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PubMed2006

Genetic and environmental contributions to hay fever among young adult twins.

BACKGROUND: The susceptibility to develop hay fever is putatively the result both of genetic and environmental causes. We estimated the significance and magnitude of genetic and environmental contributions to hay fever among young adult twins. METHODS: From the birth cohorts 1953-82 of The Danish Twin Registry 11,750 twin pairs were identified through a nationwide questionnaire survey. Subjects were regarded hay fever cases when responding affirmatively to the question 'Do you have, or have you ever had hay fever?' Latent factor models of genetic and environmental effects were fitted to the observed data using maximum likelihood methods. RESULTS: The overall cumulative prevalence of hay fever was 12.6%. Identical twins were significantly more likely to be concordant for hay fever than were fraternal twins (P<0.001). Additive genetic effects accounted for 71% and non-shared environmental effects accounted for 29% of the individual susceptibility to hay fever. The same genes contributed to the susceptibility to hay fever both in males and in females. In families with asthma, the susceptibility to develop hay fever was, in addition to genes, to a great extent ascribable to family environment, whereas the aetiology of 'sporadic' hay fever was mainly genetic. CONCLUSIONS: The susceptibility to develop hay fever is attributable to major genetic influences. However, effects of family environment and upbringing are also of importance in families where asthma is present. These results indicate that different sub-forms of hay fever may have different aetiologies.

Adolescent↗
PubMed1980

Infection with Mycoplasma hominis in postpartum fever.

A follow-up of 535 patients after vaginal delivery showed that 9% had a fever of 37.7 degrees C or greater, and 2% had a fever of 38 degrees C or more, on two days. The commonest cause of both categories of fever was Mycoplasma hominis infection as defined by a fourfold or greater rise in mycoplasmacidal antibody titre. Among women for whom sera were available this agent caused 50% (14/28) of all fevers and 71% (5/7) of the higher fevers. Absence or low titre (< 1:8) of antibody against M. hominis was the strongest single predictor of otherwise unexplained fever (16/40 patients with low antibody titre were febrile vs 7/50 with high antibody titre, p < 0.01). Among women with absent or low antibody titres, both rise in titre of antibody to this organism and lochial colonisation by it were significantly associated with fever (p < 0.001, p < 0.025, respectively). Standard microbiological and clinical techniques identified probable causes in only 18% (5/28) of all fevers and 29% (2/7) of higher fevers. Patients who had postpartum infection caused by M. hominis remained in hospital 31% longer than the non-infected patients (4.57 vs 3.49 days, p < 0.001). Low antibody to and lochial colonisation with M. hominis occurred together in 17% of patients, who accounted for 71% of all higher fevers. Since these risk factors for postpartum fever can be identified before delivery, prophylactic measures applied selectively to women with these risk factors may prevent a large proportion of postpartum fevers and the excess hospital stay associated with them.

Adult↗
PubMed1994

Doppler echocardiography and the early diagnosis of carditis in acute rheumatic fever.

BACKGROUND: The incidence of acute rheumatic fever in New Zealand remains relatively high. Reliable early diagnosis of carditis is difficult and important in management. AIM: To determine if Doppler echocardiography contributed to the early diagnosis of carditis in acute rheumatic fever. METHODS: Forty-seven patients admitted to hospital with suspected acute rheumatic fever and 19 control patients, with a febrile illness due to a documented non-cardiac bacterial infection, were assessed two days and two weeks following admission. Presence or absence of clinical carditis was determined by a cardiologist unaware of the suspected diagnosis, from clinical examination, chest radiograph, electrocardiogram (ECG) and two dimensional echocardiogram. Doppler echocardiography was then performed and interpreted by a second cardiologist unaware of the diagnosis. After completion of the study the Jones criteria were applied, to categorise the patients with suspected acute rheumatic fever into four groups for the final diagnosis: no acute rheumatic fever, possible acute rheumatic fever, definite acute rheumatic fever without carditis, and definite acute rheumatic fever with carditis. RESULTS: In 19 patients with a final diagnosis of acute rheumatic fever and carditis at the baseline assessment carditis was detected by clinical assessment in 15 patients, compared with 19 patients with evidence of significant valve regurgitation by Doppler echocardiography. Following the two week assessment, all 19 patients had both clinical and Doppler evidence of carditis. Five patients with a final clinical diagnosis of possible acute rheumatic fever or definite acute rheumatic fever without carditis, had a Doppler abnormality detected. There was no clinical or Doppler abnormality in the febrile controls. CONCLUSIONS: Doppler echocardiography is more sensitive than clinical assessment in the detection of carditis in acute rheumatic fever, and can contribute to earlier diagnosis.

