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Mucormycosis is an opportunistic infection that affects immunocompromised patients, especially those with uncontrolled diabetes. Clinical presentation depends on the site of infection. Complications arise when the pathogen invades the host tissue causing vascular necrosisand distortion. Disease course is fast, and most of the time it has a poor or fatal outcome. Rhino-orbito-cerebral mucormycosis is the most common presenting form. Although initial complaints include fever, sinusitis, nasal discharge, headache, facial pain, and swelling, it should be kept in mind that patients might present during the complication period with a hemiparesis or altered mental status. Here, we present a case of patient who presented with a stroke and further workup revealed the presence of mucormycosis. According to our knowledge, this is the first case of mucormycosis complicated with stroke that was managed with thrombolysis.
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We report a patient presenting with unique neuroophthalmological features of contraversive ocular tilt reaction and concomitant contralesional pseudo-abducens palsy. Magnetic resonance imaging confirmed the presence of an acute infarct in the right thalamomesencephalic region. We discuss the clinical topography of these unique neuroophthalmological findings.
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Basal ganglia calcifications have been linked to a wide range of conditions. Mostly it is an idiopathic finding, especially in the elderly. Endocrinological and neurological disorders are two significant entities causing this radiological finding. Here, we report the first case that suggests a possible correlation between Graves' disease and basal ganglia calcifications.
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INTRODUCTION: Cerebrovascular accidents in sickle cell disease (SCD) patients carry a high socioeconomic impact and represent the most important cause of morbidity, neurological deficits, and impaired quality of life in SCD young population.Patent foramen ovale (PFO) is prevalent in 25% of the general population and it is associated with ischemic stroke in the young population via paradoxical embolism, yet there are no specific guidelines to address how to manage SCD patients with PFO who suffer a stroke. PATIENT CONCERNS AND DIAGNOSIS: Here we present a young SCD patient, aged 24 years, who suffered a stroke in childhood and later was discovered to have a PFO on subsequent echocardiography. The patient has been receiving blood transfusion therapy since 3 years of age. INTERVENTIONS AND OUTCOMES: No treatment was administered to the patient.The intervention that was done was echocardiography with a bubble study to detect PFO. CONCLUSION: Recommendations need to be put in place regarding screening for PFO in patients with SCD, in addition to highlighting issues of whether screening needs to be done in patients who have not developed stroke, and if PFO were to be found, what would be the best management approach and how will prognosis be affected.
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Anemia Falciforme , Forame Oval Patente , Acidente Vascular Cerebral , Anemia Falciforme/complicações , Pré-Escolar , Forame Oval Patente/complicações , Forame Oval Patente/diagnóstico por imagem , Humanos , Qualidade de Vida , Fatores de Risco , Acidente Vascular Cerebral/complicaçõesRESUMO
Due to SARS-COV-2 (COVID-19) pandemic and its catastrophic impact on society, the FDA granted emergency use authorization for some vaccines. Possible rare side effects could not have been observed in this relatively short period. We are reporting an elderly lady with multiple comorbidities who presented with progressive lower limb weakness that started seven days after receiving the first dose of the COVID-19 vaccine. The electrodiagnostic study showed demyelinating polyneuropathy with secondary axonal degeneration consistent with Guillain-Barré syndrome. We ruled out other possible causes for GBS, suggesting a postvaccine nature for her presentation. The patient received intravenous immunoglobulin (IVIG) for five days and gradually improved, which supports our initial diagnosis.
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Both Sickle cell disease (SCD) and Tuberculosis (TB) are prevalent, and mostly concentrated in similar geographic areas. Since there is an overlap of the possible presenting symptoms of SCD complications and TB, a low threshold for suspicion of TB in these patients is recommended. We present a case of an active TB infection in a SCD patient that presented mainly with chronic cough.
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Owing to autoantibody production and thrombophilic disorders in COVID-19, physicians must have low threshold to investigate secondary IIH and demyelinating disorders in patients with headache and decreased vision following recent COVID-19 infection.
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Extramedullary hematopoiesis (EMH) is a well-known complication of beta thalassemia major and frequently occurs in typical sites such as liver or spleen. However, when presenting in unusual sites as sacrum, other diagnosis should be excluded by histopathology prior to deciding on treatment plan.
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Gastrointestinal manifestations of leukemias have been well recognized. Typically, acute leukemias cause typhlitis or appendicitis more commonly than chronic leukemias. Our case points to appendicitis as possible manifestation of chronic myelogenous leukemia.
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Even though most data suggest favorable outcome in patients with SCD and COVID-19 infection, close monitoring remains essential as acute complication may develop unexpectedly. Offering RBC exchange early in the course of infection might improve prognosis.
