Annular Lichenoid Dermatitis (of Youth)

About 20 years after its first description, Annular Lichenoid Dermatitis of Youth (ALDY) is recognized as a distinctive lichenoid dermatosis with specific clinical and histological features. The disease occurs mostly in young persons all over the world, runs a chronic course, and has an obscure etiopathogenesis. Clinically, lesions consist of persistent, asymptomatic erythematous macules and round-oval annular patches with a red-violaceous non-scaling border and central hypopigmentation, mostly localized on the groin and flanks. Histology shows a peculiar lichenoid dermatitis characterized by irregular epidermal hyperplasia with an alternation of thinned and quadrangular rete ridges and a dense band-like lichenoid infiltrate of lymphocytes in the papillary dermis. Typically, there is infiltration of lymphocytes into the lower epidermal layers with massive necrosis/apoptosis of keratinocytes, which is limited to the tips of rete ridges. Dermal lymphocytes are usually CD3+, CD4+, while most of the intraepidermal T cells are CD8+. Analysis of TCR-γ-chain gene rearrangement displayed polyclonality in all cases examined. Differential diagnosis mainly includes morphea, mycosis fungoides, annular erythemas and inflammatory lesions of vitiligo. Topical corticosteroids and topical tacrolimus represent the most effective drugs for ALDY treatment.

SR Ca2+ handling in unbranched, immediately post-necrotic fast-twitch mdx fibres is similar to wt littermates

There is a lack of consensus in the literature regarding the effects of dystrophin deficiency on the Ca2+ handling properties of the sarcoplasmic reticulum (SR) in mdx mice, an animal model of Duchenne muscular dystrophy. One possible reason for this is that only a few studies control for the presence of branched fibres. Fibre branching, a consequence of degenerative-regenerative processes such as muscular dystrophy, has in itself a significant influence on the function of the SR. In our present study we attempt to detect early effects of dystrophin deficiency on SR Ca2+ handling by using unbranched fibres from the immediate post-necrotic stage in mdx mice (just regenerated following massive necrosis). Using kinetically-corrected Fura-2 fluorescence signals measured during twitch and tetanus, we analysed the amplitude, rise time and decay time of Δ[Ca2+]i in unfatigued and fatigued fibres. Decay was also resolved into SR pump and SR leak components. Fibres from mdx mice were similar in all respects to fibres from wt littermates apart from: (i) a longer rise time and slower rate of rise of [Ca2+]i during a tetanus; and (ii) a mitigation of the fall in Δ[Ca2+]i amplitude during the course of fatigue. Our findings suggest that the early effects of a loss of dystrophin on SR Ca2+ handling are only slight, and differ from the widely held view that there is significant Ca2+ pathology in mdx mice. It may be that Ca2+pathology is magnified by progressive branching and degeneration.

Histological Appearance Of The Liver In Experimental Injury

In this work, the morphofunctional state has been studied at various times after the simulation of experimental syphilis. It is noted that discirculatory and dystrophic changes develop in the early stages of the study. The appearance of focal and massive necrosis of hepatocytes is accompanied by the development of an inflammatory process in the form of lymphoid infiltration around necrosis and hypertrophy of Kupffer cells. Subsequently, lymphohistiocytic infiltration spreads along the portal tracts, in which plasma cells and eosinophils appear, which are characteristic of syphilitic inflammation.

Clinical and pathologic features of acute bovine liver disease in Australia

Acute bovine liver disease (ABLD) is a sporadic hepatic disease affecting cattle in southern Australia, characterized histologically by striking periportal hepatocellular necrosis. The cause of ABLD is unknown; however, the seasonality and acute presentation of outbreaks suggest mycotoxin involvement. We describe here the clinical and pathologic findings of ABLD in 45 naturally affected cattle from 13 outbreaks occurring from 2010 to 2019 in Victoria, Australia. Outbreaks occurred in herds located along the southern coastal plain of Victoria and were observed most frequently in lactating dairy cattle. Clinical signs commonly included a combination of mild photosensitization, progressive neurologic signs, and hypogalactia, which preceded death by ≤ 48 h. All affected animals had marked elevations in activities of glutamate dehydrogenase, aspartate aminotransferase, and gamma-glutamyl transferase. At autopsy, the most common lesions were serosal petechiae and/or gastrointestinal hemorrhage, and hepatomegaly with a pronounced hepatic reticular pattern. The principal histologic lesion was widespread—severe periportal hepatocellular coagulative necrosis and erythrocyte pooling—which often extended to massive necrosis. Lesions in other organs were uncommon. Our study of ABLD suggests involvement of a potent hepatotoxin that is either directly cytopathic or requires bioactivation by periportal-specific enzymes.

