistochemistry. We used a control group of 175 pathologic specimens with plasma cell-rich interstitial infiltrates that can mimic IgG4-TIN to examine the diagnostic utility of IgG4 immunostaining. Excluding pauci-immune necrotizing and crescentic glomerulonephritis, IgG4 immunohistochemistry had a sensitivity of 100% (95% CI 90-100%) and a specificity of 92% (95% CI 86-95%) for IgG4-TIN. Of the 19 patients with renal failure for whom treatment and follow-up data were available, 17 (89%) responded to prednisone. In summary, because no single test definitively diagnoses IgG4-related systemic disease, we rely on a combination of histologic, immunophenotypic, clinical, radiographic, and laboratory features. When the disease manifests in the kidney, our data support diagnostic criteria that can distinguish IgG4-TIN from other types of TIN.

Teenage cervical screening in a high risk American population.

BACKGROUND: The new 2009 ACOG guideline for cervical cytology screening changed the starting age to 21 years regardless of the age of onset of sexual intercourse. However, many recent studies have shown a dramatic increase in the incidence of cervical epithelial abnormalities among adolescents within the past two decades. MATERIALS AND METHODS: For this study, the reports of 156,342 cervical cytology were available of which 12,226 (7.8%) were from teenagers. A total of 192 teenagers with high grade intraepithelial lesion (HSIL) cervical cytology were identified. The ages ranged from 13 to 19 years with a mean of 17.7 years and a median of 18 years. Among them, 31.3% were pregnant, 12.0% were postpartum, and 13.5% were on oral contraceptive. Ninety-eight had prior cervical cytology. RESULTS: The teenagers had statistically significant higher detection rates of overall abnormal cervical cytology (23.6% vs. 6.6%, P = 0), with 15.4% vs. 3.2% (P = 0) of low grade intraepithelial lesion (LSIL) and 1.8% vs. 1.0% (P = 2.56 × 10(-13) ) of HSIL compared to women ≥20 years. The teenage group had the highest abnormal cytology among all age groups. The LSIL/HSIL ratio was 8.5:1 for teenagers and 3.1:1 for women ≥20 years. A total of 131 teenagers had cervical biopsies within 12 months of the HSIL cytology, with diagnoses of 39 CIN 3, 1 VAIN 3, 15 CIN 2, 62 CIN 1, and 14 had a negative histology (CIN 0). Only in 19 of these 39 women, the CIN 2/3 lesion proved to be persistent. CONCLUSION: We conclude that cytology screening of high risk teenagers is effective in detecting CIN 2/3 lesions. Moreover, treatment and careful follow-up can be realized.

Fine needle aspiration of parapharyngeal space adult rhabdomyoma: a case report.

BACKGROUND: Rhabdomyomas are rare benign tumors of striated muscle and include cardiac and extracardiac types. Extracardiac rhabdomyomas are divided in three subtypes (adult, fetal, genital). The adult type is usually found in the head and neck regions of elderly persons. Misinterpretations in initial diagnosis of adult rhabdomyomas on fine needle aspiration have been reported. CASE: A 64-year-old man presented with gurgling and difficulty swallowing for approximately 3 months. Computed tomography and magnetic resonance imaging showed a 5.8-cm solid mass located in the right parapharyngeal space. Fine needle aspiration smears were cellular, showing cohesive clusters of cells with scattered individual cells. Cells had abundant eosinophilic glassy cytoplasm, peripherally placed round nuclei, and prominent nucleoli. Many traversing vessels were noted, but cross-striations were not seen. The cell block demonstrated clusters of cells with abundant eosinophilic granular cytoplasm, some with clear and/or vacuolated cytoplasm, and possible cross-striations. Tumor cells were positive for desmin. The lesion closely resembled normal muscle tissue. Electron microscopy showed many cells containing actin and myosin filaments with Z-band material. CONCLUSION: Correct diagnosis can be achieved with a combination of awareness of the lesion, familiarity with the characteristic cytologic features, and application of appropriate immunohistochemistry markers. Classic electron microscopic findings can support the diagnosis.

Lymphatic differentiation in renal angiomyolipomas.

