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Objective Previous studies have reported low incidence of carboplatin-related drug fever in early cancer treatment cycles. This study describes and analyzes relatively higher incidence rate of carboplatin-related drug fever associated with gynecologic cancer chemotherapy in order to allay anxiety in patients and avoid unnecessary interventions. Materials and methods All gynecologic cancer cases treated with carboplatin in a women's hospital in 2017 and 2018 were retrospectively reviewed and analyzed. Data for patients who experienced carboplatin-induced drug fever and those who received the same treatment but did not experience drug fever were compared for statistical significance. Risk factors for drug fever were identified by logistic regression analysis. Results In total, 318 females with a mean age of 52 years were included in the analysis. Drug fever was observed in 25 patients (7.86%) in 45 cycles of total 1605 carboplatin-containing infusions. Fever occurred at a median of the third (range: 1–7) cycle, starting at 10.62 h (range: 1.18–50.35 h) after carboplatin infusion, and was generally controlled within 3 days. After chemotherapy rechallenge, the mean frequency of drug fever was 2 times per patient (range: 1–4 times). There were 35/45 drug fever incidents (77.78%) that were classified as grade II; in 15/45 cases (33.33%), antibiotic treatment was immediately initiated to prevent infection. Younger age was found to be a risk factor for drug fever following carboplatin treatment (odds ratio = 0.126, 95% confidence interval: 0.025–0.628; p Conclusions The retrospective analysis demonstrated that carboplatin-induced drug fever, which occurred on post treatment 3 days, was a type of delayed hypersensitivity reaction with an incidence rate of 7.86% in gynecologic cancer. Younger age was identified as a risk factor. Drug fever is generally tolerated by patients, who insist on chemotherapy. Knowledge of carboplatin-induced drug fever may help physicians reach timely recognition for appropriate interventions.

As of October 2020, there is still no specific drug to treat COVID-19 as it rages around the world. Favipiravir, indicated for the treatment of new and re-emerging influenza infections, has been suggested to be effective against SARS-CoV-2, although this has not yet been fully validated. We administered favipiravir to a 64-year-old female patient with COVID-19. Her symptoms resolved quickly after the start of treatment, with reduction of SARS-CoV-2 viral load, but she developed a fever again on day 12. Since the fever was relieved by discontinuation of favipiravir, and based on positive results with a drug-induced lymphocyte stimulation test, we diagnosed her with favipiravir-induced drug fever. Decrease in the serum concentration of favipiravir was observed along with resolution of the fever. The present case suggests that drug fever should be considered in the differential diagnosis of relapsing fever episodes in COVID-19 patients receiving favipiravir.

Resume Propos L’hydroxyuree (HU) est une chimiotherapie antimetabolite frequemment utilisee dans le traitement des syndromes myeloproliferatifs chroniques. Ce traitement est habituellement bien tolere par les patients, mais des cas de fievre induite par l’HU ont ete rapportes dans la litterature. L’objectif de ce travail etait de definir les caracteristiques cliniques et biologiques d’hyperthermie induite par l’HU. Methodes Etude retrospective de quatre cas d’hyperthermie induite par l’hydroxyuree pris en charge dans un service de medecine interne entre 2006 et 2012. Les cas cliniques sont associes a une revue de la litterature dans les bases de donnees de Pubmed et de la Cochrane. Resultats Trente-huit cas, incluant notre serie personnelle, d’hyperthermie induite par l’hydroxyuree ont ete rapportes depuis 1981. L’âge moyen etait de 65 ± 10,9 ans. Il y avait 50 % d’homme. La mediane de survenue de l’hyperthermie etait de 21 jours. La mediane de temperature etait de 40 °C, cliniquement bien toleree. Le syndrome inflammatoire biologique etait modere avec une CRP moyenne a 131 ± 92 mg/L. Un traitement d’epreuve par antibiotherapie probabiliste etait realise chez 34 % des patients. Un test de reintroduction etait realise chez 50 % patients, un seul patient avait un test de reintroduction negatif. Un tiers des patients presentait une atteinte hepatique ou pulmonaire associee. La fievre regressait a l’arret du traitement avec une mediane de 24 heures. Conclusion Les fievres induites par l’hydroxyuree sont stereotypees. Un bilan infectieux standard doit etre propose. Si l’enquete infectieuse est negative, un arret precoce du traitement permet une regression rapide de la symptomatologie permettant de confirmer le diagnostic.

