Autopsies represent medical procedures through which the causes of patients' deaths are determined or, through tissue sampling and microscopic examination of slides in usual stains or special tests, one can offer the basis for understanding the physiopathological mechanisms that contribute to the patients' death Histological findings of tissue samples from patients who have died of COVID-19 have been mainly orientated to lung, heart, liver, kidney damage with a small percent of them following other organs, but none has, to our knowledge, studied skeletal muscle.

Idiopathic inflammatory myopathies (IIM) represent a heterogeneous group of autoimmune diseases whose treatment is often a challenge. Many patients, even after immunosuppressive therapy, do not respond to treatment, so new alternatives have been sought for this. Therefore, other signaling pathways that could contribute to the pathogenesis of myositis have been investigated, such as the expression of myokines in skeletal muscle in response to the inflammatory process. In this review, we will refer to these muscle cytokines that are overexpressed or downregulated in skeletal muscle in patients with various forms of IIM, thus being able to contribute to the maintenance of the autoimmune process. Some muscle cytokines, through their antagonistic action, may be a helpful contributor to the disease modulation, and thus, they could represent personalized treatment targets. Here, we consider the main myokines involved in the pathogenesis of myositis, expressing our view on the possibility of using them as potential therapeutic targets: interleukins IL-6, IL-15, and IL-18; chemokines CXCL10, CCL2, CCL3, CCL4, CCL5, and CCL20; myostatin; follistatin; decorin; osteonectin; and insulin-like 6. An interesting topic regarding the complex connection between myokines and noninflammatory pathways implied in IIM has also been briefly described, because it is an important scientific approach to the pathogenesis of IIM and can be a therapeutic alternative to be considered, especially for the patients who do not respond to immunosuppressive treatment.

Introduction. In forensic pathology the autolytic process has been observed and documented in order to determine the postmortem interval as accurately as possible. The observation and experiments have been carried out on cadavers exposed to environmental conditions -heat, humidity, air currents, soil, water. Methods. For this study hematoxylin and eosin (HE) stained sections of organ samples from 30 autopsied bodies were examined under the microscope. Modifications of tissue and cell structures were noted in correlation with the bodies' time spent in the Morgue's mortuary refrigerator until the autopsy was performed, which varied between 24 hours and 22 days. Results. All the organs sampled (lung, heart, liver and pancreas) showed severe autolytic alterations after 5 to 8 days. The most heavily affected was the pancreas, cells within Langherhans islets becoming complete autolyzed at the 36 hours mark. Inside organs, autolytic processes occur at different rates depending on the locations within that organ -deeply or superficial; in the heart after 4 or more days subendocardic myocardium shows less severe autolytic changes than the subepicardial one. Conclusion. Autolytic processes have a delayed onset and a much lower progression rate in a cold controlled environment. Different organs suffer different rates of autolysis in correlation to their structure and enzymatic content.

Objectives. Congenital myopathies (CM) are a highly heterogeneous group of disorders with genetic cause, characterized by motor deficit and weakness usually manifesting in the neonatal period, with slowly progressive or non-progressive course and affecting both sexes. MC classification has undergone many changes over time, and in recent years molecular genetic studies have enabled identification of novel genes and mutations, thus increasing the diagnostic complexity. We wanted to study the incidence and morphological features of the CM cases diagnosed by muscle biopsy in the Pathology Department of Colentina University Hospital over a period of 10 years (09.2005- 09.2015). Materials and methods. We retrospectively reviewed all the muscle biopsies diagnosed with different types of CM. Muscle biopsies were performed and specifically processed using routine and special stains on cryosections, semithin and ultrathin sections for ultrastructural examination. In all the cases we reassessed the clinical and laboratory data. Results. From a number of 1,530 peripheral nerve and muscle biopsies performed and analyzed in the 10 years period we diagnosed CM in 15 cases, representing 1.03% of the total. Of these, five were “central core myopathies”, five centronuclear/myotubular myopathies, one case of nemaline myopathy, one case of “reducing body myopathy” and three cases with congenital fi ber type disproportion. Reassessment of morphological data in the clinical context allowed us to identify numerous overlaps between subtypes both in the clinical and pathological picture. Conclusions. The reduced number of MC identified in our country suggests that these diseases are probably underdiagnosed or diagnosed late, requiring a better understanding of the various clinical and pathological particularities. In the accurate diagnostic algorithm, muscle biopsy remains essential to establish the type of CM and thus to direct genetic tests.

Limb-girdle muscular dystrophies (LGMD) are an extremely heterogeneous and rapidly expanding group of diseases characterized by progressive weakness of pelvic, scapular and trunk muscles with sparing of facial and distal musculature in most of the subtypes, onset in childhood or in adults of both sexes, very variable clinical severity ranging from mild to severe phenotypes, some associated with cardio-pulmonary and extraskeletal impairment and high serum creatine-kinase (CK) levels. In the past years, huge advances have been recorded in the various identification methods and new distinct entities were discovered. However, it is not yet clear why some muscle groups are affected and others spared in a specific subtype of LGMD, why similar clinical pictures are associated with different genes and mutations, while the same gene or mutation may present with very various clinical phenotypes. In this review we summarize the main aspects of positive and differential diagnosis in LGMD.

Primary penile melanomas are exceedingly rare (less than 1% of primary penile cancers), 221 cases being reported to date in PubMed indexed medical literature. More than half of the cases occur on the gland, usually in older people than on cutaneous counterpart and have unfavourable prognosis mainly due to the belated diagnosis. We report the case of a 77 years old male diagnosed with a pigmented ulcerated nodular melanoma of the gland with maximal thickness of 4.5 mm, mitotic index 8 mitoses/mm2 and vascular emboli. No lymph node enlargements or distant metastases were identified at presentation. Six months after the diagnosis the patient was well, free of disease. Clinically, penile melanomas may be mistaken for several lesions such as squamous carcinoma, penile nevi, pyogenic granuloma, Kaposi sarcoma. Histopathologic diagnosis is usually straight forward except for highly pleomorphic tumors; discrimination between primary penile tumor and penile metastatic melanoma is the most delicate problem of differential diagnosis. The treatment is not standardized; surgical wide excision or partial/total penectomy completed with sentinel lymph node biopsy are the most frequent methods of treatment; multi-agent chemotherapy and/or high-dose interferon alpha 2b therapy are recommended for patients with locally un-controllable disease and/or metastases.