--especially that second one, which indicates a clinical utility for skin biopsy in examining small myelinated fibers in non-hairy human skin.

In essence, it makes perfect sense to try to use skin biopsy wherever it can be used. The great advantages of the technique over nerve biopsy are that it is far less invasive and much easier to recover from, it can be used in the same area multiple times to track the extent of neuropathic damage, and it can access nerves--the smaller ones--that standard nerve conduction studies or electromyography cannot measure. But, in areas in which myelinated nerve bundles are accessible through skin--admittedly, these areas are few--it would make sense to access them through this less invasive technique (though one would have to go a little deeper, into the dermis, rather than epidermis, for myelinated nerve access). Doing this could conceivably shed new light on systemic neuropathies with a demyelinating component.

Some ideas on what cycleops is musing over:

Many neuropathies have both demyelinating and axonal degenerating components. There are many acquired neuropathies that are primarily demyelinating (sometimes with secondary axonal damage) or axonal. This group does not only include those of small fibers--many vasculitic neuropathies damage larger axons preferentially, resulting in mononeuropathy multiplex situations. And, it is common for predominantly small-fiber syndromes to have some large sensory fiber involvement (this happens often in diabetes, for example). But some acquired neuropathies, especially those that involved rogue monoclonal antibodies, and a number that are toxic (ethylene glycol comes to mind), degrade both myelin and axons. B12 deficiency results in both axonal and myelin damage. It seems as if a number of hereditary conditions may degrade both as well, and it may well be a chicken-egg question as to whether, in many of these (especially those with mitochondrial components) nerve loss causes muscle damage or the muscle breakdown results in de-enervation.

I don't know if a loss of intraepidermal nerve fiber density in glaborous skin would be a DEFINITIVE indication of a mixed hereditary nerve disorder, such as some of the CMT variants, but it would be suggestive of a condition that attacks several different types of fibers (as opposed to one attacking only small fibers found in hairy skin). Remember, depending on the point of progression at which the test is done, one could be seeing axonal loss secondary to demyelination.

CIDP is the "classic" demyelinating paradigm, and one would expect in advanced CIDP that skin biopsy of myelinated glaborous skin would show the characteristic "onion bulbing" and other damage. It's this, and the fact that the autoimmune attack is macrophage mediated, that earns the condition its diagnosis rather than the fact of reduced sensory nerve action potentials, slow latencies, or conduction block (which happen in a number of conditions):

http://www.neuro.wustl.edu/NEUROMUSC...mdem.html#cidp