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We present a rare case of hypertrophic gastropathy associated with protein loss. A 35-year-old man was hospitalized for bowel habit changes, abdominal pain, generalized edema and symptomatic anemia. Pertinent laboratory findings included iron deficiency anemia (Hb 6.7g/dl, ferritin 5 ng/ml) and marked hypoalbuminemia (albumin 2.5 g/dl). Endoscopic biopsy samples of giant gastric folds observed along the greater gastric curvature revealed foveolar hyperplasia and significant parietal cell loss. Endoscopic ultrasonography showed gastric parietal thickening with preserved architecture and normal gastric wall layers. Menetrier disease was diagnosed and the patient treated with cetuximab, a monoclonal antibody that inhibits ligand binding of transforming growth factor alpha (TGFa), preventing gastric mucosa cell proliferation. After twelve months of treatment, the patient referred symptoms improvement, and gastric biopsy levels of the proliferation marker protein Ki-67 had decreased.

Presentamos un caso infrecuente de gastropatía hipertrófica asociada a pérdida de proteínas. Un hombre de 35 años fue hospitalizado por cambios en los hábitos intestinales, dolor abdominal, edema generalizado y anemia sintomática. Los hallazgos de laboratorio pertinentes incluyeron anemia ferropénica (Hb 6.7 g/dl, ferritina 5 ng/ml) e hipoalbuminemia marcada (albúmina 2.5 g/dl). Las muestras de biopsia endoscópica de pliegues gástricos gigantes observados a lo largo de la curvatura mayor gástrica revelaron hiperplasia foveolar y pérdida significativa de células parietales. La ecografía endoscópica mostró engrosamiento parietal gástrico con arquitectura conservada y capas de pared gástrica normales. Se diagnosticó enfermedad de Menetrier y se trató al paciente con cetuximab, un anticuerpo monoclonal que inhibe la unión del ligando del factor de crecimiento transformante alfa (TGFa), evitando la proliferación de células de la mucosa gástrica. Después de doce meses de tratamiento, el paciente refirió mejoría de los síntomas y los niveles de la proteína marcadora de proliferación Ki-67 en biopsia gástrica habían disminuido.

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Abstract We present a rare case of hypertrophic gastropathy associated with protein loss. A 35-year-old man was hospitalized for bowel habit changes, abdominal pain, generalized edema and symptomatic anemia. Pertinent laboratory findings included iron deficiency anemia (Hb 6.7g/dl, ferritin 5 ng/ml) and marked hypoalbuminemia (albumin 2.5 g/dl). Endoscopic biopsy samples of giant gastric folds observed along the greater gastric curvature revealed foveolar hyperplasia and significant parietal cell loss. Endoscopic ultrasonography showed gastric parietal thickening with preserved architecture and normal gastric wall layers. Menetrier disease was diagnosed and the patient treated with cetuximab, a monoclonal antibody that inhibits ligand binding of trans forming growth factor alpha (TGFa), preventing gastric mucosa cell proliferation. After twelve months of treatment, the patient referred symptoms improvement, and gastric biopsy levels of the proliferation marker protein Ki-67 had decreased.

Resumen Presentamos un caso infrecuente de gastropatía hipertrófica asociada a pérdida de proteínas. Un hombre de 35 años fue hos pitalizado por cambios en los hábitos intestinales, dolor abdominal, edema generalizado y anemia sintomática. Los hallazgos de laboratorio pertinentes incluyeron anemia ferropénica (Hb 6.7 g/dl, ferritina 5 ng/ml) e hipoal buminemia marcada (albúmina 2.5 g/dl). Las muestras de biopsia endoscópica de pliegues gástricos gigantes observados a lo largo de la curvatura mayor gástrica revelaron hiperplasia foveolar y pérdida significativa de células parietales. La ecografía endoscópica mostró engrosamiento parietal gástrico con arquitectura conservada y capas de pared gástrica normales. Se diagnosticó enfermedad de Menetrier y se trató al paciente con cetuximab, un anticuerpo monoclonal que inhibe la unión del ligando del factor de crecimiento transformante alfa (TGFa), evitando la proliferación de células de la mucosa gástrica. Después de doce meses de tratamiento, el paciente refirió mejoría de los síntomas y los niveles de la proteína marcadora de proliferación Ki-67 en biopsia gástrica habían disminuido.

