Severe fenitrothion poisoning complicated by rhabdomyolysis in psychiatric patient

Non-traumatic rhabdomyolysis associated with organophosphate intoxication has not been generally reported. We report here in a severe case of fenitrothion poisoning complicated by rhabdomyolysis. A 43-year-old woman ingested approximately 100 ml of fenitrothion emulsion (50%) in an attempt to commit suicide. On day 3 after admission, her creatine phosphokinase (CPK) peaked at 47,762 IU/L. She received supportive treatment included sodium bicarbonate and fluid resuscitation. However, muscarinic symptoms including excessive miosis and salivation developed on day 5 when her CPK levels decreased. The delay in cholinergic symptoms might have been due to the trihexyphenidyl she took with the antipsychotic drugs. Fortunately, the present patient recovered from the acute cholinergic crisis, and acute renal failure was prevented by early diagnosis. This is a case of organophosphate poisoning complicated by rhabdomyolysis in a psychiatric patient. The masking of acute cholinergic symptoms should be taken into consideration in such patients.     

Delayed hypercalcemia after non-oliguric acute renal failure associated with rhabdomyolysis

Alterations in the calcium metabolism are a characteristic paraclinical finding in patients with oliguric acute renal failure associated with rhabdomyolysis. A 20-year-old male operated on under general anesthesia developed non-oliguric acute renal failure due to malignant hyperthermia with rhabdomyolysis (urine myoglobin greater than 20,000 nmol/l; reference range less than 0.85 nmol/l). On the 20th postoperative day hypercalcemia was found, reaching a maximum serum level of 3.74 mmol/l (reference range 2.18-2.65 mmol/l) on the 27th postoperative day. Delayed hypercalcemia in non-oliguric acute renal failure associated with rhabdomyolysis has not been reported previously. This case suggests that prolonged control of the serum calcium level should be performed in patients with rhabdomyolysis, even in the absence of oliguria.     

Rhabdomyolysis induced by simvastatin-fluconazole combination

Rhabdomyolysis is a potential adverse consequence of statin therapy. Here, we report a patient with prostate cancer being treated with simvastatin who developed rhabdomyolysis after coadministration with fluconazole. The rhabdomyolysis promptly resolved after discontinuation of fluconazole, suggesting the possible role of drug interaction in the development of rhabdomyolysis with coadministration of the two medications. Both simvastatin and fluconazole were promptly discontinued, and the patient was admitted to the intensive care unit, where vigorous hydration along with urine alkalinization led to resolution of rhabdomyolysis. Since statins are commonly prescribed treatments for individuals with hyperlipidemia, caution is advised in coadministration with azoles such as fluconazole. Although supportive treatment remains the mainstay of therapy for patients with rhabdomyolysis, fatal consequences can arise from hyperkalemia, cardiac arrhythmia, renal failure and disseminated intravascular coagulation.     

Multiple organ dysfunction syndrome,an unusual complication of heroin intoxication: a case report and review of literature

Multiple organ dysfunction syndrome (MODS) has rarely been described in patients with heroin intoxication. Here, we report a rare case of MODS involving six organs, due to heroin intoxication. The patient was a 32-year-old Chinese man with severe heroin intoxication complicated by acute pulmonary edema and respiratory insufficiency, shock, myocardial damage and cardiac insufficiency, rhabdomyolysis and acute renal insufficiency, acute liver injury and hepatic insufficiency, toxic leukoencephalopathy, and hypoglycemia. He managed to survive and was discharged after 10 weeks of intensive care. The possible pathogenesis and therapeutic measures of MODS induced by heroin intoxication and some suggestions for preventing and treating severe complications of heroin intoxication, based on clinical evidence and the pertinent literature, are discussed in this report.     

