RESUMO
INTRODUCTION: Multiseptate gallbladder is a rare congenital condition that may be asymptomatic or may lead to symptoms consistent with biliary colic, even in the absence of cholelithiasis. DISCUSSION: We present the case of a 19-year-old female who underwent an extensive gastrointestinal workup before she was referred for cholecystectomy, which led to resolution of her symptoms. The distinct imaging features of this entity are presented.
Assuntos
Doenças Biliares/cirurgia , Colecistectomia Laparoscópica/métodos , Diagnóstico por Imagem/métodos , Vesícula Biliar/anormalidades , Dor Abdominal/diagnóstico , Dor Abdominal/etiologia , Doenças Biliares/diagnóstico , Doenças Biliares/etiologia , Cólica/diagnóstico , Cólica/etiologia , Diarreia/diagnóstico , Diarreia/etiologia , Feminino , Seguimentos , Humanos , Doenças Raras , Medição de Risco , Tomografia Computadorizada por Raios X , Resultado do Tratamento , Ultrassonografia Doppler , Adulto JovemRESUMO
We describe the generation of two genetically related human immunodeficiency virus type 1 (HIV-1) isolates highly (>20,000-fold) resistant to the small molecule CCR5 inhibitor, SCH-417690 (formerly SCH-D). Both viruses were cross-resistant to other small molecules targeting entry via CCR5, but they were inhibited by some MAbs against the same coreceptor on primary CD4+ T-cells. The resistant isolates remained sensitive to inhibitors of other stages of virus entry, and to replication inhibitors acting post-entry. Neither escape mutant could replicate detectably in peripheral blood mononuclear cells (PBMC) from two donors homozygous for the CCR5-Delta32 allele and both were insensitive to the CXCR4-specific inhibitor, AMD3100. Hence, the SCH-D escape mutants retained the R5 phenotype. One of the resistant isolates was, however, capable of replication in U87.CD4.CXCR4 cells and, after expansion in those cells, was sensitive to AMD3100 in primary CD4+ T-cells. Hence, some X4 variants may be present in this escape mutant swarm. A notable observation was that the SCH-D escape mutants were also cross-resistant to PSC-RANTES and AOP-RANTES, chemokine derivatives that are reported to down-regulate cell surface CCR5 almost completely. However, the extent to which CCR5 is down-regulated was dependent upon the detection MAb. Hence, the escape mutants may be using a CCR5 configuration that is only detected by some anti-CCR5 MAbs. Finally, two SCH-D-resistant clonal viruses revealed no amino acid changes in the gp120 V3 region relative to the parental viruses, in marked contrast to clones resistant to the AD101 small molecule CCR5 inhibitor that possess 4 such sequence changes. Several sequence changes elsewhere in gp120 (V2, C3 and V4) were present in the SCH-D-resistant clones. Their influence on the resistant phenotype remains to be determined.
