Coincidentally, searching on the internet for correlation of elevated GGT
and Lyme and saw your subject.  Some literature exists on elevated GGT and
Lyme.  (GGT is hepatic)  so gastroparesis would not surprise me.  In my
case I also have positive ANA and Anti-sm ab so lupus is also likely.  But
before I donate my liver to biopsy I am interested in any information re:
GGT&Lyme's exists.

Article abstract:  "We describe a patient with documented Lyme disease whose
major complaint was increasing abdominal distention.  Electrophysiologic
studies demonstrated denervation of the lower thoracic paraspinal muscles and
the rectus abdominis.  Expanding abdominal girth can be  an unusual
manifestation of the polyradiculoneuropathy associated with Lyme disease.
    "Neurologic manifestations of Lyme disease most typically include
meningitis, cranial neuropathies, especially {*filter*} palsies, and
polyradiculopathies.  Encephalitis, cerebellar ataxia, chorea, and transverse
myelitis (as though the spinal cord has been severed) are less common features.
 Most often, radiculoneuropathic symtoms  are composed of pain, dysthesias, and
limb weakness.  We report a patient presenting with an unusual manifestation of
a Lyme polyradiculoneuropathy ---dramatic abdominal distention.
    "Case report-A 60 year-old, right handed  man, devoted to muscle enlarging
and toning exercise, developed excessive fatigue, spiking fever, and chills
while summering on Cape Cod.  After a few weeks he defervesced but complained
of "sandpaper and tingling" dysesthesias involving the chest, back , and
abdomen bilaterally, and the right thigh.  Four weeks after the onset of his
illness, he noted progressive abdominal distention despite no alteration in
diet and continued efforts to adhere to his exercise regime.  This formerly
trim and fit man became increasingly upset over his growing abdomen.  In  the
course of  his illness, his pants waist size increased from 34 to 42, requiring
him to purchase a new wardrobe."   I bet the insurance company didn't pick up
that bill.  "Previously, he performed 100 sit ups every morning; now, he could
do none.  There was no significant alteration in dietary or bowel habits.
Cathartics did not reduce his abdominal bloating.  Six weeks after his symptoms
began, he awoke with frank right {*filter*} weakness and was referred for
neurologic consultation.
    "He was unaware of exposure to ticks, but recalled many insect bites.  A
pruritic, (itchy) erythematous rash on the right forearm, which he attributed
to poison ivy , had occurred several months prior to presentation.  Medical
history was notable for nephrolithiasis, glaucoma, and vocal cord  polyps.
There was no family history of neurologic impairment.
     "Examination disclosed a well-developed man with normal vital signs.  His
abdomen was protuberant, but soft and nontender, without organmegaly.  {*filter*}
spincter tone was normal.  Mental status was normal."  He must have passed the
Lyme- buster mini mental status test that can tell if you are faking it.
"Cranial nerve exam demonstrated moderate weakness of the right side of the
face, including the brow and lower face, with impaired taste sensation of the
right anterior tongue.  Motor exam was normal.  There was no ataxia.  DTRs were
1+.  Plantar responses were equivocal bilaterally.  Sensation was preserved for
joint position, vibration, and light touch.  He reported dysesthetic sensations
when the skin over his chest and abdomen was stroked...........
    "Discussion,  Our patient exhibited many of the salient features of 2-nd
stage Lyme disease, including dysesthesias, {*filter*} palsy, and csf pleocytosis.
Systemic symptoms, as he experienced weeks prior to the onset of his neurologic
complaints, and the absence of a documented history of erythema migrans, are
NOT UNCOMMON in Lyme disease. (references for this last statement----1.
Pachner, Steere.  The triad of neurologic manifestations of Lyme disease:

1988;45:99-104.  4.  Reik,  Burgdorfer, Donaldson.  Neurologic abnormalities in
Lyme disease without erythema chronica migrans.  Am J Med.  1986;81:73-78)
Elavated IgM and IgG titers against B. burgdorferi in serum and SCSF confirmed
the diagnosis.
    "The patient's most persistent complaint during his illness was abdominal
distention with  associated discomfort and weakness.  Although his abdominal
girth increased markedly and he lost the ability to perform sit-up exercises,
he exhibited neither significant weight gain nor change in eating or bowel
habits.  Common causes of abdominal distention such as ileus, colonic
obstruction....were ruled out by an extensive workup.
    "The most parsimonious explanation for this patient's expanding abdominal
girth is a lower thoracic polyradiculoneuropathy secondary to neuroborreliosis
.  Supporting this interpretation are EMG/NCS that revealed denervation of
thoracic paraspinal muscles as well as the rectus abdominis and the gradual
resolution of his symptoms and signs after effective antibiotic
treatment.......
    "Polyradiculopathies rarely have been reported to lead to marked abdominal
distention.  Diabetes occasionally causes a syndrome of thoraco-abdominal
neuropathy involving multiple thoracic roots.  However, this entity most
typically produces sensory loss and pain and only rarely weakness of abdominal
or intercostal muscles.  One explanation is that the oblique and rectus
abdominis muscles, innervated by T7-L1 and T7-T12, respectively, receive a
multisegmented supply and thus rarely manifest clinical weakness.  We believe
that our patient is the first fully documented example of
polyradiculoneuropathy of Lyme disease causing abdominal weakness and
distention. While approximatly 1/3 of Lyme disease patients with neurologic
manifestations develop peripheral neuropathic symptoms, these typically include
 a sensory radiculoneuropathy of the thorax and a sensory-motor
radiculoneuropathy of the extremities.  The thoracic radiculopathy, which
preferentially involves the lower thoracic roots, most commonly presents as
intense pain or pressure within a few dermatomes, at times associated with
hypoesthesia.
    "...Ackerman et al noted that 1 patient of 100 had paresis" (and that is
only accounting for the cases they know of) " of abdominal muscles, apparently
without sensory disturbances or cranial neuropathy.  This series was collected
between 1956 and 1983, before serologic confirmation of diagnosis was
available, so the diagnosis of Bannwarth's syndrome was rendered on clinical
grounds..
     "The fundamental pathophysiologic mechanisms of Lyme
polyradiculoneuropathy remain uncertain. .....We suspect that if patients with
the more common thoracic dysesthesias were subjected to electrophysiologic
studies of paraspinal and rectus abdominis muscles, subtle, clinically
imperceptible abnormalities would be demonstrated."

georgia