Aeromonas sobria infection with severe soft tissue damage and segmental necrotizing gastroenteritis in a patient with alcoholic liver cirrhosis

A 49-year-old man, who had a 3-year history of liver dysfunction but had not been treated, was admitted to the hospital with a sudden onset of fever and generalized muscle pain. He subsequently developed generalized purpura with scattered hemorrhagic bullae of the skin and massive bloody stools. Aeromonas sobria was proven by culture of both blood and bullous fluid. In spite of the extensive treatment with antibiotics and other medications in the intensive care unit (ICU), the patient went into septic shock and died 2 days after admission. Pathological examination on autopsy revealed segmental necrotizing gastroenteritis with bacterial colonies and alcoholic liver cirrhosis, in addition to extensive severe soft tissue damage involving cellulitis and rhabdomyolysis and epidermolysis. Although the prognosis for Vibrio vulnificus infection with severe soft tissue damage in patients with liver cirrhosis, malignancy, diabetes mellitus or other pre-existing diseases is poor, the unfavorable progression of Aeromonas species, especially A. sobria infection is rare. This is thought to be the first report of an autopsied case.     

Case of fatal sickle cell intrahepatic cholestasis despite use of exchange transfusion in an African-American patient

Sickle cell intrahepatic cholestasis (SCIC) is a rare complication of sickle cell anemia, characterized by marked hyperbilirubinemia and acute hepatic failure with an often fatal course. However, the few reported adult cases that were treated with exchange transfusion had a favorable outcome. We herein describe a 48-year-old African-American man with hemoglobin S/B thalassemia and previously treated hepatitis C with compensated cirrhosis, who presented with a total bilirubin of 59.7 mg/dL and direct bilirubin of 43.6 mg/dL in the absence of choledocholithiasis. Despite an exchange transfusion and aggressive packed red blood cell transfusions, which successfully decreased the hemoglobin S levels to <15%, he perished from progressive hepatic and renal failure. Autopsy demonstrated extensive intrahepatocellular and intracanalicular cholestasis in a background of cirrhosis. Our case suggests that poor prognostic factors for adult SCIC patients treated with exchange transfusion may include older age and underlying hepatic disease.     

Meloxicam-induced rhabdomyolysis in the context of an acute ross river viral infection

Acute rhabdomyolysis is a clinical and laboratory syndrome resulting from the breakdown of skeletal muscle, with the release of intracellular contents into the circulatory system, which can cause potentially lethal complications. Here, we present the case of a patient who developed acute rhabdomyolysis after consumption of meloxicam for jaw pain and experienced generalized myalgias in the context of an acute febrile illness with generalized urticaria. Further investigation indicated elevated muscle enzymes and acute renal failure. Serological analysis revealed that the patient was positive for Ross River virus (RRV) IgM. Genetic studies to detect CYP2C9 polymorphisms were negative. Meloxicam was discontinued. He responded to conservative measures within 2 weeks. Oral aspirin challenge was negative, suggesting a drug-specific effect of meloxicam rather than a class effect. Our case indicates a causative role for meloxicam and/or acute RRV in rhabdomyolysis.     

A case of Goodpasture's syndrome with massive pulmonary hemorrhage

We present a typical case of Goodpasture's syndrome with massive pulmonary hemorrhage and acute deterioration of renal function. A 20-year-old male was admitted due to severe azotemia (blood urea nitrogen 214.7 mg/dL, serum creatinine 30.2 mg/dL) and was treated with emergency hemodialysis. On the 4th hospital day, a sudden onset of pulmonary hemorrhage developed. The circulating level of anti-glomerular basement membrane antibody was then elevated highly, and the kidney biopsy showed crescentic glomerulonephritis and linear deposition of IgG along the glomerular capillary. The patient was treated with intravenous high dose-steroid, oral cyclophosphamide and plasma exchanges. The pulmonary hemorrhage improved with the therapy, however, his renal function did not improve. He is currently on a regular schedule of hemodialysis.     