Drug fever (DF) is a febrile reaction induced by a drug without additional clinical features like skin eruption. This adverse drug reaction is probably common but under diagnosed. While its outcome is generally favourable, DF generates unnecessary diagnostic procedures as well as hospitalisations or hospitalisation prolongations. Clinical presentation and biological findings are not specific. Fever is generally well tolerated but may be accompanied by general symptoms mimicking sepsis. Moderate biological disorders could be expected, including elevation or decrease in white blood cell count, eosinophilia, liver cytolysis, and increased C-reactive protein. An infection should be systematically ruled out. Clinical or biological signs of severity should question DF diagnosis. When DF is suspected, the involved drug(s) should be stopped after a reliable assessment of imputability. Antibiotics represent the most often implicated drugs. Fever disappearance after discontinuing the suspected drug is the cornerstone of DF diagnosis. Before stopping the administration of the suspected drug(s), a risk/benefit ratio assessment is necessary. Consistently, it may be complicated to stop an antimicrobial drug when treating an infection or an immunosuppressive drug if required.

The differential diagnosis for fever of unknown origin in solid organ transplantation is vast and includes rejection, malignancy, adrenal insufficiency, drug fever, and infection. A 64 year-old man's post-cardiac transplantation course was complicated by 6 weeks of fevers and failure to thrive. He

PubMedID: 20673585 This prospective multicenter phase III clinical trial was designed to assess efficacy and safety of G-CSF as an adjunct to de novo AML remission induction therapy (www.clinicaltrials.gov. NCT00820976). Patients' characteristics were similar in both arms. G-CSF improved severity and duration of leukopenia. Three-year OS were similar (25.6 ± 5.1% vs. 31.8 ± 5.6%) in both arms except for patients with myeloblastic features. Significant factors for better survival were the use of G-CSF (p= 0.049), female sex (p= 0.05) and single induction cycle (p< 0.001) in multivariate analysis. Female patients performed better than male patients. Better survival obtained among female AML patients needs to be validated within the context of cytogenetic analysis. © 2010 Elsevier Ltd. The authors are indebted to the efforts of all the institutions who participated in the trial and their data management teams. Also the authors would like to thank to all physicians including Dr. Semra Dundar, who died in 2005, and their patients for this collaborative effort. Filgrastim was supplied by Roche, This study was partially supported by the Turkish Academy of Sciences. Monitoring and statistical analysis were performed by an independent clinical research organization (OMEGA, Ankara, Turkey). And a special thank you to the following hospitals and investigators that participated in this trial: Akdeniz University, Antalya, Turkey (L. Undar); Ankara University, Ankara, Turkey (M.B., M.O., O. l., G.G., A.U., H.A., E.A.); Cukurova University, Adana, Turkey (S.P.); Dokuz Eylul University, Izmir, Turkey (B. Undar); Ege University, Izmir, Turkey (S. Cagirgan); Erciyes University, Kayseri, Turkey (A. Unal, M. Cetin); Gulhane Military University, Ankara, Turkey (A. U. Ural, C. Beyan); Hacettepe University, Ankara, Turkey (S. Dundar, O.O., Y.B.); Inonu University, Malatya, Turkey (I. Aydogdu); Istanbul University of Cerrahpasa, Istanbul, Turkey (B. Ferhanoglu); Istanbul University of Istanbul, Istanbul, Turkey (D. Sargin, Sevgi Kalayoglu-Besisik); Marmara University, Istanbul, Turkey (M.B.); Osmangazi University, Eskisehir, Turkey (Z. Gulbas); Uludag University, Bursa, Turkey (A.T., R.A., F.O., T.O.). Contributions : M.B. provided the conception and design of the study, or acquisition of data, or analysis and interpretation of data; drafting the article or revising it critically for important intellectual content and final approval of the version to be submitted; M.O., E.A.S. and A.T. provided the conception and design of the study, or acquisition of data, or analysis and interpretation of data and final approval of the version to be submitted; R.A. and T.O. provided the drafting the article or revising it critically for important intellectual content and final approval of the version to be submitted and O.O, M.B., S.P., Y.B., O.I., F.O., G.G., A.U. and H.A. provided the final approval of the version to be submitted.