Acute Disease↗
PubMed2000

Differential diagnosis of fever of unknown origin in children.

Fever of unknown origin in children follows two main clinical patterns, namely fever of unknown origin and chronic episodic fever of unknown origin. Fever of unknown origin is characterized by daily fever persisting for more than 3 weeks. The main causes are infectious, rheumatologic disorders, and malignancy. Chronic episodic fever of unknown origin is characterized by fever lasting for a few days to a few weeks, followed by a fever-free interval and a sense of well-being. The main causes are familial Mediterranean fever, the hyper-immunoglobulin D syndrome, familial Hibernian fever, Behcet disease, the syndrome of periodic fever, aphthous stomatitis, pharyngitis and adenitis, and cyclic neutropenia.

Behcet Syndrome↗
PubMed1998

[Viral hemorrhagic fever].

Viral haemorrhagic fevers, such as Lassa fever and yellow fever, cause tens of thousands of deaths annually outside the Netherlands. The viruses are mostly transmitted by mosquitoes, ticks or via excreta of rodents. Important to travellers are yellow fever, dengue and Lassa and Ebola fever. For yellow fever there is an efficacious vaccine. Dengue is frequently observed in travellers; prevention consists in avoiding mosquito bites, the treatment is symptomatic. Lassa and Ebola fever are extremely rare among travellers; a management protocol can be obtained from the Netherlands Ministry of Health, Welfare and Sports. Diagnostics of a patient from the tropics with fever and haemorrhagic diathesis should be aimed at treatable disorders such as malaria, typhoid fever, rickettsiosis or bacterial sepsis, because the probability of such a disease is much higher than that of Lassa or Ebola fever.

Dengue↗
PubMed1975

Effects of etiocholanolone-induced fever on plasma antipyrine half-lives and metabolic clearance.

The plasma half-life and metabolic clearance rate of antipyrine, a drug metabolized by hepatic microsomal enzymes, were determined in 33 normal volunteers during a basal state and during fever induced with a single intramuscular injection of etiocholanolone. Of the 14 normal volunteers who achieved significant fever (fever index greater than 50), in 11 plasma antipyrine half-life was prolonged after a single oral dose of 10 mg/kg and antipyrine metabolic clearance rate was decreased. There was no significant change of these mean values in 19 normal volunteers who failed to develop significant fever (fever index smaller than 50). Therefore, under the conditions of this study plasma antipyrine half-life was prolonged, probably due to impaired hepatic metabolism, during etiocholanolone-induced fever, although no correlation was observed between the magnitude of fever and the extent to which plasma antipyrine half-life was prolonged. Failure to obtain such a correlation may be attributable to the very small range of temperature elevation, extending from 37.9 degrees C to 39.2 degrees C, in the group of 14 subjects achieving significant etiocholanolone-induced fever (fever index greater than 50). A higher dose of antipyrine (18 mg/kg) suppressed induction of fever by etiocholanolone; antipyrine is the only orally administered drug thus far shown to be effective in repressing etiocholanolone-induced fever.

Adolescent↗
PubMed2005

Neoplastic fever: a neglected paraneoplastic syndrome.

Neoplastic fever, a paraneoplastic syndrome caused by cancer itself, represents a diagnostic challenge for the clinician and is an important issue in supportive oncology. Timely recognition of this febrile condition by differentiating it from other cancer-associated fevers, such as infection and drug reaction, is essential for effective patient management. Although the pathophysiology of neoplastic fever is not well understood, it is suspected to be cytokine mediated. In clinical practice, when a patient with cancer presents with unexplained fever, extensive diagnostic studies are needed to differentiate neoplastic fever from nonneoplastic fever. Only after excluding identifiable etiologies of fever can the diagnosis of neoplastic fever be suspected. According to our experience, the naproxen test is a safe and useful test in differentiating neoplastic fever from infectious fever in patients with cancer. In addition, naproxen and other nonsteroidal anti-inflammatory drugs have been effective in the management of neoplastic fever and offer a significant palliative benefit for the patient.

