SomeGram-positive bacteria have developed resistance to doxycycline. Tetracycline resistance rates vary by geographic region; for example, resistance inStreptococcus pyogenes ranges from about 1% in Sweden to over 80% in China, and a pooled global resistance rate of approximately 67% has been reported forEnterococcus faecalis.[26][27] When bacteriologic susceptibility testing indicates appropriate susceptibility to the drug, doxycycline may be used to treat these infections caused byGram-positive bacteria:[26][27]
Subantimicrobial-dose doxycycline (SDD) is widely used as an adjunctive treatment toscaling and root planing forperiodontitis.[39] SDD is also used to treat skin conditions such as acne and rosacea,[19][40][41] includingocular rosacea. In ocular rosacea, treatment period is 2 to 3 months. After discontinuation of doxycycline, recurrences may occur within three months; therefore, many studies recommend either slow tapering or treatment with a lower dose over a longer period of time.[42]
As prophylaxis against sexually transmitted infections
Doxycycline is used aspost-exposure prophylaxis (PEP) to prevent certainsexually transmitted infections, known as doxycycline post-exposure prophylaxis (doxyPEP). A landmark randomized trial in San Francisco found that a single 200 mg dose of doxycycline taken within 72 hours after condomless sex reduced the overall incidence of bacterial STIs by approximately two-thirds amongmen who have sex with men (MSM) andtransgender women, with reductions of 87-88% forchlamydia, 73-87% forsyphilis, and 55% forgonorrhea.[10] However, a separate trial found doxyPEP was not effective in cisgender women.[43]
In June 2024, theUS Centers for Disease Control and Prevention (CDC) issued clinical guidelines recommending doxyPEP for MSM and transgender women with at least one bacterial STI in the prior 12 months.[9] TheAustralasian Society for HIV Medicine issued a more cautious consensus statement recommending doxyPEP only for syphilis prevention in MSM, citing concerns that the risk of increasingantimicrobial resistance, especially inNeisseria gonorrhoeae, outweighed the benefits for other STIs.[44] Use of doxyPEP has been associated with tetracycline resistance inN. gonorrhoeae.[45]
The first-line treatment forbrucellosis is a combination of doxycycline andstreptomycin. The second-line treatment is a combination of doxycycline andrifampicin (rifampin).[46]
Doxycycline is active against theerythrocytic stages ofPlasmodium falciparum, a protozoan parasite that causes malaria, but it is not active against thegametocytes ofP. falciparum.[47] As such, doxycycline is used to preventmalaria,[48] but not recommended alone for initial treatment of malaria, even when the parasite is doxycycline-sensitive, because the antimalarial effect of doxycycline is delayed by 48 to 96 hours owing to a "delayed death" mechanism in which parasites complete their current replication cycle before dying in the next cycle. For this reason, doxycycline prophylaxis must be continued for four weeks after leaving a malarious area, compared with only seven days foratovaquone/proguanil.[49]
Doxycycline blocks protein production in theapicoplast (anorganelle) ofP. falciparum. This disrupts the parasite's ability to producefatty acids, which are essential for its growth, and impairs the production ofheme, acofactor. These effects occur late in the parasite's life cycle during the blood stage (theerythrocytic cycle, when the parasite replicates inside humanred blood cells).[50] By blocking important processes in the parasite, doxycycline both inhibits the growth and prevents the replication ofP. falciparum. It does not directly kill livingP. falciparum, but creates conditions that prevent their growth and replication.[51]
Doxycycline can be used against parasiticnematodes (worms) that causefilariasis. It killssymbiotic bacteria of the genusWolbachia in the reproductive tracts of the nematodes, making the nematodessterile (unable to reproduce).[53] This reduces transmission of diseases such asonchocerciasis andelephantiasis.[54] A randomized controlled trial showed that an eight-week course of doxycycline almost eliminates the release ofmicrofilariae (larval offspring of the nematodes).[55]