Rhabdomyolysis and acute renal failure following an overdose of doxepine and nitrazepam

A 50-year-old woman developed rhabdomyolysis and myoglobinuric renal impairment after an oral dose of 250 mg nitrazepam and 1,250 mg doxepin. Serum creatinine increased from 70 mumol/l to 472 mumol/l in two days. Serum creatine phosphokinase reached a maximal level of 391 mu kat/l (reference range less than 2.5 mu kat/l) on the third day and serum myoglobin was maximally 910 nmol/l (reference range less than 4.5 nmol/l) on the fourth day after the overdose. Passive and active movements of the knees and ankles became increasingly restricted, but the patient felt no muscle pain. Diuresis decreased to 20-22 ml/hour in spite of repetitive doses of furosemide, but was enforced to greater than 100 ml/hour by vigorous infusion of saline. Haemodialysis was avoided on this regimen. It is suggested that in patients intoxicated with nitrazepam and/or doxepin, rhabdomyolysis should be suspected when a rapidly increasing serum concentration of creatinine is found, even in the absence of muscle pain.     

Polyangitis overlap syndrome: a fatal case combined with adult Henoch-Schönlein purpura and polyarteritis nodosa

Henoch‐Schönlein purpura (HSP) is a rather common disease characterized by systemic hypersensitivity vasculitis in the skin and other visceral organs. It has a favorable prognosis unless it is complicated by severe glomerular disease. We report a distinctive fatal case of systemic vasculitis combined with HSP and polyarteritis nodosa (PN) in a 56‐year‐old man who died of progressive renal failure one month after the onset of the disease. He complained of arthralgia, purpura of both lower extremities, nasal bleeding and tarry stool, and acute renal failure was noted at the time of admission to hospital. A skin biopsy from the purpura lesion exhibited leucocytoclastic vasculitis with IgA deposition, and HSP was considered. However, renal failure progressed rapidly and subsequently was complicated by acute myocardial infarction. Postmortem examination revealed PN type necrotizing vasculitis in the kidneys, heart and mesentery resulting in acute multiple infarctions of these organs. We think the current case was a polyangitis overlap syndrome. It is important to suspect the polyangitis overlap syndrome positively when progressive acute renal failure is seen in a patient with HSP and to begin appropriate therapy immediately.     

Severe human infections caused by Vibrio metschnikovii.

Vibrio metschnikovii is largely distributed in the aquatic environment; human infections are rarely observed. A fatal case of septicemia in a patient with liver cirrhosis, renal insufficiency, and diabetes is described. A second case in a 82-year-old woman with septicemia, respiratory problems, and infected leg lesions is reported; she was successfully treated.     

Effects of blood purification therapy on a patient with ifosfamide-induced neurotoxicity and acute kidney injury

Ifosfamide combined with other antineoplastic agents has been effective in the treatment of osteosarcoma, although adverse effects are reported in the increasing use of ifosfamide. The most serious complications among the ifosfamide intoxications are neurotoxicity and nephrotoxicity. We report on a patient who suffered from ifosfamide-induced neurotoxicity and nephrotoxicity and rhabdomyolysis after chemotherapy, and was successfully treated with blood purification therapy. The patient had osteosarcoma with multiple lung metastases, wherein the chemotherapy included ifosfamide (3 g/m²) and VP-16 (60 mg/m²) per day for 3 days. The first day after chemotherapy, the patient experienced impaired consciousness and renal function. Based on the clinical course and laboratory data, the diagnosis was ifosfamide-induced neurotoxicity and the acute kidney injury caused by ifosfamide-induced nephrotoxicity and rhabdomyolysis. As a detoxification treatment, blood purification procedures were performed daily for 3 days. Thirty-six hours after the first hemodialysis session, the symptoms of neurotoxicity disappeared. In the lead-up to the 10th day following intoxication, the serum creatinine recovered to the baseline level. Serum ifosfamide concentration decreased from 41.9 to 12.1 ng/ml by the second session of blood purification. Despite the absence of an established detoxification method when complications present simultaneously, blood purification therapy should be considered for treating severe concurrent neurotoxicity and nephrotoxicity and rhabdomyolysis.     

