Experience With the Use of Baricitinib and Tocilizumab Monotherapy or Combined, in Patients With Interstitial Pneumonia Secondary to Coronavirus COVID19: A Real-World Study / Experiencia con el uso de baricitinib y tocilizumab en monoterapia o combinados, en pacientes con neumonía intersticial secundaria al coronavirus COVID-19: Un estudio del mundo real

Objective: To describe the experience of treatment with baricitinib (BARI) and/or tocilizumab (TCZ), in monotherapy or combined, in patients admitted for interstitial pneumonia secondary to COVID19, and for 30 days after discharge. Methods: Medical records of patients admitted with COVID19 and IP with PaO2/FiO2<300, treated with BARI and/or TCZ, and compared with patients who did not, were retrospectively reviewed. Results: Sixty patients were included; 43 (72%) are males, mean age 67 (SD: 14) years (<50 years: 17%; 51–70: 30%; >70: 53%), with 8.5 (SD: 1) days of symptoms. Sixteen (27%) patients required ICU (94% in <70 years). Fifteen (25%) patients died, 67% in >70 years; 11 (18%) patients died in the first 15 days of admission and 4 (7%) between days 16 to 30. Twenty-three (38%) patients received BARI, 12 (52%) monotherapy (Group 1), during 6 (SD: 2.6) days on average, none required ICU and 2 (17%) died. Thirty-one (52%) patients received TCZ, 20 (33%) as monotherapy (Group 2), 16 (52%) patients required ICU and 4 (20%) died. In the 11 (18%) patients who received BARI (2.8 [SD: 2.5] days average) and TCZ combined (Group 3), 3 (27%) required ICU and died. There were no severe side effects in BARI or TCZ patients. In the 17 (28%) patients who received neither BARI nor TCZ (Group 4), none required ICU and 6 (35%) died. Mean (SD) PaO2/FiO2 at admission between groups was respectively: 167 (82.3), 221 (114.9), 236 (82.3), 276 (83.2). Conclusion: Treatment with BARI and TCZ did not cause serious side effects. They could be considered early in patients with NI secondary to COVID19 and impaired PaO2/PaFi.(AU)

Objetivo: Describir la experiencia con baricitinib (BARI) y/o tocilizumab (TCZ), en monoterapia o combinados en pacientes ingresados por neumonía intersticial (NI) por COVID-19 y durante los 30 días después del alta. Método: Se revisaron retrospectivamente las historias clínicas de los pacientes ingresados por COVID-19 y NI, con PaO2/FiO2<300, tratados con BARI y/o TCZ y se compararon con pacientes que no los recibieron. Resultados: Se incluyeron 60 pacientes; 43 (72%) varones, edad media 67 (DE: 14) años (< 50 años: 17%; 51-70: 30%; > 70: 53%), y 8,5 (DE: 1) días de síntomas. Dieciséis (27%) ingresaron en la unidad de cuidados intensivos (UCI) (94% < 70 años). Quince (25%) fallecieron (67% > 70 años); 11 (18%) de ellos en los primeros 15 días del ingreso y cuatro (7%) entre los días 16 y 30. Veintitrés (38%) pacientes recibieron BARI, 12 (52%) en monoterapia (Grupo 1), durante seis (DE: 2.6) días de promedio, ninguno de ellos ingresó en UCI y dos (17%) fallecieron. Treinta y un (52%) pacientes recibieron una dosis de TCZ, 20 (33%) en monoterapia (Grupo 2), 16 (52%) ingresaron en UCI y cuatro (20%) fallecieron. Entre los 11 (18%) pacientes que recibieron BARI (2,8 [DE: 2,5] días de promedio) y TCZ combinados (Grupo 3), tres (27%) ingresaron en UCI y fallecieron. No hubo efectos secundarios graves entre los que recibieron BARI y/o TCZ. Entre los 17 (28%) pacientes que no recibieron ni BARI ni TCZ (Grupo 4), ninguno ingresó en UCI y seis (35%) fallecieron. La PaO2/FiO2 media (DE) al ingreso entre los grupos fue respectivamente: 167 (82,3), 221 (114,9), 236 (82,3), 276 (83,2). Conclusión: El tratamiento con BARI y TCZ no provocó efectos secundarios graves. Podrían considerarse precozmente en pacientes con NI secundaria a COVID-19 y deterioro de PaO2/PaFi.(AU)

Experience with the use of baricitinib and tocilizumab monotherapy or combined, in patients with interstitial pneumonia secondary to coronavirus COVID19: a real-world study / Experiencia con el uso de baricitinib y tocilizumab en monoterapia o combinados, en pacientes con neumonía intersticial secundaria al coronavirus COVID-19: un estudio del mundo real

