Thin Arrow Research Articles

O-02 A RARE COLLISION TUMOR OF THE PITUITARY: CO-EXISTENCE OF CRANIOPHARYNGIOMA AND PROLACTINOMA

Abstract Introduction Pituitary adenomas are the most common lesions of the sellar region. The most common (40%) functional pituitary adenomas are prolactinomas. Craniopharyngiomas are epithelial tumors of embryonal origin originating from Rathke's sac. Very few cases of collision tumors co-existing with pituitary adenoma and craniopharyngioma have been described in the literature. Clinical Case We present a case of histopathologically proven craniopharyngioma accompanying prolactinoma in a 63-year-old female patient diagnosed with prolactinoma 40 years ago. She was treated with bromocriptine after the diagnosis, and the treatment was switched to cabergoline four years later. Although the biochemical remission was achieved, there was no significant decrease in tumor size. She had not received any treatment during last 4 years before the administration. She was admitted to our clinic with a complaint of headache. Her serum prolactin level was 1550 ng/ml ((Reference:4,79-23 ng/ml). According to the pituitary Magnetic Resonans Imaging(MRI); reports were as follows in 2007; an isolated 8x6x13 mm adenoma was observed, and then in 2015; another cystic lesion (craniopharyngioma?) was detected adjacent to the infindibular stalk in addition to the defined pituitary adenoma (Figure 1a). In the last pituitary MRI (2022); a cystic lesion extending from the sellar cavity to the suprasellar cistern and a solid mass lesion located left to the cavernous sinus, was observed (Figure 1b). Upon a dramatic increase of the tumor volume on pituitary MRI, she underwent pituitary surgery. The histopathological diagnosis was adamantinomatous craniopharyngioma. Postoperative prolactin level decreased to 10 ng/ml. Since prolactin levels decreased after the diagnosis of craniopharyngioma, the surgical material was re-evaluated by the pathologist. No evidence of prolactinoma was found. Significant regression was observed in the patient's 1st month follow-up pituitary MRI compared to the preoperative MRI. Postoperatively, prolactin levels remained within the normal range for the first 6 months. After the 6th month, cabergoline treatment was started when prolactin levels increased to 497 ng/ml. Conclusion Pituitary adenoma and craniopharyngioma collision tumors are extremely rare. Only 6 patients with the coexistence of craniopharyngioma and prolactinoma have been reported in the literature, including our case. Histopathological diagnosis may be necessary to differentiate craniopharyngioma from cystic macroprolactinoma.Figure 1:Magnetic Resonans ImagingFigure 1: a. Post-contrast coronal pituitary MRI examination revealed a pituitary adenoma (thick arrow) located in the left cavernous sinus. aAnother cystic mass lesion (thin arrow) was detected adjacent to the infindibular stalk.; b. Coronal contrast-enhanced pituitary MRI image showed cystic (arrow) and

P-48 Post-traumatic Panhypopitutarism after an in-vehicle traffic accident: A case report

Abstract Introduction Hypopituitarism, occurs most commonly from pituitary tumors and a head injury, though a fracture of the base of the skull is considered a rare cause. Traumatic brain injury causes severe disability and endocrine dysfunction in a significant proportion of patients. Hypopituitarism diagnosed with endocrine symptoms related to hypoadrenocorticotropinemia, hypothyroidism and hypogonadism. We describe a case of posttraumatic panhypopitutarism presenting with symptoms of secondary amenorrhea, loss of appetite, nausea, vomiting, hearing loss and hypoglycemia after an in-vehicle traffic accident. Clinical Case A 28-year-old female patient with no medical history was admitted with symptoms of nausea, vomiting, anorexia, amenorrhea, and hypoglycemia after an in-vehicle traffic accident. It was learned that the patient's menstrual periods were regular before the accident and she did not have any complaints. Panhypopitutarism was observed in the examinations performed (Table 1). In the follow-ups, 10% intravenous dextrose solution and 20 mg prednisolone every 6 hours were started due to the hypoglycemic course. Prednisolone was reduced and discontinued, and hydrocortisone treatment was started from 30 mg/day. L-thyroxine replacement was started one week after the steroid treatment. Computed tomography (CT) showed deformity and collapse secondary to the fracture at the base of the sella and on contrast-enhanced pituitary magnetic resonance (MRI) imaging, it was observed that the morphology of the sella was distorted in T1-weighted sections, pituitary tissue could not be clearly distinguished, and there was collapse at the base of the sella in the right lateral section; the present findings were thought to support pituitary insufficiency (Figure 1). Hormone replacement therapy was given for secondary amenorrhea. One year after the accident, she wanted to be a pregnant and ovulation was induced by the injection of human menopausal gonadotrophin (HMG) following human chorionic gonadotrophin (HCG) at a large dose. She got pregnant in the first cycle. Conclusion In a patient with Panhypopituitarism, who could not be pregnant spontaneously, clinical practice of ovulation–induction treatment including administration of hCG and follicle-stimulating hormone, pulsatile GnRH (gonadotropin-releasing hormone), and in vitro fertilization, enabled the hypopituitary women to become ovulation and pregnancy. In our case, pregnancy was achieved after adequate hormone replacement therapy.Figure 1.CT and MRI images of the patientFigure. (a) Coronal CT section showing deformity-subsidence at the base of the sella secondary to fracture, (b and c) sagittal and coronal contrast-enhanced MRI showing subsidence at the base of the sella (thick arrow) with herniation of pituitary tissue (short arrow) and distorted-deformed infundibular stalk (thin arrow), respectively. Table 1.Laboratory workup*ACTH: Adrenocorticotropic hormone; FSH: follicle-stimulating hormone; LH: Luteinizing hormone; TSH: thyroid stimulating hormone; fT4: thyroxine; GH: Growth hormone; IGF-1: Insulin-like growth factor 1

Retropharyngeal Abscess with Clival Osteomyelitis Caused by Staphylococcus intermedius and Staphylococcus aureus in a 6-Year-old Boy.