Anti-Inflammatory Agents, Non-Steroidal↗
PubMed1993

Fever of nosocomial origin: etiology, risk factors, and outcomes.

OBJECTIVES: To identify the etiologies and risk factors associated with fever of nosocomial origin and compare the outcomes of patients with and without nosocomial fever. DESIGN: A prospective study with a case-control component. SETTING: The three medical services of a university hospital. PATIENTS AND METHODS: We evaluated 100 patients with fever of nosocomial origin. Etiologies were assigned by the consensus of three independent reviewers using Centers for Disease Control guidelines. Predictors of bacterial etiology were identified using logistic regression methods. Controls matched for age (+/- 5 years), sex, and comorbidity were identified for 65 of the nosocomial fever cases. Cases and controls were compared with conditional logistic regression to identify risk factors for fever of nosocomial origin. Cases and controls were followed at 1 month to compare length of stay, mortality, and hospital readmission rates. MEASUREMENTS AND MAIN RESULTS: An etiology was assigned in 81 cases: 51 had bacterial infection, 5 had nonbacterial infection, and 25 had a noninfectious etiology. Multivariate predictors of bacterial infection were the presence of diabetes mellitus (odds ratio [OR] = 5.74; 95% confidence interval of the odds ratio [CI] = 1.61 to 20.40), length of stay to fever onset after admission greater than 10 days (OR = 3.98, CI = 1.04 to 15.22), maximum temperature greater than 38.7 degrees C (OR = 3.37, CI = 1.28 to 8.88), and white blood cell count greater than 10 x 10(9)/L (OR = 4.64, CI = 1.68 to 12.77). Comparison of cases and controls indicated that patients with nosocomial fever had more invasive procedures in the 72 hours preceding enrollment in the study than controls (OR = 1.46, CI = 1.03 to 2.08). Although cases were hospitalized almost twice as long as controls (21.5 versus 12.5 days; p < 0.0001), neither 30-day mortality nor hospital readmission rates differed between cases and controls. CONCLUSION: Nosocomial fever often does not represent nosocomial infection and may constitute a wide variety of other conditions. Since bacterial etiology of fever is a major concern, clinical and laboratory findings can be used to predict patients at high risk for an infectious process. A reduction in the number of invasive procedures may decrease the incidence of nosocomial fever. New-onset nosocomial fever leads to an increase in length of hospital stay but is not a significant predictor of mortality.

Case-Control Studies↗
PubMed1995

Unexplained fever after aortic valve replacement with cryopreserved allografts.

The incidence of fever of unknown origin was studied in 3 groups of patients undergoing aortic valve replacement. Fever of unknown origin was defined as a fever greater than 38.3 degrees C detected after the third postoperative day and which initiated a negative "fever work-up." Fifty patients underwent aortic valve replacement using cyropreserved allografts. Of the 49 patients who survived the operation, 13 (26%) developed fever of unknown origin. Only 1 (2%) of 51 patients, and 4 (8%) patients undergoing aortic valve replacement with a mechanical prosthesis and porcine xenograft, respectively, developed fever of unknown origin (p = 0.0034). Fever of unknown origin after allograft aortic valve replacement developed between the fourth and sixth postoperative days, with no other associated symptoms or signs. It lasted for 24 to 48 hours, and resolved without treatment. Univariate analysis revealed that fever of unknown origin occurred in younger patients (39.9 +/- 9.4 versus 50.8 +/- 11.8 years of age). The mean white blood cell count in fever of unknown origin and afebrile patients were similar (10.4 +/- 3.2 and 8.9 +/- 2.3, p = NS), both of which were significantly lower than the white blood cell count in patients with documented infection (15.0 +/- 5.2, p = 0.02; p < 0.001). No association could be demonstrated between the fever of unknown origin and gender, previous endocarditis, operative technique, cardiopulmonary bypass or cross-clamp times, ABO match, or perioperative blood transfusions. We conclude that a significant number of patients undergoing allograft aortic valve replacement develop noninfectious postoperative fever. The etiology remains unknown, but low-grade rejection cannot be excluded.

