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2.
Braz. j. med. biol. res ; 32(10): 1211-5, Oct. 1999. ilus, tab, graf
Article in English | LILACS | ID: lil-252270

ABSTRACT

Chemotherapy with oxazaphosphorines, such as cyclophosphamide (CYP), is often limited by unacceptable urotoxicity. Without uroprotection, hemorrhagic cystitis (HC) becomes dose-limiting. To compare the uroprotective efficacy of classical 2-mercaptoethanesulfonic acid (Mesna) treatment with dexamethasone in CYP-induced HC, male Wistar rats (150-200 g; N = 6 in each group) were treated with saline or Mesna (40 mg/kg, ip) immediately and 4 and 8 h after ip administration of CYP (200 mg/kg). One, 2 or 3 doses of Mesna were replaced with dexamethasone (1 mg/kg, ip). The animals were sacrificed 24 h later. Cystitis was evaluated by determining the changes in bladder wet weight (BWW) and by macroscopic and microscopic analysis. CYP treatment induced a marked increased in BWW 162 percent 0.05, which was significantly inhibited by treatment with 3 doses of Mesna 0.05; 80 percent. The replacement of 1 or 2 doses of Mesna with dexamethasone reduced the increase in BWW by 83.3 and 95 percent, respectively. Macroscopic analysis of the bladder of rats with CYP-induced HC showed severe edema and hemorrhage, confirmed by microscopic analysis, that also showed mucosal erosion, inflammatory cell infiltration and ulcerations. The replacement of 1 or 2 doses of Mesna with dexamethasone inhibited the CYP-induced increase in BWW and almost abolished the macroscopic and microscopic alterations, with no significant difference between the effects of Mesna and dexamethasone, indicating that both drugs were efficient in blocking HC. However, although the replacement of all Mesna doses with dexamethasone reduced the edema, it did not prevent HC, suggesting that Mesna is necessary for the initial uroprotection


Subject(s)
Animals , Male , Rats , Cyclophosphamide/toxicity , Cystitis/chemically induced , Dexamethasone/therapeutic use , Hemorrhage/chemically induced , Mesna/therapeutic use , Protective Agents/therapeutic use , Analysis of Variance , Hematuria/chemically induced , Hematuria/pathology , Rats, Wistar , Urinary Bladder/pathology
5.
Rev. nefrol. diál. traspl ; (28): 9-15, dic. 1990. ilus
Article in Spanish | LILACS | ID: lil-100736

ABSTRACT

Se presenta una mujer de 20 años de edad tratada con 2000 mg/día de DPA desde los 17 años por enfermedad de Wilson. Consultó en agosto de 1988: tenía artropatía, hematuria parda, fiebre, amenorrea, úlcera de lengua, pancitopenia, FAN y anti-DNA positivos, síndrome nefrótico y función renal alterada con antiestreptolisina O, hepatograma, coagulograma, completo y tensión arteriales normales. Al suspender DPA desaparecieron la artropatía, la úlcera de lengua y la fiebre y se negativizaron FAN y anti-DNA. En setiembre de 1988 tuvo fiebre y disnea con infiltrado parahiliar izquierdo algodonoso; se descartaron colagenopatías e infecciones, remitiendo en forma espontánea. La biopsia renal mostró alteraciones avanzadas de una glomerulonefritis necrotizante y proliferativa, moderada arteriolonefroesclerosis y ausencia de inmunodepósitos. Recibió pulsos de corticoides y ciclofosfamida sin beneficio. En los seis meses siguientes desapareció la hematuria, reapareció el período menstrual y redujo la proteinuria. Al reiniciar la DPA aumento la proteinuria, suspendiéndose la droga. En julio de 1989 la proteinuria era moderada y la creatinina normal. No se describe glomerulopatía asociada al Wilson; los síntomas y la serología de LES desaparecieron al suprimir la droga. El síndrome urinario, el síndrome pulmonar sin hemoptisis que coincidió con deterioro de la función renal al momento de la biopsia y el tipo de lesión, hallada en la paciente permitirían inscribir este cuadro entre las formas atípicas de púrpura pulmonar y nefritis, cuya incidencia fue estimada en menos del 0,5%en pacientes tratados con DPA por enfermedad de Wilson


Subject(s)
Humans , Adult , Female , Penicillamine/adverse effects , Glomerulonephritis/chemically induced , Hepatolenticular Degeneration/drug therapy , Penicillamine/therapeutic use , Proteinuria/chemically induced , Glomerulonephritis/pathology , Hematuria/chemically induced
6.
Bol. Asoc. Méd. P. R ; 82(9): 423-4, Sept. 1990. tab
Article in English | LILACS | ID: lil-96169

ABSTRACT

Cocaine abuse is associated with a constellation of serious medical complications. An unrecognized and recently described complication of cocaine use is rhabdomyolysis with acute renal failure. We describe the first patient identified in our institution with this entity, admitted to the medical services with oliguric acute renal failure. Three days prior to admission the patient had a cocaine snorting binge. He presented with bilateral flank pain, gross hematuria, vomiting and chills. No history of crush injury, prolonged immobilization and or seizures was reported. On admission the vital signs were normal, physical exam revealed periorbital edema and marked soft tissue neck swelling. Lab values: Bun 120 mgs%, Creat. 10.7 mgs%, Na 132 meq/lt, Co2 13mq/lt, Cl, 103meq/lt, Co2 13meq/lt, Ca5.3 mgs%, CPK 30,800 U/L with a MM fraction of 98%, LDH 600 U/L, SGOT 300 U/L. The urine was dark red with a ph of 6.5 and 100 rbc/hpf. The anti-GBM antibody and blood cultures were negative. An abdominal sonogram was normal. He received peritoneal dialysis and was discharged on his 14th hospital day with a CPK of 2,800 U/L and decreasing azotemia. Cocaine associated rhabdomyolysis has only been recently described in the literature (AJM April, 88). Acute myoglobinuric renal failure needs to be added to the growing list of medical complications of cocaine use


Subject(s)
Humans , Adult , Male , Acute Kidney Injury/chemically induced , Cocaine/adverse effects , Rhabdomyosarcoma/chemically induced , Substance-Related Disorders/complications , Hematuria/chemically induced
7.
Rev. bras. reumatol ; 28(5): 141-3, set.-out. 1988. tab
Article in Portuguese | LILACS | ID: lil-72745

ABSTRACT

Estuda o presente trabalho o resultado do tratamentoa áurico precoce em onze pacietnes portadores de artrite reumatóide juvenil. Avalia a evoluçäo clínica e laboratorial dos doentes observados ao longo de oito anos e conclui que a precocidade do tratamento modifica a evoluçäo natural da artrite reumatóide. Ressalta a importância da história psicossomática das crianças observadas e o trauma familiar conseqüente desempenhando papel de relevo na gênese e na evoluçäo da artrite reumatóide


Subject(s)
Infant , Child, Preschool , Child , Adolescent , Humans , Male , Female , Arthritis, Juvenile/drug therapy , Blood Sedimentation , Gold Sodium Thiomalate/therapeutic use , Arthritis, Juvenile/blood , Eosinophilia/chemically induced , Gold Sodium Thiomalate/adverse effects , Hematuria/chemically induced
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