Autopsy findings of miliary tuberculosis in a renal transplant recipient.

Miliary tuberculosis is a lethal form of disseminated tuberculosis (TB), deriving its name from the millet-seed-sized granulomas in multiple organs. As TB still remains a leading cause of morbidity and mortality in India, its disseminated forms need to be diagnosed early to ensure more aggressive treatment at the earliest possible time. However, a considerable number of cases are missed ante-mortem. We discuss the case of a 32-year-old immunocompromised, non-HIV patient with an ante-mortem diagnosis of pulmonary TB. However, multiple organ involvement by Mycobacterium tuberculosis was demonstrated on autopsy. This case highlights the role of autopsy as a research and learning tool, and prudential clinico-pathologic correlation, which will improve clinical outcomes in the future.

Autopsy findings of miliary tuberculosis in a renal transplant recipient

Miliary tuberculosis is a lethal form of disseminated tuberculosis (TB), deriving its name from the millet-seed-sized granulomas in multiple organs. As TB still remains a leading cause of morbidity and mortality in India, its disseminated forms need to be diagnosed early to ensure more aggressive treatment at the earliest possible time. However, a considerable number of cases are missed ante-mortem. We discuss the case of a 32-year-old immunocompromised, non-HIV patient with an ante-mortem diagnosis of pulmonary TB. However, multiple organ involvement by was demonstrated on autopsy. This case highlights the role of autopsy as a research and learning tool, and prudential clinico-pathologic correlation, which will improve clinical outcomes in the future.

Association of Helicobacter pylori restriction endonuclease-replacing gene, hrgA with overt gastrointestinal diseases.

BACKGROUND AND AIM: Helicobacter pylori has been proven to be responsible for causing various gastrointestinal disorders including gastric adenocarcinoma. Several genes of pathogen (the genes of the cag-PAI, vacA, iceA, and babA) either in combination or independently have been reported to significantly increase the risk of ulceration/gastric carcinoma, with the cagA gene having the strongest predictive value. Pursuit to identify new genes which could serve as a marker of overt disease progression, lead to the discovery of hrgA gene. METHODS: Fifty-six indigenous strains of H. pylori from subjects with various gastric disorder were screened to assess the status of hrgA gene along with the cagA gene using simple polymerase chain reaction using specific oligonucleotide primers. Post-amplification, amplicons were subjected for sequencing to identify any strain specific variations in sequences from the H. pylori isolated from different disease manifestations. Histopathological analysis was done to ascertain any significant change in the histological scores of subjects infected with cagA+/hrgA+ and cagA-/hrg+ strains. RESULTS: All the 56 (100%) subjects amplified with the oligonucleotide primers specific to hrgA gene, whereas 81.71% subjects showed the presence of cagA gene. Sequencing of the amplimers showed 99% homology. Histology of the cagA+/hrgA+ and cagA-/hrg+ subjects did not show any significant difference. CONCLUSION: hrgA gene of Helicobacter pylori is not a ideal surrogate marker for identifying individuals with higher risk of developing overt gastro-duodenal diseases such as neoplasia of the stomach.

Association of Helicobacter pylori restriction endonuclease-replacing gene, hrgA with overt gastrointestinal diseases / Associação entre o hrgA (Helicobacter pylori restriction endonuclease-replacing gene) com as principais doença gastrointestinais

BACKGROUND and AIM: Helicobacter pylori has been proven to be responsible for causing various gastrointestinal disorders including gastric adenocarcinoma. Several genes of pathogen (the genes of the cag-PAI, vacA, iceA, and babA) either in combination or independently have been reported to significantly increase the risk of ulceration/gastric carcinoma, with the cagA gene having the strongest predictive value. Pursuit to identify new genes which could serve as a marker of overt disease progression, lead to the discovery of hrgA gene. METHODS: Fifty-six indigenous strains of H. pylori from subjects with various gastric disorder were screened to assess the status of hrgA gene along with the cagA gene using simple polymerase chain reaction using specific oligonucleotide primers. Post-amplification, amplicons were subjected for sequencing to identify any strain specific variations in sequences from the H. pylori isolated from different disease manifestations. Histopathological analysis was done to ascertain any significant change in the histological scores of subjects infected with cagA+/hrgA+ and cagA-/hrg+ strains. RESULTS: All the 56 (100 percent) subjects amplified with the oligonucleotide primers specific to hrgA gene, whereas 81.71 percent subjects showed the presence of cagA gene. Sequencing of the amplimers showed 99 percent homology. Histology of the cagA+/hrgA+ and cagA-/hrg+ subjects did not show any significant difference. CONCLUSION: hrgA gene of Helicobacter pylori is not a ideal surrogate marker for identifying individuals with higher risk of developing overt gastro-duodenal diseases such as neoplasia of the stomach.

RACIONAL e OBJETIVOS: O Helicobacter pylori tem sido incriminado como causador de vários distúrbios digestivos, incluindo o adenocarcinoma gástrico. Diversos genes patogênicos (os genes do cag-PAI, vacA, iceA e babA), em combinação ou independentes, têm sido reportados como fatores de aumento de risco para ulceração/carcinoma gástrico, tendo o gene cagA forte valor preditivo. A procura da identificação de novos genes que possam vir a ser marcadores da progressão da doença levaram à descoberta do gene hrgA. MÉTODOS: Cinqüenta e seis amostras de H. pylori provenientes de pacientes com diversas afecções gástricas foram examinadas para caracterizar a presença do hrgA juntamente ao cagA, usando iniciadores específicos da reação de cadeia da polimerase. Após amplificação, os produtos amplificados pela PCR foram seqüenciados para a identificação de variações específicas nas seqüências do H. pylori isolado de diferentes doenças gastroduodenais. A análise histopatológica foi feita para assegurar qualquer mudança significativa nos escores dos indivíduos infectados com cagA+hrgA+ e cagA-/hrgA+. RESULTADOS: Todas as 56 amostras (100 por cento) foram amplificadas com iniciadores específicos para o hrgA, enquanto que 81,71 por cento mostraram a presença do cagA. O seqüenciamento do produto amplificado pela PCR mostrou 99 por cento de homologia. A histologia entre os grupos cagA+/hrgA+ e cagA-/hrgA+ não mostrou nenhuma diferença significante. CONCLUSÃO: O gene hrgA do H. pylori não é o marcador ideal para identificar indivíduos com alto risco de desenvolvimento de doenças gastrointestinais como a neoplasia de estômago.