Agustos 2016
Asiri yükselmis ve uzun süreli devam eden hiperbilirubineminin nadir sebebi: Weil hastaligi
A rare cause of long-standing and severe hyperbilirubinemia: Weil’s disease
- Ana Sayfa
- Sayılar
- Agustos 2016
- Asiri yükselmis ve uzun süreli devam eden hiperbilirubineminin nadir sebebi: Weil hastaligi...
Özet
Leptospirozis vakalarinin büyük çogunlugunda grip benzeri hafif klinik tablo görülürken, %10’u sarilik ve böbrek yetmezligi bulgularinin oldugu ve Weil hastaligi olarak adlandirilan klinik formda görülür. Çalis- mamizda Weil hastaligi tanisi konulan, yas ortalamasi 36.2±1.7 olan bes erkek hasta sunulmustur. Tüm hastalarda ates, yaygin kas agrisi, karin agrisi, sarilik, konjunktivalarda kizariklik ve sislik, üç vakada ka- sinti ve yaygin cilt döküntüleri mevcuttu. Biyokimya tetkiklerinde tüm vakalarda bilirubin ve kreatin kinaz seviyesinde belirgin artma ve normal protrombin düzeyi ile beraber aspartat amino transferaz, alanin amino transferaz, alkalen fosfataz ve gama glutamil transferaz seviyesinde hafif artma; dört vakada kreatin seviyesinde belirgin artma saptandi. Tam kan sayiminda tüm vakalarda trombositopeni ve lökositoz vardi. Weil hastaligi tanisi mikroskobik aglutinasyon testi ile dogrulandi. Tüm hastalara yatisinin ilk gününden itibaren genis spektrumlu antibiyotik tedavisi baslandi. Akut böbrek yetmezligi olan üç hastamiz hemodiyaliz tedavisine alindi. Tüm hastalara tedavinin ilk gününden karaciger fonksiyon testlerinin normale dönmesine kadar ursodeoksikolik asit tedavisi verildi. Hastalardan biri yatisinin birinci gününde akciger içi kanama nedeniyle vefat etti. Geriye kalan dört hastanin diger klinik ve laboratuvar bulgulari erken düzelirken, serum bilirubin düzeyleri ortalama 99.2±7.4 gün sonra normale döndü. Sonuç olarak, akut enfeksiyon belirtileriyle baslayan ve uzun süreli devam eden sarilik olgularinin ayirici tanisinda Weil hastaligi da düsünülmelidir.
Abstract
Although a mild, flu-like clinical picture is seen in the great majority of cases with Leptospirosis, jaundice, and acute renal failure are seen in 10% of cases. This clinical picture is named Weil’s disease. In our study, we present five male patients (mean age 36.2±1.7 years) with a diagnosis of Weil’s disease. There was fever, generalized muscle pain, abdominal pain, jaundice, and conjunctival suffusion in all patients, and skin rashes and itching in three patients. Biochemistry showed significant elevations in bilirubin and creatine kinase levels associated with moderately elevated aspartate aminotransferase, alanine aminotrasferase, alkaline phosphatase, and gamma glutamyl transferase levels in all patients; significant elevations in creatine levels were present in four patients. Prothrombin time was normal in all patients. Complete blood count showed thrombocytopenia and leukocytosis in all patients. The diagnosis of Weil disease was confirmed by microscopic agglutination test in all patients. Broad-spectrum antibiotics were given to all patients on admission to our clinic. Ursodeoxycholic acid was given continuously to all patients until death or improvement of liver function tests. One patient died within the first day of hospitalization due to intra-alveolar hemorrhage. In the remaining four patients, although early improvement was observed in other clinical and laboratory findings, serum bilirubin returned to normal levels after a mean of 99.2±7.4 days. In conclusion, Weil disease should be considered in the differential diagnosis of patients with symptoms and signs of acute infection and long-standing jaundice.