To the Editors: In the March 2023 issue of PIDJ, we read a case report of septic arthritis of the atlanto-occipital joint caused by Staphylococcus intermedius, Di Siena, and coworkers. In our hospital, we treated a similar case of a 6-year-old boy with a retropharyngeal abscess and clival osteomyelitis caused by S. intermedius and S. aureus. Our patient was a 6-year-old previously healthy boy. He presented with a low-grade fever (38.3 max.), headaches and torticollis. At a local hospital, computed tomography of the head and neck was performed, and a diagnosis of retropharyngeal abscess was established. The patient was sent to our clinic for additional workup and therapy. His blood count was 8600 L/cmm with a neutrophil predominance of 76%. C-reactive protein was 81.7 mg/L. The rest of the routine biochemical tests were unremarkable. The throat swab test results were negative. Two sets of blood cultures taken before antimicrobial therapy were sterile. We consulted an otolaryngology specialist who performed an adenoidectomy with incision and drainage of the retropharyngeal abscess on the third day of hospitalization. A sample of pus sent for culture showed growth of S. intermedius sensitive to penicillin, ampicillin, ceftriaxone and vancomycin. A wound swab taken during the operation showed the growth of S. intermedius (same sensitivity) and S. aureus, sensitive to penicillin and flucloxacillin but resistant to clindamycin. The patient gradually defervesced in 3 days and was continuously afebrile until discharge. First few days, he had mild dysphagia with apparent torticollis, and his head was slightly inclined to the left. After the operation, his neck movements gradually increased, and his headache and dysphagia ceased. We started treatment with cefazoline and clindamycin for the first 2 days and then with vancomycin and meropenem for 7 days, pending microbiological results. After gaining insight into the microbiology results, we changed the therapy to penicillin G. Total intravenous therapy was 21 days. After discharge from the hospital, treatment with amoxicillin was continued for the next 3 weeks. On the 10th day of hospitalization, we performed magnetic resonance (MR) of the head and neck, which showed liquid collection (18 × 5 mm, laterolateral and anterioposterior, respectively) at the site of the retropharyngeal abscess incision downwards to C3. It also showed destruction of the clivus 11 × 8 × 10 mm (craniocaudal, anterioposterior and laterolateral, respectively), reaching the periosteum and dura mater but without forming an epidural liquid collection. The remaining MR images were unremarkable (Fig. 1A and C).FIGURE 1.: A: Sagittal short tau inversion recovery image: hyperintense signal in clivus indicates bone edema (thick arrow); hyperintense signal in epipharynx indicates edema and fluid collection (thin arrow). B: Sagittal short tau inversion recovery image: minimal residual hyperintense signal in the clivus—almost complete regression (thick arrow); normal finding in the epipharynx (thin arrow). C: Axial T2 image: hyperintense signal in the epipharynx indicates edema and fluid collection (white arrow). D: Axial T2 image: normal finding of epipharynx (white arrow).On the control visit, the patient was completely well and had free neck movement, with no fever or pain. His inflammatory markers (erythrocyte sedimentation rate and C-reactive protein) and blood count were normal. Control MR of the head and neck showed minimal residual changes (Fig. 1B and D). In conclusion, we treated a 6-year-old, previously healthy boy with a retropharyngeal abscess and clival osteomyelitis caused by S. intermedius and penicillin-sensitive S. aureus. Treatment consisted of incision and drainage of the retropharyngeal abscess and antimicrobial treatment for 6 weeks, including 3 weeks of intravenous and 3 weeks of oral therapy. The patient did well, and the treatment ended with the complete resolution of the inflammatory changes. We think that it is important to bear in mind that children with pyogenic processes of the head and neck, such as retro/parapharyngeal or peritonsillar abscess, paranasal sinusitis and otitis/mastoiditis, could also have osteomyelitis of the base of the skull because it requires prolonged antimicrobial therapy.1–4

Clinics in diagnostic imaging (216).

Clinics in diagnostic imaging (216).