OBJECTIVE: To describe the experience of treatment with baricitinib (BARI) and/or tocilizumab (TCZ), in monotherapy or combined, in patients admitted for interstitial pneumonia secondary to COVID19, and for 30 days after discharge. METHODS: Medical records of patients admitted with COVID19 and IP with PaO2/FiO2<300, treated with BARI and/or TCZ, and compared with patients who did not, were retrospectively reviewed. RESULTS: Sixty patients were included; 43 (72%) are males, mean age 67 (SD: 14) years (<50 years: 17%; 51-70: 30%; >70: 53%), with 8.5 (SD: 1) days of symptoms. Sixteen (27%) patients required ICU (94% in <70 years). Fifteen (25%) patients died, 67% in >70 years; 11 (18%) patients died in the first 15 days of admission and 4 (7%) between days 16 to 30. Twenty-three (38%) patients received BARI, 12 (52%) monotherapy (Group 1), during 6 (SD: 2.6) days on average, none required ICU and 2 (17%) died. Thirty-one (52%) patients received TCZ, 20 (33%) as monotherapy (Group 2), 16 (52%) patients required ICU and 4 (20%) died. In the 11 (18%) patients who received BARI (2.8 [SD: 2.5] days average) and TCZ combined (Group 3), 3 (27%) required ICU and died. There were no severe side effects in BARI or TCZ patients. In the 17 (28%) patients who received neither BARI nor TCZ (Group 4), none required ICU and 6 (35%) died. Mean (SD) PaO2/FiO2 at admission between groups was respectively: 167 (82.3), 221 (114.9), 236 (82.3), 276 (83.2). CONCLUSION: Treatment with BARI and TCZ did not cause serious side effects. They could be considered early in patients with NI secondary to COVID19 and impaired PaO2/PaFi

OBJETIVO: Describir la experiencia con baricitinib (BARI) y/o tocilizumab (TCZ), en monoterapia o combinados en pacientes ingresados por neumonía intersticial (NI) por COVID-19 y durante los 30 días después del alta. MÉTODO: Se revisaron retrospectivamente las historias clínicas de los pacientes ingresados por COVID-19 y NI, con PaO2/FiO2<300, tratados con BARI y/o TCZ y se compararon con pacientes que no los recibieron. RESULTADOS: Se incluyeron 60 pacientes; 43 (72%) varones, edad media 67 (DE: 14) años (< 50 años: 17%; 51-70: 30%; > 70: 53%), y 8,5 (DE: 1) días de síntomas. Dieciséis (27%) ingresaron en la unidad de cuidados intensivos (UCI) (94% < 70 años). Quince (25%) fallecieron (67% > 70 años); 11 (18%) de ellos en los primeros 15 días del ingreso y cuatro (7%) entre los días 16 y 30. Veintitrés (38%) pacientes recibieron BARI, 12 (52%) en monoterapia (Grupo 1), durante seis (DE: 2.6) días de promedio, ninguno de ellos ingresó en UCI y dos (17%) fallecieron. Treinta y un (52%) pacientes recibieron una dosis de TCZ, 20 (33%) en monoterapia (Grupo 2), 16 (52%) ingresaron en UCI y cuatro (20%) fallecieron. Entre los 11 (18%) pacientes que recibieron BARI (2,8 [DE: 2,5] días de promedio) y TCZ combinados (Grupo 3), tres (27%) ingresaron en UCI y fallecieron. No hubo efectos secundarios graves entre los que recibieron BARI y/o TCZ. Entre los 17 (28%) pacientes que no recibieron ni BARI ni TCZ (Grupo 4), ninguno ingresó en UCI y seis (35%) fallecieron. La PaO2/FiO2 media (DE) al ingreso entre los grupos fue respectivamente: 167 (82,3), 221 (114,9), 236 (82,3), 276 (83,2). CONCLUSIÓN: El tratamiento con BARI y TCZ no provocó efectos secundarios graves. Podrían considerarse precozmente en pacientes con NI secundaria a COVID-19 y deterioro de PaO2/PaFi

Diagnóstico del déficit de alfa 1-antitripsina: limitaciones de las pruebas de laboratorio de diagnóstico rápido / Diagnosis of Alpha-1 Antitrypsin Deficiency: Limitations of Rapid Diagnostic Laboratory Tests

El déficit hereditario de alfa 1-antitripsina ( 1-AT) predispone al desarrollo de enfisema pulmonar. Elobjetivo de este trabajo es evidenciar las limitaciones de algunos métodos de laboratorio utilizados en elestudio del déficit, cuya interpretación puede inducir a error en la detección de alelos poco frecuentes.Se describen dos casos clínicos: la paciente índice, que presentaba enfisema pulmonar con niveles de 1-AT inferiores a 12 mg/dL, catalogada erróneamente como homocigota de la variante alélica normalPI MM mediante un método de genotipificado rápido; la madre de la paciente, asintomática, con nivelesbajos (60 mg/dL), catalogada también como PI MM.La secuenciación del gen catalogó a la paciente índice como portadora del alelo nulo PI Clayton y deldeficitario PI Mmalton. La madre resultó portadora heterocigota PI Clayton/PI M.Los resultados ponen de relieve las dificultades de diagnóstico del déficit así como la necesidad deconsensuar métodos para este estudio(AU)