Doxycycline has a highoral bioavailability, as it is almost completely absorbed in thestomach and proximalsmall intestine.[19] Unlike older tetracyclines, whose absorption is substantially reduced by food, doxycycline absorption is only modestly affected: co-administration of dairy products reduces the serum concentration of doxycycline by about 20%, compared with a 50% reduction for tetracycline.[19] Doxycycline absorption is inhibited bycations with a 2+ or 3+ charge (divalent andtrivalent cations), such as iron,bismuth, aluminum, calcium, and magnesium.[19] Doxycycline forms unstablecomplexes with these metal ions in theacidic environment of the stomach; most of these complexes dissociate in thesmall intestine, allowing the drug to be absorbed. However, some doxycycline remains complexed with metal ions in theduodenum, resulting in a slight decrease in absorption.[19]
Doxycycline is categorized by theFDA as aclass D drug in pregnancy, meaning there is evidence of risk to the fetus but the benefits may outweigh the risks in certain situations. Doxycycline crosses intobreast milk and is therefore a concern duringbreastfeeding.[61] Other tetracycline antibiotics are contraindicated in pregnancy and up to eight years of age, due to the potential for disrupting bone and tooth development.[62] The FDA includes a class warning for all tetracyclines aboutstaining of teeth (typically yellow to brown discoloration) and decreased development ofdental enamel in children exposed to tetracyclinesin utero, duringbreastfeeding, or during early childhood (under eight years of age).[63] However, the FDA has acknowledged that the actual risk of dental staining of primary teeth is undetermined for doxycycline specifically. The best available evidence indicates that doxycycline has little or no effect onhypoplasia (underdevelopment) of dental enamel or on staining ofprimary teeth (baby teeth). The USCenters for Disease Control and Prevention (CDC) recommends the use of doxycycline for treatment ofQ fever and tick-bornerickettsial diseases in children of all ages, and some researchers advocate for its use in children with malaria as well.[64]
Adverse effects of doxycycline are similar to those of other members of thetetracycline antibiotic group. Doxycycline can cause gastrointestinal upset.[65][66] Oral doxycycline can causepill esophagitis, particularly when it is swallowed without adequate fluid, or by persons with difficulty swallowing or reducedgastrointestinal motility.[67] Doxycycline is less likely than other antibiotic drugs to causeClostridioides difficilecolitis.[68]
Anerythematous (red) rash in sun-exposed parts of the body has been reported to occur in 7.3-21.2% of persons taking doxycycline as prophylaxis against malaria. The rash resolves upon discontinuation of the drug. One study examined the tolerability of various malaria prophylactic regimens and found doxycycline did not cause a significantly higher percentage of skin events (such as rash, itching, or photosensitivity) when compared with other antimalarials.[69]
Unlike some other members of the tetracycline group, doxycycline may be used in those withrenal impairment, because it is primarily excreted via the feces rather than the kidneys, and does not accumulate to toxic levels when kidney function is reduced.[70]
Previously, doxycycline was believed to impair the effectiveness of many types ofhormonal contraception due to induction ofCYP450 enzymes (a family of liver enzymes that break down drugs, potentially accelerating the metabolism of hormonal contraceptives). Research has shown no significant loss of effectiveness in oral contraceptives while using most tetracycline antibiotics (including doxycycline), although many physicians still recommend the use ofbarrier contraception for people taking the drug to prevent unwanted pregnancy.[73][74][70]
Doxycycline, like other tetracycline antibiotics, isbacteriostatic. It works by preventing bacteria from reproducing by inhibitingprotein synthesis.[75]
Doxycycline is highlylipophilic, so it can easily enter cells, meaning the drug is readily absorbed and has a largevolume of distribution (it distributes widely throughout body tissues rather than remaining in the blood). It can also be re-absorbed in therenal tubules andgastrointestinal tract due to its high lipophilicity, giving it a longelimination half-life. In patients withkidney failure, doxycycline does not accumulate to toxic levels because the body compensates by increasing excretion through thefeces.[66][76] Doxycycline-metal ion complexes are unstable inacidic conditions, therefore more doxycycline enters the duodenum for absorption than older tetracycline compounds such astetracycline andoxytetracycline. In addition, food has less effect on the absorption of doxycycline than on other tetracyclines, with doxycycline serum concentrations being reduced by about 20% by test meals compared with 50% for tetracycline.[77]
