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Psoriasis: The Story Worsens
We have already come a long way from thinking that psoriasis is merely a cutaneous disease caused by a defect in cellular replication; we now recognize that psoriasis is a systemic inflammatory process that has broad health implications. This association is manifested by comorbidities such as the occurrence of the metabolic syndrome and an increased risk for myocardial infarction. An increased incidence of chronic obstructive pulmonary disease also has been demonstrated in patients with psoriasis, especially those who smoke. Unfortunately, recent publications have highlighted investigative work that expands the scope of psoriatic comorbidity into new realms.
Li and colleagues (Ann Rheum Dis. 2013;72:1200-1205) performed a retrospective analysis of 174,476 women enrolled in several large national health studies. They found an increased risk for incident Crohn disease (relative risk [RR], 4.00; 95% confidence interval [CI], 1.72-9.27) among women with psoriasis. This increased risk rose (RR, 6.43; 95% CI, 2.04-20.32) if both psoriasis and psoriatic arthritis were present. Although the risk for those who already have Crohn disease to develop psoriasis has been previously noted, this study provides the first convincing clinical evidence that the converse association also is true, which is is not totally surprising when one considers common genetic and aberrant cytokine profiles between Crohn disease and psoriasis to suggest an overlap in pathogenic mechanisms.
Perhaps more ominous was the recently published work of Wan and associates (BMJ. 2013;347:f5961). In this massive retrospective analysis utilizing detailed British electronic medical records, 136,529 patients with mild psoriasis and 7354 patients with severe psoriasis based on treatment patterns were matched to 689,702 unaffected patients. The investigators found a clear increased risk for chronic renal disease (RR, 1.93; 95% CI, 1.79-2.08) among those with severe psoriasis. The risk was higher in younger patients; for example, among those aged 30 years, the RR rose to 3.82 (95% CI, 3.15-4.64). The risk for developing renal disease was independent of well-known predisposing factors, such as diabetes mellitus and hypertension. The association between severe psoriasis and renal disease also appeared to be independent of medications administered for psoriasis (eg, cyclosporine).
Also alarming was a recently published systematic review and meta-analysis of 1080 publications concerning the potential association between psoriasis and cancer (J Eur Acad Dermatol Venereol. 2013;27[suppl 3]:36-46). Pouplard et al found that there may be an increased risk for the following solid cancers in psoriasis patients: respiratory tract cancer (RR, 1.52; 95% CI, 1.35-1.71), upper aerodigestive tract cancer (RR, 3.05; 95% CI, 1.74-5.32), urinary tract cancer (RR, 1.31; 95% CI, 1.11-1.55), and liver cancer (RR, 1.90; 95% CI, 1.48-2.44). To the authors, the association seemed particularly strong with these neoplasms, which are associated with excessive alcohol ingestion and smoking.
What’s the issue?
Why might these comorbidities occur? Perhaps chronic inflammation due to abnormal cytokine production and/or deviant immune defenses may promote these new (or better documented) psoriatic comorbidities. Why are they of importance to dermatologists? Because we are the primary source of care for patients with psoriasis, especially those with severe disease. We cannot stop our historical reviews and physical examination with the skin and joints; rather, we must consider the whole patient. We probably should at least perform a comprehensive history at each visit, being carefully attune to any new concerns that suggest gastrointestinal, pulmonary, and renal disease or internal neoplasia, which places an extra (and perhaps unwanted) burden of care on the dermatologist. However, the way I see it is that our role in early detection of an ever-expanding list of serious psoriatic comorbidities may be crucial to the ultimate long-term health of our patients. Are you ready to accept that intensified and enhanced medical responsibility?
We have already come a long way from thinking that psoriasis is merely a cutaneous disease caused by a defect in cellular replication; we now recognize that psoriasis is a systemic inflammatory process that has broad health implications. This association is manifested by comorbidities such as the occurrence of the metabolic syndrome and an increased risk for myocardial infarction. An increased incidence of chronic obstructive pulmonary disease also has been demonstrated in patients with psoriasis, especially those who smoke. Unfortunately, recent publications have highlighted investigative work that expands the scope of psoriatic comorbidity into new realms.
