Patient: Female, 68Final Diagnosis: Hepatic sarcoidosisSymptoms: Abdominal pain • nausea • weaknessMedication: —Clinical Procedure: Liver biopsySpecialty: Gastroenterology and HepatologyObjective:Rare diseaseBackground:Sarcoidosis is a systemic disease that can affect any organ, including the liver. It is manifested by the presence of non-caseating granulomas within involved organs, most commonly the pulmonary, lymphatic, and hepatic system. Unlike pulmonary or lymphatic involvement, hepatic involvement is usually asymptomatic and it is underdiagnosed. Here, we report a case of a patient with a history of pulmonary sarcoidosis who developed hepatic sarcoidosis.Case Report:68-year-old female with pulmonary sarcoidosis with a 2-week history of severe abdominal pain and epigastric tenderness presented to our center. Abdominal magnetic resonance imaging (MRI) demonstrated mild hepatic fibrosis and cirrhosis. A thorough workup was performed including a liver biopsy which showed chronic non-necrotizing granulomas consistent with sarcoidosis. She was started on prednisone and subsequently improved. The patient was symptom-free on follow-up 1 month later.Conclusions:The majority of patients with hepatic sarcoidosis are usually asymptomatic, with only 5–30% presenting with abdominal pain, jaundice, nausea, vomiting, and hepatosplenomegaly. In rare cases, hepatic sarcoidosis can lead to cholestasis, portal hypertension, cirrhosis, or Budd-Chiari syndrome. Treatment with steroids is the mainstay of therapy; however, in severe cases, patients may require liver transplantation. This case report demonstrates that hepatic sarcoidosis is a serious condition, and if not treated, can lead to portal hypertension and cirrhosis. In patients with sarcoidosis, early detection and longitudinal follow-up is important in preventing overt liver failure.
Patient: Male, 67Final Diagnosis: Nodal marginal zone lymphoma and chronic myelomonocyticSymptoms: Cervical lymphadenopathy and leukocytosisMedication: —Clinical Procedure: —Specialty: OncologyObjective:Rare co-existance of disease or pathologyBackground:Leukemias and lymphomas can arise from myeloid or lymphoid stem cells. Combined myeloid leukemia and non-Hodgkin’s lymphoma (NHL), either synchronous or metachronous, rarely occur in the same patient. This report is of a 67-year-old man with a synchronous diagnosis of both bone marrow chronic myelomonocytic leukemia (CMML) and nodal marginal zone lymphoma (NMZL), which a peripheral low-grade B-cell NHL.Case Report:A 67-year-old Caucasian man, who was a long-term cigarette smoker, presented with a five-year history of leukocytosis and cervical lymphadenopathy. He had no symptoms of night sweats, fever, or weight loss. Review of his medical records showed a progressively increasing leukocytosis with a peak of 58×109/L. Computed tomography (CT) imaging of the chest and abdomen showed lymphadenopathy, including enlarged cervical, axillary, mediastinal, and retroperitoneal lymph nodes. Bone marrow biopsy and histology showed CMML. Lymph node biopsy and histology showed NMZL. The patient was treated for NMZL with weekly intravenous rituximab infusions. Although his CMML was stable, the patient requested an evaluation for treatment with hematopoietic allogeneic stem cell transplantation (ASCT). At the time of this report, the patient remains asymptomatic.Conclusions:The synchronous occurrence of bone marrow CMML and NMZL in a single patient is rare and may be attributed to a genetic mutation common to both. There are no current treatment guidelines for this group of patients, and treatment strategies should be individualized to provide an optimum outcome or symptomatic improvement.
Patient: Male, 39Final Diagnosis: Trigger-point induced hypokalemiaSymptoms: Bilateral lower extremity weaknessMedication: Epinephrine • Bupivacaine • MethylprednisoloneClinical Procedure: Trigger-point InjectionSpecialty: Nephrology and RadiologyObjective:Unknown etiologyBackground:Trigger-point injection (TPI) therapy is an effective modality for symptomatic treatment of myofascial pain. Serious adverse effects are rarely observed. In this report, we present the case of a 39-year-old man who experienced severe, transient hypokalemic paralysis in the context of TPI therapy with methylprednisolone, bupivacaine, and epinephrine. He was successfully treated with electrolyte replacement in a closely monitored setting.Case Report:A 39-year-old man with no past medical history except for chronic left hip pain from a work-related injury received a TPI with methylprednisolone and bupivacaine. The TPI targeted the left iliopsoas tendon and was administered using ultrasound guidance. There were no immediately perceived complications, but within 12 h he presented with severe hypokalemic paralysis with a serum potassium 1.7 mmol/L. Judicious potassium repletion was initiated. Repeated tests after 6 h consistently showed normal potassium levels of 4.5 mmol/L.Conclusions:Severe hypokalemic paralysis in the context of trigger-point injection is an incredibly rare occurrence and this is the first case report in English literature. A high index of clinical suspicion and a systematic approach are therefore required for prompt diagnosis and management of this obscure iatrogenic entity. Clinicians can enhance patient safety by allowing the primary pathology to guide them.
