The undergraduate thesis rather than a requirement to graduate, are a way of doing research. Previous studies show a thesis To describe the characteristics of the undergraduate thesis of a medical school. Material and Methods: assess publication. Descriptive statistics were used. The undergraduate thesis were characterized as descriptive, in hospitals, in adults, based on out dated literature
Summary Cushing’s syndrome is an endocrine disorder that causes anovulatory infertility secondary to hypercortisolism; therefore, pregnancy rarely occurs during its course. We present the case of a 24-year-old, 16-week pregnant female with a 10-month history of unintentional weight gain, dorsal gibbus, nonpruritic comedones, hirsutism and hair loss. Initial biochemical, hormonal and ultrasound investigations revealed hypokalemia, increased nocturnal cortisolemia and a right adrenal mass. The patient had persistent high blood pressure, hyperglycemia and hypercortisolemia. She was initially treated with antihypertensive medications and insulin therapy. Endogenous Cushing’s syndrome was confirmed by an abdominal MRI that demonstrated a right adrenal adenoma. The patient underwent right laparoscopic adrenalectomy and anatomopathological examination revealed an adrenal adenoma with areas of oncocytic changes. Finally, antihypertensive medication was progressively reduced and glycemic control and hypokalemia reversal were achieved. Long-term therapy consisted of low-dose daily prednisone. During follow-up, despite favorable outcomes regarding the patient’s Cushing’s syndrome, stillbirth was confirmed at 28 weeks of pregnancy. We discuss the importance of early diagnosis and treatment of Cushing’s syndrome to prevent severe maternal and fetal complications. Learning points: Pregnancy can occur, though rarely, during the course of Cushing’s syndrome. Pregnancy is a transient physiological state of hypercortisolism and it must be differentiated from Cushing’s syndrome based on clinical manifestations and laboratory tests. The diagnosis of Cushing’s syndrome during pregnancy may be challenging, particularly in the second and third trimesters because of the changes in the maternal hypothalamic-pituitary-adrenal axis. Pregnancy during the course of Cushing’s syndrome is associated with severe maternal and fetal complications; therefore, its early diagnosis and treatment is critical.
Adrenal hemorrhage is the most common cause of adrenal mass in newborns. We present a case of a fullterm male, born by cesarean section due to acute fetal distress from a mother with severe coronavirus disease 2019 (COVID-19) infection. He was diagnosed with hypoxic-ischemic encephalopathy, multifactorial shock, and early neonatal sepsis. On the seventh day of hospitalization, hemoglobin dropped and thus blood transfusion was required, and abdominal ultrasound showed bilateral adrenal hemorrhage. He developed relative adrenal insufficiency without either hemodynamic instability or electrolyte imbalances. The use of parenteral corticosteroids was not required. Follow-up ultrasonography and adrenal axis laboratory examination revealed complete resolution of adrenal hemorrhage. Neonatal adrenal hemorrhage has a wide variety of clinical manifestations. Ultrasound is preferred for both initial screening and follow-up evaluation. Adrenal insufficiency occurs rarely in neonatal adrenal hemorrhage. Treatment is usually conservative. We emphasize the importance of a timely diagnosis and clinical follow-up of adrenal hemorrhage in neonates with fetal distress born from mothers with severe COVID-19.
Summary Type B insulin resistance syndrome (TBIR) is a rare autoimmune disease caused by antibodies against the insulin receptor. It should be considered in patients with dysglycaemia and severe insulin resistance when other more common causes have been ruled out. We report a case of a 72-year-old male with a 4-year history of type 2 diabetes who presented with hypercatabolism, vitiligo, acanthosis nigricans, and hyperglycaemia resistant to massive doses of insulin (up to 1000 U/day). Detection of anti-insulin receptor antibodies confirmed TBIR. The patient received six pulses of methylprednisolone and daily treatment with cyclophosphamide for 6 months. Response to treatment was evident after the fourth pulse of methylprednisolone, as indicated by weight gain, decreased glycosylated haemoglobin and decreased requirement of exogenous insulin that was later discontinued due to episodes of hypoglycaemia. Remission was eventually achieved and the patient is currently asymptomatic, does not require insulin therapy, has normal glycaemia and is awaiting initiation of maintenance therapy with azathioprine. Thus, TBIR remitted without the use of rituximab. This case highlights the importance of diagnosis and treatment in a timely fashion, as well as the significance of clinical features, available laboratory findings and medication. Large controlled studies are required to standardise a therapeutic protocol, particularly in resource-constrained settings where access to rituximab is limited. Learning points: Type B insulin resistance syndrome is a rare autoimmune disorder that should be considered in patients with dysglycaemia, severe insulin resistance and a concomitant autoimmune disease. Serological confirmation of antibodies against the insulin receptor is not necessary in all cases due to the high associated mortality without timely treatment. Although there is no standardised immunosuppressive treatment, a protocol containing rituximab, cyclophosphamide and steroids has shown a significant reduction in previously reported mortality rates. The present case, reports successful remission in an atypical patient using cyclophosphamide and methylprednisolone, which is an effective therapy in countries in which rituximab is not covered by health insurance. When there is improvement in the hypercatabolic phase, the insulin dose should be reduced and/or discontinued to prevent hypoglycaemia; a mild postprandial hyperglycaemic state should be acceptable.
