That's what gave me my first signs of adrenal suppression many years
ago.  Same thing. I recall reading some studies a few years ago of
early, low dose scalp solutions with it, and within 2 weeks of daily
use, 50% of users showed HPA suppression, while it took longer for the
rest to catch up.  :-/

I hope it improves.

Susan

Since we're on the topic: for years I would get some knee pain when I
had an infection. Then, this summer I had a headache/fever and 6 weeks
of subsequent joint pain. I order ticked serology, which literally
ticked off my PCP, so I switched to her partner who is double boarded
in infectious diseases. The tick serology was negative, and she
hypothesized it could have been West Nile Virus, but didn't check
serology.
 Then, I had a couple of less intense recurrences, following what
appear to be viral illnesses. The last episode left me with lots of
joint inflammation in the hands.
 I called my PCP, and her office made an appointment, and I asked
about labs prior to the visit--but her health assistant called back
and reported the PCP said "no labs first", so I called my buddy the
rheumatologist and ordered the labs he suggested. I saw the PCP who
thanked me for the labs (to the point I'm sure she never told me not
to order them), which didn't suggest an etiology, and she still thinks
it's a post viral thing, but reminds her of Lyme as well, and asked me
to see the rheumatologist--I already had an appointment to see him
after the phone call, and was just seeing the PCP to be polite. (Also
to get her take on the West NIle thing.)
 My office staff gave me hell for not calling someone on the "no
labs" issue, but what's the point?
 It's always something....
Judy

Most cases of autoimmunity appear to get started in the gut in some
fashion.  Infections can generate antibodies against a common molecular
target also found in the body (e.g., Tourette's, SARS) but if parasites
are there helping keep regulatory T-cells (Tregs) and immunoglobulins
properly balanced, this cross-reaction is much less likely.  The gut is
where the body expects Tregs to get activated.

there is an inverse relationship between parasitic infection (especially
worms/helminths) and allergy; as parasitic infections dropped on the
Pacific island of Mauke, allergies increased proportionately; one theory
is that when freed of parasitic targets, the immune system has time on
its hands and turns on innocuous allergens; the body¹s Y-shaped IgG
antibodies usually target bacteria and viruses by latching directly on
to target proteins and recruiting immune cells; parasites activate a
different mechanism - Y-shaped IgE antibodies - which attach their tails
to the surface of mast cells; mast cells are found wherever the body
comes into contact with the outside world and thus multicellular
parasites - mucous membranes of the eyes, nose, and throat, and in the
lining of the lungs and gut; once the initial IgE response is complete,
each mast cell has 100,000 to 500,000 Y-shaped antibodies protruding
from its surface with outstretched arms; usually within two weeks of
worm infestation, the immune system is primed and each mast cell
contains a thousand or more large, globular granules; a worm protein
sticks to the arms of two adjacent IgE antibodies and sets off a
reaction causing the mast cell to burst and spew its granules (mast cell
degranulation) of histamines and other inflammatory chemicals that
infiltrate local tissues; this causes itching; blood vessels dilate and
leak; tissues swell and mucus production increases; this response may
prevent worms from infiltrating further through the skin; other cells
are attracted to dump toxins on the parasites; intestinal worms, on the
other hand, come in through the mouth and attack the GI tract; in this
case, an inflamed gut producing fluid and mucus causes in diarrheamaybe
to flush out worms before they can attach; some worms can also spend
part of their life cycle in the human lung (like schistosomiasis); this
may trigger coughing and sneezing; this responses are all more acute to
newcomers in the tropics when first exposed to parasites; some worms do
get through though mostly the system works to protect people; in the
absence of helminths, IgE antibodies can zero in on airborne allergens
(causing asthma or hayfever) or ingested foods instead; worm infested
rats have weak allergy responsesl their IgE antibodies are tied up
fighting worms; however, in rural New Guinea, worm infestation doesn¹t
lessen the asthma rate; there¹s an IgG antibody that competes with IgE;
this G antibody (IgG4) grabs the worm protein before it bumps into the E
antibody attached to a mast cell and this prevents the mast cell
degranulation; IgG4 (1-2%) is the rarest of the IgG¹s; IgG1 targets
viruses and bacteria and is the most common; in people with parasites;
IgG4 jumpts to 18%
<http://www.discover.com/issues/sep-93/features/ofparasitesandpo264/>

the hygiene hypothesis was advanced in 1989 by David Strachan of the
London School of Hygiene and Tropical Medicine; the immune system
expects a dirty environment and when it isn¹t living in on it becomes
hyperactive; Gabonese children with worm infestations have fewer
allergies (and more IL-10, which blocks inflammatory signals among
immune cells); children treated for worms became much more sensitive to
dust mites; Alan Brown of Britain's University of Nottingham has treated
his hayfever with intestinal hookworms; they cause anemia and require
overeating; Joel Weinstock (once at the University of Iowa, now Tufts)
used pig whipworms (Trichuris suis; TSO from Ovamed) to treat ulcerative
colitis <http://www.cosmosmagazine.com/node/695>

twenty-four patients with multiple sclerosis were followed for
four-and-a-half years; half had signs of parasitic infections -
pinworms, tapeworms, whipworms and nematodes; those infected had three
relapses compared to 56 in the uninfected group and fewer MRI lesion
changes; the infected had higher levels of Tregs than the non-infected
and reported substantially less disability; helminth-infected Vietnamese
children also have much fewer allergies; bacterial and viral infections
trigger Th1 cells; Th2 cells mediate allergies; Tregs control both Th1
and Th2 responses; in the infected group, myelin basic protein-specific
responses in peripheral blood had a significant increase in IL-10 and
TGF-beta and a drop in IL-12 and interferon-gamma-secreting cells;
myelin basic protein-specific T cells cloned from infected subjects
lacked IL-2 and IL-4 production, but had high IL-10 and/or TGF-beta
secretion, showing a cytokine profile similar to the T-cell subsets Tr1
and Th3; cloning frequency of CD4+CD25+ FoxP3+ Tregs was substantially
increased in infected patients; Smad7 messenger RNA was not detected in
T cells from infected MS patients secreting TGF-beta; increased
production of IL-10 and TGF-beta, together with induction of CD25+CD4+
FoxP3+ T cells, suggests Tregs induced by parasite infection alter the
course of MS <http://news.bbc.co.uk/1/hi/health/6268585.stm>,
<http://www.newscientist.com/article/dn10964.html>, [PMID 17230481]