Dengue hemorrhagic fever is a more serious form of disease characterised by plasma leakage syndrome,thrombocytopenia and disseminated intravascular coagulation.We present a 51 year old male who presented with fever,pe...Dengue hemorrhagic fever is a more serious form of disease characterised by plasma leakage syndrome,thrombocytopenia and disseminated intravascular coagulation.We present a 51 year old male who presented with fever,petechiae and acute onset of breathlessness.Emergency chest rhoentogram showed a massive riglit sided pleural effusion.On insertion of intercostal drain,there was a sudden gush of blood tinged fluid suggestive of hemothorax.There was no history of trauma or bleeding tendencies.Laboratory investigations revealed a raised hematocrit and severe thrombocytopenia.Dengue IgM was surprisingly positive.After aggressive supportive management the patient gradually improved and was discharged.While bilateral pleural effusion is a known occurrence in dengue hemorrhagic fever,massive hemothorax is unheard of.We report the first case in literature ol dengue hemorrhagic fever presenting as unilateral massive hemothorax.A suspicion of dengue must also be borne in mind in cases of non-traumatic hemothorax especially in endemic areas.展开更多
We present this rare occurrence of a 17 yr old boy,a known case of congenital hypoparathyroidism, who presented with fever and jaundice for 8 days and 2 episodes of generalised tonic-clonic seizures.Premorbidly patien...We present this rare occurrence of a 17 yr old boy,a known case of congenital hypoparathyroidism, who presented with fever and jaundice for 8 days and 2 episodes of generalised tonic-clonic seizures.Premorbidly patient was on regular oral calcium supplementations with normal serum calcium levels.Investigations revealed severe hypocalcaemia(3.2 mg/dL),low 25 hydroxyvitamin D levels and hypomagnesacmia.The marked elevation of serum bilirubin was accompanied by derangement of liver enzymes.Microbiological investigations were confirmatory for both hepatitis A and typhoid fever.In spite of the aggressive management with intravenous calcium gluconate infusion,refractory hypocalcaemia persisted with recovery only after gradual decline in the bilirubin levels.We inferred that the cholestatic process produced by both acute viral hepatitis A and typhoid fever precipitated this state of refractory hypocalcaemia in the previously well preserved patient.展开更多
BACKGROUND The expression of amino acid transporters is known to vary during acute pancreatitis(AP)except for LAT1(slc7a5),the expression of which remains stable.LAT1 supports cell growth by importing leucine and ther...BACKGROUND The expression of amino acid transporters is known to vary during acute pancreatitis(AP)except for LAT1(slc7a5),the expression of which remains stable.LAT1 supports cell growth by importing leucine and thereby stimulates mammalian target of rapamycin(mTOR)activity,a phenomenon often observed in cancer cells.The mechanisms by which LAT1 influences physiological and pathophysiological processes and affects disease progression in the pancreas are not yet known.AIM To evaluate the role of LAT1 in the development of and recovery from AP.METHODS AP was induced with caerulein(cae)injections in female and male mice expressing LAT1 or after its knockout(LAT1 Cre/LoxP).The development of the initial AP injury and its recovery were followed for seven days after cae injections by daily measuring body weight,assessing microscopical tissue architecture,mRNA and protein expression,protein synthesis,and enzyme activity levels,as well as by testing the recruitment of immune cells by FACS and ELISA.RESULTS The initial injury,evaluated by measurements of plasma amylase,lipase,and trypsin activity,as well as the gene expression of dedifferentiation markers,did not differ between the groups.However,early metabolic adaptations that support regeneration at later stages were blunted in LAT1 knockout mice.Especially in females,we observed less mTOR reactivation and dysfunctional autophagy.The later regeneration phase was clearly delayed in female LAT1 knockout mice,which did not regain normal expression of the pancreas-specific differentiation markers recombining binding protein suppressor of hairless-like protein(rbpjl)and basic helixloop-helix family member A15(mist1).Amylase mRNA and protein levels remained lower,and,strikingly,female LAT1 knockout mice presented signs of fibrosis lasting until day seven.In contrast,pancreas morphology had returned to normal in wild-type littermates.CONCLUSION LAT1 supports the regeneration of acinar cells after AP.Female mice lacking LAT1 exhibited more pronounced alterations than male mice,indicating a sexual dimorphism of amino acid metabolism.展开更多
文摘Dengue hemorrhagic fever is a more serious form of disease characterised by plasma leakage syndrome,thrombocytopenia and disseminated intravascular coagulation.We present a 51 year old male who presented with fever,petechiae and acute onset of breathlessness.Emergency chest rhoentogram showed a massive riglit sided pleural effusion.On insertion of intercostal drain,there was a sudden gush of blood tinged fluid suggestive of hemothorax.There was no history of trauma or bleeding tendencies.Laboratory investigations revealed a raised hematocrit and severe thrombocytopenia.Dengue IgM was surprisingly positive.After aggressive supportive management the patient gradually improved and was discharged.While bilateral pleural effusion is a known occurrence in dengue hemorrhagic fever,massive hemothorax is unheard of.We report the first case in literature ol dengue hemorrhagic fever presenting as unilateral massive hemothorax.A suspicion of dengue must also be borne in mind in cases of non-traumatic hemothorax especially in endemic areas.