Adult↗
PubMed1996

Hypothalamic prostaglandin E2 during lipopolysaccharide-induced fever in guinea pigs.

Prostaglandin E2 (PGE2) is postulated to be a central mediator of fever. It is generally believed that it is produced in the preoptic area of the anterior hypothalamus (POA) because, among other evidence, its level increases both in the third ventricle and in the POA in response to pyrogens. However, lately, the question has arisen whether PGE2 might, in fact, be formed outside of the brain substance and then penetrate it, in particular through the organum vasculosum laminae terminalis. If produced outside the brain substance, the peripheral blockade of its synthesis should prevent lipopolysaccharides (LPS)-induced fever, whereas the intracarotid infusion of PGE2 should produce an increase in core temperature (T(C)) as well as in preoptic PGE2. To verify this hypothesis, continuous measurements of T(C) and preoptic PGE2 levels were made in conscious guinea pigs administered the PGE2 synthase inhibitor, indomethacin (10 or 50 mg/kg, im) 30 min before S. enteritidis LPS (2 mu g/kg, iv) or before PGE2 microdialyzed into the POA (1 mu g/mu l at 2 mu g/min for 2.5 h) and during PGE2 infused into a carotid artery (1 mu g and 10 mu g/mu l at 2 mu g/min for 1 h). LPS induced a biphasic 1.4 degrees C fever that was consistently associated with an increase in the level of PGE2 in the POA. Indomethacin at 10 mg/kg attenuated the course of the LPS-induced fever and prevented the associated increase in preoptic PGE2 for 90 min after fever onset; thereafter, PGE2 was significantly reduced by comparison with controls. Indomethacin at 50 mg/kg completely abolished both the fever and the increased levels of PGE2 in the POA; the fever induced by PGE2 microdialyzed into the POA was not affected by indomethacin pretreatment The intracarotid infusion of PGE2 produced T(C) falls and no increase in preoptic PGE2 levels. The indomethacin-induced blockade of fever and inhibition of the associated increase in preoptic PGE2 levels further substantiates the presumptive link between PGE2 in the POA and fever caused by LPS. The failure of exogenous PGE2 infusion to induce increases in T(C) and preoptic PGE2 levels excludes the possibility that PGE2 formed outside of the brain penetrates the POA and induces fever. Thus, in guinea pigs, the PGE2 associated with LPS-induced fever may be synthesized in the POA.

Animals↗
PubMed2006

Influence of ambient temperature on peripherally induced interleukin-1 beta fever in young and old rats.

We have previously demonstrated that old and young rats mount similar fevers after intraperitoneal (i.p.) LPS injection at a warm ambient temperature (Ta) of 31 degrees C, but not at a cooler Ta of 21 degrees C. LPS stimulates the synthesis and release of proinflammatory cytokines, particularly interleukin-1 beta (IL-1 beta), necessary for fever development, and possibly this is attenuated at the lower Ta. If so, then administration of exogenous IL-1 beta should enable old rats to mount fevers equivalent to those of young rats regardless of Ta. Here, young (3-5 months) and old (23-29 months) Long-Evans rats were maintained at Ta 21 or 31 degrees C for 3 days prior to i.p. or intravenous (i.v.) injection of rat recombinant IL-1 beta (1 microg/kg) or vehicle. Three days later, rats were given the alternate injection at the same T(a). At least 5 days later, the same rats were injected at the other Ta. Body temperature was continuously monitored throughout the experiments. Young rats mounted fevers after LPS at both Ta's and i.p. fevers were lower than i.v. fevers. Old rats developed fevers that were equivalent to those of young rats at 31 degrees C regardless of route of administration, but no fever responses were evident at 21 degrees C. These data suggest that the attenuated fever of old rats is not due to an inability to produce IL-1 beta, but rather to a deficiency further along in the fever pathway. In addition, these results show that, as with LPS, Ta plays a role in the ability of old rats to mount fever in response to IL-1 beta.

Aging↗
PubMed1995

Reliability of infrared tympanic thermometry in the detection of rectal fever in children.

