Role of HRCT in evaluation of Interstitial Lung Disease

In this study, HRCT is the examination technique of choice as it is quickly accomplished, readily available and does not require ancillary studies using other imaging technologies in most cases. In this given study, A total of 40 patients were included in which 16 patients were found to be having ILDs , there were 10 male patients (62.5%) and 6 were female patients i.e., (37.5%) of total number of patients .Idiopathic pulmonary fibrosis were found in 3 (18.75%) patients, Usual interstitial pneumonia in 2 (12.5%) patients, Chronic Hypersensitive pneumonitis in 1 (6.25%) patient , Fibrotic hypersensitive pneumonitis in 4 (25%) patients and Pulmonary interstitial edema in 6 (37.5%). The maximum patients were found in pulmonary interstitial edema and minimum patients in Chronic Hypersensitive pneumonitis, the highest number of patients with interstitial lung disease were from the 60-80 Years age group category, which was 8 Out of 16 i.e. 50% of the total number of the patients and no patients were found from the age group 0-18 years age group and 80-100 years age group.

Stasis Ulcers – The Unifying Concept

Chronic stasis dermatitis, usually confined to the lower legs, is a complication of longstanding interstitial edema and inflammation, due either to venous hypertension or disorders having in common excessive lymph overload. Heart failure, renal failure, liver cirrhosis, secondary and primary diseases of lymph vessels may complicate with stasis dermatitis. The same mechanisms causing stasis dermatitis can also generate skin ulcers superimposed on stasis dermatitis. In the appropriate context such skin ulcers are called "venous ulcers" or, in different situations, “stasis ulcers”. The distinction between venous and other stasis ulcers is usually possible at the bedside. Also, some general measures of therapy are similar for venous and other stasis ulcers: such are elastic compression, topical skin care and ulcer care. In having in common the pathophysiological mechanisms, in bearing clinical resemblance, and responding to similar therapies, a unifying concept may be opportune to comprise the spectrum of stasis dermatitis, venous and other stasis ulcers. The present work is an appeal to this aim.

REPERFUSION INJURY AND INTRA-ABDOMINAL HYPERTENSION SYNDROME IN PATIENTS WITH ACUTE PANCREATITIS: CAUSES, CURRENT APPROACHES TO PREVENTION AND TREATMENT (LITERATURE REVIEW)

The aim of the work is to analyze and summarize current data on the problem of reperfusion injury and intra-abdominal hypertension syndrome in patients with acute pancreatitis: the causes of their occurrence, approaches to their prevention and treatment. Results. The analysis is based on sources that were searched in scientometric databases Google Scholar, MedLine, Web of Science, Scopus for 2013-2019. Disorders of microcirculation are one of the factors influencing the development of acute pancreatitis, namely, stimulate the increase of pancreatic enzymes level, interstitial edema and infiltration by inflammatory response cells. On the other hand, ischemia can complicate the course of the disease with the development of ischemia-reperfusion syndrome and intra-abdominal hypertension. The analyzed data concerning the prevention and treatment of these syndromes in acute pancreatitis are contradictory, which does not allow to form a unified approach to the treatment of the above conditions. Conclusions. In order to reduce mortality in acute pancreatitis, it is important to study possible ways to prevent and further manage patients with acute pancreatitis, accompanied by reperfusion injury and intra-abdominal hypertension.

The Pathogenesis of COVID-19 Myocardial Injury: An Immunohistochemical Study of Postmortem Biopsies

