Keywords Kawasaki disease · Pyuria · C-reactive protein · Erythrocyte sedimentation rate Sirs,We read with interest the article by Ristoska-Bojkovska et al. [1]. The authors reported that Japanese pediatricians are very familiar with pyuria coexisting with the nonspecific findings of severe inflammation, such as increased C-reactive protein (CRP) and erythrocyte sedimentation rate (ESR) in Kawasaki disease (KD). A possible diagnosis of urinary tract infection (UTI) is not automatically considered.It is sometimes difficult to differentiate KD from infections such as sepsis, streptococcosis, or pyelonephritis in the early period of KD. Upon admission, we routinely perform the septic work-up, including urine culture, even if the most likely diagnosis is KD. We describe here a patient with KD associated with acute pyelonephritis.A 2-year-old boy was admitted to our center with a 4-day history of high fever (40.0C) and anorexia with moderate throat pain and malaise. He had conjunctivitis, injected pharynx, and lymphadenopathy, but no rash or changes of the peripheral extremities. Initial laboratory results showed an increased ESR of 119 mm/h and CRP of 5.44 g/dl. White blood cell count showed 11,190/mm 3 with neutrophilia (79%). Pyuria was present. Past history included KD with intravenous immunoglobulin therapy (IVIG) (400 mg/kg daily, given for 5 days) and aspirin (30 mg/kg daily) treatment at the age of 11 months. At that time, his urinalysis was normal.A presumptive diagnosis of recurrent KD was made but bacterial lymphadenitis or UTI was undeniable. He was treated initially with intravenous cefotiam hydrochloride (100 mg/kg per 24 h). Two days later, he remained febrile with a temperature of 40.0 º C. Blood analysis showed a CRP of 9.08 g/dl and a white blood cell count of 16,880/mm 3 . We diagnosed recurrent KD and stopped antibiotic therapy. IVIG and flubiprofen (4.2 mg/ kg daily), because of hepatitis (aspartate aminotransferase 169 IU/l, alanine aminotransferase 111 IU/l), were administered. Within 1 day of initial IVIG infusion, the boy became afebrile. On the 14th hospital day, he had periungual desquamation of the fingers and toes, and he met the five clinical signs of KD. His electrocardiogram and echocardiography were normal.The urine culture performed upon admission showed 10 6 colonies of Escherichia coli. On the 2nd hospital day renal ultrasonography demonstrated left hydronephrosis. A diagnosis of acute pyelonephritis was established and additional cefotiam hydrochloride was administered. On the 18th hospital day a voiding cystourethrogram showed left vesicoureteral reflux.KD often presents with abnormal urinary findings that are due to urethritis in most cases as shown by RistoskaBojkovska et al. [1]. The clinical manifestations of KD are similar to severe infections. We diagnose KD after confirming the negative results of cultures of all specimens because the etiology of KD still remains unclear [2]. Moreover, there is no specific diagnostic marker for KD except the clinical criteria. Had we not or...
Internal hernia through a mesenteric defect, called mesenteric hernia, is an uncommon cause of acute intestinal obstruction in newborns. Strangulated mesenteric hernia results in intestinal necrosis or perforation and progressive deterioration with fatal outcome, especially when it occurs in low-birthweight infants. We report two very low-birthweight (VLBW) infants, who presented with acute intestinal obstruction related to mesenteric defect. The initial diagnosis was meconium obstruction in those cases, which is a common cause of bowel obstruction occurring in VLBW infants. Correct diagnosis of mesenteric hernia was difficult in these cases because of rapid deterioration and non-specific radiological findings. Awareness of the possibility of rare mesenteric hernia causing acute intestinal obstruction and surgical intervention in an appropriate timeframe are important for rescuing VLBW infants with such organic abnormalities.
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