- ISSN 1008-5734
- CN 11-4015/R
- 1999年创刊
- 主管: 中国科学技术协会
- 主办: 中华医学会
Objective: To investigate the clinical characteristics and treatment of fluoroquinolone-induced acute interstitial nephritis. Methods: Clinical data on patients who were definitely diagnosed as having fluoroquinolone-induced acute interstitial nephritis in Department of Medicine and Institute of Nephrology, Peking University First Hospital between January 2002 and September 2010 were collected and retrospectively analyzed. The baseline characteristics, fluoroquinolone usage, combined therapy, laboratory tests, pathological examination of the kidney, and follow-up were recorded. Results: Five patients ［3 males and 2 females with average age of (48.6±6.1) years］ were enrolled in the study. Of them, 3 patients received levofloxacin and 2 received pefloxacin for urinary infections or fever. The duration of the treatment was 1 to 12 days. The time to onset of an elevated serum creatinine level after drug administration was 7 to 15 days ［average (11±3) days］. The patients developed nausea，vomiting，congestive rash， fever, and chills. Laboratory tests showed that 12-60 days after treatment start, the 5 patients developed elevated serum creatinine and urine protein levels, and abnormal urine acidification capability in varying degrees, accompanied by haematuria (4 cases), renal glycosuria (4 cases), elevated urinary α1-MG level（3 cases）, and aseptic leukocyturia（2 cases）.Clinical symptoms disappeared 1 to 2 days after drug withdrawal, but serum creatinine levels, routine urine test results, microscopic examination of urinary sediment, and urine acidification capability did not return to normal. After 1 to 6 weeks of glucocorticoid therapy,serum creatinine levels returned to the normal ranges, urine protein levels decreased, and haematuria, glycosuria and aseptic leukocyturia disappeared, but urinary α1-MG and urine acidification capability in some patients remained abnormal. Conclusion: The clinical presentation of fluoroquinolone-induced acute interstitial nephritis is lack of specificity. Routine blood and urine tests and kidney function test should be performed regularly during the period of fluoroquinolone therapy. If acute interstitial nephritis occurs, the drug should be discontinued immediately, and glucocorticoid therapy might be given.
Statins are broadly used in the prevention of coronary heart disease and ischemic stroke. However, several studies indicate that statins may increase the risk of hemorrhagic stroke. The mechanism might be associated with cholesterol level, microbleed, and pharmacological action of statins. Manifestation of statins-induced hemorrhagic stroke is intracerebral hemorrhage which includes lobar hemorrhage and deep hemorrhage. A previous history of drug use is an important basis for a causal relationship assessment. Treatment measures include drug discontinuation, reducing intracranial pressure, control of blood pressure, and symptomatic treatment.
Leflunomide is an isoxazole agent and has immunosuppressant effects. It is mainly used in treatment of rheumatoid arthritis. Common adverse reactions of leflunomide include gastrointestinal disturbances, elevated liver enzyme levels, hypertension, headache, and alopecia. Recent studies have showed that leflunomide can cause peripheral neuropathy. The time to symptom onset of peripheral neuropathy is about 6 months after leflunomide treatment start. Clinical presentations are bilateral numbness, tingling, burning sensation, and pain in the extremities, cold peripheral extremities, and weakness of the extremities. The mechanism of leflunomide-induced peripheral neuropathy might be related to a direct neurotoxicity of the drug. The risk factors for peripheral neuropathy development include advanced age, diabetes mellitus, and combination therapy. Once symptoms of peripheral neuropathy associated with leflunomide occur，the drug should be withdrawn within 30 days.
Thiourea antithyroid drugs have an inhibitory effect on the production of thyroid hormone and are used in the treatment of hyperthyroidism in clinical practice. The commonly used thiourea antithyroid drugs are methimazole and propylthiouracil. Their adverse reactions include drug eruption, granulocytosis, serious hepatic injures, ANCA-associated vasculitis and teratogenicity. Severe hepatic injures and ANCA-associated vasculitis are mainly related to propylthiouracil, while teratogenicity is caused by methimazole. Methimazole is a first-choice drug for treating children and non-pregnant women with hyperthyroidism, while propylthiouracil is a first-choice drug for treating pregnant and breast-feeding women. The measures of the prevention and treatment of adverse reactions to thiourea antithyroid drugs are as follows: rational drug use, regular monitoring, drug withdrawl immediately after developing related adverse reactions and treatment.