辛伐他汀致横纹肌溶解1例

患者女,76岁,因“全身肌肉疼痛,伴乏力1周”入院。因冠心病长期服用降脂药“辛伐他汀(舒将之)20 mg/晚”,约2月前改用“辛伐他汀(京新)40 mg/晚”。入院后完善相关检查,肌酸激酶明显升高,肾功能轻度受损。诊断上考虑为：辛伐他汀导致的横纹肌溶解症。该病例特点：1)长期服用辛伐他汀未见不良反应,更换厂家及增加剂量2月后出现不良反应;2)肌酸激酶水平的显著升高;3)如此高的肌酶水平却并没有出现严重的肾功能损害,预后良好。     

Ciprofloxacin-induced acute liver injury: case report and review of literature

Ciprofloxacin is a fluorinated quinolone antibiotic with relatively low occurrence of adverse side effects. However, increasing evidence suggests that ciprofloxacin may cause severe liver damage. Until now, 14 cases of ciprofloxacin-associated liver injuries have been reported. We describe a case of a 22-year-old male who developed hepatic failure after intake of ciprofloxacin. The patient had been treated with 2×250 mg ciprofloxacin per day. He presented with symptoms of acute liver failure 14 days later. Liver biopsy revealed extensive hepatocellular necrosis involving zones 3 and 2 of hepatic acini and a mixed inflammatory infiltration containing abundant eosinophils. Symptoms resolved after corticoidsteroid therapy. In the present paper, we report the clinico-pathological characteristics of a case of ciprofloxacin-associated acute hepatic failure and discuss the current literature.     

Bacteremia caused by Laribacter hongkongensis misidentified as Acinetobacter lwoffii: report of the first case in Korea

Laribacter hongkongensis is an emerging pathogen in patients with community-acquired gastroenteritis and traveler's diarrhea. We herein report a case of L. hongkongensis infection in a 24-yr-old male with liver cirrhosis complicated by Wilson's disease. He was admitted to a hospital with only abdominal distension. On day 6 following admission, he complained of abdominal pain and his body temperature reached 38.6℃. The results of peritoneal fluid evaluation revealed a leukocyte count of 1,180/μL (polymorphonuclear leukocyte 74%). Growth on blood culture was identified as a gram-negative bacillus. The isolate was initially identified as Acinetobacter lwoffii by conventional identification methods in the clinical microbiology laboratory, but was later identified as L. hongkongensis on the basis of molecular identification. The patient was successfully treated with cefotaxime. To the best of our knowledge, this case is the first report of hospital-acquired L. hongkongensis bacteremia with neutrophilic ascites.     

Recurrence of Kawasaki disease in an adult patient with cholecystitis

We report recurrence of Kawasaki disease in a 20-year-old man eighteen years after the primary episode. Athough sixty-nine cases have been reported among adults in the literature, this represents only the second case of Kawasaki disease recurring in an adult patient after childhood presentation. Our patient presented with the characteristic mucocutaneous features, fever, arthralgia, epigastric pain and cholecystitis. His presentation was complicated by arthralgias and abnormal liver function tests, which are more common in the adult patient. The diagnosis was made based on clinical findings after the exclusion of other causes of persistent febrile illness. He was successfully treated with high dose aspirin and intravenous immunoglobulin therapy. Despite a second presentation of Kawasaki disease our patient did not have any demonstrable coronary arterial involvement. Although typically a self-limiting disease, cardiac complications can cause significant morbidity and mortality in those not treated with aspirin and IVIG. This report serves to highlight that late recurrence of Kawasaki disease may develop in adults many decades after the initial presentation. A twenty-year-old male, presented to the Emergency department with a one-week history of general malaise. He complained of sore throat, 5-day history of fever (39 degree celsius), epigastric discomfort, rash, nausea, vomiting, generalised arthralgia and myalgia. He was jaundiced with dark urine and pale stools. He had been commenced on oral penicillin three times a day for possible streptococcal infection after the rash had occurred. Past medical history was notable for a previous episode of Kawasaki disease (KD) at 2 years of age, after which there were no adverse sequelae, a history of asthma and non-alcoholic fatty liver disease.     