RationaleMyocardial injury associates significantly and independently with mortality in COVID-19 patients. However, the pathogenesis of myocardial injury in COVID-19 remains unclear, and cardiac involvement by SARS-CoV-2 presents a major challenge worldwide.ObjectiveThis histological and immunohistochemical study sought to clarify the pathogenesis and propose a mechanism with pathways involved in COVID-19 myocardial injury.Methods and ResultsPostmortem minimally invasive autopsies were performed in six patients who died from COVID-19, and the myocardium samples were compared to a control group (n=11). Histological analysis was performed using hematoxylin-eosin and toluidine blue staining. Immunohistochemical (IHC) staining was performed using monoclonal antibodies against targets: caspase-1, caspase-9, gasdermin-d, ICAM-1, IL-1β, IL-4, IL-6, CD163, TNF-α, TGF-β, MMP-9, type 1 and type 3 collagen. The samples were also assessed for apoptotic cells by TUNEL. Histological analysis showed severe pericardiocyte interstitial edema and higher mast cells counts per high-power field in all COVID-19 myocardium samples. The IHC analysis showed increased expression of caspase-1, ICAM-1, IL-1β, IL-6, MMP-9, TNF-α, and other markers in the hearts of COVID-19 patients. Expression of caspase-9 did not differ from the controls, while gasdermin-d expression was less. The TUNEL assay was positive in all the COVID-19 samples supporting endothelial apoptosis.ConclusionsThe pathogenesis of COVID-19 myocardial injury does not seem to relate to primary myocardiocyte involvement but to local inflammation with associated interstitial edema. We found heightened TGF-β and interstitial collagen expression in COVID-affected hearts, a potential harbinger of chronic myocardial fibrosis. These results suggest a need for continued clinical surveillance of patients for myocardial dysfunction and arrythmias after recovery from the acute phase of COVID-19.

Multi-Organ Histopathological Changes in a Mouse Hepatitis Virus Model of COVID-19

Infection with SARS-CoV-2, the virus responsible for the global COVID-19 pandemic, causes a respiratory illness that can severely impact other organ systems and is possibly precipitated by cytokine storm, septic shock, thrombosis, and oxidative stress. SARS-CoV-2 infected individuals may be asymptomatic or may experience mild, moderate, or severe symptoms with or without pneumonia. The mechanisms by which SARS-CoV-2 infects humans are largely unknown. Mouse hepatitis virus 1 (MHV-1)-induced infection was used as a highly relevant surrogate animal model for this study. We further characterized this animal model and compared it with SARS-CoV-2 infection in humans. MHV-1 inoculated mice displayed death as well as weight loss, as reported earlier. We showed that MHV-1-infected mice at days 7–8 exhibit severe lung inflammation, peribronchiolar interstitial infiltration, bronchiolar epithelial cell necrosis and intra-alveolar necrotic debris, alveolar exudation (surrounding alveolar walls have capillaries that are dilated and filled with red blood cells), mononuclear cell infiltration, hyaline membrane formation, the presence of hemosiderin-laden macrophages, and interstitial edema. When compared to uninfected mice, the infected mice showed severe liver vascular congestion, luminal thrombosis of portal and sinusoidal vessels, hepatocyte degeneration, cell necrosis, and hemorrhagic changes. Proximal and distal tubular necrosis, hemorrhage in interstitial tissue, and the vacuolation of renal tubules were observed. The heart showed severe interstitial edema, vascular congestion, and dilation, as well as red blood cell extravasation into the interstitium. Upon examination of the MHV-1 infected mice brain, we observed congested blood vessels, perivascular cavitation, cortical pericellular halos, vacuolation of neuropils, darkly stained nuclei, pyknotic nuclei, and associated vacuolation of the neuropil in the cortex, as well as acute eosinophilic necrosis and necrotic neurons with fragmented nuclei and vacuolation in the hippocampus. Our findings suggest that the widespread thrombotic events observed in the surrogate animal model for SARS-CoV-2 mimic the reported findings in SARS-CoV-2 infected humans, representing a highly relevant and safe animal model for the study of the pathophysiologic mechanisms of SARS-CoV-2 for potential therapeutic interventions.

Clinical cases of rarely diagnosed forms of choroidal osteoma

Purpose. To analyze the 3 cases of choroidal osteomas, revealed in histological study after evisceration of eye. Material and methods. 3 patients (3 eyes) with chronic uveitis of different origin. Results. On histological examination, the bone tissue consisted of a network of bone beams of not fully mature type, with irregularly pronounced fibroreticular tissue between them. There was insignificant proliferation of endosteal cells in the fibroreticular component. There was marked interstitial edema, increased vascularization with hyperemia in the choroidal vascular plate. Conclusion. Preoperative diagnosis of choroidal osteomas is difficult because of the opacity of the eye media. Long term chronic uveitis of different origin was common to all given cases. Choroidal osteomas was an intraoperative finding and ossification process of choroid was indused by inflammatory process of the eye. Key words: choroidal osteomas, chronic uveitis.

Endogenous Hydrogen Sulfide Is an Important Factor in Maintaining Arterial Oxygen Saturation

The gasotransmitter H2S is involved in various physiological and pathophysiological processes. The aim of this study was to investigate the physiological functions of H2S in the lungs. In the model of mouse with genetic deficiency in a H2S natural synthesis enzyme cystathionine-γ-lyase (CSE), we found that arterial oxygen saturation (SaO2) was decreased compared with wild type mice. Hypoxyprobe test showed that mild hypoxia occurred in the tissues of heart, lungs and kidneys in Cse-/- mice. H2S donor GYY4137 treatment increased SaO2 and ameliorated hypoxia state in cardiac and renal tissues. Further, we revealed that lung blood perfusion and airway responsiveness were not linked to reduced SaO2 level. Lung injury was found in Cse-/- mice as evidenced by alveolar wall thickening, diffuse interstitial edema and leukocyte infiltration in pulmonary tissues. IL-8, IL-1β, and TNF-α levels were markedly increased and oxidative stress levels were also significantly higher with increased levels of the pro-oxidative biomarker, MDA, decreased levels of the anti-oxidative biomarkers, T-AOC and GSH/GSSG, and reduced superoxide dismutase (SOD) activity in lung tissues of Cse-/- mice compared with those of wild type mice. GYY4137 treatment ameliorated lung injury and suppressed inflammatory state and oxidative stress in lung tissues of Cse-/- mice. A decrease in SaO2 was found in normal mice under hypoxia. These mice displayed lung injury as evidenced by alveolar wall thickening, interstitial edema and leukocyte infiltration. Increased levels of inflammatory cytokines and oxidative stress were also found in lung tissues of the mice with hypoxia insult. GYY4137 treatment increased SaO2 and ameliorated lung injury, inflammation and oxidative stress. Our data indicate that endogenous H2S is an important factor in maintaining normal SaO2 by preventing oxidative stress and inflammation in the lungs.

MO142A SINGLE-CENTER CASE SERIES OF 150 PATIENTS WITH RENAL FANCONI SYNDROME

Background and Aims Renal Fanconi syndrome (RFS) is characterized by generalized dysfunctions of renal proximal tubular (PT) transport. The causes of FS can be inherited or acquired, the latter of which mostly includes drugs, heavy metals, monoclonal light chains (LC), and primary Sj gren’s syndrome (pSS). We intended to observe the clinico-pathological features of RFS with different etiologies. Method From January 2012 to September 2018, all the patients diagnosed as RFS in our hospital were enrolled. Their clinicopathological records were retrospectively reviewed. The diagnosis of RFS was defined as existence of ≥ 3 of the following five items alone or ≥ 2 items combined with an evidence of PT damages in kidney pathology: (I) normoglycemic glycosuria; (II) generalized aminoaciduria; (III) hypophosphatemia and hyperphosphaturia; (IV) hypouricemia and hyperuricosuria; (V) proximal RTA. Results: 1. Clinical characteristics We identified 150 RFS patients, with an average age of (45.9±14.2) years old and male: female ratio 1.3:1. They presented with different degrees of PT dysfunctions and the most common were hypophosphatemia (83.2%) and aminoaciduria (80.6%). Their mean eGFR levels were 76.3 (4.5-188.6) ml/min/1.73m2 with 73.5% had proteinuria. 2. Renal pathological features 47 RFS patients received kidney biopsy and the most common pathological diagnosis was interstitial nephritis. They all presented with different degrees of proximal tubule atrophy, defective brush border, interstitial edema and fibrosis. 3. Etiology-related clinicopathologic features The most common causes of our RFS were LC (14.0%), drugs (13.3%), and pSS (9.3%). Compared to pSS associated RFS, LC associated RFS patients showed a higher prevalence of bone involvement, more severe proteinuria and less severe hypokalemia (P < 0.05) despite similar eGFR levels. Specific renal pathological features were seen in different etiology groups, including crystalline formation and increased lysosomes in PT cells under electron microscope in LC associated RFS, and CD21 positive ectopic germinal center formation in renal interstitum in parts of the pSS associated RFS. Conclusion We identified 150 RFS with different etiologies and they showed etiology-specific patterns of PT dysfunctions and renal pathologic changes.