ABSTRACT
CASE REPORT: A 61-year-old woman with type 2 diabetes mellitus for 7 years for which she was prescribed insulin therapy. Rosiglitazone (4 mg once daily) was introduced with adequate blood glucose control. One month later, she presented with complaints of systemic oedema and loss of vision. Fundoscopy showed bilateral macular oedema. A systemic study demonstrated peripheral oedema. Rosiglitazone was stopped and she was managed conservatively with a rapid resolution of the oedemas and at fundus examination there was no decrease in the macular oedema. DISCUSSION: This case reminds us of the importance of identifying potential toxicities of glitazone regimens. Glitazone use appears to be a cause of macular oedema, and stopping the drug may not resolve this oedema.
Subject(s)
Diabetes Mellitus/drug therapy , Hypoglycemic Agents/adverse effects , Macular Edema/chemically induced , Thiazolidinediones/adverse effects , Female , Humans , Middle Aged , RosiglitazoneABSTRACT
Caso clínicoMujer de 61 años diabética tipo 2 de 7 años de evolución en tratamiento con insulina. Se añade rosiglitazona (4mg al día) para conseguir un control glucémico adecuado. Un mes después, la paciente presenta edema generalizado y pérdida de visión. El estudio fundoscópico mostró edema macular bilateral. En la exploración sistémica destacaban edemas periféricos. La rosiglitazona fue suspendida y la paciente fue tratada de forma conservadora, con resolución rápida de los edemas periféricos pero no de los maculares.DiscusiónEste caso nos indica la importancia de identificar los efectos secundarios de las glitazonas. El tratamiento con glitazonas puede causar edema macular que podría permanecer aun después de su supresión(AU)
Case reportA 61-year-old woman with type 2 diabetes mellitus for 7 years for which she was prescribed insulin therapy. Rosiglitazone (4mg once daily) was introduced with adequate blood glucose control. One month later, she presented with complaints of systemic oedema and loss of vision. Fundoscopy showed bilateral macular oedema. A systemic study demonstrated peripheral oedema. Rosiglitazone was stopped and she was managed conservatively with a rapid resolution of the oedemas and at fundus examination there was no decrease in the macular oedema.DiscussionThis case reminds us of the importance of identifying potential toxicities of glitazone regimens. Glitazone use appears to be a cause of macular oedema, and stopping the drug may not resolve this oedema(AU)
Subject(s)
Humans , Female , Aged , Diabetes Mellitus, Type 2/drug therapy , Macular Edema/chemically induced , Hypoglycemic Agents/adverse effects , Diabetes Mellitus, Type 2/complicationsABSTRACT
CASE REPORT: We report a 34-year-old woman with biopsy proven type II mesangiocapillary glomerulonephritis (MCG II) who had an ophthalmic fundal appearance similar to that seen in patients with age-related macular degeneration (ARMD). DISCUSSION: All patients with MCG II should be reviewed regularly by an ophthalmologist to assess and treat any retinal complications.
Subject(s)
Glomerulonephritis, Membranoproliferative/complications , Macular Degeneration/etiology , Adult , Female , HumansSubject(s)
Cyclosporine/adverse effects , Hyperglycemia/chemically induced , Female , Humans , Middle AgedABSTRACT
Severe metabolic alkalosis in a patient while being hemodialysed with dialysate of bicarbonate is presented. The evolution was satisfactory after a session of hemodialysis with a bath of acetate. Disorders in the acid-base balance which appear following dialytic technics more complex each time are discussed.
Subject(s)
Alkalosis/etiology , Renal Dialysis/adverse effects , Acute Disease , Acute Kidney Injury/complications , Acute Kidney Injury/therapy , Alkalosis/diagnosis , Bicarbonates/adverse effects , Female , Hemodialysis Solutions/adverse effects , Humans , Middle AgedABSTRACT
We show the case of a patient suffering from a chronic renal failure in hemodialysis. He had a ischemic necrosis that was quickly progressive in his fingers and toes. It was necessary to amputate them. Diffuse vascular calcifications were recorded so radiologically than pathologically. PTH and phosphocalcic product were raised. Parathyroidectomy was practised with a quick initial improvement but immediately new distal ischemic lesions and keratotic papules with histologic perforation, that became necrosed, appeared in his buttocks and inferior extremities. The coexistence of acquired perforating disease and calciphylaxis in uremic patients has not been reported until now.