Objetivo: identificar los factores asociados a la presencia de fisura labial y/o palatina en recién nacidos en el Hospital Nacional Edgardo Rebagliati Martins, localizado en Lima – Perú, durante el periodo noviembre 2012 - diciembre 2016. Materiales y métodos: estudio observacional, analítico, de casos y controles emparejado, con datos del Estudio Colaborativo Latinoamericano de Malformaciones Congénitas (ECLAMC). Se analizaron 61 casos y 61 controles. La variable dependiente fue la presencia de fisura labial y/o palatina. Se recogieron también variables clínicas, epidemiológicas, obstétricas y prenatales. Resultados: la fisura labiopalatina con extensión completa, en el sexo masculino, fue la forma más frecuente y estuvo presente en 36 neonatos (59%), con cariotipo normal 44 (75,9%) y sin diagnóstico prenatal 40 (65,6%). Las malformaciones observadas con más frecuencia fueron las faciales 27 (44,2%) seguidas de malformaciones cardiacas (29,6%). Se construyó un modelo estadístico mediante análisis multivariado conformado por tres variables: enfermedad crónica durante el embarazo (odds ratio [OR]: 3,8; intervalo de confianza al 95% [IC 95%]: 1,11 - 13,08), edad materna mayor a 35 años (OR: 6,85; IC 95%: 2,69 - 17,43) y antecedente familiar (OR: 14,5; IC 95%: 1,68 - 125,56). Conclusiones: las enfermedades crónicas en el embarazo, la edad materna avanzada y el antecedente familiar fueron factores que aumentaron la presencia de fisura labial y/o palatina.
Background Fanconi syndrome and diabetes insipidus are rare adverse effects of ifosfamide. They usually present with high cumulative doses of this medication. They are mainly related to type II proximal renal tubular dysfunction. These complications typically present with severe polydipsia and polyuria accompanied by glycosuria, proteinuria, and some electrolyte abnormalities including hypokalemia, hypophosphataemia, and non-anion gap metabolic acidosis. Clinical case: A 15-year-old male with, a diagnosis of metastatic osteoblastic osteosarcoma in the right distal treated with ifosfamide three years prior to this hospitalization, was admitted to the emergency department complaining of 3 episodes of vomiting, 6 days history of increase volume of the right lower limb and fever. On admission, blood pressure of 80/50 mm Hg, heart rate of 110 beats / minute, respiratory rate of 30 breaths / minute, axillary temperature of 38.3 ° C. It was evident phlogosis at level of the proximal third of the right lower limb. CBC revealed pancytopenia (WBC 5 x10 9 L, Hb 6.8 g/dL, platelets 25×10 3 /mm 3) and ABG and CMP were compatible with mild metabolic acidosis normal AG (pH 7.285, K 1.9 meq / L, Na 156 meq / L, lactate: 0.9 meq / L, HCO3: 17 meq / L). A diagnosis of sepsis was made and the patient was started on meropenem 2g IV every 8 hours, vancomycin 1 g IV every 12 hours, filgastrim 120 ug/daily and one unit of packed RBC. Patient improved after 5 days over the course of his hospitalization. However, on the 18 th day after his hospital admission, he developed a new episode of polyuria, associated with hypocalcemia (7 mg/dL), hypokalemia (2 mEq/L), hypomagnesemia (0.95 mg/dL), hypophosphatemia (0.9 mg/dL) and metabolic acidosis (pH 7.2, bicarbonate 15 mEq/L). Urine analysis revealed glucosuria and proteinuria. Desmopressin test did not showed increase urinary osmolarity thus nephrogenic diabetes insipidus and Fanconi syndrome were diagnosed due to the multiple laboratory abnormalities and sign/symptoms. Patient received electrolyte replacement and ifosfamide was stopped from his chemotherapy regimen. After this, patient recovers and he was discharge at 25 th day of his admission. Conclusion : Ifosfamide causes tubular cell dysfunction leading to both nephrogenic diabetes insipidus and Fanconi syndrome. These complications might event present several years after receiving this chemotherapeutic agent. Full electrolyte repletion and hydration are the gold standard for management The present case report emphasizes the importance of the prevention of nephrotoxicity associated with ifosfamide, since its presentation could increase poor outcomes in patients receiving chemotherapy regimens that include ifosfamide. Presentation: No date and time listed
This review provides an update on the epidemiology, pathophysiology, symptoms, diagnosis and treatment of neuroendocrine neoplasms (NENs) of the small bowel (SB). These NENs are defined as a group of neoplasms deriving from neuroendocrine cells. NENs are currently the most common primary tumors of the SB, mainly involving the ileum, making the SB the most frequently affected part of the gastrointestinal tract. SB NENs by definition are located between the ligament of Treitz and the ileocecal valve. They are characterized by small size and induce an extensive fibrotic reaction in the small intestine including the mesentery, resulting in narrowing or twisting of the intestine. Clinical manifestations of bowel functionality are related to the precise location of the primary tumor. The majority of them are non-functional NENs and generally asymptomatic; in an advanced stage, NENs present symptoms of mass effect by non-specific abdominal pain or carcinoid syndrome which appears in patients with liver metastasis (around 10%). The main manifestations of the carcinoid syndrome are facial flushing (94%), diarrhea (78%), abdominal cramps (50%), heart valve disease (50%), telangiectasia (25%), wheezing (15%) and edema (19%). Diagnosis is made by imaging or biochemical tests, and the order of request will depend on the initial diagnostic hypothesis, while confirmation will always be histological. All patients with a localized SB NEN with or without near metastasis in the mesentery are recommended for curative resection. Locoregional and distant spread may be susceptible to several therapeutic strategies, such as chemotherapy, somatostatin analogs and palliative resection.
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