Li and colleagues (Ann Rheum Dis. 2013;72:1200-1205) performed a retrospective analysis of 174,476 women enrolled in several large national health studies. They found an increased risk for incident Crohn disease (relative risk [RR], 4.00; 95% confidence interval [CI], 1.72-9.27) among women with psoriasis. This increased risk rose (RR, 6.43; 95% CI, 2.04-20.32) if both psoriasis and psoriatic arthritis were present. Although the risk for those who already have Crohn disease to develop psoriasis has been previously noted, this study provides the first convincing clinical evidence that the converse association also is true, which is is not totally surprising when one considers common genetic and aberrant cytokine profiles between Crohn disease and psoriasis to suggest an overlap in pathogenic mechanisms.
Perhaps more ominous was the recently published work of Wan and associates (BMJ. 2013;347:f5961). In this massive retrospective analysis utilizing detailed British electronic medical records, 136,529 patients with mild psoriasis and 7354 patients with severe psoriasis based on treatment patterns were matched to 689,702 unaffected patients. The investigators found a clear increased risk for chronic renal disease (RR, 1.93; 95% CI, 1.79-2.08) among those with severe psoriasis. The risk was higher in younger patients; for example, among those aged 30 years, the RR rose to 3.82 (95% CI, 3.15-4.64). The risk for developing renal disease was independent of well-known predisposing factors, such as diabetes mellitus and hypertension. The association between severe psoriasis and renal disease also appeared to be independent of medications administered for psoriasis (eg, cyclosporine).
Also alarming was a recently published systematic review and meta-analysis of 1080 publications concerning the potential association between psoriasis and cancer (J Eur Acad Dermatol Venereol. 2013;27[suppl 3]:36-46). Pouplard et al found that there may be an increased risk for the following solid cancers in psoriasis patients: respiratory tract cancer (RR, 1.52; 95% CI, 1.35-1.71), upper aerodigestive tract cancer (RR, 3.05; 95% CI, 1.74-5.32), urinary tract cancer (RR, 1.31; 95% CI, 1.11-1.55), and liver cancer (RR, 1.90; 95% CI, 1.48-2.44). To the authors, the association seemed particularly strong with these neoplasms, which are associated with excessive alcohol ingestion and smoking.
What’s the issue?
Why might these comorbidities occur? Perhaps chronic inflammation due to abnormal cytokine production and/or deviant immune defenses may promote these new (or better documented) psoriatic comorbidities. Why are they of importance to dermatologists? Because we are the primary source of care for patients with psoriasis, especially those with severe disease. We cannot stop our historical reviews and physical examination with the skin and joints; rather, we must consider the whole patient. We probably should at least perform a comprehensive history at each visit, being carefully attune to any new concerns that suggest gastrointestinal, pulmonary, and renal disease or internal neoplasia, which places an extra (and perhaps unwanted) burden of care on the dermatologist. However, the way I see it is that our role in early detection of an ever-expanding list of serious psoriatic comorbidities may be crucial to the ultimate long-term health of our patients. Are you ready to accept that intensified and enhanced medical responsibility?
We have already come a long way from thinking that psoriasis is merely a cutaneous disease caused by a defect in cellular replication; we now recognize that psoriasis is a systemic inflammatory process that has broad health implications. This association is manifested by comorbidities such as the occurrence of the metabolic syndrome and an increased risk for myocardial infarction. An increased incidence of chronic obstructive pulmonary disease also has been demonstrated in patients with psoriasis, especially those who smoke. Unfortunately, recent publications have highlighted investigative work that expands the scope of psoriatic comorbidity into new realms.
Li and colleagues (Ann Rheum Dis. 2013;72:1200-1205) performed a retrospective analysis of 174,476 women enrolled in several large national health studies. They found an increased risk for incident Crohn disease (relative risk [RR], 4.00; 95% confidence interval [CI], 1.72-9.27) among women with psoriasis. This increased risk rose (RR, 6.43; 95% CI, 2.04-20.32) if both psoriasis and psoriatic arthritis were present. Although the risk for those who already have Crohn disease to develop psoriasis has been previously noted, this study provides the first convincing clinical evidence that the converse association also is true, which is is not totally surprising when one considers common genetic and aberrant cytokine profiles between Crohn disease and psoriasis to suggest an overlap in pathogenic mechanisms.
Perhaps more ominous was the recently published work of Wan and associates (BMJ. 2013;347:f5961). In this massive retrospective analysis utilizing detailed British electronic medical records, 136,529 patients with mild psoriasis and 7354 patients with severe psoriasis based on treatment patterns were matched to 689,702 unaffected patients. The investigators found a clear increased risk for chronic renal disease (RR, 1.93; 95% CI, 1.79-2.08) among those with severe psoriasis. The risk was higher in younger patients; for example, among those aged 30 years, the RR rose to 3.82 (95% CI, 3.15-4.64). The risk for developing renal disease was independent of well-known predisposing factors, such as diabetes mellitus and hypertension. The association between severe psoriasis and renal disease also appeared to be independent of medications administered for psoriasis (eg, cyclosporine).
Also alarming was a recently published systematic review and meta-analysis of 1080 publications concerning the potential association between psoriasis and cancer (J Eur Acad Dermatol Venereol. 2013;27[suppl 3]:36-46). Pouplard et al found that there may be an increased risk for the following solid cancers in psoriasis patients: respiratory tract cancer (RR, 1.52; 95% CI, 1.35-1.71), upper aerodigestive tract cancer (RR, 3.05; 95% CI, 1.74-5.32), urinary tract cancer (RR, 1.31; 95% CI, 1.11-1.55), and liver cancer (RR, 1.90; 95% CI, 1.48-2.44). To the authors, the association seemed particularly strong with these neoplasms, which are associated with excessive alcohol ingestion and smoking.
What’s the issue?
Why might these comorbidities occur? Perhaps chronic inflammation due to abnormal cytokine production and/or deviant immune defenses may promote these new (or better documented) psoriatic comorbidities. Why are they of importance to dermatologists? Because we are the primary source of care for patients with psoriasis, especially those with severe disease. We cannot stop our historical reviews and physical examination with the skin and joints; rather, we must consider the whole patient. We probably should at least perform a comprehensive history at each visit, being carefully attune to any new concerns that suggest gastrointestinal, pulmonary, and renal disease or internal neoplasia, which places an extra (and perhaps unwanted) burden of care on the dermatologist. However, the way I see it is that our role in early detection of an ever-expanding list of serious psoriatic comorbidities may be crucial to the ultimate long-term health of our patients. Are you ready to accept that intensified and enhanced medical responsibility?
Beta-blockers and Melanoma
I have taken beta-blockers for nearly 30 years to combat a non–life-threatening but very disconcerting supraventricular arrhythmia. Also being fair skinned and having suffered through many a blistering sunburn in my youth, I was excited to read the most recent publication regarding the relationship between beta-blocker ingestion and survival from melanoma by De Giorgi et al (Mayo Clin Proc. 2013;88:1196-1203). The Italian investigators collected data from all melanoma patients diagnosed in the dermatology department at the University of Florence (1993-2009). After excluding patients who presented with metastatic disease, they then compared the courses of the remaining patients based on whether or not they had been prescribed beta-blockers for at least 1 year before or after their cutaneous melanoma diagnosis. Of 741 consecutive patients who fit the retrospective study criteria, 79 (11%) had been taking beta-blockers and the remaining 662 (89%) had not been taking beta-blockers.
An analysis based on the multivariate Cox model indicated that the beta-blocker group had improved overall survival after a median follow-up of 4.2 years (P=.005). Looked at in another way, significantly more patients in the untreated group (8%) than the beta-blocker group (3%) experienced disease progression or death (P<.001). The “protective” effect of beta-blockers was so striking that it could be quantified; for each year of beta-blocker use, the risk for death was reduced by 38%. More notable was the fact that the beneficial effect of beta-blocker administration was consistent, even among patients with inherently unfavorable prognostic factors, such as advanced age, thicker lesions, higher frequency of mitoses and ulceration, and nodular melanoma subtype. This large study confirms the results of a much smaller study (N=121) published by the same group in 2011 (Arch Intern Med. 2011;171:779-781).