A systematic approach is presented for the patient with antibiotic failure. Noninfectious mimics of infection and nontreatable infections must first be excluded. Then, the clinician must identify those patients who have responded but have a surgical component of their infection or have complications separate from their initial infection. Such complications could include drug fever, phlebitis, decubiti, urinary tract infection, aspiration, and pulmonary embolism. Other patients may deteriorate clinically because of incorrect antibiotic coverage, failure of antibiotic to reach the site of infection, local inactivation of antibiotic, paradoxical response, immune compromise, or because they have reached the point of no return.

Fever of unknown origin (FUO) is now often defined as a fever higher than 38.3°C on several occasions during at least 3 weeks with uncertain diagnosis after several obligatory tests. Infection accounts for about one-third of cases of FUO, followed by neoplasm and non-infectious inflammatory diseases. No diagnosis is reached in 25–35% of cases. In patients with periodic fever, this percentage is higher. A diagnostic algorithm is proposed in which the most important steps are history-taking, physical examination and obligatory investigations in a search for potentially diagnostic clues (PDCs). First, factitious fever and drug fever should be excluded. Further diagnostic procedures should be guided by a list of most probable diagnoses. In patients without useful PDCs, certain diagnostic procedures, divided into first-stage and second-stage investigations, should be performed. If no diagnosis is reached and the clinical condition is stable, waiting for new PDCs is recommended. In patients with recurrent fever, diagnosis should comprise only a search for PDCs matching known recurrent syndromes. Scintigraphic methods such as gallium-67 citrate-labelled leucocytes and 18F-fluorodeoxyglucose positron emission tomography (FDG-PET) are often used in patients with FUO. Because of the favourable characteristics of FDG-PET, conventional scintigraphic techniques may be replaced by FDG-PET in institutions where it is available. If undiagnosed fever persists, supportive treatment with non-steroidal anti-inflammatory drugs can be helpful. Most patients with undiagnosed FUO have benign self-limiting or recurrent fever. Other therapeutic trials should be considered only in patients who deteriorate.

The case history of a haemodialysis patient with fever and rigors is presented. This diagnostic problem turned out to be a hypersensitivity reaction to azathioprine, with identical complaints recurring after a rechallenge with azathioprine, findings which resolved on discontinuation of this drug. The more extended indications for use of azathioprine warrant attention to the possibility of side-effects like drug fever.

Although drug fever is a clinical entity that has received considerable attention in textbooks and review articles, only recently have such writings been subjected to critical analysis. In the present review, mechanisms responsible for drug fever are examined. In addition, published characterizations of the syndrome are compared with the results of a recently published systematic analysis of 148 cases of drug fever. This comparison identified a number of important areas in which descriptions of the clinical entity in textbooks and review articles are at odds with the clinical profile exhibited by actual cases of drug fever.

Summary Twenty-three children with influenzal meningitis have been treated at the Charity Hospital in the past two years with sulfadiazine. Sixteen patients have been discharged as cured and have remained well except one patient who developed and still has a residual generalized spasticity. Six fatalities occurred, all in young infants below 8 months of age. In this group only one recovery occurred in an infant 4 months old. In our series no fatalities occurred above the age of 8 months. Since sulfadiazine alone does not seem sufficient in these young infants, it is imperative that type-specific rabbit antiserum be given together with large doses of sulfadiazine. In older infants and children the recovery rate is very high with sulfadiazine alone. Very few spinal punctures and drainages were performed. Leucopenia in one patient, hematuria in one patient, and drug fever in one patient were the only toxic conditions encountered that can be attributed to the drug.