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INTRODUCTION: Corynebacterium coyleae is a Gram-stain-positive non-lipophilic coryneform rod first described in blood samples and pleural fluid. There is scarce information about the clinical relevance of C. coyleae and none on complicated urinary tract infections has been described so far. CASE PRESENTATION: A 36-year-old woman with a history of chronic kidney failure, under thrice-weekly haemodialysis since 2014 due to polycystic kidney disease, presented with hypogastric pain, lower left quadrant pain and nausea. Since 1997, the patient had developed several episodes of urinary tract infection. On admission, the patient presented tenderness in the lower abdomen and fist positive lumbar percussion. Urine culture showed significant bacterial growth (>105 c.f.u. ml-1). Slightly glistening colonies of 1 mm in diameter were observed after a 24 h incubation. Gram staining showed coryneform Gram-stain-positive rods. The patient was diagnosed as having a complicated urinary tract infection. A bilateral nephrectomy was performed on the fourth day of hospitalization. Two samples of kidney tissue were sent for culture. Direct examination of the material revealed the presence of abundant inflammatory reaction and Gram-positive diphtheroid rods. The organism was identified using MALDI-TOF and conventional biochemical tests; in both isolates further identification was performed by PCR amplification and sequence analysis of the rpoB gene as Corynebacterium coyleae. CONCLUSIONS: C. coyleae is an infrequent species among the genus Corynebacterium that should be considered as an emerging pathogen that can be involved in nosocomial infections and complicated urinary tract infections.

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The paradoxical response to tuberculosis treatment consists in the appearance of new clinical or radiologic manifestations or worsening of previous injuries after an initial improvement with anti-tuberculosis therapy. It can be observed in 6 to 30 percent of the cases of tubercular meningitis. It is the consequence of an exaggerated immune reaction that should be considered since the treatment is based on the use of immunomodulators and not in the change of anti-tuberculous drugs. We present the case of an HIV negative adult with tuberculous meningitis with a good initial response to specific therapy who showed, 10 weeks later, a paradoxical reaction to treatment that responded successfully to corticosteroids.

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La respuesta paradojal al tratamiento tuberculoso es la aparición de manifestaciones clínico-radiológicas nuevas, o el empeoramiento de las previas, luego de una mejoría inicial con el tratamiento específico. Se puede observar en 6-30% de los casos de tuberculosis meníngea. Es una reacción inmunológica exagerada y debe tenerse presente ya que su tratamiento se basa en el uso de inmunomoduladores y no en el cambio de las drogas antituberculosas. Presentamos el caso de una paciente adulta HIV negativa con meningitis tuberculosa que, luego de una adecuada respuesta inicial al tratamiento, intercurre a las 10 semanas con una reacción paradojal tratada satisfactoriamente con corticoides.

The paradoxical response to tuberculosis treatment consists in the appearance of new clinical or radiologic manifestations or worsening of previous injuries after an initial improvement with anti-tuberculosis therapy. It can be observed in 6 to 30 percent of the cases of tubercular meningitis. It is the consequence of an exaggerated immune reaction that should be considered since the treatment is based on the use of immunomodulators and not in the change of anti-tuberculous drugs. We present the case of an HIV negative adult with tuberculous meningitis with a good initial response to specific therapy who showed, 10 weeks later, a paradoxical reaction to treatment that responded successfully to corticosteroids.

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Ergotism is a clinical condition known since old times and whose main characteristics are ischemia and even limb gangrene. Some drugs have the capacity of interacting with small amounts of ergotamine or its derivatives producing ergotism as a side effect. This is the case of ritonavir, a widely used anti-HIV drug. Here we present a case of ergotism that developed in an HIV positive 39 year old male under treatment with ritonavir, after taking 1 mg of ergotamine tartrate. His clinical picture, apart from showing the basic manifestations of the disease, was associated with splenic infarction. For this reason, we consider important to advise patients about the potential pharmacological interaction between ergotamines and others common drugs and, in particular, ritonavir in HIV positive patients.

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El ergotismo es una enfermedad conocida desde la antig³edad, que se caracteriza por isquemia y, en algunos casos, gangrena de las extremidades. Muchas drogas de uso corriente tienen la capacidad de interactuar con los ergotamínicos desarrollando ergotismo como efecto adverso. Un ejemplo de ello es el ritonavir, un inhibidor de la proteasa utilizado en pacientes con el virus de la inmunodeficiencia humana (HIV). Presentamos un caso de ergotismo en un varón de 39 años con infección por HIV en tratamiento con ritonavir que, después de ingerir 1 mg de tartrato de ergotamina, además de presentar manifestaciones clásicas de la enfermedad, desarrolló un infarto esplénico. Por lo tanto, consideramos importante advertir a los pacientes sobre la posible interacción farmacológica entre los ergotamínicos y otras drogas de uso frecuente y, en particular, el ritonavir en pacientes portadores de HIV.(AU)