What’s the issue?
Why might this phenomenon occur? Perhaps blocking sympathetic nervous system neurotransmitters might help avoid the suspected immunosuppression that accompanies stress. Sympathetic neurotransmitters also are known to interact with molecular pathways implicated in abnormal cellular replication, such as the p38/MAPK pathway. Thus, blunting the effects of epinephrine and norepinephrine by blocking some of their receptors might produce a salutatory benefit in the cancer (in this case, melanoma) patient.
Before we all rush out and give all our melanoma patients daily doses of metoprolol, however, De Giorgi et al noted in the most recent study that about two-thirds of the patients were already taking a beta-blocker when their melanoma was diagnosed. Although this study suggests that beta-blockers reduce the risk for recurrence and disease-specific mortality, these drugs clearly do not prevent melanoma in the first place. Furthermore, it should be noted that the number of melanoma patients receiving beta-blockers was small, and conclusions should always be tempered in a retrospective study. The authors duly admit that their investigation indicates the strong need for a truly randomized prospective clinical trial. Of course, administration of beta-blockers is not a totally benign endeavor, as serious hypotension and/or bradycardia may occur, leading to syncope or even worse problems. Finally, the evidence of beta-blocker benefit in melanoma patients is contradictory! A Dutch cohort of 709 melanoma patients recently was studied (Eur J Cancer. 2013;49:3863-3871); this set of investigators found that exposure to beta-blockers did not impact overall melanoma survival regardless of the timing, duration, or dosage of beta-blocker use. In summary, therefore, we still need to determine many things about the relationship between beta-blockers and melanoma survival. That is, if there is a relationship at all. What do you think?
I have taken beta-blockers for nearly 30 years to combat a non–life-threatening but very disconcerting supraventricular arrhythmia. Also being fair skinned and having suffered through many a blistering sunburn in my youth, I was excited to read the most recent publication regarding the relationship between beta-blocker ingestion and survival from melanoma by De Giorgi et al (Mayo Clin Proc. 2013;88:1196-1203). The Italian investigators collected data from all melanoma patients diagnosed in the dermatology department at the University of Florence (1993-2009). After excluding patients who presented with metastatic disease, they then compared the courses of the remaining patients based on whether or not they had been prescribed beta-blockers for at least 1 year before or after their cutaneous melanoma diagnosis. Of 741 consecutive patients who fit the retrospective study criteria, 79 (11%) had been taking beta-blockers and the remaining 662 (89%) had not been taking beta-blockers.
An analysis based on the multivariate Cox model indicated that the beta-blocker group had improved overall survival after a median follow-up of 4.2 years (P=.005). Looked at in another way, significantly more patients in the untreated group (8%) than the beta-blocker group (3%) experienced disease progression or death (P<.001). The “protective” effect of beta-blockers was so striking that it could be quantified; for each year of beta-blocker use, the risk for death was reduced by 38%. More notable was the fact that the beneficial effect of beta-blocker administration was consistent, even among patients with inherently unfavorable prognostic factors, such as advanced age, thicker lesions, higher frequency of mitoses and ulceration, and nodular melanoma subtype. This large study confirms the results of a much smaller study (N=121) published by the same group in 2011 (Arch Intern Med. 2011;171:779-781).
What’s the issue?
Why might this phenomenon occur? Perhaps blocking sympathetic nervous system neurotransmitters might help avoid the suspected immunosuppression that accompanies stress. Sympathetic neurotransmitters also are known to interact with molecular pathways implicated in abnormal cellular replication, such as the p38/MAPK pathway. Thus, blunting the effects of epinephrine and norepinephrine by blocking some of their receptors might produce a salutatory benefit in the cancer (in this case, melanoma) patient.
Before we all rush out and give all our melanoma patients daily doses of metoprolol, however, De Giorgi et al noted in the most recent study that about two-thirds of the patients were already taking a beta-blocker when their melanoma was diagnosed. Although this study suggests that beta-blockers reduce the risk for recurrence and disease-specific mortality, these drugs clearly do not prevent melanoma in the first place. Furthermore, it should be noted that the number of melanoma patients receiving beta-blockers was small, and conclusions should always be tempered in a retrospective study. The authors duly admit that their investigation indicates the strong need for a truly randomized prospective clinical trial. Of course, administration of beta-blockers is not a totally benign endeavor, as serious hypotension and/or bradycardia may occur, leading to syncope or even worse problems. Finally, the evidence of beta-blocker benefit in melanoma patients is contradictory! A Dutch cohort of 709 melanoma patients recently was studied (Eur J Cancer. 2013;49:3863-3871); this set of investigators found that exposure to beta-blockers did not impact overall melanoma survival regardless of the timing, duration, or dosage of beta-blocker use. In summary, therefore, we still need to determine many things about the relationship between beta-blockers and melanoma survival. That is, if there is a relationship at all. What do you think?
I have taken beta-blockers for nearly 30 years to combat a non–life-threatening but very disconcerting supraventricular arrhythmia. Also being fair skinned and having suffered through many a blistering sunburn in my youth, I was excited to read the most recent publication regarding the relationship between beta-blocker ingestion and survival from melanoma by De Giorgi et al (Mayo Clin Proc. 2013;88:1196-1203). The Italian investigators collected data from all melanoma patients diagnosed in the dermatology department at the University of Florence (1993-2009). After excluding patients who presented with metastatic disease, they then compared the courses of the remaining patients based on whether or not they had been prescribed beta-blockers for at least 1 year before or after their cutaneous melanoma diagnosis. Of 741 consecutive patients who fit the retrospective study criteria, 79 (11%) had been taking beta-blockers and the remaining 662 (89%) had not been taking beta-blockers.
An analysis based on the multivariate Cox model indicated that the beta-blocker group had improved overall survival after a median follow-up of 4.2 years (P=.005). Looked at in another way, significantly more patients in the untreated group (8%) than the beta-blocker group (3%) experienced disease progression or death (P<.001). The “protective” effect of beta-blockers was so striking that it could be quantified; for each year of beta-blocker use, the risk for death was reduced by 38%. More notable was the fact that the beneficial effect of beta-blocker administration was consistent, even among patients with inherently unfavorable prognostic factors, such as advanced age, thicker lesions, higher frequency of mitoses and ulceration, and nodular melanoma subtype. This large study confirms the results of a much smaller study (N=121) published by the same group in 2011 (Arch Intern Med. 2011;171:779-781).
What’s the issue?
Why might this phenomenon occur? Perhaps blocking sympathetic nervous system neurotransmitters might help avoid the suspected immunosuppression that accompanies stress. Sympathetic neurotransmitters also are known to interact with molecular pathways implicated in abnormal cellular replication, such as the p38/MAPK pathway. Thus, blunting the effects of epinephrine and norepinephrine by blocking some of their receptors might produce a salutatory benefit in the cancer (in this case, melanoma) patient.
Before we all rush out and give all our melanoma patients daily doses of metoprolol, however, De Giorgi et al noted in the most recent study that about two-thirds of the patients were already taking a beta-blocker when their melanoma was diagnosed. Although this study suggests that beta-blockers reduce the risk for recurrence and disease-specific mortality, these drugs clearly do not prevent melanoma in the first place. Furthermore, it should be noted that the number of melanoma patients receiving beta-blockers was small, and conclusions should always be tempered in a retrospective study. The authors duly admit that their investigation indicates the strong need for a truly randomized prospective clinical trial. Of course, administration of beta-blockers is not a totally benign endeavor, as serious hypotension and/or bradycardia may occur, leading to syncope or even worse problems. Finally, the evidence of beta-blocker benefit in melanoma patients is contradictory! A Dutch cohort of 709 melanoma patients recently was studied (Eur J Cancer. 2013;49:3863-3871); this set of investigators found that exposure to beta-blockers did not impact overall melanoma survival regardless of the timing, duration, or dosage of beta-blocker use. In summary, therefore, we still need to determine many things about the relationship between beta-blockers and melanoma survival. That is, if there is a relationship at all. What do you think?
Antibiotic Use: Yet Another Threat?
The issue of increasing antibiotic resistance has become a serious global threat. The World Health Organization proclaimed that World Health Day 2011 would be dedicated to a comprehensive consolidated strategy to prevent regression to a preantibiotic era when infections were the single leading causes of death. At the 2013 G8 summit, the health ministers of the 8 wealthiest nations in the world proclaimed that antibiotic resistance is the single biggest threat to health security facing the 21st century. In addition to the problem of resistance, the use of antibiotics can lead to long-lasting alterations in the gut flora, making posttraumatic septicemia due to enteric organisms difficult to manage. Antibiotic use also has been associated with the development of inflammatory bowel disease in a number of well-done studies. Acute antibiotic side effects have included dyschromia, photosensitivity, potential hepatic and/or renal dysfunction, gastrointestinal tract distress, and various cutaneous events ranging from morbilliform eruptions to hives and even toxic epidermal necrolysis. All of the foregoing begs for more rational, appropriate, and circumspect use of antibiotic medications by all health care providers.
If the preceding commentary didn’t catch your attention, perhaps the findings from a recent article published online in the British Journal of Dermatology will. In this thoughtful and comprehensive review, a meta-analysis was performed on 20 large-scale observational studies involving individuals aged 0 to 25 years, which assessed the impact of antibiotic exposure in utero or within the first year of life on the subsequent risk for developing eczema. Both cross-sectional and longitudinal studies demonstrated a consistently increased risk (odds ratio, 1.4) of developing atopic eczema associated with postnatal antibiotic exposure. In fact, this association was so reliable that a dose-response association could be determined, suggesting a 7% increased risk for eczema for each additional oral or parenteral antibiotic course received during the first year of life. Why this effect happens remains uncertain, but the association is clear.
What’s the issue?
Think about your use of antibiotics! Do you use open-ended and prolonged courses for acne, rosacea, hidradenitis suppurativa, dissecting cellulitis of the scalp, and other conditions in adults? Are you contributing to the ever-expanding pool of antibiotic-resistant microbes carried by the adult population? When you do utilize antibiotics, do you always verify the presence of infection by culture? Do you always obtain sensitivities on bacterial isolates? Do you explicitly admonish antibiotic recipients or their parents/guardians to finish the antibiotic course and not save or share? This recent article now makes concerns about antibiotic use early in life highly relevant. Do you treat impetigo, for example, with one of the several approved topical agents or still routinely administer oral antibiotics? How would you manage neonatal acne or furunculosis in a young child? This paper from the British Journal of Dermatology supplies us with yet another good reason to evaluate and refine our own prescribing habits when it comes to antibiotics.
The issue of increasing antibiotic resistance has become a serious global threat. The World Health Organization proclaimed that World Health Day 2011 would be dedicated to a comprehensive consolidated strategy to prevent regression to a preantibiotic era when infections were the single leading causes of death. At the 2013 G8 summit, the health ministers of the 8 wealthiest nations in the world proclaimed that antibiotic resistance is the single biggest threat to health security facing the 21st century. In addition to the problem of resistance, the use of antibiotics can lead to long-lasting alterations in the gut flora, making posttraumatic septicemia due to enteric organisms difficult to manage. Antibiotic use also has been associated with the development of inflammatory bowel disease in a number of well-done studies. Acute antibiotic side effects have included dyschromia, photosensitivity, potential hepatic and/or renal dysfunction, gastrointestinal tract distress, and various cutaneous events ranging from morbilliform eruptions to hives and even toxic epidermal necrolysis. All of the foregoing begs for more rational, appropriate, and circumspect use of antibiotic medications by all health care providers.
