Conclusion: The suspicion of hepatic cystadenoma is fundamental in the therapeutic, are infrequent tumors less than 5%, and its malignant potential makes this surgery indicated. Normality in tumor markers such as CA19-9 and carcinoembryonic antigen does not exclude the diagnosis. Rule out differential diagnoses as in our first case, hepatic echinococcosis. Major hepatectomies or lobectomies should be taken into consideration depending on the tumor location and resulting hepatic reserve. Not indicating another type of minor surgical treatment, such as drainage or unroofing of the lesion, due to the high probability of recurrence or to that it is a malignant lesion after the complete histological study of the piece.
INTRODUCTION: Systemic lupus erythematosus (SLE) and human immunodeficiency virus (HIV) infection are both systemic disorders presenting with nonspecific constitutional symptoms including fever, fatigue, weight loss, myalgia and arthralgias. Patients with SLE and HIV infection may both develop severe multiorgan dysfunction requiring intensive care unit (ICU) admission. We report a case of misdiagnosed HIV infection in a new-onset SLE patient due to falsely positive HIV antigen/ antibody (Ag/Ab) test resulting in ICU admission.CASE PRESENTATION: A 37-year-old female presented for fatigue, diffuse muscle aches, joint swelling, and oral thrush with dysphagia. She was found to be leukopenic and lymphopenic, with a positive preliminary HIV Ag/Ab Combo test, and absolute CD4 count of 247 cells/mcl. Additional findings included positive cytomegalovirus IgM and nephrotic-range proteinuria. Chest imaging revealed bilateral pleural effusions. She was started on fluconazole for the oral thrush and highly active antiretroviral therapy (HAART) for HIV. However, she further deteriorated clinically with recurrent fevers, declining mental status requiring intubation and ICU admission. The lack of response to therapy prompted alternative diagnosis. Surprisingly, her HIV confirmatory tests was negative, but rheumatologic serology was positive, including high ANA 1:1280 speckled, low complements C3 and C4, positive for anti-Smith antibodies, ds-DNA antibodies, RNP, SSA and SSB, RF, direct coombs, and anticardiolipin antibodies. HAART was discontinued and pulse intravenous (IV) steroid therapy was initiated, which resulted in marked improvement; she was subsequently extubated. Renal biopsy confirmed the diagnosis of lupus nephritis. HIV viral load real-time PCR and genotype analysis were both negative, confirming the false-positive initial test. The patient was optimized and discharged with outpatient follow-up.DISCUSSION: SLE and HIV infection have significant overlapping clinical features. Initial screening HIV tests may be falsely positive due to SLE and antiphospholipid autoantibodies, making it difficult to differentiate the two diseases. A lack of response to initial treatment in our patient prompted the consideration of an alternative diagnosis. Acutely critically-ill SLE patients with major organ involvement are treated with high dose IV methylprednisolone to decrease systemic inflammation. Other immunosuppressive agents such as cyclophosphamide and mycophenolate may also be used. In cases of severe antiphospholipid syndrome with systemic thrombosis and end-organ damage, plasma exchange and IVIG are indicated. CONCLUSIONS:Rarely patients with SLE may present with false-positive HIV screening test, and thus masking and delaying treatment for critical systemic SLE. Clinicians should understand the limitations of initial screening tests and have high suspicion and consideration of diagnoses of both diseases.
INTRODUCTION: Carbon Monoxide (CO) is a colorless, odorless gas found in fumes produced from carbon fuels in engines, stoves, and fireplaces. CO binds to hemoglobin forming a molecule called carboxyhemoglobin (CO-Hb), which has higher affinity to O2 than hemoglobin itself which leads to symptoms of hypoxia and ischemia. Given an adequate history, clinicians can quickly initiate treatment but differentials for shortness of breath (SOB) must be sought and ruled out. Our case report will discuss the importance of CO poisoning and its involvement in thrombus formation and development of a pulmonary embolism (PE).CASE PRESENTATION: 62 year old female with history of COPD was brought to ED due to acute SOB and lethargy. Upon EMS arrival, CO level was 800. While in transport in EMS, the patient's CO-Hb level was 34 (trended to 11.4). The patient was found to have sp02 of 86% on room air (RA), and was placed on 10L nonrebreather mask. Patient was hemodynamically stable and afebrile. Labs revealed WBC 17.96, platelet 409k (clumped), troponin 0.08 ng/mL, LDH 405 units/L, and CRP 22.3 mg/L. Patient was deemed not a candidate for hyperbaric oxygen therapy. CT Head without contrast ruled out intracranial pathology and UA ruled out UTI. Chest X-ray revealed bilateral hazy opacities. CTPE revealed RUL/RML segmental and subsegmental PE as well as bilateral GGO reflecting interstitial edema in the setting of CO poisoning. Echo revealed EF of 65% with no wall motion abnormalities. COVID PCR test resulted negative making PE more likely as cause for SOB and patient was started on therapeutic Lovenox and empiric Azithromycin and Ceftriaxone. Within 24 hours, patient clinically improved and was discharged on Xarelto. DISCUSSION: PE in patients with CO poisoning should be suspected if the patient does not clinically improve with initial treatment. CO toxicity has been known to cause inflammatory and obstructive changes to arterioles and venules. Furthermore, it may induce vasospasms and increase platelet aggregation, leading to venous thrombus formation. CO poisoning may also increase oxidative stress with nitric oxide and oxygen free radicals causing further damage to endothelial lining1 and leading to further platelet dysfunction. 2 This combination of vessel wall injury and stasis in blood flow are important for development of thrombus. Treatment of given thrombus will lead to moderate resolution of symptoms.CONCLUSIONS: Treatment may be delayed in patients with coexisting PE and CO poisoning as it may be misdiagnosed. It is especially difficult to identify PE in patients with stable O2 saturation. However, the combination of endothelial damage and eventual increased platelet aggregation plays a critical role in thrombus formation in patients with CO toxicity. As a result, it is an important differential for patients with CO poisoning especially when symptoms do not respond to initial treatment.
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