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To optimize care for patients with hemoglobinopathies, frequent screening for COVID-19 is prudent as viral kinetics in asplenic patients are unknown and differentiating prolonged viral shedding versus reinfection remains a challenge.
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Due to the overlap between ACS and COVID-19 pneumonia, we recommend close monitoring for those patients and offering them RBC exchange early in the course of the disease to avoid clinical deterioration.
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Although the possibility of asymptomatic course for COVID-19 infection in splenectomized thalassemia beta major patients is present, screening them for COVID-19 is important as the progression is still not clear.
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INTRODUCTION: Marfan syndrome, G6PD deficiency, systemic lupus erythematosus (SLE), and Castleman disease are four distinctive, thoroughly investigated entities whose coincidence was never reported. However, occurrence in pairs was sporadically mentioned in literature. CASE PRESENTATION: We report a 15-year-old Caucasian G6PD deficient Marfan male patient, who presented with tonic-clonic seizures, fever, a hemolytic episode, and general symptoms. After the discovery of hepatosplenomegaly, malar rash, and painless lymphadenopathy, further testing diagnosed a multifocal Castleman disease of the hyaline vascular subtype and systemic lupus erythematosus with lupus nephritis that got 35 points on the 2019 EULAR/ACR criteria. G6PD deficiency, SLE & Castleman disease, and seizures were handled medically with eventual improvement in the patient's condition. DISCUSSION AND CONCLUSION: It is extremely rare to discover the gathering of these four diseases in the same patient. Marfan syndrome and G6PD deficiency were proven by respective clinical and laboratory examinations. Castleman disease that tends to occur in older age groups was confirmed via pathological study of a lymph node biopsy, which was compatible with the HHV-8 negative type reported in Asian countries. SLE is part of the differential diagnosis for Castleman disease, yet the newest evidence strongly supports its presence as a distinct entity. However, no concrete proof is available to suggest a causative relationship between the four of them, rather than a coincidental occurrence.
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Pleural effusion is a rare presentation of plasma cell myeloma, occurring in around 6% of patients during the course of their disease, most commonly as a consequence of a concurrent disease process like heart failure secondary to amyloid deposition. Direct infiltration of the pleural fluid by malignant cells leading to myelomatous pleural effusion is a rare mechanism occurring in less than 1% of patients with plasma cell myeloma, and it is associated with a worse prognosis. There are few case reports of myelomatous pleural effusion as an initial presentation of multiple myeloma. Pleural fluid infiltration by monoclonal plasma cells in the absence of an underlying plasma cell myeloma was not reported before in the literature. Tuberculosis is a known cause of polyclonal gammaglobulinemia, however few case reports described the coexistence of monoclonal gammopathy of undetermined significance and tuberculosis. Here we present an interesting case of pleural fluid infiltration by an abnormal looking clonal plasma cells associated with active pulmonary tuberculosis and parapneumonic effusion in a patient with a background of acute myeloid leukemia. Interestingly, the clonal plasma cell proliferation was confined to the pleural fluid without any evidence of an underlying plasma cell neoplasms (including monoclonal gammopathy of undetermined significance and plasmacytomas). Since our patient had an underlying meyloid neoplasm, we though about the possibility of secondary malignancy. However, in almost all patients with coexisting myeloid and plasma cell neoplasms, myeloid neoplasms developed following chemotherapeutic treatment of plasma cell neoplasms not the other way around. Given that, one must conclude localized extramedullary (pleural) plasma cell proliferation probably represents a transient reactive process to pulmonary tuberculosis which is an extremely rare phenomenon and not described before.
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Secondary iron overload in patients with chronic kidney disease (CKD) due to iatrogenic iron replacement is an emerging medical challenge. There are limited options to manage secondary iron overload in patients with CKD as most iron chelators are contraindicated due to low creatinine clearance. In addition to that, accuracy of serum ferritin in monitoring is questionable since it is affected by different variables including inflammation and liver disease. Moreover, correlation of serum ferritin with liver iron concentration (LIC) and heart iron concentration is not well studied in CKD patients. There is no established cut-off value in the current guidelines, and this warrants further investigation with more accurate methods. There are few studies that evaluated the relationship between serum ferritin and LIC determined by different MRI protocols. Limited data in the literature concluded that a positive correlation exists between serum ferritin and LIC determined by MRI T2* and that serum ferritin more than 290 mcg/L is equivalent to severe iron overload on MRI T2*. However, we had a different observation of a patient with CKD on a prolonged course of iron replacement who was monitored with serum ferritin, and despite having a serum ferritin level of more than 1,000 mcg/L, LIC determined by MRI T2* was 5.3 mg/g of liver dry tissue, which is equivalent to mild iron overload. This observation opens the door for further studies to examine the correlation between serum ferritin and LIC determined by MRI and to establish a safe cut-off value of serum ferritin so that further investigation would be indicated in patients with CKD.