Acute renal failure associated with acute type A hepatitis with a mild liver damage

Acute renal failure associated with acute type A hepatitis was successfully treated with hemodialysis. Though acute renal failure is usually associated with severe liver damage of end stage cirrhosis or fulminant hepatitis, liver damage of our case was only slight. The etiology of the renal failure is discussed.     

Use of erythropoietin in the treatment of anemia induced by ribavirin/interferon in patients with hepatitis C

We are presenting 20 patients with hepatitis C, who developed anemia on interferon alpha-2b/ribavirin treatment and were treated with recombinant human c alpha. Median age was 43 years (range 25-72). Four patients received previous treatment. Interferon-alpha-2b was given at six million units three times a week to 10 patients and at three million units three times a week to five patients. PEG-interferon-alpha-2b (80-120 mug/week) was given to five patients. The dose of ribavirin was 800-1200 mg/day (19 patients) and 200 mg/day (one patient with renal failure). Duration of an interferon/ribavirin treatment was 6-12 months. Baseline median hemoglobin was 13.3 g/dl (range 12.2-15.8); median hemoglobin nadir: 9.8 g/dl (range 8.4-11.2). On erythropoietin, the hemoglobin increased to median 11.7 g/dl (range 9.6-12.8). The ribavirin dose had been decreased to 800 mg in four patients, to 600 mg in four patients, to 400 mg in one patient. Thirteen patients responded to interferon/ribavirin treatment, six patients (all genotype 1) did not. Of the 13 initial responders 11 had sustained response, one still under treatment and two patients relapsed. In conclusion, in our patients with chronic hepatitis C treated with interferon/ribavirin combination therapy, erythropoietin was beneficial in the treatment of ribavirin-induced anemia.     

Life-threatening hypophosphataemia in a cirrhotic patient with jaundice

We report the case of a 51-year-old patient with a history of liver cirrhosis, who presented with jaundice (total bilirubin 50 mg/dl [855 µmol/l], direct bilirubin 20 mg/dl [342 µmol/l]) and life-threatening hypophosphataemia (serum phosphate 0.5 mg/dl [0.16 mmol/l]), accompanied by inappropriate phosphaturia. The patient also manifested hypouricaemia (serum uric acid 1.7 mg/dl [101 µmol/l]) with renal uric acid wasting and renal glycosuria. This generalized proximal tubular defect may occasionally be seen in deeply jaundiced patients. Therefore, serum phosphate levels should be closely monitored in these patients.     

Beethoven's triad: Diarrhoea,deafness and cirrhosis. A plausible solution to the 195-year-old controversy

Beethoven suffered from episodes of severe diarrhoea starting in his late teens, and increasing deafness from around the age of 28. He died from cirrhosis of the liver at the age of 57 in 1827. The nature of his diseases has been controversial ever since. Until recently, no one has invoked a single disease that would explain the chronic afflictions of his bowel, ears and liver. Suggested diagnoses have included lead poisoning, alcoholic cirrhosis, viral hepatitis, inflammatory eye disease, rheumatism, inflammatory bowel disease, Paget's disease of bone, Cogan's syndrome, systemic lupus erythematosus, otosclerosis, chronic pancreatitis, tuberculosis, sarcoidosis, Whipple's disease, renal papillary necrosis and syphilis. In 2005, Karmody and Bachor suggested that Beethoven suffered from chronic ulcerative colitis and its sequels. It is now known that ulcerative colitis may be complicated by sensorneural deafness and sclerosing cholangitis which progresses to cirrhosis, liver failure and death. These apparently diverse diseases are now believed to share an autoimmune pathogenesis. This explanation neatly joins together Beethoven's triad of diarrhoea, deafness and cirrhosis.