Doxycyclinemetabolism (breakdown by the body) is negligible. It is actively excreted into the gut (in part via the gallbladder, in part directly fromblood vessels), where some of it is inactivated by formingchelates. About 40% are eliminated via the kidneys, much less in people withend-stage kidney disease. Thebiological half-life is 18 to 22 hours (16 ± 6 hours according to another source[79]) in healthy people, slightly longer in those with end-stage kidney disease, and significantly longer in those withliver disease.[59][79][80]
Expired tetracyclines or tetracyclines allowed to stand at a pH less than 2 are reported to benephrotoxic due to the formation of a degradation product, anhydro-4-epitetracycline[82][83] causingFanconi syndrome.[84] In the case of doxycycline, the absence of ahydroxyl group in C-6 prevents the formation of the nephrotoxic compound.[83] Nevertheless, tetracyclines and doxycycline itself have to be taken with caution in patients with kidney injury, as they can worsenazotemia due tocatabolic effects.[84]
Afterpenicillin revolutionized the treatment of bacterial infections inWorld War II, many chemical companies moved into the field of discovering antibiotics bybioprospecting.American Cyanamid was one of these, and in the late 1940s chemists there discoveredchlortetracycline, the first member of thetetracycline class of antibiotics.[6] Shortly thereafter, scientists at Pfizer discoveredoxytetracycline and it was brought to market. Both compounds, like penicillin, were natural products and it was commonly believed that nature had perfected them, and further chemical changes could only degrade their effectiveness. Scientists at Pfizer led byLloyd Conover modified these compounds, which led to the invention oftetracycline itself, the first semi-synthetic antibiotic. Charlie Stephens' group at Pfizer worked on further analogs and created one with greatly improved stability and pharmacological efficacy: doxycycline. It was clinically developed in the early 1960s and approved by the USFood and Drug Administration (FDA) in 1967.[6]
As its patent grew near to expiring in the early 1970s, the patent became the subject of lawsuit between Pfizer andInternational Rectifier[85] that was not resolved until 1983; at the time it was the largest litigated patent case in US history.[86] Instead of a cash payment for infringement, Pfizer took the veterinary and feed-additive businesses of International Rectifier's subsidiary, Rachelle Laboratories.[86]
In January 2013, the FDA reported shortages of some, but not all, forms of doxycycline "caused by increased demand and manufacturing issues".[87] Companies involved included an unnamed major generics manufacturer that ceased production in February 2013,Teva (which ceased production in May 2013),Mylan,Actavis, andHikma Pharmaceuticals.[88][89] The shortage came at a particularly bad time, since there were also shortages of an alternative antibiotic, tetracycline, at the same time.[90] The market price for doxycycline dramatically increased in the United States in 2013 and early 2014 (from $20 to over $1800 for a bottle of 500 tablets),[91][92][93] before decreasing again.[94][95]
Doxycycline-activatedTet-ON (tetracycline-controlled transcriptional activation) system driving inducible short hairpin RNA (shRNA) expression for controlled gene silencing via the RNA interference pathway. The Tet-ON inducible shRNA system is a regulated gene-silencing platform where short hairpin RNA (shRNA) expression is switched on only in the presence of a tetracycline-class antibiotic, such as doxycycline. Doxycycline binds to a modifiedTet repressor (TetR) protein, enabling it to activate transcription from aTet-responsive promoter, producing shRNA that is processed into small interfering RNA (siRNA) by the cell's RNA interference (RNAi) machinery. This allows researchers to precisely control the timing and level of targetgene knockdown, minimizing off-target effects and enabling studies of essential genes without permanent silencing.[97][98]
