Hep B

 https://www.youtube.com/watch?v=3cP2kvPq7iQ


m.c form of acquiring Hep B in Asia - Vertically

m.c form of acquiring Hep B in western coutnries: Parenterally (sexual / needles etc)


  • Neonates have immature immune system, so they cant 'fight-off' vertically acquired virus. Over 90% of babies infected with Hep B, go on to have chronic Hep B infection
  • 95% of adults if they acquire Hep B - fight it off!


  • HBV is a DNA virus - replicates efficiently. But is error-prone. Plagued with mutants. 
  • e-antigen negative mutant - tend to be in older patients, tend to be more aggressive.
  • 30-50% of HCC in HBV occurs in absence of cirrhosis






Reveal study - 15 year follow-up study of untreated patients with HEp B. The only factor that was relevant in predicting risk of HCC was viral load at base-line!

Viral load more than 10*4 (2000 IU/ml) was predictive of risk of HCC or Cirrhosis (similar graph for Cirrhosis as for HCC)




Immune Tolerant Phase: typically after vertical infection. DNA remains very high, no inflammation, no fibrosis. Immune system is not trying to fight-off the virus.

Over time - 
The immune tolerant phase -> Active heaptitis B
Viral load comes down, inflammation in liver goes up, ALT goes up. 

Some patients will spontaneously lose e-Antigen, eantibody becomes positive. (IgM for core antibody becomes positive) - usually with an acute bout of hepatitis /jaundice. 
Rate of spontaneous seroconversion is few% per year. There is resolution / improvement of fibrosis to a certain degree. 

Patients with inactive / seroconversion  - have low ALT, low viral count (immune control phase).


E-negative Hep B:
E-gene is located in the pre-core region of HBV. Not necessary for replication. However is the target for immune response. 
If there is mutation in E-gene, it produces no detectable E-antigen, it prevents immune response. 

So basically, after the Immune Control phase - where e-antigen seroconversion has taken place, the virus 'Escapes' and moves in to 'Immune Escape' phase when e-antigen mutates. These patients still might have E-antibody


Comments

Post a Comment

Popular posts from this blog

Pancreatic Cyst

Image
 MCN - (Mother cyst) >95% in pre-menopausal women Mostly in body and tail of pancreas Thick-walled cyst, lined by Ovarian type stroma. Cyst contains mucinous / hemorrhagic material. Does not communicate with PD (unlike IPMN) 10-20% have in-dwelling cancer One review found - no dysplasia in cysts <3 cm in size LN mets is rare. Distal pancreatectomy usually suffices.  Doesnt result in metachronous lesions. Surveillance isnt really necessary SCA - (Grandmother cyst) 75% of SCAs seen in post-menopausal women Can be anywhere in pancreas Honeycombing, with tiny cysts containing clear fluid distributed around central scarring. Central scarring may bear calcification in 30% cases Microcystic SCAs can undergo degeneration and become macrocystic variants zero risk of malignancy, but they can continue to grow and cause obstructive symptoms SPN - (daughter lesion) - Solid Pseudopapillary Neoplasm 90% of lesion occur in young women, in teens / twenties Anywhere  in pancreas Solid / Solid-cys
Read more

Pancreatic cyst fluid examiantion

  CEA Levels:   CEA >192 is 60% sensitive and 90% specific for mucinous cysts (ipmn/mcn) This was based on a study of 70 lesions in 2004 and has stuck till date   CEA < 5 has excellent negative predictive value for mucinous cysts   CEA > 5, therefore can still be a mucinous neoplasm and needs to be taken in context. Other markers such as Ca 72-4, CA 19-9, CA 15-3, CA 125 have lower accuracy than CEA   Amylase levels: ·        Amylase < 250 IU/L is highly unlikely to be connected to PD (eg  SCA) ·        MCN usually have very low / low amylase (one study suggested it has similar amylase to ipmn)   Glucose: ·        Glucose is very low in mucinous tumors & pseudocysts (those with communication to PD)– usually less than 2.8 mmol/l     Glucose < 2.8 mmol/l has Sens/Spec of 90/90 ( more accurate)  compared to CEA >192 (sens/spec 60/90) for identification of mucinous cysts
Read more

Iron deficiency anaemia

IDA   Ferritin: (BSG 2021 / UTD)   Ferritin is the universal intracellular protein containing Iron – a soluble and non-toxic form. It is the primary iron storage protein in prokaryotes and eukaryotes. Ferritin w/o iron is called apo-ferritin . Each ferritin molecule can store up to 4,500 atoms of iron within it.     Iron deficiency anaemia:   1)     Low MCH is more sensitiv e for Iron deficiency than Low MCV. 2)     Low Ferritin is single most important serological marker of IDA. Serum ferritin assessed by assays is usually apo-ferritin, but reflects intra-cellular ferritin stores in RES (macrophages in liver, spleen, LN etc ) in absence of inflammation.   Fe < 15 – indicative of absent iron stores Fe <45 – indicative of low iron stores   In anaemia of chronic disease / CHF  - TSat <20% with Fe <100 is suggestive of Fe deficiency     Fe > 150 unlikely to represent low iron stores even in face of inflammation .   3)     Transf
Read more