ABSTRACT
La retinopatía por descompresión es una complicación infrecuente de la cirugía ocular. Aunque después de una trabeculectomía con o sin antimetabolitos se ha reportado la mayoría de los casos, también se ha comunicado en otros procederes oculares. La presión intraocular preoperatoria elevada y sus bruscas variaciones intra- y posoperatorias juegan un rol en su fisiopatología. Las hemorragias retinales son su signo distintivo y la oclusión de la vena central de la retina su diagnóstico diferencial más complejo. En la mayoría de los pacientes se resuelve el cuadro clínico en las primeras ocho semanas sin necesidad de intervención terapéutica. Para minimizar su riesgo, se recomienda una reducción gradual y controlada de la presión intraocular pre- e intraoperatoria. Para la actualización del conocimiento sobre retinopatía por descompresión se realizó una revisión de las publicaciones más relevantes relacionadas con el tema durante los últimos años, con el objetivo de profundizar y mejorar el entendimiento sobre retinopatía por descompresión(AU)
Decompression retinopathy is an infrequent complication of ocular surgery. Most cases have been reported after trabeculectomy with or without antimetabolites, but it has also been described in other ocular procedures. High preoperative intraocular pressure and its sudden intra- and postoperative variations play a role in its physiopathology. Retinal hemorrhage is its distinguishing sign, and central retinal vein occlusion its most complex differential diagnosis. In most patients the clinical picture is resolved within the first eight weeks without any therapeutic intervention. A gradual, controlled reduction in pre- and intraoperative intraocular pressure is recommended to minimize risk. With the purpose of updating knowledge about decompression retinopathy, a review was conducted of the most relevant studies about the topic published in recent years(AU)
Subject(s)
Humans , Retinal Hemorrhage , Trabeculectomy/methods , Diagnosis, Differential , Antimetabolites/adverse effects , Review Literature as Topic , Intraocular PressureABSTRACT
Allopurinol-induced hypersensitivity syndrome is characterized by an idiosyncratic reaction involving multiple-organs, which usually begins 2 to 6 weeks after starting allopurinol. In rare cases, the adverse reactions to allopurinol are accompanied by a variety of liver injury, such as reactive hepatitis, granulomatous hepatitis, vanishing bile duct syndrome, or fulminant hepatic failure. Here we report a case with granulomatous hepatitis and ductopenia. A 69-year-old man with chronic renal failure, hyperuricemia, and previously normal liver function presented with jaundice, skin rash, and fever 2 weeks after taking allopurinol (200 mg/day). In histopathology, a liver biopsy specimen showed mild spotty necrosis of hepatocytes, marked cholestasis in parenchyma, and some granulomas in the portal area. There were vacuolar degeneration in the interlobular bile ducts and ductopenia in the portal tracts. Pathologic criteria strongly suggested the presence of allopurinol-induced granulomatous hepatitis with ductopenia and cholestasis. The patient fully recovered following the early administration of systemic corticosteroid therapy.
Subject(s)
Aged , Humans , Male , Allopurinol/adverse effects , Antimetabolites/adverse effects , Bile Duct Diseases/chemically induced , Bile Ducts, Intrahepatic/drug effects , Cholestasis/chemically induced , Drug Eruptions/pathology , Granuloma/chemically induced , Chemical and Drug Induced Liver Injury/pathology , Kidney Failure, Chronic/complicationsABSTRACT
Acute pancreatitis is a serious disease with fatality rate up to 15%. We recently experienced a case of acute pancreatitis induced by multiple drugs in a patient with ulcerative colitis. A 20-year-old female visited with abdominal pain and hematochezia and diagnosed of ulcerative colitis. Sulfasalazine and prednisolone were used. However, acute pancreatitis occurred after 4 weeks of treatment with additional azathioprine treatment. Drug-induced pancreatitis was suspected, and she was recovered with conventional therapy for acute pancreatitis. Therefore, it was proposed that acute pancreatitis was induced by azathioprine. However, after the administration of sulfasalazine, pancreatitis relapsed. Furthermore, even the re-administration of 5-ASA and azathioprine induced relapse of acute pancreatitis. We concluded that acute pancreatitis was induced by multiple drugs in this patient with ulcerative colitis.
Subject(s)
Female , Humans , Young Adult , Acute Disease , Anti-Inflammatory Agents, Non-Steroidal/adverse effects , Antimetabolites/adverse effects , Azathioprine/adverse effects , Colitis, Ulcerative/diagnosis , Colonoscopy , Mesalamine/adverse effects , Pancreatitis/chemically induced , Sulfasalazine/adverse effects , Tomography, X-Ray ComputedABSTRACT
Antimetabolite, 5-fluorouracil (5-FU) is known to cause testicular damage by epithelial sloughing and cell killing. However, it is not known whether 5-FU induces tubular atrophy and the fate of exfoliated germ cells. Present study was conducted to evaluate these effects of 5-FU on rat testis. Animals were injected, single dose of 5-FU (10.50 & 100 mg/kg, i.p.) and sampled at 1, 3, 15 and 30 day following the treatment. The testes were perfusion fixed by Bouin's fluid. Five micron thick paraffin sections of testes and epididymis were stained with haematoxylin and eosin. Slides were examined for the incidence of abnormal tubules (per 200 tubules), tubular diameter (STD), epithelial height (SEH) and for the presence of germ cells in the epididymis. Data were analysed by Mann-Whitney 'U' test. The testes weight, STD, SEH were decreased (P < 0.05-0.01) in treated animals. The abnormal tubules were increased in a dose dependent manner with atrophic tubules seen on 30 d. The exfoliated germ cells have not blocked the post testicular ductal system and found in the epididymis in a dose dependent manner. The present study concludes that 5-FU causes tubular shrinkage and atrophy. Further, epididymis is involved in the phagocytosis of germ cells.