I have a 47-year-old male patient who appeared healthy when he was found to have a gamma-glutamyl transferase (GGT) level of 106iu/e about eight years ago.
Three months ago it reached 398iu/e. He had been drinking about 42 units of alcohol a week, but stopped completely at that point. His GGT dropped to 276iu/e but is now back up to 315iu/e. His alkaline phosphatase level was normal but is now 500iu/e, his alanine aminotransferase is now 68iu/e, and his ESR is 59mm/hr.
Apart from one episode of tiredness and shivering attacks, he has been asymptomatic. What could be causing his GGT levels to rise now he has stopped drinking and why is the ESR so high?
If this man's alcohol history is accurate, it seems unlikely that he has alcoholic liver disease.
GGT is reasonably sensitive for diagnosing alcohol abuse, but it is not specific. GGT is increased in cholestasis and hepatocellular disease and an increase in liver alkaline phosphatase will always be accompanied by a rise in GGT.
Now that this man has an elevated alkaline phosphatase as well as an increased GGT, it is important to exclude obstruction. An ultrasound scan would be the easiest way of doing this. This will also tell you whether there is a focal lesion or infiltration of the liver.
The elevated ESR is another non-specific sign and could reflect infection or inflammation. The history of shivering might suggest infection, particularly cholangitis, but more clinical information is needed.
It is possible the patient has chronic liver disease that is now becoming symptomatic. A low serum albumin would support this. The ultrasound will also give important information on the spleen size and regularity of the liver, which may help determine whether this is acute or chronic disease.
Professor David Adams, consultant hepatologist at Queen Elizabeth Hospital, Birmingham, and professor of hepatology at Birmingham University
A patient has had a raised mean cell volume (MCV) for the past three years. I did some blood tests and found she had a folate deficiency.
She is 43, has a reasonable diet and low alcohol consumption. Despite treatment with vitamin B12 injections and folic acid, she still has a raised MCV. How long does this take to resolve and should I now do further tests?
Vitamin B12 and folate deficiency give rise to identical blood pictures because they are both involved in the same metabolic pathway. The MCV is usually high and the haemoglobin, white blood count and platelets may be low.
If you do not know which vitamin is deficient, it is best to give both while you wait for assays, because giving folate to someone who is B12 deficient may worsen a neuropathy. This is based on minimal evidence but it does make sense.
Red cells have a life span of 120 days. After you replace the vitamin it will take several weeks for the MCV to come back down to normal, since the old red cells need to be replaced by young ones.
I think that, if after three months the MCV is unchanged, you need to look for another cause, such as hypothyroidism or myelodysplasia. It would also be worth checking anti-endomysial and anti-gliadin antibodies (always check immunoglobulins first because these are IgA antibodies). Look through the patient's history for features of coeliac disease or other causes of malabsorption.
To see whether someone is responding to B12 or folate replacement, we generally check the reticulocyte count after five to seven days. There is usually a marked rise as fresh young red cells are produced.
Dr Drew Provan, consultant haemotologist at St Bart's Hospital and The Royal London School of Medicine and Dentistry
What is the best treatment for patients with Bell's palsy?
In most people, Bell's palsy gets better naturally in days, weeks or months.
Steroids are often used to try to accelerate recovery, although the data on benefit is less than compelling.
If steroids are used, they should be given early and only for a few days.
I would not start steroids more than a day or two after the onset, and would avoid them where there is any possible contraindication.
Anti-viral drugs are sometimes used because some cases may be due to Varicella zoster, but the evidence for benefit is weaker than for steroids.
Patients appreciate being given some treatment and it is arguable that a treatment of low risk that may have some benefit is worthwhile. A minority of patients with Bell's palsy recover poorly and are upset if treatment is not offered.
Neurologists occasionally see patients erroneously diagnosed with Bell's palsy. It is not the explanation for all facial weakness.
Dr Giles Elrington, consultant neurologist, Harley Street Neurological Clinic and The Oaks Hospital, Colchester.