Magnetic resonance imaging (MRI) chest in post-COVID-19 pneumonia

A 61-year-old male, reverse transcription-polymerase chain reaction (RT-PCR) positive for COVID-19, was admitted to our hospital with features of moderate acute respiratory distress syndrome (ARDS). He was a known case of type-2 diabetes mellitus and was treated with steroids, remdesivir, and high-flow oxygen through a Venturi mask. He was discharged in a stable condition. However, the patient complained of persistent dyspnea on walking and climbing stairs. During his post recovery phase, his baseline partial oxygen saturation was 96%, which decreased to 90% after 6-min walk test.[1] He underwent computed tomography (CT) and magnetic resonance imaging (MRI) chest after 53 and 55 days of symptom onset, respectively. The CT chest was acquired on SOMATOM Definition Flash (Siemens Healthcare, Forchheim, Germany), and the images shown [Figure 1, left pane] are reconstructed images of 1 mm thickness with pulmonary B80F kernel. MRI images [Figure 1, right pane] are respiratory-gated, fast-BLADE turbo spin-echo images acquired on 1.5 Tesla MAGNETOM Aera (Siemens Medical Solutions, Malvern, PA, USA). The information provided by both modalities was similar. Both showed areas of parenchymal bands, septal thickening, traction bronchiectasis and bronchiolectasis, crazy-paving, and pleural thickening. The patient was diagnosed with “fibrotic-like” changes as sequelae of COVID-19 pneumonia.[2]Figure 1: Axial sections of CT chest (left pane) and corresponding sections of MRI chest (right pane) showing sequelae of COVID-19 pneumonia as areas of septal thickening and traction bronchiectasis (thick arrows in a) and pleural thickening (curved arrows in a), traction bronchiectasis (thin arrows in b) and parenchymal bands (dashed arrows in b), and crazy-paving (boxes in c). Both imaging modalities provided comparable image quality and informationThe advancing age, ARDS, longer hospital stay, mechanical ventilation, high severity score on baseline CT, raised erythrocyte sedimentation rate, and eosinophil counts are reported to be the independent predictors of fibrotic lung changes in patients recovering from COVID-19.[2] MRI has been emerging as a radiation-free alternative, comparable to CT, combining functional and morphological information. MRI provides high tissue contrast, which is beneficial in identifying fibrotic changes in the lung.[3] High signal-to-noise ratio has been achieved in MRI by developing rapid image acquisition with the help of parallel imaging and under-sampling methods, as well as by reducing susceptibility artifacts caused by air.[4] In patients with sequelae of COVID-19 infection, repeat imaging by CT is often needed to evaluate the progression and severity of the sequelae, thus giving considerable radiation exposure to the patients. A recent study by Torkian et al.[5] showed that MRI lung has similar capabilities as CT scan in depicting changes of COVID-19 pneumonia. Our present case also shows the comparable image quality of lung MRI and CT in delineating the extent and features of post-COVID-19 pneumonia. Thus, MRI being the radiation-free modality can be utilized more frequently as follow-up imaging tool in patients with COVID-19 pneumonia. Declaration of patient consent The authors certify that they have obtained all appropriate patient consent forms. In the form the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed. Financial support and sponsorship Nil. Conflicts of interest There are no conflicts of interest.

Commentary: Development of a Comparative European Orthohantavirus Microneutralization Assay With Multi-Species Validation and Evaluation in a Human Diagnostic Cohort.

In this otherwise excellent article (Hoornweg et al., 2020) cited “Three human SEOV infections were confirmed, of which one was previously described as the first [2018] proven SEOV case in The Netherlands, based on IFT [immuno-fluorescence test] serology and an epidemiological link to SEOV RNA-positive [wild] rats) (Swanink et al., 2018), and now confirmed by comparative VNT [virus neutralization test].” This is historically incorrect: 27 years before Swanink et al, Groen et al. already reported wild rat-induced human SEOV infections in The Netherlands, moreover, in the same Dutch Institute of Public Health and Environmental Protection, Bilthoven, and with the same IFT (or IFA) technique (Groen et al., 1991). In addition, this 1991 report compared 14 non-laboratory cases of hemorrhagic fever with renal syndrome (HFRS), caused by the common European arvicolid orthohantavirus Puumala (PUUV), to 13 cases infected by the then rare (at least in early 1990s Western literature) orthohantavirus Seoul (SEOV), a juxtaposition in one single paper of two different local Dutch pathogenic orthohantaviruses, thus constituting at that moment the earliest such confrontation in nascent Western hantavirus literature (Figure 1). Moreover, not only 11 Dutch and/or Belgian laboratory rat-induced early 1980s SEOV-HFRS cases were detected, but also two wild rat-induced cases (arrows in Figure 1), thereby scoring yet another “first” in western hantavirus literature. Open in a separate window Figure 1 IFA: immuno-fluorescence assay or immuno-fluorescence test (IFT). ELISA, enzyme-linked immunosorbent assay. CTB ELISA, complex-trapping blocking, an inhibition ELISA variant. Closed circles: 1980s laboratory rat-acquired human hantavirus infections. Open circles: non-laboratory rat-acquired or “wild” human hantavirus infections, mostly being 1980s PUUV-induced, except for two “wild” cases (arrows), being 1980s wild rat-induced SEOV infections. Thick arrow: Dutch farmer, thin arrow: Belgian homeless vagabond, both with wild rat-exposure. In these two cases, SEOV infection was missed in IFA, showing surprisingly high cross-reacting PUUV titers (A), but confirmed, albeit with lower titers, in ELISA (B), and unmistakably ascertained in CTB-ELISA (C). Consequently, these two cases would have been mistaken for PUUV infections, if relying only on IFT/IFA. Adapted from Groen et al., 1991. Copyright © 1991 Wiley‐Liss, Inc., A Wiley Company.

The Pressure Profiles of the Equilibrium States of Osmosis across Plant and Animal Cell Membranes

Introduction In our previous abstract titled “The Nature and Measures of Osmotic Pressure” in EB2021, we illustrated that 1) in a simple osmosis system where a solution compartment and a water compartment are separated by a selectively permeable membrane (m), πachieved, πapplied, and πTM (TM refers to transmembrane) are the three common ways osmotic pressure (π) is defined, where πTM is the nature of osmotic pressure that drives osmosis; and 2) in a composite osmosis system where a cell membrane separates two solutions (extracellular and intracellular fluids, i.e., ECF and ICF), the driving pressure of osmosis is the osmotic pressure difference/gradient (ΔπTM) across the m. In this presentation, we apply the concepts of a composite ECF-m-ICF and the ΔπTM to illustrate how three different types of pressure characterize the equilibrium states of osmosis (after water enters the cells) across plant and animal cell membranes. Method 1) Deconstructing a composite ECF-m-ICF (Fig 1) into two simple osmosis systems (ECF-m-H2O and H2O-m-ICF) to understand the ΔπTM. 2) Graphical (logical) analysis of the three pressures in plant and animal ECF-m-ICF (Fig 2). Results 1) As shown in Fig 1, ΔπTM = πTM(ECF-m-H2O) - πTM(H2O-m-ICF). 2) After water enters a cell and reaches equilibrium of osmosis, ΔπTM is reduced to Δπeq (Fig 2). 3) In a plant ECF-m-ICF (Fig 2a and 2b), large Δπeq (close to ΔπTM), high hydrostatic pressure (ΔPH2O, thick grey arrows in Fig 2b) inside the cell, and high tension in the call wall (ΔTwall, thick white bidirectional arrows, Fig 2b) characterize this equilibrium state. To focus on the pressure profiles and simplify the Fig 2, the vacuoles that store water in the plant cell are not shown. In contrast, in an animal ECF-m-ICF, smaller Δπeq, lower PH2O (the thin grey arrows, Fig 2d), and lesser tension in the cell membrane (ΔTCM, the white bidirectional arrows, Fig 2d) characterize the equilibrium state. Conclusion This is the first work to illustrate in detail the differences in the three pressure profiles across plant and animal cell membranes after water enters the cells due to osmosis using the method of deconstruction of ICF-m-ECF and the concept of ΔπTM.

The radiofrequency interference on CRT-D functioning during AV node ablation: An educational case.

We have described some unusual findings of radiofrequency interference with ICD functioning during AV nodal ablation, guiding the reader to the possible explanation of the phenomena.

Retroperitoneal perforation of the descending colon diverticulitis presenting with systemic emphysema.

A 75-year-old man was admitted to the cardiac care unit because of congestive heart failure (CHF) secondary to non-ST elevated myocardial infarction (NSTEMI). His medical history included CHF, hypertension, diabetes, bronchial asthma, and hyperuricemia. He denied any past surgical interventions. At admission, the patient was intubated and underwent percutaneous coronary angioplasty (PCA). His hospital course was complicated with refractory respiratory failure due to pulmonary edema, pneumonia, and bronchial asthma. He was intubated three times in 18 days. Steroids used to treat his asthma included intravenous methylprednisolone 40 mg for 3 days, which was switched to oral prednisone 30 mg, tapering to 5 mg over 12 days. Ceftriaxone was administered on hospital days 4–11 to treat pneumonia. He was finally extubated on hospital day 18, at which time routine chest radiography showed pneumomediastinum, subcutaneous emphysema, and subdiaphragmatic free air (figure 1). He was afebrile and his vital signs were normal except for mild tachycardia (heart rate 105 bpm). He presented with abdominal bloating but denied abdominal pain. He exhibited crepitation all over his body. His abdomen was distended and soft. His white cell count was 1.21x10∧9/L, blood urea nitrogen 89.6 mg/dL, and creatinine 4.35 mg/dL. Non-contrast CT showed extensive subcutaneous emphysema over the chest and abdominal wall, pneumomediastinum without pneumothorax, massive pneumoperitoneum, and pneumoretroperitoneum. Diffuse mesenteric emphysema was observed without ascites (figure 2). The acute care surgery service was consulted. Figure 1 Chest radiograph shows pneumomediastinum (thin arrows), subcutaneous emphysema …

Entwined Pattern of Coronary Arteries

A 67-year-old asymptomatic man with a history of the Bentall procedure 20 years ago for aortic root dilatation and severe aortic regurgitation underwent a routine evaluation, for residual aortic root dilatation, by coronary computed tomography angiography. The image analysis highlighted a crossing of the mid left circumflex (thin white arrows) with the obtuse marginal artery (wide black arrows) in their proximal segments both in volume rendering (Supplemental Figs. S1 and S2) and in maximum intensity projection (Supplemental Fig. S3) reconstructions. The basic information about the scanner and the scanning protocol is available in Supplemental Appendix S1. Very few cases of crossing coronary arteries have been previously described in the literature, and it remains considered as a normal variant of coronary anatomy.1Trivellato M. Angelini P. Leachman R.D. Variations in coronary artery anatomy: normal versus abnormal.Cardiovasc Dis, Bull Tex Heart Inst. 1980; 7: 357-370Google Scholar Other coronary arteries, as left anterior descending and diagonal branches, may also be involved.2Pandey N.N. Sharma A. A curious case of crossing coronary arteries.Asian Cardiovasc Thorac Ann. 2020; 28: 219Crossref PubMed Scopus (1) Google Scholar It's frequently a fortuitous diagnosis as performing coronary computed tomography angiography or coronary angiogram for another purpose. There is currently no evidence of functional significance attributed to this condition. Precise data on epidemiology remain unknown. We herein add a supplementary exception to the generally accepted anatomic postulate describing the major branches of the coronary arteries running parallel to one another without any crossing pattern.3Silverman J.F. Coronary Angiography. Addison Wesley, Inc., Menlo Park, CA1984: 66Google Scholar Albeit mostly asymptomatic, this condition may have a therapeutic impact by influencing the revascularization strategy either by percutaneous coronary intervention or coronary artery bypass grafting in multivessel disease involving left circumflex coronary artery branches. Indeed, crossing coronary arteries suggest that one vessel may be intramyocardial and thus cannot be bypassed.4Bilazarian S.D. Jacobs A.K. Fonger J.D. Faxon D.P. Case report of a coronary anomaly: crossing obtuse marginal arteries.Cathet Cardiovasc Diagn. 1991; 23: 130-132Crossref PubMed Scopus (3) Google Scholar In such cases, it has been proposed to perform an arterioarterial shunt at the crossing point in case of a significant stenosis involving the proximal segment of one branch5Muyldermans L.L. van den Heuvel P.A. Ernst S.M. Epicardial crossing of coronary arteries: a variation of coronary arterial anatomy.Int J Cardiol. 1985; 7: 416-419Abstract Full Text PDF PubMed Scopus (6) Google Scholar when coronary artery bypass grafting is planned, provided the other is healthy.Novel Teaching Points•Major branches of the coronary arteries may cross each other rather than running parallel to one another as generally stipulated.•Crossing coronary arteries may influence the revascularization strategy, especially when coronary artery bypass grafting is planned. •Major branches of the coronary arteries may cross each other rather than running parallel to one another as generally stipulated.•Crossing coronary arteries may influence the revascularization strategy, especially when coronary artery bypass grafting is planned.

Elastin Damage and Vascular Smooth Muscle Cell Alterations Are the Initial Changes in a Novel Model of Tobacco Smoke-induced Aortic Injury

Tobacco smoke exposure is a major risk factor for aortic aneurysm development. However, the initial aortic response to tobacco smoke, preceding aneurysm formation, is not well understood. We developed a novel model to examine early effect of solubilized tobacco smoke (STS) on the thoracic and abdominal aorta of mice as well as on cultured human aortic smooth muscle cells (HASMC). Nineteen Male C57BL6 mice received an infusion of STS or vehicle via osmotic minipumps for 2 weeks. Six mice were treated with vehicle-containing pumps, eight mice received STS pumps in the peritoneal position and five mice received STS pumps in the subcutaneous position. The thoracic and abdominal aortas were assessed for elastic lamellar damage, smooth muscle cell response, and infiltration of inflammatory cells. Elastin breaks were counted by two independent investigators and differences between groups were assessed using a two-tailed Student t-test. Cultured HASMC were exposed to STS after growth in differentiation media and assessed for α-smooth muscle actin (αSMA) and Mac-2 expression using immunofluorescence and western blot analysis. STS exposure caused increased numbers of breaks in the elastic lamellae of the thoracic and abdominal aorta (Fig 1; P < .001). Elastin breaks occurred more frequently in the abdominal aorta than the thoracic aorta (3.7 breaks per cross-section vs 2.3 breaks per cross-section; P < .001). In vivo, STS exposure caused microdissections of the aorta and a phenotypic switch in vascular smooth muscle cells characterized by downregulation of αSMA (Fig 2) and expression of Mac-2. Cultured HASMC exposed to solubilized tobacco smoke demonstrated loss of αSMA compared to HASMC not exposed to STS. Western blot analysis confirmed the loss of αSMA in HASMC exposed to tobacco smoke. HASMC exposed to STS demonstrated altered, rounded morphology within 2 days of tobacco smoke exposure, correlating with the αSMA loss. In initial experiments, Mac-2 expression was not different between HASMC exposed to STS and those exposed to vehicle. We demonstrate a new model for investigating the initial structural and cellular aortic changes in response to tobacco smoke exposure. Our findings suggest that STS exposure causes aortic elastic lamellar damage and phenotypic changes in VSMC, involving αSMA downregulation and possible Mac-2 upregulation. The VSMC phenotypic changes indicate a loss of normal contractile phenotype and expression of inflammatory markers. Utilizing this model, the mechanism of early tobacco smoke-induced aortic injury and strategies for early detection and prevention of aortic injury prior to clinical disease development can be investigated.Fig 2Immunofluorescence staining of aortic microdissection showing Mac-2 expression (bright green) and α-smooth muscle actin (αSMA) expression (red). The area of microdissection (*) shows increased Mac-2 expression (thick arrow, right) and decreased αSMA expression (thick arrow, left) compared to normal area or aorta showing no Mac-2 expression and normal αSMA expression (thin arrows).View Large Image Figure ViewerDownload Hi-res image Download (PPT)

Using a hybrid approach to management of a common femoral arterial dissection

A middle-aged (fifth decade) patient was brought to the emergency department after a motorcycle collision during which the lower abdomen-to-pelvis area was trapped between a traffic sign pole and the...

Giant Pulmonary Aneurysms in Behçet’s Disease Presenting with Hemoptysis—Embolization with Cyanoacrylate Glue and Coils

A 28-year-old man with Behçet’s disease presented with a 3-day history of 1 cup/day hemoptysis. He was diagnosed 2 years earlier with recurrent oral and genital ulcers, erythema nodosum, saccular pulmonary aneurysms, and lung biopsy showing necrotizing vasculitis, with a Behçet’s syndrome activity score of 14. His medications included prednisolone, azathioprine, and infliximab (after the hemoptysis began). Computed tomography showed 3 right lung aneurysms, measuring 21, 39, and 44 mm in diameter, and 2 left lung aneurysms, measuring 72 and 77 mm in diameter (Fig 1). Vascular involvement in Behçet’s disease can occur in up to 15% of cases, causing arteritis of both small and large arteries, most frequently of the pulmonary circulation. Pulmonary artery aneurysms also occur in combination with thrombophlebitis—a syndrome known by the eponym Hughes–Stovin—in the absence of criteria for a diagnosis of Behçet’s disease. The European League Against Rheumatism recommends immunosuppressive agents for major vessel disease in Behçet’s disease, and surgery is discouraged because of the high risk of complications and recurrence. The aneurysms were embolized with detachable coils (AZUR CX; Terumo, Shibuya City, Tokyo, Japan) and a cyanoacrylate glue (Glubran2; GEM, San Benedetto del Tronto AP, Italy)/Lipiodol (Guerbet, Villepinte, France) mixture in a 1:4 ratio (Figure 2, Figure 3, Figure 4 and Videos 1–8 [available online on the article’s Supplemental Material page at www.jvir.org]). In total, 25 ml of cyanoacrylate glue was used with 100 cc of Lipiodol (Guerbet), without immediate complications. The patient recovered well and was discharged 2 days later. He remained free of hemoptysis. Follow-up computed tomography 2.5 months after the treatment (Fig 5) demonstrated exclusion of all aneurysms, with no signs of perfusion. Figure 2(a) Sagittal maximum intensity projection of the left lung showing a giant aneurysm of the lower lobe, arising from a pulmonary artery branch. (b) Fluoroscopy image showing the aneurysm embolized with glue and Lipiodol (Guerbet) (1:4) only. View Large Image Figure Viewer Download Hi-res image Figure 3Fluoroscopy image showing the 2 left lung aneurysms embolized with a mixture of glue and Lipiodol (Guerbet) (1:4) and detachable coils (block arrow) and with glue and Lipiodol (Guerbet) only (thin arrow). View Large Image Figure Viewer Download Hi-res image Figure 4Fluoroscopy image showing the 3 right lung aneurysms embolized with detachable coils only (long block arrow), with a mixture of glue and Lipiodol (Guerbet) (1:4) and detachable coils (short block arrow), and with glue and Lipiodol (Guerbet) only (thin arrow). View Large Image Figure Viewer Download Hi-res image Figure 5Curved multiplanar reformation from computed tomography of the thorax showing 4 of the 5 embolized aneurysms 2.5 months after the treatment, with no signs of perfusion View Large Image Figure Viewer Download Hi-res image

