Aubrey Blumsohn wrote:
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I'm not sure about the assertion that the symptoms are due to
increased viscosity at cold temperatures. Skin temperature rarely
reaches 4 degrees (or indeed anything near). Furthermore some
clinical features occur in organs at core temperature. Most patients
with high viscosity (eg most patients with MGUS) do not have similar
clinical features.
Cryoglobins and their detection is a bit of a black art, and I
have never understood what it all means. Maybe we should look at the
viscosity (or whatever) slope as temperature crosses some physiologically
plausible threshold? Investigation of the shape of the
viscosity/temperature
curve sounds potentially attractive in any event.
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Obviously the detection of cryoglobulins is a problem in many laboratories.
One of you suggested that I should publish my experiences with viscosity.
However, a scientific publication needs a lot of subjects. In this case you
must have not only a healthy reference population (this is commonly not
difficult to achieve) but also a number of patients having hyperviscosity
caused by other factors (e g hyperfibrinogenemia, MGUS) besides patients
having more or less severe symtoms of cryoglobulinemia.
Without any intention to be 100% scientifically correct, I can therefore
convey my experiences to this mailbase. Probably the method may be of
interest and maybe sombody want to set it up.
When introducing viscosimetry in the laboratory in the middle of the 70-s I
observerd that some plasmas did not reach a stable reading using a
Brookfield cone-plate viscosimeter at 37 C. After introducing the sample
(0.5 mL) in the cone-plate chamber, readings were made each minute and for
most samples the viscosity stabilized within 3 minutes.
Freqeuently, however, the readings did not stabilize until 30-90 minutes in
37 C. At first this observation was considered to be a technical error, but
after contact with the clinician we realized that this phenomenon was
always associated with clinical symtoms of cryoglobulins.
Neither the clinicians nor the laboratory chief realized that this could be
a better method for the detection of cryoglobulins, because the main reason
for introducing viscosimetry was hyperviscosity and not cryoglobulins.
In the middle of the 90-s we replaced the old Brookfield viscosimeter with
a modern one with digital readings. Then readings could then be done
automatically each minute by a computer. This considerably facilitated the
method, because you could start the viscosimeter and the program and then
look at the result half an hour later. The difference between common
hyperviscosity and cryoglobulins is then obvious: If there is a negative
trend in the viscosity after 3 minutes cryoglobulins are present. If the
readings are stable after 3 minutes the patient may have other sources of
hyperviscosity, but not cryoglobulins.
Before measurement the samples are stored at 4 C, and this is obviously not
a temperature achieved in vivo. However, cryoglobulins are known to
aggregate and (in severe cases precipitate) at temperatures as high as 30
C. In cold environment the temperature in hands and feet (where the
characteristic symtoms of cryoglobulins appear) can fall below this level.
If you want to test this method, simply use a digital Brookfield cone-plate
viscosimeter (lowest possible range) thermostated to 37 C. Connect the
RS232 output to a computer and let it read the measurement each minute
after triggering. Calibrate with water (0.6915 mPaS) and then introduce 0.5
mL EDTA-plasma stored at 4 C for at least 2 hours. Start the motor and the
program.
Normal subjects have viscosities below 1.60 mPaS (reference limit), but no
symtoms appear below about 2.0 mPaS. If cryoglobulins are present the
viscosity can initially be very high (>10 mPaS within 3 minutes) but no
stable reading (negative trend) is achieved until after a considerable time
(30-90 minutes).
Mr Sten Öhman, PhD
Sten Öhman, PhD
Elfin Lab & Milieuconsult
P O Box 133
S-590 70 Ljungsbro
Sweden
Tel Nat: 013-368940 Int: +46 13 368940
Fax Nat: 013-368941 Int: +46 13 368941
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