Histopathological Analysis of the Pro-Arrhythmogenic Changes in a Suspected Chagas Disease Sudden Death

Background Sudden death is the principal cause of fatality in Chagas disease, afflicting to non-symptomatic patients younger than 50-years. For this, sudden death associated with chagasic malignant arrhythmias is underdiagnosed and their pathophysiological basis is poorly understood. Aims In this sense, this work aimed to analyze the histopathological alterations in cardiac structures specialized in the generation/conduction of action potential in an anatomopathological case of non-diagnosed sudden death living in a Chagasic endemic area. Methods The donor was a woman, 62-year-old, which ingressed without vital signs to the emergency room of “Antonio María Pineda” hospital, without any apparent antecedents of cardiac disease. The gross examination was normal, with no external evidence of structural/ischemic disease. Results Microscopic examination revealed nodal like cell depopulation, microvascular disturbances, chronic myocarditis with mononuclear and mast cell infiltrate plus extracellular matrix reaction, and profuse damage of neural structures placed in nodal region. Amastigote nest of Trypanosoma cruzi (T. cruzi) was detected. Conclusion These findings suggest a complex association among parasite persistence, sinus disease, micro-ischemia foci, and neural inflammation in the genesis of malignant arrhythmias of Chagas disease despite the absence of structural disease or massive necrosis. It is important to perform a protocol of examination for no explained sudden death cases in chagasic endemic countries, to avoid misdiagnosed of sudden death associated with Chagas disease.

Massive gastric necrosis associated with delayed presentation of congenital diaphragmatic hernia—is salvage possible?

Background Delayed presentation of congenital diaphragmatic hernia is an uncommon event. Occurrence of gastric volvulus with massive necrosis in this setting is unusual. In this difficult scenario, the surgeon is faced with the dilemma of conservation or resection. Case presentation A 1-year-old boy with vague gastrointestinal symptoms was found to have congenital diaphragmatic hernia with gastric volvulus, on imaging. The stomach showed massive necrosis secondary to volvulus, and after removal of the necrotic body of the stomach, the remnant was sutured together. Conclusion Congenital diaphragmatic hernia is difficult to diagnose in late presenters beyond the neonatal period due to lack of respiratory symptoms. Stomach salvage is feasible even in severe vascular compromise due to extensive collaterals.

COVID-19, MERS and SARS with Concomitant Liver Injury—Systematic Review of the Existing Literature

The novel coronavirus SARS-CoV-2 (severe acute respiratory syndrome coronavirus 2) infection has been predominantly linked to respiratory distress syndrome, but gastrointestinal symptoms and hepatic injury have also been reported. The mechanism of liver injury is poorly understood and may result as a consequence of viral hepatitis, systemic inflammatory response, gut barrier and microbiome alterations, intensive care treatment or drug toxicity. The incidence of hepatopathy among patients with coronavirus disease 2019 (COVID-19) is unclear, but studies have reported liver injury in patients with SARS and Middle East respiratory syndrome (MERS). We aimed to systematically review data on the prevalence of hepatic impairments and their clinical course in SARS and MERS Coronaviridae infections. A systematic literature search (PubMed/Embase/Cinahl/Web of Science) according to preferred reporting items for systematic review and meta-analysis protocols (PRISMA) was conducted from database inception until 17/03/2020 for studies that evaluated the incidence of hepatic abnormalities in SARS CoV-1, SARS CoV-2 and MERS infected patients with reported liver-related parameters. A total of forty-three studies were included. Liver anomalies were predominantly mild to moderately elevated transaminases, hypoalbuminemia and prolongation of prothrombin time. Histopathology varied between non-specific inflammation, mild steatosis, congestion and massive necrosis. More studies to elucidate the mechanism and importance of liver injury on the clinical course and prognosis in patients with novel SARS-CoV-2 infection are warranted.

Sorafenib treatment has the potential to downstage advanced hepatocellular carcinoma before liver resection

Sorafenib is acknowledged as the standard therapy for advanced hepatocellular carcinoma (HCC) but in the clinical practice the treatment of these patients is extremely complex and needs to be personalized. New evidence suggests that surgical resection-based multimodal treatments may improve outcome in these patients. There is no strong evidence supporting the ability of sorafenib in downstage HCC before surgery. We presented a case of a 53-year-old man with well-compensated HCV-cirrhosis complicated with HCC and neoplastic portal vein thrombosis. The patient was treated initially with sorafenib with optimal radiological and serological response and subsequently with liver resection. Pathological examination showed necrotic portal thrombosis and massive necrosis of a metastatic regional node confirming radiological evidence. This finding suggests that sorafenib exhibits a potential to downstage advanced HCC which is not irrelevant. A possible combination of different modalities has to be considered in the view of a personalized medicine.

Severe damage of respiratory muscles in polymyositis

Objectives - to present a clinical case of polymyositis in a 55-year-old man. The patient was admitted with a diagnosis "transient ischemic attack", quickly followed by an acute respiratory failure, which required the continuous use of mechanical ventilation. Other clinical symptoms included: a high diaphragm position up to the 4-th ribs, the concurrent purulent endobronchitis, bilateral pneumonia, pleurisy, multiple atelectasis, myocardial dysfunction with a decrease in ejection fraction to 46%, local hypokinesia according to EchoCG data. Despite the severe condition of the patient, there was not registered any distinct impairment of the proximal limb muscles and an increase in creatinphosphokinase blood level. The antinuclear myositis-specific antibodies, the signs of primary muscular damage according to the limb muscles ENMG data were also absent. The paraneoplastic process was excluded. The results of clinical examination made the diagnosis of polymyositis uncertain. To clarify the cause of the respiratory muscles damage, an intercostal muscle biopsy was performed.It revealed expressed changes in the muscle, with massive necrosis areas, and perivascular lymphohistiocytic infiltration. Conclusion. The described case of polymyositis is extremely rare, has a severe course and is complicated for diagnosis and treatment. In this case, the most informative examination method can be a biopsy of the intercostal muscles, which allows to identify the inflammatory origine of the disease and to determine the pathogenetic therapy.