Renal angiomyolipomas are mesenchymal neoplasms with varying proportions of smooth muscle, adipose tissue, and abnormal blood vessels. Although the presence of lymphangiomatous-like foci is frequently noted in large series of angiomyolipoma, lymphatic differentiation has not been previously studied. Twelve angiomyolipomas from 10 patients were identified. All tumors expressed a melanocytic marker, HMB-45 or Melan-A. Twenty-eight paraffin blocks (1-4 per tumor) were stained for lymphatic endothelial cell markers, podoplanin, and D2-40, and the presence and distribution of lymphatic differentiation were recorded. The angiomyolipomas ranged from typical triphasic tumors to leiomyoma-like and lipoma-like tumors. All 12 tumors showed positive staining with podoplanin, and all 6 tumors stained for D2-40 were also positive, indicative of lymphatic differentiation. Lymphatic differentiation was variably observed throughout the tumors. It was most prevalent in myoid areas of the triphasic angiomyolipomas and in the leiomyoma-like variant, but infrequent and widely scattered within the adipose regions of triphasic angiomyolipoma and in the lipoma-like variant. The lymphatics were usually small, often irregularly shaped, and isolated vessels in fat, whereas in myoid regions lymphatics were clustered and in some areas formed a sinusoidal or labyrinth-like pattern. Lymphatics were commonly adjacent to abnormal arteries. However, unlike the lymphatics in the normal renal cortex, a consistent adventitial association was not observed and the clustering around arteries is regarded as reflecting the myoid regions that typically exist in these areas. In conclusion, lymphatic differentiation is common in angiomyolipomas, preferentially located in myoid regions. These data expand the mesenchymal pluripotential profile of renal angiomyolipomas.

Eosinophilic gastroenteritis of the pancreas: an unusual cause of obstructive jaundice.

Eosinophilic gastroenteritis (EG) is a rare gastrointestinal disorder of undetermined etiology and is manifest by eosinophilic infiltration of any area of gastrointestinal tract, most frequently stomach and small intestine. Peripheral eosinophilia is present in about 80% of patients. Definitive diagnosis requires histologic evidence of eosinophilic infiltration; which is usually patchy in distribution. Steroids are the mainstay of treatment. We present a case of 47-year-old man with abdominal pain, jaundice, and marked eosinophilia. Endoscopic retrograde cholangio-pancreatogram revealed a dilated common bile duct. There was biopsy proven eosinophilic infiltration in stomach, duodenum, gall bladder, and pancreas. Obstructive jaundice is an extremely rare manifestation of EG. This unusual case illustrates the wide variety of gastrointestinal manifestations caused by EG and emphasizes the importance of clinical suspicion and endoscopic mucosal biopsies in diagnosis of EG. This entity should be considered in the patients with chronic and relapsing gastrointestinal symptoms.

Increased transferrin receptor expression following 11q23 deletion as a mechanism of malignant progression in chronic lymphocytic leukemia.

Chronic lymphocytic leukemia (CLL) is a common adult leukemia characterized by the accumulation of mature neoplastic B-lymphocytes. Typically, CLL follows an indolent course, with most patients surviving for many years. However, 10-20% of CLL patients carry 11q23 chromosomal deletions and often exhibit a more severe disease course, with earlier onset of symptoms, shortened lymphocyte doubling time, poor response to therapy, and shortened survival. The molecular basis for 11q23 deletions resulting in a poor prognosis is currently poorly understood. The tumor suppressor gene, ataxia-telangiectasia mutated (ATM, 11q22.3-23.1), is considered a likely candidate gene whose loss could result in the poor prognosis associated with 11q23 deletion and is mutated in a significant percentage of CLL cases. Recently, recombinant ATM expression in ATM-deficient cells was found to decrease transferrin receptor (TfR) expression, suggesting that deletion of the chromosomal region carrying ATM results in increased TfR expression. TfR imports iron into cells, an event necessary for DNA synthesis and cell growth. Additionally, rapidly growing malignant cells, including lymphomas and CLL, often express high TfR levels. Based on this, we propose that one molecular mechanism by which 11q23 deletions confer a poor prognosis in CLL is via increased TfR expression secondary to ATM loss, resulting in the increased cellular iron import, and hence increased capacity for malignant growth. Our hypothesis may also partially explain why gallium, an atomically iron-like toxic metal that binds to transferrin and the TfR is incorporated into cells and was previously demonstrated to have anti-tumor activity in patients with lymphomas refractory to other chemotherapeutic treatments.