STUDY OBJECTIVE: Recently published clinical guidelines for the management of febrile children are based on studies that used rectal temperature data to stratify the risk of bacteremia and septic complications. Appropriate management decisions rely on accurate detection and categorization of fever. Accordingly, this study compared the newer infrared tympanic thermometry (ITT) to rectal thermometry in this regard. DESIGN: Prospective observational study. SETTING: Urban teaching hospital ED with annual census of 60,000. PARTICIPANTS: Consecutive children 6 months to 6 years old who had rectal temperatures measured. INTERVENTIONS: Triage nurses recorded rectal temperatures and bilateral ITT temperatures. Temperatures were correlated by Pearson correlation coefficients and compared using paired t tests with significance set at P < .01. Children were categorized by degree of fever using rectal temperature (afebrile, less than 100.4 degrees F; low fever, 100.4 to 102.9 degrees F; and high fever, more than 102.9 degrees F), and the accuracy of ITT in detecting fever and high fever was determined. RESULTS: Three hundred seventy patients were enrolled in the study. The mean age was 18.4 +/- 11.3 months; boys comprised 56% of patients. The mean temperatures were rectal, 101.0 +/- 2.0 degrees F; right tympanic membrane, 100.4 +/- 1.9 degrees F; and left tympanic membrane, 100.3 +/- 1.9 degrees F. The tympanic membrane temperatures were significantly lower than rectal readings (P << .001 for both right and left versus rectal). Rectal temperatures showed good correlation with both right and left tympanic membrane temperatures (r = .83 and .85, respectively). ITT was 76% sensitive and 92% specific in detecting fever of 100.4 degrees F or more (positive predictive value, 0.92; negative predictive value, 0.76). In the detection of high fever, ITT was only 57% sensitive but 98% specific (positive predictive value, 0.90; negative predictive value, 0.90). Rectal and TM temperatures differed by at least 0.5 degree F in 70% of the patients, 1.0 degree F in 41%, 2.0 degrees F in 12%, and 3.0 degrees F in 3%. CONCLUSION: Despite the statistical correlation between ITT and rectal temperatures, the modalities may yield significantly different temperatures. The poor sensitivity of ITT in detecting fever and high fever may result in clinically important miscategorizations of individual patients. Current clinical management that is based on the presence and height of fever may be adversely affected if ITT is used.

Child↗
PubMed2000

Association between epidural analgesia and intrapartum fever.

The objective of this paper is to determine whether or not epidural analgesia is an independent risk factor for intrapartum fever. Maternal temperature was measured every 4 h during labor to 1004 consecutive women in term labor. Women with fever or on antibiotics were excluded. Epidural analgesia was administered upon patients' request. Of the 406 (40%) women who received epidural analgesia, 11.8% (n = 48) developed a fever > or = 37.8 degrees C during labor compared with only 0.2% (n = 1) of women not receiving epidural analgesia. Women who received epidural analgesia were more likely to have one or more risk factors for intrapartum infection. Their labor and ruptured membranes were longer, they were more likely to have internal monitoring and have more vaginal examinations. Compared with women who received epidural analgesia and did not develop intrapartum fever, women that did develop fever had longer epidurals and more risk factors for infection. However, in a logistic regression analysis with fever as dependent variable, only the duration of epidural was significantly associated with the occurrence of fever. The rate of fever increased with longer labors, from 5% with labor < 3 h to 28% with labor > 6 h. In 90% of women the fever resolved within a few hours after delivery. Sepsis evaluation was negative in all of the newborns to mother who had intrapartum fever. Our data support a noninfectious etiology for intrapartum fever in the vast majority of our patients. However, infection must be ruled out before a decision is made to withhold antibiotic therapy.

Adult↗
PubMedDate not supplied

Hemorrhagic fevers, with special reference to recent outbreaks in southern Africa.