Doxycycline and other members of thetetracycline class of antibiotics are often used as researchreagents inin vitro andin vivo biomedical research experiments involving bacteria as well in experiments in eukaryotic cells and organisms with inducible protein expression systems usingtetracycline-controlled transcriptional activation. The mechanism of action for the antibacterial effect of tetracyclines relies on disrupting protein translation in bacteria, thereby damaging the ability of microbes to grow and repair; however protein translation is also disrupted in eukaryoticmitochondria impairing metabolism and leading to effects that canconfound experimental results.[99][100] Doxycycline is also used in "tet-on" (gene expression activated by doxycycline) and "tet-off" (gene expression inactivated by doxycycline)tetracycline-controlled transcriptional activation to regulatetransgene expression in organisms andcell cultures.[101] Doxycycline is more stable than tetracycline for this purpose.[clarification needed][101] At subantimicrobial doses, doxycycline is an inhibitor ofmatrix metalloproteases,[23] and has been used in various experimental systems for this purpose, such as for recalcitrantrecurrent corneal erosions.[102]
Although doxycycline is approved to treatLyme disease, the optimal dosing and duration of treatment for this condition is a topic of ongoing research.[105][33] it can be used in adults and children. For treatment or prophylaxis of Lyme disease in children, it can be used for a duration of up to 21 days in children of any age.[4] Doxycycline is specifically indicated to treat Lyme disease for patients presenting witherythema migrans. As for the optimal duration of treatment of this disease, guidelines vary, with some recommending a 10-day course of doxycycline, while others suggest a 14-day course; still, recent data suggest that even a 7-day course of doxycycline can be effective. Compared to other drugs, there are no significant differences in treatment response across antibiotic agents, doses, or durations when comparing 14 days versus 21 days; as such, the optimal duration of treatment of Lyme disease remains uncertain, as prolonged antibiotic courses have drawbacks, including diminishing returns in terms of patient outcomes, heightened risks of adverse events, superinfections, increased healthcare costs, and the potential for development of antibiotic resistance. Therefore, the consensus remains to treat patients with the shortest effective duration of antibiotics, as is the case with doxycycline for Lyme disease as well.[105]
Some studies show doxycycline as a potential agent to possess anti-inflammatory properties acting by inhibiting proinflammatory cytokines such asinterleukin-1 (IL-1),interleukin-6 (IL-6),tumor necrosis factor-alpha (TNF-α), andmatrix metalloproteinases (MMPs)[23] while increasing the production of anti-inflammatorycytokines such asinterleukin-10 (IL-10). Cytokines are small proteins that are secreted by immune cells and play a key role in the immune response. Some studies suggest that doxycycline can suppress the activation of thenuclear factor-kappa B (NF-κB) pathway, which is responsible forupregulating several inflammatory mediators in various cells, includingneurons; therefore, it is studied as a potential agent for treatingneuroinflammation.[106][107][108]
A potential explanation of doxycycline's anti-inflammatory properties is its inhibition ofmatrix metalloproteinases (MMPs),[23] which are a group ofproteases known to regulate the turnover ofextracellular matrix (ECM) and thus are suggested to be important in the process of several diseases associated withtissue remodeling and inflammation.[109][110][111][112] Doxycycline has been shown to inhibit MMPs,[23] includingmatrilysin (MMP7), by interacting with the structural zinc atom and/or calcium atoms within the structural metal center of the protein.[113][114][115]
Doxycycline also inhibits allikrein-related peptidase 5 (KLK5).[112] The inhibition of MMPs and KLK5 enzymes subsequently suppresses the expression of LL-37, acathelicidin antimicrobial peptide that, when overexpressed, can trigger inflammatory cascades. By inhibiting LL-37 expression, doxycycline helps to mitigate these downstream inflammatory cascades, thereby reducing inflammation and the symptoms of inflammatory conditions.[112]