Ergotism is a clinical condition known since old times and whose main characteristics are ischemia and even limb gangrene. Some drugs have the capacity of interacting with small amounts of ergotamine or its derivatives producing ergotism as a side effect. This is the case of ritonavir, a widely used anti-HIV drug. Here we present a case of ergotism that developed in an HIV positive 39 year old male under treatment with ritonavir, after taking 1 mg of ergotamine tartrate. His clinical picture, apart from showing the basic manifestations of the disease, was associated with splenic infarction. For this reason, we consider important to advise patients about the potential pharmacological interaction between ergotamines and others common drugs and, in particular, ritonavir in HIV positive patients.(AU)

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El ergotismo es una enfermedad conocida desde la antigüedad, que se caracteriza por isquemia y, en algunos casos, gangrena de las extremidades. Muchas drogas de uso corriente tienen la capacidad de interactuar con los ergotamínicos desarrollando ergotismo como efecto adverso. Un ejemplo de ello es el ritonavir, un inhibidor de la proteasa utilizado en pacientes con el virus de la inmunodeficiencia humana (HIV). Presentamos un caso de ergotismo en un varón de 39 años con infección por HIV en tratamiento con ritonavir que, después de ingerir 1 mg de tartrato de ergotamina, además de presentar manifestaciones clásicas de la enfermedad, desarrolló un infarto esplénico. Por lo tanto, consideramos importante advertir a los pacientes sobre la posible interacción farmacológica entre los ergotamínicos y otras drogas de uso frecuente y, en particular, el ritonavir en pacientes portadores de HIV.

Ergotism is a clinical condition known since old times and whose main characteristics are ischemia and even limb gangrene. Some drugs have the capacity of interacting with small amounts of ergotamine or its derivatives producing ergotism as a side effect. This is the case of ritonavir, a widely used anti-HIV drug. Here we present a case of ergotism that developed in an HIV positive 39 year old male under treatment with ritonavir, after taking 1 mg of ergotamine tartrate. His clinical picture, apart from showing the basic manifestations of the disease, was associated with splenic infarction. For this reason, we consider important to advise patients about the potential pharmacological interaction between ergotamines and others common drugs and, in particular, ritonavir in HIV positive patients.

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Leflunomide, a disease-modifying antirheumatic drug, has been shown to be effective in the management of rheumatoid arthritis (RA). Among other side effects, systemic hypertension has been described, and also a case of possible pulmonary hypertension (PH) has been reported. Symptomatic PH in RA is rare. We present a 28-year-old woman with a history of RA who consulted our hospital because of severe symptomatic pulmonary hypertension. Two years before admission, she was started on leflunomide. Due to previous evidence of the association of leflunomide with pulmonary hypertension, the drug was stopped. The patient became asymptomatic with normal pulmonary arterial pressure within a year. Given the poor prognosis of idiopathic pulmonary arterial hypertension, the recognition of potentially reversible causes is crucial. Until further evidence is available in a patient who develops pulmonary arterial hypertension, stopping leflunomide should be considered.

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El síndrome pulmón-riñón se define como una combinación de hemorragia alveolar difusa y glomerulonefritis. La coexistencia de estas dos afecciones clínicas se produce por enfermedades con distintos mecanismos patogénicos. Las vasculitis sistémicas primarias y el síndrome de Goodpasture son las etiologías más frecuentes. El lupus eritematoso sistémico, otras colagenopatías, las vasculitis con anticuerpos anticitoplasma de los neutrófilos negativos y las secundarias a drogas son causas mucho menos comunes. El diagnóstico temprano basado en criterios clínicos, radiológicos, de laboratorio e histológicos, permite iniciar el tratamiento disminuyendo su elevada morbi-mortalidad. La terapéutica se basa en altas dosis de corticoides, inmunosupresores, inhibidores del factor de necrosis tumoral y plasmaféresis.

The pulmonary-renal syndrome is defined as a combination of diffuse alveolar hemorrhage and glomerulonephritis. The coexistence of these two clinical conditions is due to diseases with different pathogenic mechanisms. Primary systemic vasculitis and Goodpasture syndrome are the most frequent etiologies. Systemic lupus erythematosus, connective tissue diseases, negative anti neutrophil cytoplasmic antibody vasculitis and those secondary to drugs are far less common causes. An early diagnosis based on clinical, radiologic, laboratory and histologic criteria enables early treatment, thus diminishing its high morbility-mortality rate. Therapy is based on high doses of corticosteroids, immunosuppressants, tumor necrosis factor inhibitors and plasmapheresis.

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