In considering the diagnosis of a patient admitted to the Johannesburg Hospital, suffering from an illness characterized by high fever and complicated by a hemorrhagic state from which he died, a list of possible causes of his illness was drawn up. This list included the arthropodborne viral infections prevalent in southern Africa, namely, chikungunya fever, Sindbis fever, West Nile fever, yellow fever, and Rift Valley fever; viral infections associated with rodents, such as Lassa fever; the viral infection associated with monkeys, Marburg virus disease; the rickettsial infections; tick-bite fever (the variety of spotted fever of tick typhus occurring in southern Africa) and Q fever; the bacterial infections, especially the coccal infections, plague septicemia, and meningococcal, staphylococcal, and streptococcal septicemia; and the blood protozoal infections malaria and trypanosomiasis. In addition, rubella, Gasser's syndrome, Henoch-Schönlein purpura, and viperine snakebite were briefly described in this review. All of these conditions may be complicated by the development of a hemorrhagic state. The circulation of large numbers of infecting organisms, by they viruses, rickettsiae, bacteria, or protozoa, may initiate the coagulation cascade, the formation of fibrin and its deposition in the finer blood vessels, and the aggregation and entanglement of platelets resulting in marked thrombocytopenia and bleeding. This bleeding tendency is greatly aggravated when the infection specifically involves the parenchymal cells of the liver; such a condition results in defective formation of coagulation factors such as prothrombin. The proper care of patients in whom a hemorrhagic state has developed requires urgent and accurate diagnosis followed by immediate and appropriate treatment that will combat the infection and alleviate the hemorrhagic state and liver disorder. If the hemorrhagic state is due to one of the dangerous infectious fevers, adequate protection of the medical, nursing, and laboratory staff concerned is also vital.

Adolescent↗
PubMed2005

Fever in pulmonary embolism.

This study was planned to investigate the characteristics of clinical and laboratory findings of patients with fever diagnosed as pulmonary embolism (PE) in comparison with PE patients without fever and patients with community-acquired pneumonia (CAP). Thirty-nine PE patients with fever without other identifiable causes (18 received antibiotics and 21 did not receive antibiotics) (study groups) were included in the study. 22 patients with PE without fever and 21 patients diagnosed with CAP were retrospectively selected as control groups. Daily peak body temperature, risk factors for PE, symptoms, and physical and laboratory findings at admission were recorded. Patients with CAP demonstrated higher body temperature than PE patients with fever (38.5+/-0.6 versus 37.8+/-0.6 degrees C, P=0.0001). Fever patterns were similar between the three groups of patients who had fever. The leukocyte count and the erythrocyte sedimentation rate (ESR) were slightly higher in the group of PE with fever versus PE without fever (11,465.6+/-4229.4/mm, 51.1+/-34.7/mm/h versus 10,777.3+/-4927.6/mm, 35.2+/-30.1/mm/h, respectively) (P>0.05). The group of CAP showed significantly highest values of leukocyte count and ESR (15,490.5+/-5606.3/mm, 69.1+/-35.9/mm per h, respectively) (P<0.05). This study suggested that fever might accompany with PE. The presence of slight leukocytosis and increased ESR may not securely differentiate PE patients with fever from patients with CAP.

Adolescent↗
PubMed1998

The use of knockout mice to understand the role of cytokines in fever.

1. In most instances, data obtained using knockout mice to dissect the role of cytokines in fever are similar to data obtained by other, more traditional experimental techniques. 2. Interleukin (IL)-1beta appears to be critically involved in fever caused by some routes of infection/inflammation (e.g. localized inflammation with turpentine). This cytokine has only a small role in fevers caused by i.p. injection of lipopolysaccharide (LPS). These IL-1beta-induced fevers in knockout mice appear to be via the induction of IL-6, similar to LPS-induced fevers in rats. Interleukin-6 also appears to be critically involved in turpentine-induced fever. 3. The precise role of tumour necrosis factor (TNF) in fever is controversial. Data obtained from knockout mice lacking both TNF receptors do not support a pyrogenic role for TNF in fever either to i.p. injection of LPS, s.c. injection of turpentine or following caecal ligation and puncture. 4. The roles of these cytokines in fevers induced by injection of LPS, IL-1beta, turpentine and caecal ligation and puncture are summarized. The data show the complexity of the febrile response. Depending on the types of inflammatory/infectious stimuli, different cytokines play important roles. Because other cytokines are thought to be involved in fever (e.g. macrophage inflammatory protein, interferons), considerable work is still needed to dissect the precise roles of cytokines in fever.

Animals↗
PubMed2001

Familial Mediterranean fever and menstruation.