文摘We present this rare occurrence of a 17 yr old boy,a known case of congenital hypoparathyroidism, who presented with fever and jaundice for 8 days and 2 episodes of generalised tonic-clonic seizures.Premorbidly patient was on regular oral calcium supplementations with normal serum calcium levels.Investigations revealed severe hypocalcaemia(3.2 mg/dL),low 25 hydroxyvitamin D levels and hypomagnesacmia.The marked elevation of serum bilirubin was accompanied by derangement of liver enzymes.Microbiological investigations were confirmatory for both hepatitis A and typhoid fever.In spite of the aggressive management with intravenous calcium gluconate infusion,refractory hypocalcaemia persisted with recovery only after gradual decline in the bilirubin levels.We inferred that the cholestatic process produced by both acute viral hepatitis A and typhoid fever precipitated this state of refractory hypocalcaemia in the previously well preserved patient.
基金Swiss National Science Foundation,Grant No.31_166430/1(to Verrey F)。
文摘BACKGROUND The expression of amino acid transporters is known to vary during acute pancreatitis(AP)except for LAT1(slc7a5),the expression of which remains stable.LAT1 supports cell growth by importing leucine and thereby stimulates mammalian target of rapamycin(mTOR)activity,a phenomenon often observed in cancer cells.The mechanisms by which LAT1 influences physiological and pathophysiological processes and affects disease progression in the pancreas are not yet known.AIM To evaluate the role of LAT1 in the development of and recovery from AP.METHODS AP was induced with caerulein(cae)injections in female and male mice expressing LAT1 or after its knockout(LAT1 Cre/LoxP).The development of the initial AP injury and its recovery were followed for seven days after cae injections by daily measuring body weight,assessing microscopical tissue architecture,mRNA and protein expression,protein synthesis,and enzyme activity levels,as well as by testing the recruitment of immune cells by FACS and ELISA.RESULTS The initial injury,evaluated by measurements of plasma amylase,lipase,and trypsin activity,as well as the gene expression of dedifferentiation markers,did not differ between the groups.However,early metabolic adaptations that support regeneration at later stages were blunted in LAT1 knockout mice.Especially in females,we observed less mTOR reactivation and dysfunctional autophagy.The later regeneration phase was clearly delayed in female LAT1 knockout mice,which did not regain normal expression of the pancreas-specific differentiation markers recombining binding protein suppressor of hairless-like protein(rbpjl)and basic helixloop-helix family member A15(mist1).Amylase mRNA and protein levels remained lower,and,strikingly,female LAT1 knockout mice presented signs of fibrosis lasting until day seven.In contrast,pancreas morphology had returned to normal in wild-type littermates.CONCLUSION LAT1 supports the regeneration of acinar cells after AP.Female mice lacking LAT1 exhibited more pronounced alterations than male mice,indicating a sexual dimorphism of amino acid metabolism.
