Perianal streptococcal disease in childhood: systematic literature review.

Group A Streptococcus has been associated with a perianal infection. We conducted a systematic review of the literature on childhood streptococcal perianitis in three databases: Excerpta Medica, National Library of Medicine, and Web of Science. The main purposes were to document the clinical features, the tendency to recur, the association with an asymptomatic streptococcal throat carriage, the accuracy of rapid streptococcal tests, and the mechanism possibly underlying the acquisition of this infection. More than 80% of cases are boys ≤7.0 years of age with defecation disorders, perianal pain, local itch, rectal bleeding, or fissure and a sharply demarcated perianal redness. Perianitis is associated with a streptococcal tonsillopharyngitis in about every fifth case. The time to diagnosis is ≥3 weeks in 65% of cases. Recurrences occur within 3½ months in about 20% of cases. An asymptomatic group A streptococcal throat carriage occurs in 63% of cases. As compared with perianal Streptococcus A culture, the rapid streptococcal tests have a positive predictive value of 80% and a negative predictive value of 96%. It is hypothesized that digital inoculation from nasopharynx to anus underlies perianitis. Many cases are likely caused directly by children, who are throat and nasal carriers of Streptococcus A. Some cases might occur in children, who have their bottoms wiped by caregivers with streptococcal tonsillopharyngitis or carriage of Streptococcus.Conclusion: Perianitis is an infection with a distinctive presentation and a rather long time to diagnosis. There is a need for a wider awareness of this condition among healthcare professionals. What is Known: • Group A Streptococcus may cause perianitis in childhood. • Systemic antimicrobials (penicillin V, amoxycillin, or cefuroxime) are superior to topical treatment. What is New: • The clinical presentation is distinctive (defecation disorders, perianal pain, local itch, rectal bleeding, or fissure and a sharply demarcated perianal redness). • The time to diagnosis is usually ≥3 weeks. Recurrences occur in about 20% of cases.

Dietary Chloride Deficiency Syndrome: Pathophysiology, History, and Systematic Literature Review.

Metabolic alkalosis may develop as a consequence of urinary chloride (and sodium) wasting, excessive loss of salt in the sweat, or intestinal chloride wasting, among other causes. There is also a likely underrecognized association between poor salt intake and the mentioned electrolyte and acid-base abnormality. In patients with excessive loss of salt in the sweat or poor salt intake, the maintenance of metabolic alkalosis is crucially modulated by the chloride-bicarbonate exchanger pendrin located on the renal tubular membrane of type B intercalated cells. In the late 1970s, recommendations were made to decrease the salt content of foods as part of an effort to minimize the tendency towards systemic hypertension. Hence, the baby food industry decided to remove added salt from formula milk. Some weeks later, approximately 200 infants (fed exclusively with formula milks with a chloride content of only 2-4 mmol/L), were admitted with failure to thrive, constipation, food refusal, muscular weakness, and delayed psychomotor development. The laboratory work-up disclosed metabolic alkalosis, hypokalemia, hypochloremia, and a reduced urinary chloride excretion. In all cases, both the clinical and the laboratory features remitted in ≤7 days when the infants were fed on formula milk with a normal chloride content. Since 1982, 13 further publications reported additional cases of dietary chloride depletion. It is therefore concluded that the dietary intake of chloride, which was previously considered a "mendicant" ion, plays a crucial role in acid-base and salt balance.

Nicolau syndrome caused by non-steroidal anti-inflammatory drugs: Systematic literature review.

AIM: Intramuscular or, more rarely, local drug injection is occasionally followed by immediate local pain, livedoid skin lesions and, some days later, the development of ischemic lesions. This very uncommon but potentially severe reaction, termed Nicolau syndrome, is traditionally associated with bismuth and ß-lactam antimicrobials. The aim of this report was to review the literature associating Nicolau syndrome with the administration of non-steroidal anti-inflammatory drugs. METHODS: The National Library, Excerpta Medica, Web of Science and Cochrane library databases were used. RESULTS: Sixty-two cases (40 females and 22 males aged from 13 to 81, median 57 years) of Nicolau syndrome were published after 1992. Fifty-three cases occurred after diclofenac. The remaining nine cases were associated with ketoprofen (N = 2), ketorolac (N = 2), phenylbutazone (N = 2), etofenamate (N = 1), ibuprofen (N = 1) and piroxicam (N = 1). CONCLUSION: Although Nicolau syndrome is extremely uncommon, physicians must be aware of this complication after intramuscular administration of non-steroidal anti-inflammatory drugs and should avoid unnecessary injections.