Rhabdomyolysis and muscle infarcts associated with intra-operative compression

Rhabdomyolysis and muscle infarcts associated with intra-operative compression

Computer-aided Quantification of Pulmonary Fibrosis in Patients with Lung Cancer: Relationship to Disease-free Survival.

Background Interstitial lung abnormalities (ILAs) are present at CT in about 10% of individuals undergoing lung cancer screening. The relationship between histologic findings of ILAs and their influence on patient prognosis remains unknown. Purpose To evaluate the percentage of ILAs at preoperative CT, as measured by radiologists and a computer-aided detection (CAD) software, as a predictor of disease-free survival in patients with lung cancer. Materials and Methods This retrospective study evaluated 217 consecutive patients who underwent complete resection of lung cancer from April 2010 to December 2015. Two radiologists, blinded to the patients' clinical information, scored percentage fibrosis extent and determined whether ILAs and the usual interstitial pneumonia (UIP) pattern were present. They assessed ILA progression at follow-up CT. Two pathologists determined the presence of an UIP pattern. Percentage fibrosis extent was also measured by using CAD. Binary logistic regression analysis was performed to determine whether the CAD percentage fibrosis extent was associated with ILA at CT. Multivariable Cox regression analysis was used to evaluate the significance of CAD percentage fibrosis extent as a predictor of prognosis. Results The radiologists classified 47 patients with ILAs and 24 patients with a UIP pattern at chest CT. The pathologists detected a UIP pattern in 25 patients. CT abnormalities showed progression over a 2-year period in all patients with histologic evidence of UIP. After adjustment for age, sex, and smoking index, the CAD percentage fibrosis extent was independently associated with ILA (odds ratio: 3.1; 95% confidence interval [CI]: 2.1, 4.7; P < .001). After adjustment for age, forced expiratory volume in 1 second (percentage predicted) radiologist-assessed percentage fibrosis extent, and pathologic stage, CAD percentage fibrosis extent was independently associated with worse disease-free survival (hazard ratio: 1.3; 95% CI: 1.1, 1.6; P < .001). Conclusion Greater computer-aided detection percentage fibrosis extent at preoperative CT independently predicted worse disease-free survival in patients with lung cancer. © RSNA, 2019 Online supplemental material is available for this article. See also the editorial by Goo in this issue.

Proton Pump Inhibitor-Induced Liver Injury

Proton Pump Inhibitors (PPIs) are one of the most widely prescribed medications in the world and for a long time they were regarded as one of the safest medications. Recent studies have linked them with numerous adverse effects like dementia, interstitial nephritis, bone fractures, clostridium difficile infection, pneumonia etc. however, acute liver injury is not one of them. A 65-year-old female with no known liver disease presented with jaundice, dark urine and light stool 3 days after starting esomeprazole for heartburn which prompted her to stop the medication and seek medical attention. Outpatient laboratory studies were significant for total bilirubin of 12.4 mg/dl, AST 374 U/L, ALT 678 U/L, ALP 114 U/L and INR of 2. The patient was promptly sent to emergency department by her primary physician for further evaluation. Her mental status remained intact. Inpatient studies showed consistent elevation of liver test as well as positive ANA (antinuclear antibody) of 1:320 and AMA (antimitochondrial antibody) of 1:20. Due to concern for drug induced liver injury and possible autoimmune liver disease given positive autoimmune markers, liver biopsy was performed which showed acute cholestatic hepatitis compatible with drug induced liver injury (DILI). The patient's serum aminotransferase levels improved to AST 113 U/L, ALT 278 U/L respectively and total bilirubin of 10 upon discharge. At outpatient visit 6 week later, her labs were back to normal. DILI is one of the most common causes of acute hepatitis in the United States. Majority of the studies have not documented association of PPIs with liver injury. However, a few cases of PPI induced liver injury with minor elevation of liver enzymes which normalized after discontinuation of PPI have been documented. Omeprazole and pantoprazole are the main culprits among the PPIs but there are a few cases associated with esomeprazole as well. To our knowledge this is the first case of biopsy proven acute liver injury caused by esomeprazole. DILI may cause serious liver failure which warrants early diagnosis and treatment including referral to liver transplantation. Our case provides a convincing evidence that esomeprazole linked to acute liver injury. Once thought the safest and the most prescribed group of medications, is it time to add one more adverse effect on their extensive list of adverse effects?2422_A Figure 1. The normal architecture of the liver is preserved without scarring. There is marked portal and lobular inflammatory infiltrates and mild steatosis.2422_B Figure 2. Portal tracts contain a mild mixed inflammatory infiltrate including eosinophils (thin arrow). Lobular hepatitis is evidenced by collections of pigment laden macrophages (angled arrow), focal mixed inflammatory infiltrates and scattered acidophil bodies (thick arrow)2422_C Figure 3. Cholestatic features are evidenced by prominent bilirubinostasis in zone 3 hepatocytes (thin arrow), focal canalicular bile plugs (thick arrow), and bile pigment in macrophages (angled arrow).

Extensive Gastric Metaplasia Presenting as a Duodenal Mass

A 56-year-old woman was referred for EGD due to abdominal pain, nausea, and emesis for one month. This revealed a 3 cm semi-pedunculated mass in the third portion of the duodenum (FIGURE A arrows), biopsies of which showed only gastric metaplasia. Given concern for a more sinister nature, she underwent endoscopic submucosal dissection of the mass with microscopic evaluation. FIGURE B (H&E x 40) and FIGURE C (H&E x 100) depict normal duodenal mucosa (left, thin arrow) with the lesional tissue on the right, highlighting hyperplastic and reactive changes including villous blunting and extensive gastric metaplasia with mucinous epithelium (thick arrow) with gastric heterotopia characterized by the presence of parietal and chief cells (star). FIGURE B also depicts neutrophilic inflammation and plasma cell infiltrates (top inset, arrow) (H&E x 200) and prolapse-type changes (bottom inset, arrow) (H&E X 100). Duodenal gastric heterotopia and foveolar gastric metaplasia are long-recognized but poorly understood phenomena. They may exist on a spectrum of a purely congenital lesion to one associated with significant peptic duodenitis or mucosal injury(1), and rarely present as a mass(2, 3) that is excised. NBI and EUS may help characterize these masses(2, 4). In follow-up, the patient reported symptomatic improvement.2517_A Figure 1. Endoscopic view of 3 cm semi-pedunculated mass in the third portion of the duodenum2517_B Figure 2. H&E stain of excised mass under low power2517_C Figure 3. H&E stain of excised mass under high power

Aortic Root Sign

Appearance: The aortic root sign describes an anomalous circumflex coronary artery (ACCA) that emerges from the contralateral coronary sinus, and travels underneath the aorta to supply blood to its normal vascular territory. Explanation: The moniker, “aortic root sign,” was first coined by Page et al1 on conventional angiography to describe ACCA as arising from the proximal right coronary artery or right coronary sinus. The aberrant vessel courses inferiorly behind the aortic root within the groove between the left atrium and aorta,2 hence the term “aortic root sign” (Fig. 1).FIGURE 1: Fifty-six-year-old patient with atypical chest pain. A, Right anterior oblique ventriculogram from left heart catheterization demonstrates anomalous course of the left circumflex (LCX) en face below the aortic root (classic aortic root “dot” sign; thin arrow) (LV=left ventricle). B, Electrocardiogram-gated cardiac computed tomography (CT) matched in projection of the cardiac catheterization reveals the same signature appearance of the anomalous LCX (thin arrow). C, CT correlate of the conventional aortic root “dot” sign seen on an axial image from an electrocardiogram-gated CT reveals the anomalous LCX coursing inferior to the noncoronary sinus of the aortic root (medium arrow) (RA=right atrium, RV=right ventricle, LA=left atrium). D, Volume-rendered image of the aortic root demonstrates coronary origin from the right sinus of Valsalva (asterisk) with immediate takeoff of the anomalous LCX (arrowhead) from the normal right coronary artery (large arrow).Discussion: Traditionally coronary artery anomalies (CAAs) were thought to have little significance, and were often discovered as incidental findings on angiography. However, patients may present with clinically significant disease.2 In fact, CAAs are the second most common cause of sudden cardiac death in young athletes in the United States.2 ACCA was first described by Antopol and Kugel.3 The prevalence of ACCA reported in the coronary angiography literature ranges from 0.18% to 0.67%, making it the most common CAA. Some authors postulate that the oblique angulation of its origin predisposes ACCA to atherosclerosis. However, most clinicians agree that ACCA is a benign, asymptomatic anomaly. Indeed, the retroaortic course of ACCA, as described by the aortic root sign, rarely leads to ischemia or sudden cardiac death. On the contrary, CAAs that travel along an interarterial course between the aorta and pulmonary artery are more prone to ischemia during strenuous exercise.2 Despite the low risk of ischemia and sudden death with ACCA, recognition of this anomaly is still of great clinical importance because failure to identify this aberrant vessel can lead to adverse patient outcomes, especially during cardiac surgery. Therefore, it is crucial for the angiographer as well as the radiologist to be adept at recognizing ACCA and the other coronary anomalies, especially given the ease of diagnosis with noninvasive coronary imaging techniques, such as multidetector computed tomography4 and cardiac magnetic resonance imaging.5

A Unique Triad of Ulcerative Colitis With Autoimmune Hemolytic Anemia and Primary Sclerosing Cholangitis

