Cytomegalovirus Esophagitis in an Immunocompromised Patient.

Cytomegalovirus (CMV) can present with end-organ disease (EOD), particularly in patients with a CD4 cell count <50/mm3. While EOD in immunocompromised patients commonly presents as CMV retinitis (30%) and CMV colitis (5-10%), CMV esophagitis is rare. CMV is the third most common infectious esophagitis following Candida and Herpes Simplex. CMV esophagitis presents with odynophagia, dysphagia, and abdominal pain. Endoscopic exam may reveal large, linear distal esophageal ulcers. Histopathology or serology studies are diagnostic, though serology may be unreliable in the extremely immunosuppressed. Current treatment consists of antivirals such as ganciclovir and valganciclovir. Esophageal disease due to CMV carries a poor prognosis in the immunocompromised. We present the case of a 56-year-old male with a medical history of HIV/AIDS and stage III rectal squamous cell cancer who presented with shortness of breath, weakness, and chronic diarrhea. His HIV was previously well-controlled on antiretroviral therapy. However, due to his malignancy, he was undergoing treatment with chemotherapy and radiation. Initial labs revealed a CD4 count of 42. His clinical course consisted of Escherichia coli septicemia, new-onset atrial fibrillation with a rapid ventricular response, worsening pneumonia, possible metastasis, progressive diarrhea, and potential oropharyngeal candidiasis. Despite several broad-spectrum antimicrobial regimens, he remained symptomatic with new complaints of dysphagia and odynophagia. Eventually, the appearance of vesicular lesions on the lips and a repeat CD4 count of 13 garnered a suspicion of HSV or CMV. This complicated case highlights the necessity for a high index of suspicion of rare manifestations of CMV EOD in an immunocompromised patient presenting with confounding clinical symptoms and extensive diagnoses.

Adenocarcinoma of an Unknown Primary Site: Presentation, Diagnosis, and Management.

Carcinoma of unknown primary (CUP) is a rare metastatic disease in which a primary tumor site cannot be identified. CUP is a diagnosis of exclusion requiring prior workup to identify a primary site. We present a case of a 64-year-old male with vague abdominal pain, a history of gastroesophageal reflux disease (GERD), gastritis, esophagitis, hepatitis C, alcoholic pancreatitis, liver hemangioma, and Warthin tumor, and family history of cancer that was found to have CUP. The diagnosis was made after an extensive workup was done including serum tumor markers, computed tomography (CT) and ultrasound (US) imaging, flow cytometry, and an array of immunohistochemistry stains positive for only cytokeratin 7.

Bilateral Renal Vein Thrombosis in Membranous Nephropathy: Hypoalbuminemia Predictive of Venous Thromboembolism in Nephrotic Syndrome.

Nephrotic syndrome is a known clinical syndrome in which there is increased permeability in the glomerular basement membrane leading to proteinuria, >3.5g/24h, and hypoalbuminemia. The primary causes of nephrotic syndrome include membranous nephropathy, focal segmental glomerulosclerosis, and minimal change disease. Secondary causes include lupus nephritis, diabetes mellitus, multiple myeloma, amyloidosis, and other systemic conditions. Clinically, nephrotic syndrome presents with edema, hyperlipidemia, and increased risk of thromboembolism, the primary focus of this paper. Nephrotic syndrome is often associated with thromboembolic events, especially in patients with membranous nephropathy. It has been shown that hypoalbuminemia is the most significant independent predictor of venous thromboembolic risk. We present the case of a 32-year-old male who first presented with pleuritic chest pain and was found to have multiple bilateral pulmonary emboli treated with oral anticoagulation. On subsequent visits, prompted by either chest pain or edema, he was found to have increasing pulmonary emboli, as well as downtrending serum albumin levels at each visit. Eventually, bilateral non-occlusive renal vein thrombi were discovered. Lab work indicated membranous nephropathy as the most likely etiology secondary to the patient's presentation. Serum anti-phospholipase A2 receptor antibody positivity confirmed the diagnosis, and the patient was treated appropriately.

Physiological, Pathological, and Circadian Factors Impacting Skin Hydration.

Thismanuscript focuses on the physiological, environmental, nutritional, circadian, and aging factors affecting skin tissue water and hydration parameters. The literature findings indicate a multiplicity of interacting processes among these parameters, ultimately impacting skin hydration in normal skin and playing a role in conditions such as atopic dermatitis and psoriasis. The maintenance of adequate skin hydration, aided by the proper functioning of the skin's protective barrier, is facilitated by stratum corneum integrity with the presence of tight junctions and lipids such as ceramides, each of which is impacted by changes in most of the evaluated parameters. Abnormalities in aquaporin 3 (AQP3) expression and associated deficits in skin hydration appear to have a role in atopic dermatitis and psoriasis. AQP3 hydration-related aspects are influenced by circadian rhythms via modulations associated with CLOCK genes that alter AQP3 protein expression. Ultraviolet exposure, aging, and low temperatures are among those factors that affect skin ceramide composition, potentially leading to increased transepidermal water loss and negatively impacting skin hydration. Vitamin C, collagen, and probiotics may increase ceramide production and improve skin hydration. The extent to which each of the different evaluated factors affects skin hydration varies but is usually large enough to consider their potential effects when investigating skin in research and clinical settings.