1) Cephalosporins are a commonly used class of antibiotics --> what's not so commonly known is that some members of this drug class can cause major bleeding complications!
4 groups of cephalosporins have been implicated in this problem!
2) This is based on the different side chains attached to position 3 of the cephem nucleus!
The first and largest group is the NMTT (N-methylthiotetrazole) side chain containing group --> cefamandole, cefotetan, cefmatazole, moxalactam and cefoperazone!
3) Other groups include MTDT and HTT side chain containing cephalosporins as well as cefoxitin which doesn't have any side chains attached to the 3 position of the cephem nucleus!
4) Mechanism --> either direct inhibition of Vitamin K or inhibition of gut bacteria which produce Vit K (menadione or Vit K2)
The latter mechanism is more plausible because most bleeding occurred in malnourished patients!
5) Ceftriaxone has also been associated with some bleeding risk but it is believed to be much lower than the NMTT side chain containing cephalosporins!
6) This link between bleeding and cephalosporin use has been known since the 1980s but the evidence is conflicting and lacks hard evidence!
7) A recent study from South Korea in 2019 found the strongest evidence in favour of lab derived hemostatic abnormalities for cefoperazone, cefamandole and moxalactam!
But clinically significant bleeding problems was NOT STATISTICALLY SIGNIFICANT!
8) It must be remembered that septic patients are very sick and may have many other causes for bleeding --> before we blame the antibiotics!!
The youngest STEMI (heart attack) patient I ever saw was aged 23.
He was obese, hypertensive,never excercised and drank soft drinks everyday! He had lost his father and uncle to STEMI as well! We suspected FH but there was no evidence!
Young age no longer rules out ACS!
FH --> Familial hypercholesterolemia, the most common AD genetic disease --> problems with the LDL receptor --> your liver cannot clear LDL --> LDL laden cholesterol gets oxidized (more in Indians, African Americans and Hispanics) --> atherosclerosis!
Statins usually work by reducing HMG CoA reductase which helps in cholesterol synthesis in the liver --> so the liver draws in more chol. from the LDL in blood using LDL receptors. They may/may not work in FH, depending on how badly the receptors are affected.
1) Apparently, KK was a regular user of antacids. Chronic angina, as described by Heberden and Prinzmetal, is a notorious mimicker of dyspepsia - abdominal fullness, bloating, generalized ill feeling with/without a relation to meals, especially fatty, oily meals!
2) So please stop taking these PPI/H2RA/antacids by yourself (for patients) if you have these symptoms and get yourself checked out by a physician/cardiologist!
The Indian popn is genetically predisposed to ASCVD!