Inflammatory Bowel Diseases (IBD) lead to chronic intestinal inflammation along with extra-intestinal manifestations which could present prior to, subsequent with or after the diagnosis of IBD. We present a unique case of Ulcerative Colitis (UC), Autoimmune Hemolytic Anemia (AIHA) and Primary Sclerosing Cholangitis (PSC) diagnosed simultaneously in a patient. The unique triad of these diseases gives important clues to the immunological factors involved in the pathogenesis of these diseases. An 18-year-old male presented with 1 week of bloody diarrhea, abdominal cramps and nausea. Vitals were stable. Initial labs showed Hb 9.5 g/dL, MCV 102 fL, WBC 22.4 x 103/μL, total bilirubin 2.4 mg/dL, direct bilirubin 0.7 mg/dL, alkaline phosphatase 436 units/L, ALT 133 units/L and AST 83 units/L. Hepatitis panel and Clostridium difficile toxin assay were negative. Further work-up revealed reticulocyte count > 17%, LDH 529 units/L, haptoglobin < 10 mg/dl and positive direct Coomb's test. Peripheral smear showed hemolysis by a warm antibody. Hydrocortisone was started for AIHA. CT abdomen showed mild colonic wall thickening. Colonoscopy showed moderate pancolitis and biopsies showed findings consistent with UC. Mesalamine was started. MRCP showed irregular beaded appearance of intra and extrahepatic bile ducts. ERCP was performed and biopsies taken from the ducts showed chronic inflammation but no evidence of malignancy. ASMA and ANCA were positive. Liver biopsy ruled out overlap syndrome with autoimmune hepatitis. The patient clinically improved and was discharged to follow-up with a gastroenterologist. In patients with UC, extra-intestinal manifestations involving cutaneous, hepatobiliary and ocular systems are common. The concomitant presence of PSC is 2-7% and AIHA is 0.2 -1.7% in patients with UC. The extra-intestinal manifestations of UC could be due to associated autoimmune diseases or they could be immune-mediated due to damaged mucosal wall. The exact pathogenesis of PSC and AIHA is unknown. The absorption of toxins and antigenic substances from the mucosa in the circulation mediates inflammation in the biliary system leading to PSC. This also leads to warm anti-E antibody production which cross-react with intestinal microbiome and the E antigen at the surface of RBCs. In UC patients, a vigorous workup for early detection of other autoimmune diseases is important to improve the quality of life and to prevent mortality associated with them.Figure: Peripheral smear showing polychromatic RBCs and microspherocytes.Figure: Axial CT demonstrating mild wall thickening and featureless appearance of the rectosigmoid colon compatible with chronic ulcerative colitis (left). Descending colon at 4X magnification showing crypt distortion, cryptitis and crypt abscess (right).Figure: Left: Coronal thin section T2 weighted image showing a beaded appearance of the left hepatic and intrahepatic bile ducts with alternating strictures (arrows) and dilatation (arrowheads). Right: A) Fluoroscopic image from an ERCP depicting beading of the bilateral intrahepatic bile ducts due to segmental strictures (thin arrows). Guidewire in the left intrahepatic bile duct (thick arrow). B) ERCP image after biliary stent placement (arrowhead) with decompression of the biliary tree.

Something is not anymore there

A 86 years old man, with past medical history of hypertension, ischemic cardiomyopathy and gallstones, that refused the cholecystectomy a year ago, was seen at the emergency room because dark vomiting and confusion that began two days ago, the physical examination was unremarkable, the blood tests revealed: haemoglobin 12 g/L, 11.350 cells/mm3 leucocytes, protein c reactive 10.58 mg/L (normal value 5 mg/L), normal liver function, 1.9 mg/dL of creatinine and 252 mg/dL of urea. The abdominal X-ray showed some hydroaereus levels in the small bowel. He was admitted in the Internal Medicine ward, a nasogastric tube was placed, intravenous hydration was started and neuroleptics were administrated. At the ward the patient stays hemodynamically stable, without new episodes of vomiting nor confusion and the nasogastric tube drainage was minimum, he was able to drink without any symptoms after 48 h. In the 4th day, his general condition worsened because vomiting and abdominal pain appeared, these symptoms relieved with fasting and antiemetics drugs. An abdominal computerized tomography (CT) scan was performed. What is the diagnosis? The image in the panel A shows a big gallstone, panels B & C show pneumobilia (thin arrow) and the gallstone in the terminal jejunum (thick arrow) (Fig. 1). The gallstone ileus is an infrequent condition, its incidence varies from 0.5 to 4% [[1]Aguilar-espinosa F. Sangrado de tubo digestivo y delirium, retos en el diagnóstico de íleo biliar: reporte de un caso y revisión de bibliografía.Cirugía y Cirujanos. 2017; 299: 2-6Google Scholar], it's caused by a fistula that connects the gallbladder with the gastrointestinal tract. Almost 80% of affected have medical history of gallstones, symptoms are diverse as intermittent intestinal occlusion, vomiting, upper digestive haemorrhage, and diffuse abdominal pain. The Rigler's triad that consists in: gas in the biliary tree, small intestine occlusion and gallstone in the intestinal lumen, is usefull to confirm the diagnosis. This entity is more frequent in patients over 65 years old [[2]Sahsamanis G. Maltezos K. Dimas P. Tassos A. Mouchasiris C. Bowel obstruction and perforation due to a large gallstone. A case report.Int J Surg Case Rep. 2016; 26: 193-196Abstract Full Text Full Text PDF PubMed Scopus (7) Google Scholar]. The mortality is about 15–30% and depends on the timely diagnosis. The commonest complications are: intestinal occlusion, and perforation due to the gallstone in the gut [1Aguilar-espinosa F. Sangrado de tubo digestivo y delirium, retos en el diagnóstico de íleo biliar: reporte de un caso y revisión de bibliografía.Cirugía y Cirujanos. 2017; 299: 2-6Google Scholar, 2Sahsamanis G. Maltezos K. Dimas P. Tassos A. Mouchasiris C. Bowel obstruction and perforation due to a large gallstone. A case report.Int J Surg Case Rep. 2016; 26: 193-196Abstract Full Text Full Text PDF PubMed Scopus (7) Google Scholar]. This patient was undergone to laparotomy with enterotomy and gallstone extraction, he recovered well without complication with spontaneous healing of the fistula, as other cases reported [[3]Neary P.M. Dowdall J.F. Evolution of entero-biliary fistula following gallstone ileus management.BMJ Case Rep. 2012; 2012: 1-2Crossref Scopus (3) Google Scholar]. The authors want call attention about this entity that can be misdiagnosed because the unspecific symptoms can lead to major complication, and the Internal Medicine ward physicians must keep in mind this illness in order to do a timely diagnosis.