If the preceding commentary didn’t catch your attention, perhaps the findings from a recent article published online in the British Journal of Dermatology will. In this thoughtful and comprehensive review, a meta-analysis was performed on 20 large-scale observational studies involving individuals aged 0 to 25 years, which assessed the impact of antibiotic exposure in utero or within the first year of life on the subsequent risk for developing eczema. Both cross-sectional and longitudinal studies demonstrated a consistently increased risk (odds ratio, 1.4) of developing atopic eczema associated with postnatal antibiotic exposure. In fact, this association was so reliable that a dose-response association could be determined, suggesting a 7% increased risk for eczema for each additional oral or parenteral antibiotic course received during the first year of life. Why this effect happens remains uncertain, but the association is clear.
What’s the issue?
Think about your use of antibiotics! Do you use open-ended and prolonged courses for acne, rosacea, hidradenitis suppurativa, dissecting cellulitis of the scalp, and other conditions in adults? Are you contributing to the ever-expanding pool of antibiotic-resistant microbes carried by the adult population? When you do utilize antibiotics, do you always verify the presence of infection by culture? Do you always obtain sensitivities on bacterial isolates? Do you explicitly admonish antibiotic recipients or their parents/guardians to finish the antibiotic course and not save or share? This recent article now makes concerns about antibiotic use early in life highly relevant. Do you treat impetigo, for example, with one of the several approved topical agents or still routinely administer oral antibiotics? How would you manage neonatal acne or furunculosis in a young child? This paper from the British Journal of Dermatology supplies us with yet another good reason to evaluate and refine our own prescribing habits when it comes to antibiotics.
The issue of increasing antibiotic resistance has become a serious global threat. The World Health Organization proclaimed that World Health Day 2011 would be dedicated to a comprehensive consolidated strategy to prevent regression to a preantibiotic era when infections were the single leading causes of death. At the 2013 G8 summit, the health ministers of the 8 wealthiest nations in the world proclaimed that antibiotic resistance is the single biggest threat to health security facing the 21st century. In addition to the problem of resistance, the use of antibiotics can lead to long-lasting alterations in the gut flora, making posttraumatic septicemia due to enteric organisms difficult to manage. Antibiotic use also has been associated with the development of inflammatory bowel disease in a number of well-done studies. Acute antibiotic side effects have included dyschromia, photosensitivity, potential hepatic and/or renal dysfunction, gastrointestinal tract distress, and various cutaneous events ranging from morbilliform eruptions to hives and even toxic epidermal necrolysis. All of the foregoing begs for more rational, appropriate, and circumspect use of antibiotic medications by all health care providers.
If the preceding commentary didn’t catch your attention, perhaps the findings from a recent article published online in the British Journal of Dermatology will. In this thoughtful and comprehensive review, a meta-analysis was performed on 20 large-scale observational studies involving individuals aged 0 to 25 years, which assessed the impact of antibiotic exposure in utero or within the first year of life on the subsequent risk for developing eczema. Both cross-sectional and longitudinal studies demonstrated a consistently increased risk (odds ratio, 1.4) of developing atopic eczema associated with postnatal antibiotic exposure. In fact, this association was so reliable that a dose-response association could be determined, suggesting a 7% increased risk for eczema for each additional oral or parenteral antibiotic course received during the first year of life. Why this effect happens remains uncertain, but the association is clear.
What’s the issue?
Think about your use of antibiotics! Do you use open-ended and prolonged courses for acne, rosacea, hidradenitis suppurativa, dissecting cellulitis of the scalp, and other conditions in adults? Are you contributing to the ever-expanding pool of antibiotic-resistant microbes carried by the adult population? When you do utilize antibiotics, do you always verify the presence of infection by culture? Do you always obtain sensitivities on bacterial isolates? Do you explicitly admonish antibiotic recipients or their parents/guardians to finish the antibiotic course and not save or share? This recent article now makes concerns about antibiotic use early in life highly relevant. Do you treat impetigo, for example, with one of the several approved topical agents or still routinely administer oral antibiotics? How would you manage neonatal acne or furunculosis in a young child? This paper from the British Journal of Dermatology supplies us with yet another good reason to evaluate and refine our own prescribing habits when it comes to antibiotics.