OBJECTIVE: To study the prevalence, the nature and the genotype correlation of menstruation associated familial Mediterranean fever attacks. METHODS: One hundred and forty-one female patients with familial Mediterranean fever were studied. A questionnaire regarding the presence and nature of menstruation associated with familial Mediterranean fever was designed and filled in by the authors during the patients' visits to the familial Mediterranean fever clinic. The patients who had a positive history for this manifestation were analysed for their familial Mediterranean fever mutations. RESULTS: Ten out of 141 familial Mediterranean fever female patients (7%) had menstruation-associated familial Mediterranean fever attacks. These patients varied in their disease age of onset and disease duration. Increase of colchicine dose, daily or during the perimenstrual period or oral contraceptives were beneficial in preventing these familial Mediterranean fever attacks. No correlation was found with specific mutations causing familial Mediterranean fever. CONCLUSIONS: Menstruation-associated familial Mediterranean fever attacks are relatively uncommon. They are not related to the age of the women, the chronicity of their disease or to the mutations they bear. Various therapeutic approaches have to be tried in order to abolish these attacks. A decrease in oestrogen level during menstruation may have a role in this unique manifestation of familial Mediterranean fever.

Adolescent↗
PubMed1996

The role of TNF-alpha in fever: opposing actions of human and murine TNF-alpha and interactions with IL-beta in the rat.

1. The role of tumour necrosis factor-alpha (TNF-alpha) in fever is controversial. Some studies have indicated that TNF-alpha acts as a cryogen to inhibit fever, while others suggest that TNF-alpha is an endogenous pyrogen which mediates fever. The majority of studies in experimental animals supporting a cryogenic action have been conducted using human (h)TNF-alpha, which has been shown to bind only to one (p55) of the two TNF-alpha receptors in rodents. 2. The aim of the present investigation was to study the role of TNF-alpha in fever by comparing effects of hTNF-alpha, which binds only to the p55 receptor, with those of murine (m) TNF-alpha, which binds to both p55 and p75 TNF-alpha receptors, and to investigate the relationship between TNF-alpha and interleukin-1 (IL-1), an important endogenous pyrogen. 3. Injection of hTNF-alpha (0.3-10 micrograms kg-1, i.p.) had no effect on core temperature in conscious rats (measured by remote radiotelemetry), whereas mTNF-alpha (3 micrograms kg-1) induced fever which was maximal 1 h after the injection (38.2 +/- 0.2 degrees C compared to 37.3 +/- 0.1 degrees C in controls). Intracerebroventricular (i.c.v.) administration of either form of TNF-alpha elicited dose-dependent fever at doses higher than 0.12 microgram kg-1. 4. Peripheral injection of hIL-1 beta (1 microgram kg-1) resulted in fever (38.3 +/- 0.2 degree C compared to 37.2 +/- 0.1 degrees C in controls at 2 h), which was significantly attenuated (P < 0.01) by co-administration of a sub-pyrogenic dose of hTNF-alpha (1 microgram kg-1), but was unaffected by co-administration of mTNF-alpha (0.1 or 0.3 microgram kg-1, i.p.). In contrast, intracerebroventricular (i.c.v.) co-administration of a sub-pyrogenic dose (0.12 microgram kg-1) of hTNF-alpha did not attenuate fever induced by intraperitoneal (i.p.) injection of IL-1 beta, and sub-pyrogenic dose (0.12 microgram kg-1, i.c.v.) of mTNF-alpha significantly prolonged the febrile response to IL-1 beta. Pretreatment of animals with anti-TNF-alpha antiserum (i.c.v.) did not affect the febrile response to systemic IL-1 beta. 5. Animals injected i.p. with a pyrogenic dose of mTNF-alpha developed fever (38.2 +/- 0.2 degrees C compared to 37.3 +/- 0.1 degrees C in controls 2 h after the injection) that was completely abolished by peripheral administration of IL-1ra (2 mg kg-1, P < 0.001), while i.c.v. administration of IL-1ra (400 micrograms/rat) did not affect mTNF-alpha-induced fever. 6. These data indicate that endogenous TNF-alpha is probably a pyrogen and that previous results suggesting cryogenic actions of TNF-alpha resulted from the use of a heterologous protein in the rat. The markedly contrasting effects of mTNF-alpha and TNF-alpha could result from different interactions with the two TNF-alpha receptor subtypes. The data also suggest that fever induced by exogenous TNF-alpha is mediated via release of IL-1 beta in peripheral tissues, but not in the brain.

Animals↗