Ceftriaxone is a third generation cephalosporin, and it has a broad-spectrum antimicrobial activity. Ceftriaxone readily forms a precipitate of calcium-ceftriaxone salt with calcium in bile and urine, and this results in formation of pseudostone. Most patients with ceftriaxone-associated pseudolithiasis are asymptomatic. Ultrasonography is the most usual method for the diagnosis of ceftriaxone-associated pseudostone. Review of medical history and drug usage is helpful for an accurate diagnosis. The main risk factors for ceftriaxone-associated pseudolithiasis development include dosage, duration of treatment, rate of intravenous infusion, fasting, and dehydration. Ceftriaxone-associated pseudolithiasis is reversible and resolves spontaneously after drug withdrawal, there is no
need for any operations. Symptomatic treatment should be given, if necessary.
A 44-year-old man took the tuber of Alocasia macrorrhiza by mistake. Several minutes after ingestion of the tuber, he presented with numbness of lip, sore throat, nausea, vomiting, salivation, dyspnea, and dysphonia. Twenty minutes after poisoning, he was hospitalized and diagnosed as having acute laryngeal edema. He received diphenhydramine 20 mg and dexamethasone 5 mg via IV push, followed by an IV infusion of dexamethasone 10 mg. Meanwhile oxygen inhalation, liver protective treatment, and other symptomatic treatment were given. Five hours after poisoning, his symptoms gradually resolved and, 50 days later, he recovered. Alocasia macrorrhiza is a poisonous plant of Alocasia Schott in the family Araceae, and it contains sapotoxin and calcium oxalate which can induce neurological and gastrointestinal disorder after ingestion of the plant. The latent period from exposure to onset of symptoms is 10 to 30 minutes and death might occur in patients with severe poisoning. Skin contact or eye contact with Alocasia macrorrhiza juice can cause pruritus, conjunctivitis, and even blindness. Inhalation of Alocasia macrorrhiza powder can lead to severe mucosal irritation in the eye, nasal cavity, and throat. Poisoning could be diagnosed by the history of contact with the plant and clinical manifestations. There is no specific antidote for Alocasia macrorrhiza poisoning and main management is symptomatic treatment.
Four very-low-birthweight premature infants (a pair of female twins, gestational age 31 weeks; a pair of male twins, gestational age 29 weeks.) received linezolid 10 mg/kg every 8 hours via an IV pump for anti-infective treatment 22-31 days after birth. Patients 1 and 2 were given linezolid alone. Patient 3 was prescribed combination therapy with linezolid, meropenem, and amphotericin B liposome. Patient 4 was administered concomitant use of linezolid and amphotericin B liposome. On days 4, 16, 8, and 10 after drug administration, they all experienced thrombocytopenia and the minimum platelet count was 27×109/L, 74×109/L, 23×109/L, 4×109/L, respectively. Six to seventeen days after linezolid withdrawl and administration of symptomatic treatment, their platelet count returned to normal.
A 72-year-old male patient received an IV infusion of cefoperazone/tazobactam 2 g in 5% glucose 250 ml twice daily for 8 days, an IV infusion of bromhexine 4 mg twice daily for 15 days, oral aminophylline 0.1 g every 8 hours for 17 days, and two chewable tablets of montelukast sodium 10 mg every night for 16 days for acute exacerbations of chronic bronchitis. On day 17, the patient presented with upper limb tremor, especially in fingers. His symptoms was considered to be produced by montelukast sodium chewable tablets and did not recur after drug discontinuation.