Patient: Male, 24Final Diagnosis: Non-seminomatous primary mediastinal germ cell tumorSymptoms: Chest pain • dyspneaMedication: —Clinical Procedure: ChemotherapySpecialty: OncologyObjective:Rare co-existance of disease or pathologyBackground:Primary mediastinal non-seminomatous germ cell tumors (NSGCTs) are aggressive and carry a poor five-year disease free survival rate even with aggressive treatment. We describe a young adult male with primary mediastinal NSGCT presenting with airway obstruction and superior vena cava syndrome (SVCS).Case Report:The patient presented with four weeks of nonproductive cough, weight loss, and right-sided pleuritic chest pain. Chest computed topography (CT) imaging demonstrated a right-sided mediastinal mass determined as a yolk sac tumor on biopsy. The patient underwent induction chemotherapy with etoposide and cisplatin for stage III NSGCT. In the interim, he developed SVCS warranting a second cycle of chemotherapy along with intravenous steroids, with notable improvement in symptoms. However, serial alpha-fetoprotein (AFP) measurements showed progressively increasing levels up to a maximum of 18,781 ng/mL indicating treatment failure. He is currently on salvage chemotherapy.Conclusions:Obstruction of the SVC by external compression is often a manifestation of a malignant process in the thorax. SVCS is a medical emergency and occurs in 6% of patients with mediastinal GCTs. Historically, irradiation was initiated without a histologic diagnosis to relieve the life-threatening obstruction. However, newer data suggest that it is acceptable to defer therapy until a full diagnostic workup is completed. This case highlights the malignant nature of primary mediastinal NSGCTs. In addition, inasmuch as SVCS is dramatic in presentation, it is important to recognize that symptomatic obstruction often develops over weeks or longer. In a hemodynamically stable patient, an accurate histologic diagnosis prior to starting treatment is essential in guiding therapy.
Background Adrenocortical carcinoma (ACC) is a rare tumor with an incidence of one per million population per year. Overall prognosis is poor especially in the presence of distant metastasis where five-year survival rate is 10%. Aside from chemotherapy along with mitotane, second-line regimens are not well-established, and therapeutic options remain limited. Here we present a case of metastatic ACC with rapid and complete remission after salvage therapy with gemcitabine (GEM). Clinical Case A 28-year-old man presented with night sweats, 10-lb weight loss and abdominal pain for three months. An abdominal CT showed a 13x14 cm complex mass partially effacing the inferior vena cava (IVC) and a chest CT showed multiple pulmonary micronodules. Biochemical evaluation was unremarkable, confirming a non-functioning adrenal tumor. The patient underwent right adrenalectomy, hepatectomy, right diaphragm resection and cavotomy of IVC. Pathology confirmed ACC with extra-adrenal and vascular invasion. He then underwent adjuvant intensity-modulated radiation therapy with no evidence of disease on imaging thereafter. However, he was lost to follow-up for six months and returned with new enlarging pulmonary nodules. He was started on chemotherapy (cisplatin, etoposide, adriamycin) with mitotane which were discontinued after two months, due to intractable vomiting despite high dose glucocorticoids and anti-emetics. He was then enrolled in a clinical trial using immunotherapy with nivolumab and ipilimumab which led to a significant decrease in the size of pulmonary metastases. His clinical course was complicated by the development of type 1 diabetes mellitus and proliferative glomerulonephritis related to immunotherapy. After one year of immunotherapy, repeat imaging showed disease progression with new pulmonary nodules. These agents were discontinued, and he was then given a single dose of GEM. Subsequent imaging with CT chest, abdomen and pelvis three months later showed complete response with resolution of lung nodules. He has no evidence of disease one year post therapy and continues to undergo active surveillance. Discussion GEM-based chemotherapy has shown to be a modestly active regimen based on a multicenter study which demonstrated a partial response or stable disease in 4.9% and 25% of cases, respectively, with a median duration of 26 weeks. Median progression-free survival is 12 weeks (range 1 to 94). From the available data, GEM remains an important option for salvage therapy however, to date, there are no reliable predictive biomarkers to potentially identify responsive patients. Conclusion This is an extremely rare case of metastatic ACC achieving complete response after definitive surgery and a single dose of gemcitabine, despite failing first-line chemotherapy and immunotherapy. The unusual positive response may lead to the consideration of its use as a second line regimen.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
hi@scite.ai
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
Copyright © 2024 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.