Hereditary alpha-1-antitrypsin ( 1-AT) deficiency predisposes to pulmonary emphysema. The objectiveof this study is to demonstrate the limitations of some laboratory methods used in the study of thedeficiency, and which may produce errors in interpretation and detection of uncommon alleles.Two clinical cases are described: the index patient, who had pulmonary emphysema with 1-AT levelsless than 12 mg/dL, was erroneously classified as a homozygote of the normal allelic variant PIMMusinga rapid genotype method; the mother of the patient, asymptomatic, with low levels (60 mg/dL), was alsoclassified as PI MM.The gene sequencing classified the index patient as a carrier of the PI Clayton null allele and PI Mmaltondeficient. The mother was a PI Clayton/PI heterozygote carrier.These results highlight the difficulties in diagnosing the deficiency, as the well as the need to reach aconsensus on methods for this study(AU)

[Diagnosis of alpha-1 antitrypsin deficiency: limitations of rapid diagnostic laboratory tests]. / Diagnóstico del déficit de alfa 1-antitripsina: limitaciones de las pruebas de laboratorio de diagnóstico rápido.

Hereditary alpha-1-antitrypsin (α1-AT) deficiency predisposes to pulmonary emphysema. The objective of this study is to demonstrate the limitations of some laboratory methods used in the study of the deficiency, and which may produce errors in interpretation and detection of uncommon alleles. Two clinical cases are described: the index patient, who had pulmonary emphysema with α1-AT levels less than 12 mg/dL, was erroneously classified as a homozygote of the normal allelic variant PI MM using a rapid genotype method; the mother of the patient, asymptomatic, with low levels (60 mg/dL), was also classified as PI MM. The gene sequencing classified the index patient as a carrier of the PI Clayton null allele and PI Mmalton deficient. The mother was a PI Clayton/PI heterozygote carrier. These results highlight the difficulties in diagnosing the deficiency, as the well as the need to reach a consensus on methods for this study.

[Hepatopulmonary syndrome in a patient with adenocarcinoma of the colon metastatic to the liver and no apparent chronic liver disease]. / Síndrome hepatopulmonar en paciente con adenocarcinoma de colon con metástasis hepáticas y sin hepatopatía crónica conocida.

Hepatopulmonary syndrome consists of a clinical triad: arterial blood deoxygenation, intrapulmonary vasodilation, and liver disease. Both acute and chronic cases of this syndrome have been reported, and the most common cause is cirrhosis. The principle disease mechanism is dilation of the pulmonary blood vessels causing alterations in gas exchange. Increased pulmonary production of nitric acid has been implicated as the primary pathogenic mechanism of vasodilation although it has also been associated with imbalance between vasodilators and vasoconstrictors. We describe the case of a patient with hepatopulmonary syndrome and adenocarcinoma of the colon with metastases to a previously healthy liver.

Síndrome hepatopulmonar en paciente con adenocarcinoma de colon con metástasis hepáticas y sin hepatopatía crónica conocida / Hepatopulmonary syndrome in a patient with adenocarcinoma of the colon metastatic to the liver and no apparent chronic liver disease

El síndrome hepatopulmonar comprende una tríada clínica caracterizada por desoxigenación arterial, dilataciones vasculares intrapulmonares y hepatopatía. Se han descrito tanto casos agudos como crónicos, y la causa más frecuente es la cirrosis. El mecanismo fisiopatológico principal es la dilatación de los vasos pulmonares, que produce una alteración del intercambio gaseoso. Se ha implicado la mayor producción pulmonar de óxido nítrico como mecanismo patogénico principal de la vasodilatación, aunque también se ha relacionado el desequilibrio entre sustancias vasodilatadoras y vasoconstrictoras. Describimos un caso en el que se produjo un síndrome hepatopulmonar en un paciente afectado de un adenocarcinoma de colon con metástasis hepáticas en un hígado previamente sano

Hepatopulmonary syndrome consists of a clinical triad: arterial blood deoxygenation, intrapulmonary vasodilation, and liver disease. Both acute and chronic cases of this syndrome have been reported, and the most common cause is cirrhosis. The principle disease mechanism is dilation of the pulmonary blood vessels causing alterations in gas exchange. Increased pulmonary production of nitric acid has been implicated as the primary pathogenic mechanism of vasodilation although it has also been associated with imbalance between vasodilators and vasoconstrictors. We describe the case of a patient with hepatopulmonary syndrome and adenocarcinoma of the colon with metastases to a previously healthy liver