Papilledema secondary to vestibular schwannoma: An atypical case without intracranial hypertension.

In most cases, vestibular schwannomas with papilledema are associated with intracranial hypertension secondary to hydrocephalus (obstructive or communicating). We describe the atypical case of a 39-years-old man who presented with bilateral papilledema revealing a vestibular schwannoma, but without hydrocephalus and with normal intracranial pressure. Ophtalmologic signs were completely resolved after tumor removal. The pathophysiological mechanism generally described to explain bilateral papilledema in such cases is tumor-induced hyperproteinorachia. However, in the absence of hydrocephalus or intracranial hypertension, this case raises the question of the mechanisms involved in the visual impairment related to vestibular schwannoma.

Late infective endocarditis after transcatheter tricuspid valve-in-valve implantation: A pediatric case report.

In patients with congenital heart diseases, new procedures, such as transcatheter valve replacement, have been associated with a non-negligible incidence of infective endocarditis (IE): up to 4% patient-year IE incidence. Prosthetic IE after percutaneous tricuspid valve replacement (PTVR) has been scarcely reported. We report the first pediatric case of IE after percutaneous tricuspid Melody™ valve-in-valve implantation in a boy who was diagnosed with Eisenmenger syndrome, related to patent ductus arteriosus. This first pediatric case of late IE (4 years) after PTVR is added to eight previously reported cases of IE from the valve-in-valve international database registry (VIVID registry).

Respiratory syncytial virus-associated mortality in a healthy 3-year-old child: a case report.

BACKGROUND: Respiratory syncytial virus (RSV) is the most frequently identified pathogen in children with acute lower respiratory tract infection. Fatal cases have mainly been reported during the first 6 months of life or in the presence of comorbidity. CASE PRESENTATION: A 47-month-old girl was admitted to the pediatric intensive care unit following sudden cardiopulmonary arrest occurring at home. The electrocardiogram showed cardiac asystole, which was refractory to prolonged resuscitation efforts. Postmortem analyses detected RSV by polymerase chain reaction in an abundant, exudative pericardial effusion. Histopathological examination was consistent with viral myoepicarditis, including an inflammatory process affecting cardiac nerves and ganglia. Molecular analysis of sudden unexplained death genes identified a heterozygous mutation in myosin light chain 2, which was also found in two other healthy members of the family. Additional expert interpretation of the cardiac histology confirmed the absence of arrhythmogenic right ventricular dysplasia or hypertrophic cardiomyopathy. CONCLUSIONS: RSV-related sudden death in a normally developing child of this age is exceptional. This case highlights the risk of extrapulmonary manifestations associated with this infection, particularly arrhythmia induced by inflammatory phenomena affecting the cardiac autonomic nervous system. The role of the mutation in this context is uncertain, and it is therefore necessary to continue to assess how this pathogenic variant contributes to unexpected sudden death in childhood.

Chikungunya disease among infants in French West Indies during the 2014 outbreak.

BACKGROUND: We aimed to describe the clinical and laboratory features of Chikungunya disease in infants aged from 1 month to 2years. METHODS: This epidemiologic study was carried out at the Pointe-à-Pitre University Hospital from May to September 2014. We collected data prospectively from infants hospitalized for Chikungunya disease. RESULTS: A total of 154 infants were included. Hyperthermia was greater than 38.5°C the first 48h and during on average 2.7 days. Pain (on mobilization and/or cutaneous hyperesthesia and/or arthralgia) was present in 82% of the cases. Loss of appetite was reported for 62% of the infants. Initial maculopapular erythematous eruption occurred in 69% of the cases. A vesiculobullous eruption was secondarily observed in 7% of the cases. Edema on the feet and/or hands was present in 48% of the cases. Febrile seizure was observed in 12% of the cases. Lymphopenia was the most frequent laboratory finding, present in 94% of the infants. No cases of thrombocytopenia were observed. The reported complications were: bullous epidermolysis, state of epilepticus, and severe acute hepatitis. CONCLUSION: This study highlights a suggestive clinical presentation of Chikungunya diseases combining pain, fever, tachycardia, foot and/or hand edema. Lymphopenia, monocytosis, and the absence of thrombocytopenia were relevant biological signs.

Photobiomodulation of pain and inflammation in microcrystalline arthropathies: experimental and clinical results.

