Author: rdg30

I am a histopathologist based at Imperial but work one day a week in Oxford. My clinical interests are gastro-intestinal and hepato-biliary pathology. I enjoy teaching, both undergraduate and postgraduate, and this blog is aimed at adding another string to this.


This post was stimulated by a case of eosinophilic colitis I reviewed at an MDT this morning. The images are below.

They show sheets of eosinophils in the lamina propria and infiltrating crypts. They are easily recognised by their bilobed nuclei and prominent red granules.




This was an opportunity to review eosinophils.

Eosinophils are conspicuous in inflammatory reactions triggered by IgE, such as asthma, and by parasites and are increased by TH-2 activation.  IL-5 and GM-CSF increase the production of eosinophils by the bone marrow. They are associated are recruited into the tissue by eotaxins which are CC chemokines.

Eosinophils have 2 types of effector function:

  1. they release toxic granule proteins  (e.g. major basic protein which is toxic to parasites) and free radicals.
  2. they synthesise prostaglandins, leukotrienes and cytokines.

In the context of this case, likely causes include gut parasites, such as schistosomiasis, and allergic reactions to drugs.

If you want to read more try the excellent British Society of Immunology Website:

Not “Everyone Must Get Stoned” *

My first blog is going to be about gallstones. There is no special reason for this other than they are common (and, therefore, I hope this will be of interest to lots of people) and I happen to find gallbladder pathology interesting!

Below is a picture of a case I cut up yesterday:

As a medical student, I remember that the risk factors for gallstones were described as being “fat, fair, female and forty/ fertile ”  (depending on the specific version of the mnemonic).

How does this shape up now?  In this blog my core reference is Robin’s Pathology (in its range of formats) but will use a range of others. I will return to the topic of textbooks another time.

According to Robbins Basic Pathology (page 673):

Age: The prevalence of gallstones increases with age; over a 1/4 of people aged over 80 years have stones.

Sex: At every age, they are twice as common in women.

Ethnicity: They are very common in certain Native American groups.

Hereditary:  Family history and genetic disorders of bile salt metabolism. Although not mentioned in Robbins,  patients with haemolytic anaemias, including genetic ones such as Sickle Cell Anaemia, are at increased risk of pigment stones.

Environment:  Any factor that increases cholesterol excretion will increase the risk of stones. Oestrogens do this  (obviously contributing to the increased risk in women) as does obesity, rapid weight loss and drugs which increase cholesterol excretion, such as clofibrate.

Disorders affecting gallbladder motility: These includes pregnancy which contributes to the female and fertile risk.

So how does the mnemonic stand up? I came  across a paper (Postgrad Med J. 2013 Nov;89(1057):638-41. ) which directly addresses this question and concluded: “Our study found that the validated ‘students’ 5Fs’ mnemonic retains a role in clinical diagnosis of patients suspected of cholelithiasis but the factor ‘familial’ should be substituted for ‘forty’ in recognition of the role of inheritance and the changing demographics of gallstone incidence.”.

* Bob Dylan: