Cetoacidosis inducida por corticoides y gatifloxacina en una mujer joven no diabética
Objective: To communicate a case of glucocorticoid and gatifloxacin induced ketoacidosis and to discuss the mecanisms of this unusual and severe complication. Case: A 32 years old woman, was admitted for community acquired pneumonia of 5 days of evolution. History: previous diagnosis of probable...
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| Publicado en: | Revista Médica Universitaria |
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| Autores principales: | , , , , |
| Materias: | |
| Acceso en línea: | https://bdigital.uncu.edu.ar/fichas.php?idobjeto=2750 |
| Sumario: | Objective: To communicate a case of glucocorticoid and gatifloxacin induced
ketoacidosis and to discuss the mecanisms of this unusual and severe complication.
Case: A 32 years old woman, was admitted for community acquired pneumonia of 5
days of evolution. History: previous diagnosis of probable AR 4 months before
treated with intermittent methotrexate and glucocorticoids. Physical examination:
regular status, BMI 21, Tº 38ºC, RR 32/min, right pleural effusion, HR 96/min, BP
110/70, polyarthralgia without arthritis. Blood test: HCT 23%, WBC 16300/mm3, ESR
96mm/1ºh, glycemia 0.90mg/dl, liver function and amylase normal, uremia 1.19g/l,
creatinine 19mg/l. Blood cultures (2) and sputum positives for Streptococcus
pneumoniae penicillin susceptible. Pneumonia respond to gatifloxacin. She
developed renal failure becoming anuric with metabolic acidosis. Assuming this
findings as lupic rapidly progressive glomerulonephritis because of proteinuria of
2g/24hs, RF (+) 1/1280, homogeneous ANA (+) 1/320, Anti DNA (+), reduced
complement: C3 29.4mg/dl and C4 10mg/dl, Anti-Ro, Anti-La, Scl70, RNP and Anticardiolipin
positives. Therapy was initiated with IV methylprednisolone bolus
(1g/day/3 days), complicating with hyperglycemia of >6 g/l and ketoacidosis with
ketonuria (+); Anti-ICA and Anti-GAD negatives, and HbA1C 5.2%. She was
admitted to ICU and managed with insulin and hemodialysis. The patient improves,
glucocorticoids were tapered and was dismissed without insulin.
Commentary
1) The presence of normal HbA1C, negative Anti-ICA and Anti-GAD, allows us to rule
out a Tipe 1 Diabetes associated to lupus. 2) The development of ketoacidosis
during glucocorticoid and gatifloxacin therapy and the later resolution support the
etiologic rol of them. 3) Ketoacidosis can be explained by enhanced gluconeogenesis
and insulin resistance with impaired peripheral glucose uptake at receptor and postreceptor
level induced by implicated drugs associated to inflammatory state related
with lupus and sepsis which increase those effects.
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