Classical Hodgkin lymphoma (cHL) is a B-cell-derived malignant neoplasia that has a unique histological distribution, in which the scarce malignant Hodgkin and Reed-Sternberg cells are surrounded by nonmalignant inflammatory cells. The interactions between the malignant and inflammatory cells are mediated by aberrantly produced cytokines, which play an important role in tumor immunopathogenesis. Single nucleotide polymorphisms (SNPs) in genes encoding cytokines and their regulatory proteins may influence the peripheral levels of these molecules and affect disease’s pathobiology. In this study, we evaluate SNPs in the promoter regions of the genes encoding for two key cytokines in Hodgkin lymphoma: IL-10 (SNP/pIL10–592, rs1800872; and SNP/pIL10–1082, rs1800896) and TNF-α (SNP/pTNF -238, rs361525; and SNP/pTNF -862, rs1800630), as well as an SNP in the intronic region of the NFκB1 gene (SNP/iNFKB1, rs1585215), an important regulator of cytokine gene expression. We then look to their possible association with clinical and laboratory features in cHL patients. Seventy-three patients with cHL are genotyped by qPCR-high resolution melting. The SNPs’ genotypes are analyzed individually for each SNP, and when more than two allelic combinations are identified, the genotypes are also divided into two groups according to proposed biological relevance. By univariate analysis, patients harboring SNP/pTNF -238 AG genotype more frequently have EBV-associated cHL compared to homozygous GG, whereas the presence of mediastinal disease (bulky and nonbulky) is more common in the pIL10–592 AC/CC group compared to the AA homozygous group. Patients with SNP/iNFKB1 AA genotype more frequently have stage IV and extranodal disease at diagnosis. These results indicate that some SNPs’ genotypes for IL-10 and TNF-α genes are associated with prognostic parameters in cHL. For the first time, the SNP/iNFKB1 is described in association with clinical features of the disease.

Patient: Male, 55-year-old Final Diagnosis: Gout • spinal gout Symptoms: Back pain • fever • incontinence • pain • paresthesia of extremities • tachycardia Medication: — Clinical Procedure: Antibiotics • arthrocentesis • biopsy • CT scan • surgery • ultrasonography Specialty: General and Internal Medicine Objective: Unusual clinical course Background: Gout is a chronic disease characterized by deposition of monosodium urate crystals, typically manifesting as arthritis. Clinical presentation of gout usually results from activation of local inflammatory response. Despite being one of the oldest diseases in the world, gout pathophysiology is incompletely understood and clinical features are still surprising. Recent reports describe unusual manifestations including atypical joints involvement, tenosynovitis, panniculitis, and multinodular inguinal swelling. Another atypical feature is the acute polyarticular gout with severe systemic inflammatory response. Case Report: We report the case of a 55-year-old man presenting with fever, tachycardia, cauda equina syndrome, left-knee arthritis, and systemic inflammatory manifestations. Lumbar spine magnetic resonance imaging showed a 4.0×1.3×2.2 cm calcified mass inside the vertebral canal at the L4–L5 level, causing stenosis of the dural space and intervertebral foramen. Clinical diagnoses were septic knee arthritis and lumbar spine meningioma. Despite antibiotic therapy and left-knee surgical drainage, fever and increased C-reactive protein persisted, and arthritis developed in the elbows and right knee. As cultures were negatives, we then diagnosed gout flare in the affected joints accompanied by a severe systemic inflammatory reaction. A few days after starting colchicine and anti-inflammatory drugs, symptoms and inflammatory markers subsided. It was such a severe attack that we called it a “gout storm”. Conclusions: The report highlights the difficulty in diagnosing acute polyarticular gout affecting atypical joints, particularly when faced with a severe systemic inflammatory reaction.

Background: Hepatic epithelioid hemangioendothelioma (HEHE) is a rare neoplastic disease of varied presentation and unspecific radiological signs in the early stages. The diagnostic delay can lead to metastatic disease, thus increasing the tumor burden and reducing the treatment options. HEHE is usually deemed a slow-growing tumor, but its speed of growth is poorly reported and still unknown.Case Description: In this case report, we documented a HEHE diagnosed in a young woman who had complaints of abdominal pain, weight loss and bloating for a long time. The typical findings observed in histological studies were not promptly recognized in the histological analyzes, even after two laparoscopicguided liver biopsies, delaying the diagnosis until extrahepatic tumor spreading. Findings observed in computed tomography, magnetic resonance imaging and histological studies are presented. The coalescence of nodules and the rising of giant masses, occupying large parts of the liver in a specific time span, were registered and quantified. As opposed to prior reports, the results show that hepatic HEHE can grow rapidly, reinforcing the need of early diagnosis, thus avoiding the complications presented herein. Conclusions:The findings observed via radiological and histological imaging that could have avoided the diagnosis delay are depicted and discussed, showing that HEHE can rise faster than previously documented.

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Patient: Female, 27-year-old Final Diagnosis: Ischemic stroke • papillary fibroelastoma Symptoms: Motor aphasia and hemiparesis in the right dimidium Medication:— Clinical Procedure: — Specialty: Cardiology • Neurology Objective: Rare disease Background: Primary cardiac tumors represent less than 5% of total cardiac tumors. Fibroelastoma is a rare benign cardiac tumor that is usually asymptomatic but is acknowledged for its emboligenic potential for causing cardiac, neurological, and vascular symptoms and increasing patient morbidity and mortality. Case Report: This report describes the clinical case of a 27-year-old woman who entered the Emergency Department with motor aphasia and hemiparesis in the right dimidium. A brain computed tomography scan was performed at admission, which showed left frontal-parietal hypodensity. The diagnosis of ischemic stroke was made, but cerebral reperfusion therapy with intravenous recombinant tissue plasminogen activator was not instituted due to the time that had passed since ictus (15 h 40 min). On the first day of hospitalization, the patient had a fever, with no apparent infectious cause. She underwent transthoracic echocardiogram that showed a sessile, isoechoic mass adhered to the atrial surface of the anterior mitral valve leaflet, measuring 6.8×5.5 mm. Antibiotic therapy with ceftriaxone and gentamicin was initiated due to the initial diagnosis of infective endocarditis. Three blood culture samples had negative results. Given a differential diagnosis of fibroelastoma, transesophageal echocardiography and cardiac resonance imaging were performed, and the findings were compatible with a diagnosis of mitral valve fibroelastoma. After clinical discussion, the patient was referred to cardiac surgery and underwent tumor resection with anatomopathological diagnosis of papillary fibroelastoma of the heart valve. Conclusions: Young patients with ischemic stroke must be investigated with transthoracic and transesophageal echocardio-grams. Papillary fibroelastoma is potential cause of ischemic stroke in young patients, and surgical resection is curative and has excellent prognosis.