In the following Medscape article, long-term use of the macrolide antibiotic
azithromycin ("Zithromax") has been shown to have benefit in cystic
fibrosis, in children and adults, with little negative side effects. Not
used for its antibacterial properties, but for its anti-inflammatory
properties, which it has been found to have.

Has this also been prescribed in such a manner for chronic sinusitis? I
wonder if it could be helpful?

Finding a safe anti-inflammatory medication is a problem--as long-term usage
of oral corticosteroids has harmful effects, and there are also negative
effects from long-term NSAID usage.

I would guess that the azithromycin would lose its antibacterial effect if
used regularly over a long period, as the bacteria would develop resistance
to it. But if it remains effective as an anti-inflammatory, with little
negative side effects--could be a good thing, no?

(Of course--one negative for people without health insurance--could get very
expensive to use long term. With health insurance--would depend if the plan
would cover it long term like that.)

Anyone reading has prescribed or been prescribed azithromycin long-term as
an anti-inflammatory?

http://www.medscape.com/viewarticle/503819_3   (scroll down to see part
about this med)

quote of part of article---------

Azithromycin
Azithromycin is a macrolide commonly used for its antibacterial activity in
both children and adults. It is approved for treatment of acute otitis media
and community-acquired pneumonia in patients older than 6 months and for
treatment of pharyngitis or tonsillitis in those aged 2 years or older.[77]
Azithromycin has a long tissue half-life and accumulates in the sputum and
lungs of treated patients.[78] The potential role of azithro-mycin in cystic
fibrosis is extrapolated from experience with diffuse panbronchiolitis, a
respiratory disease similar to cystic fibrosis. In patients with diffuse
panbronchiolitis, long-term erythromycin therapy improved both symptoms and
survival.[79, 80]

Azithromycin has been evaluated as a treatment option for patients with
cystic fibrosis for its antiinflammatory properties.[81] The precise
mechanism through which azithromycin exerts these effects has not been
elucidated (Figure 2).[82-99] Antimicrobial classes typically used in the
treatment of acute cystic fibrosis exacerbations, such as third-generation
cephalosporins, amino-glycosides, and fluoroquinolones, do not appear to
exert any significant direct antiinflammatory action and have not been
included in this review.[100]

     Figure 2. (click image to zoom) Proposed antiinflammatory mechanisms
of macrolide antibiotics. The precise mechanism by which azithromycin
mitigates inflammation is unknown, but it affects neutrophils through
mediation of apoptosis, migration, chemotactic activity, and phagocytic
function. Azithromycin is an indirect antioxidant and may prevent lung
damage through this function. Therapy with this agent has inhibited
production of nitric oxide, prostaglandin E2, and proinflammatory cytokines
interleukin (IL)-8, IL-1?, and tumor necrosis factor (TNF)-?. Azithromycin
may also downregulate growth-related oncogene-? as well as soluble vascular
cell adhesion molecule (SVCAM)-1. Reduced sputum viscoelasticity and
improved mucociliary and cough transportability of airway secretions has
been noted. Antagonism of the virulence of Pseudomonas aeruginosa has been
proposed as a mechanism, an effect mediated through a decrease in airway
adherence, inhibition of production of various exoproducts, and interference
with Pseudomonas mucoid-alginate biofilm formation. In addition, it may
affect Pseudomonas aeruginosa's viability directly despite subinhibitory
minimum inhibitory concentrations. Restoration of the cystic fibrosis
transmembrane conductance regulator (CFTR) chloride channel is an additional
possible mechanism. X = mitigation of adverse effect.[82-89]

Treatment with either erythromycin or clarithromycin has not been beneficial
in cystic fibrosis.[101] Six trials have evaluated the effects of
azithromycin in children and adults with cystic fibrosis ( Table
2 ).[102-107] Of the three randomized, placebo-controlled trials conducted,
two involved patients younger than 18 years.[106, 107] Although a benefit
with azithromycin was observed in both of these studies, the more recent one
provides the most compelling evidence of therapeutic improvement.[107]

In a randomized, double-blind, placebo-controlled study involving 60 adults
with cystic fibrosis, treatment with azithromycin led to an improvement in
total quality of life (p=0.035), a reduction in antibiotic therapy
associated with acute respiratory exacerbations (p < 0.037), and a slowed
rate of decline in predicted FEV1 (p=0.047) and FVC (p=0.001).[105] This
benefit was observed despite baseline patient characteristics indicating the
treatment group had less lung function than the placebo group (mean FEV1
50.9% vs 62.3%, mean FVC 67.3% vs 77.5%). The treatment group also was
shorter, on average, and weighed less than the placebo group. However,
outcome changes in lung function were small, indicating maintenance rather
than improvement.

In the first trial involving patients younger than 18 years with cystic
fibrosis, pulmonary function was only modestly affected after a 6-month
course of azithromycin.[106] This study-a 15-month, prospective, randomized,
double-blind, placebo-controlled, crossover trial-included 41 children (18
boys, 23 girls) aged 8-18 years, with a median FEV1 of 61% (range 33-80%). A
history of chronic P. aeruginosa colonization was not a specific entry
criterion. Exclusion criteria were liver disease, hearing impairment,
Burkholderia cepacia colonization, previous organ transplantation, treatment
with macrolide antibiotics or oral corticosteroids for more than 14 days, or
treatment with dornase alfa begun within 2 months of enrollment.

Azithromycin dosage was based on weight; patients weighing 40 kg or less
received 250 mg once/day; those weighing more than 40 kg received 500 mg
once/day. A clinically significant change in the primary outcome measure,
FEV1, and the secondary outcome measures, FVC and FEF25-75, was defined as a
change of more or less than 13%, 13%, and 20%, respectively. At every time
point during treatment, mean FEV1, mean FVC, and mean FEF25-75 were higher
in the azithromycin-treated patients than in the placebo patients. However,
the median relative difference in predicted FEV1 between azithromycin and
placebo was only 5.4% (p > 0.05). Improvement in FEV1 greater than 13% was
noted in 13 of 41 patients, whereas deterioration of more than 13% was
observed in five (p=0.059). The median relative difference in predicted FVC
and FEF25-75 between the two groups was 3.9% and 11.4%, respectively (p >
0.05). The results of this study suggest that azithromycin treatment in
children and adolescents may exert clinically important beneficial effects
on pulmonary function in approximately 33% of patients but may result in
worsening lung function in approximately 10-20% of patients.