Doxycycline is used to treatacne vulgaris androsacea.[116][117][19] However, there is no clear understanding of what contributes more: the bacteriostatic properties of doxycycline, which affect bacteria (such asPropionibacterium acnes[19]) on the surface of sebaceous glands even in lower doses called "submicrobial"[118][119] or "subantimicrobial",[120][121][122][19] or whether doxycycline's anti-inflammatory effects, which reduce inflammation inacne vulgaris androsacea, includingocular rosacea,[42] contribute more to its therapeutic effectiveness against these skin conditions.[123] Subantimicrobial-dose doxycycline (SDD) can still have abacteriostatic effect, especially when taken for extended periods, such as several months in treating acne and rosacea.[124] While the SDD is believed to have anti-inflammatory effects rather than solely antibacterial effects, SDD was proven to work by reducing inflammation associated with acne and rosacea. Still, the exact mechanisms have yet to be fully discovered.[125] One probable mechanism is doxycycline's ability to decrease the amount ofreactive oxygen species (ROS). Inflammation in rosacea may be associated with increased production ofROS by inflammatory cells; these ROS contribute toward exacerbating symptoms. Doxycycline may reduce ROS levels and induce antioxidant activity because it directly scavengeshydroxyl radicals andsinglet oxygen, helping minimize tissue damage caused by highly oxidative and inflammatory conditions.[126] Studies have shown that SDD can effectively improve acne and rosacea symptoms,[127] probably without inducingantibiotic resistance.[128] It is observed that doxycycline exerts its anti-inflammatory effects by inhibiting neutrophil chemotaxis and oxidative bursts, which are common mechanisms involved in inflammation and ROS activity in rosacea and acne.[23]
Doxycycline's dual benefits as an antibacterial and anti-inflammatory make it a helpful treatment option for diseases involving inflammation not only of theskin, such as rosacea and acne, but also in conditions such asosteoarthritis orperiodontitis.[129] Nevertheless, current results are inconclusive, and evidence of doxycycline's anti-inflammatory properties needs to be improved, considering conflicting reports from animal models so far.[130][131][132] Doxycycline has been studied in various immunological disorders, includingrheumatoid arthritis,lupus, andperiodontitis.[133] In these conditions, doxycycline has been researched to determine anti-inflammatory and immunomodulatory effects that could be beneficial in treating these conditions. However, a solid conclusion still needs to be provided.[134][135][136][137]
Doxycycline is also studied for its neuroprotective properties which are associated withantioxidant,anti-apoptotic, and anti-inflammatory mechanisms. In this context, it is important to note that doxycycline is able to cross theblood–brain barrier. Several studies have shown that doxycycline inhibitsdopaminergicneurodegeneration through the upregulation ofaxonal andsynaptic proteins.[138][139] Axonal degeneration and synaptic loss are key events at the early stages of neurodegeneration and precede neuronal death inneurodegenerative diseases, includingParkinson's disease (PD). Therefore, the regeneration of the axonal and synaptic network might be beneficial in PD.[140] It has been demonstrated that doxycycline mimicsnerve growth factor (NGF) signaling inPC12 cells. However, the involvement of this mechanism in the neuroprotective effect of doxycycline is unknown. Doxycycline is also studied in reverting inflammatory changes related todepression.[121] While there is some research on the use of doxycycline for treatingmajor depressive disorder, the results are mixed.[121][141][142]
After a large-scale trial showed no benefit of using doxycycline in treatingCOVID‑19, the UK'sNational Institute for Health and Care Excellence (NICE) updated its guidance to not recommend the medication for the treatment of COVID‑19.[143][144] Doxycycline was expected to possess anti-inflammatory properties that could lessen thecytokine storm associated with aSARS-CoV-2 infection, but the trials did not demonstrate the expected benefit.[145] Researchers also believed that doxycycline possesses anti-inflammatory and immunomodulatory effects that could reduce the production of cytokines in COVID-19, but these supposed effects failed to improve the outcome of COVID-19 treatment.[146][147]
Research on novel drug formulations for the delivery of doxycycline in wound treatment is expanding, focusing on overcoming stability limitations for long-term storage and developing consumer-friendly, parenteral antibiotic delivery systems. The most common and practical form of doxycycline delivery is through wound dressings, which have evolved from mono- to three-layered systems to maximize healing effectiveness.[148]
Research directions on the use of doxycycline in wound healing include the continuous stabilization of doxycycline, scaling up technology and industrial production, and exploring non-contact wound treatment methods like sprays and aerosols for use in emergencies and when medical care is not readily accessible.[148]
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