OBJECTIVE: This article presents the results of laser therapy in crystal (hydroxyapatite, calcium pyrophosphate, and urates) deposition-induced arthritis in rats and the clinical applications in humans. BACKGROUND DATA: Microcrystalline arthropathies are prevalent among geriatric patients, who are more vulnerable to the side effects of drugs. The effectiveness of laser therapy for pain relief, free of side effects, has been reported in painful conditions. METHODS: Two milligrams of each of the above-mentioned crystals was injected in both joints of the back limbs in three groups of rats; these groups were then treated with laser irradiation. Three other groups received no treatment after the injections. We determined the plasmatic levels of inflammatory markers (fibrinogen, prostaglandin E2, and TNF(alpha)), tissues (prostaglandin E(2)) and conducted anatomopathological studies. Twenty-five patients with acute gout arthritis were randomized into two groups and treated over 5 days: group A, diclofenac 75 mg orally, twice a day; and group B, laser irradiation once a day. Forty-nine patients with knee chronic pyrophosphate arthropathy were randomized into two groups and treated over 21 days; group A, diclofenac 50 mg orally, twice a day; and group B, laser irradiation once a day. Thirty patients with shoulder chronic hydroxyapatite arthropathy were randomized into two groups and treated over 21 days; group A, diclofenac 50 mg orally, twice a day; and group B, laser irradiation once a day. RESULTS: Fibrinogen, prostaglandin E(2), and TNF(alpha) concentrations in the rats injected with crystals and treated with laser decreased significantly as compared with the groups injected with crystals without treatment. Both laser therapy and diclofenac achieved rapid pain relief in patients with acute gouty arthritis without significant differences in efficacy. Laser therapy was more effective than diclofenac in patients with chronic pyrophosphate arthropathy and in patients with chronic apatite deposition disease. CONCLUSION: Laser therapy represents an effective treatment in the therapeutic arsenal of microcrystalline arthropathies.

He-Ne laser on microcrystalline arthropathies.

OBJECTIVE: The objective of this work is to assess the anti-inflammatory capacity of He-Ne laser therapy as determined by the plasmatic levels of inflammatory markers, fibrinogen, and TNFalpha and by histopathological study in rats with arthropathy induced by calcium pyrophosphate crystals. BACKGROUND DATA: Microcrystalline arthropathies are a group of diseases characterized by the deposit of different crystals in joints. MATERIALS AND METHODS: Two milligrams of dicalcium pyrophosphate crystals (DCPP) were injected in both joints of the lower limbs of rats during 2 days. A group was treated with laser of He-Ne (6 mW) on the injected joints during 3 consecutive days. After 96 h of the first injection, animals were sacrificed to determine TNFalpha using the ELISA method and fibrinogen was assessed using spectrophotometry. Sections from the lower limbs were used for histopathology. RESULTS: A statistically significant increase (p < 0.001) in plasma fibrinogen levels and TNFalpha was noted between the control group and the laser-treated group. The histological transversal section of a posterior limb joint of a rat injected with DCPP showed fibroadipose tissue with diffuse chronic infiltrate. The histopathology of the group of rats injected with DCPP and subsequently treated with He-Ne laser showed no inflammatory response. CONCLUSION: He-Ne laser treatment in the microcrystalline arthropathy induced in rats by DCPP injection might have an antiinflammatory effect, evaluated by fibrinogen plasma levels and TNF-alpha (inflammatory markers) and by the histopathology regressive process.

Effects of diclofenac sodium and He:Ne laser irradiation on plasmatic fibrinogen levels in inflammatory processes.

OBJECTIVE: The aim of the present work was to determine the possible synergic effect on the concentration of plasma fibrinogen (PF) by injecting diclofenac sodium associated with laser therapy postsurgery. SUMMARY BACKGROUND DATA: Nonsteroidal anti-inflammatory drugs (NSAIDs) and He:Ne laser irradiation as a therapy were used to inhibit the effects generated by inflammation. Tissue injury produces significant increases in PF levels, which are reduced to normal values by administration of NSAIDs or laser irradiation of the injured zone. MATERIALS AND METHODS: Rate were divided into groups in which different presurgical and postsurgical treatment were used; the inflammation was induced by laparotomy. RESULTS: Parenteral diclofenac or He:Ne laser irradiation used separately in normal rats did not produce changes in the PF levels. Diclofenac and laser irradiation combined postsurgery produced a significant reduction of PF levels compared with normal values, or with groups that were injected or irradiated postsurgically. CONCLUSION: The inflammatory response could be reduced by the effect of the diclofenac sodium upon the COX-2/COX-1 inhibitory relation associated with the photobiological effect of the He:