A 74-year-old woman with herpes zoster received IM cobamamide 1 mg/d for 3 days, oral vitamine B1 10 mg thrice daily, and oral ribavirin 0.4 g every eight hours. Three days later, the patient developed dizziness, asthenia, and anorexia. Six days later, she experienced dizziness with unconsciousness lasting several seconds, followed by nausea and palpitation. Laboratory examination revealed a Hb level of 75 g/L and a reticulocyte count of 9.2%. Anemia was considered to be associated with ribavirin and then the drug was withdrawn. One week after drug withdrawl, routine blood tests showed a Hb level of 95 g/L and a reticulocyte count of 9.5%. Thirty-seven days after drug withdrawl, her routine blood test results returned to normal and her symptoms improved gradually.
A 7-year-old girl received an IV infusion of cefathiamidine 2.0 g in 0.9% sodium chloride 100 ml once daily and an IV infusion of mezlocillin 2.0 g dissolved in 0.5% glucose 100 ml once daily for nine days for preventing infection after surgery. On day 2 after withdrawl, the patient developed generalized pruritus accompanied by sporadic rashes and low-grade fever. Subsequently, her rash progressively worsen and became purple and more extensive; vesicles with erosion were seen on the lesion surface; the rash mainly involved her trunk, and erosion and purulent exudation were noted in the oral and conjunctival mucosa. She was then hospitalised and treated with azithromycin, fusidic acid, methylprednisolone, human immunoglobulin, and drugs for external use. Her symptoms of skin improved gradually and, two weeks later, she recovered and was discharged.
A 20-year-old man with heart failure received an Ⅳ infusion of deslanoside
0.4 mg twice daily, a slow intravenous injection of amiodarone 75 mg and then a continuous
infusion of 1 mg/min via a pump, and furosemide 20 mg once daily. On day 3 of treatment, he
developed obnubilation and somnolence, his blood pressure was 78/36 mm Hg. Dopamine,
nikethamide, lobeline were given immediately, meanwhile he was placed on a respirator for
assisted respiration. On the same day, his blood digoxin level reached 7.3 μg/L.
Deslanoside, amiodarone, and furosemide were stopped, nasal administration of phenytoin
sodium 0.1 g was given three times daily. On day 5, his blood digoxin level decreased to
0.82 μg/L.
A 52-year-old female patient himself took azithromycin 0.5 g once daily for upper respiratory tract infections. Three days later, the patient developed smell and taste disorders. Azithromycin was discontinued immediately. However, two weeks after cessation of the drug, her sense of smell and taste still did not return.
A 20-year-old man developed palpitations, nausea, vomiting, and dizziness 30 minutes after the patient himself took astemizole 3 mg for pruritus with rash in his entire body. His symptoms relieved after symptomatic treatment. A review of his medical history revealed that the patient had taken 2 doses of astemizole at the same dosage, and his dizziness and palpitation had occurred after taking each dose of astemizole and than the symptoms had spontaneously disappeared.
Four male patients (aged 20,40,22, and 28 years) with chronic superficial gastritis or duodenal ulcer or gastric ulcer received omeprazole 20 mg twice daily. Three of them were given oral omeprazole alone. One of them received combined treatment with omeprazole, azithromycin, and colloidal bismmth pectin. Two days later, they developed dizziness, fatigue, chest distress, and short of breath. Their heart rate decreased to 44 beats/min, 46 beats /min, 46 beats /min, and 44 beats /min, respectively. After discontinuation of omeprazole and administration of IM atropine 0.5 mg 3 times a day, four patients’ heart rate returned to baseline.
A 16-year-old female patient with progressive myoclonic epilepsy developed non-convulsive status epilepticus after receiving oral phenytoin 0.15 g every 12 hours for one week. An EEG showed continuous spike-and-slow-wave complexes in all leads. Seven weeks after that, the patient was admitted to our hospital, her phenytoin dosage was reduced to 0.05 g twice daily at once and then withdrawn 2 days later. At the same time, the patient was given sodium valproate 0.3 g every 8 hours; clonazepam 1mg every 12 hours; levetiracetam 0.25 g every 12 hours. On day 3 of treatment, the patient’s myoclonic seizures disappeared. On day 6 of treatment, the EEG revealed sporadic spike-and-slow-wave complexes and slow waves. Twelve days after admission, the patient’s condition was stable, and she was discharged.
A 59-year-old man developed a temporary skin rash on his lower limbs after taking carbamazepine 0.1 g 1-2 times daily for seven days for tinnitus. His rash disappeared after withdrawal of carbamazepine. Subsequently, he was hospitalised with worsening tinnitus and received oral carbamazepine 0.1 g twice daily and oral mecobalamin 1 mg thrice daily. On day 2 of admission, his temperature was 39.2 ℃ and, on day 3, he presented with a red maculopapular rash on his face, body, and both knees. Biochemical blood tests revealed the following values: ALT 359 U/L, AST 137 U/L, γ-GT 506 U/L, and LDH 273 U/L. Carbamazepine and mecobalamin was stopped. Methylprednisolone and anti-allergic therapy were given. Two day later, his temperature normalized and, five days later, rash and hepatic function improved gradually. On day 9 of admission, the patient had a fever again with a temperature of 38.1 ℃. Later, his rash recurred and progressed to involve his entire body. Laboratory tests showed the following levels: WBC 13.78×109/L with eosinophils 0.113, ALT 187 U/L, AST 45 U/L, γ-GT 374 U/L, and LDH 239 U/L. Carbamazepine-induced hypersensitivity syndrome was diagnosed. Methylprednisolone and human immune globulin were given and his rash and hepatic function improved. On day 16 of admission,the rash reappeared on his lower extremities, and then resolved after administration of methylprednisone and symptomatic treatment.
A 52-year-old woman with acute tonsillitis took oral levofloxacin 0.2 g trice daily. Three days later, the patient developed urinary urgency, urinary frequency, hypogastrium pain, brown urine with blood clot accompanied by dysuria. Laboratory tests showed occult blood (+++) and ultrasonography revealed acute cystitis. Levofloxacin was stopped. On day 2 after drug discontinuation, urine color normalised and, on day 5, routine urine tests were normal. Two weeks later, ultrasonography showed her bladder was normal.
A 46-year-old female patient received aspirin 0.1 g once daily，atorvastatin calcium 10 mg once daily, bezafibrate 0.2 g twice daily, and nifedipine 30 mg twice daily for 10 days for hyperlipidemia and primary hypertension. On day 8 of treatment, the patient experienced muscular pain in both lower limbs and, on day 9, the pain progressed to involve her bilateral shoulder and back, both upper extremities, and then the whole body. Thereafter, she present with aggravated generalised muscular pain, muscle stiffness in both lower limbs, and red-brown urine. Biochemical blood tests showed the following levels: creatine kinase 21 507 U/L, creatine kinase MB 5460 U/L, lactate dehydrogenase 1517 U/L, alanine aminotransferase 194 U/L, aspartate aminotransferase 895 U/L, and creatinine 268 μmol/L. The patient improved after receiving blood purification, urinary alkalinization, as well as liver and kidney protective treatment.
A 34-year-old woman received combined treatment with sulpiride 0.4 g twice daily and trihexyphenidyl 4 mg twice daily for 4 years for schizophrenia. One year ago, the patient repeatedly developed defecation and urination disorders. Her symptoms worsened more than 10 days ago. Physical examination showed mild distension of the lower abdomen and hypoactive bowel sounds. Routine blood tests showed a white blood cell count of 26.7×109/L with neutrophils 0.92. Abdominal ultrasound and CT examinations revealed paralytic ileus and urinary retention. It was considered to be associated with the concomitant long-term use of sulpiride and trihexyphenidyl. Both drugs were stopped and symptomatic and supportive treatments were given. Her symptoms improved and she was discharged.
A 45-year-old male patient himself took devilpepper root decoction(250 ml equivalent to 25 g) thrice daily for sore throat. On day 4 of treatment start, he developed yellowish urine, On day 7, he developed nausea, vomiting, asthenia, anorexia, yellowish skin and sclera. On day 9, he was hospitalized. Laboratory tests showed the following values: ALT 1735 U/L, AST 682 U/L. He was diagnosed with drug-induced hepatitis. Devilpepper root was discontinued immediately and he was given oral Yinzhihuang granule, followed by infusions of glutathione, matrine and diammonium glycyrrhizinate. On hospital day 12, repeat liver function tests revealed the following levels: ALT 97 U/L, AST 32 U/L. He recovered well and was discharged.
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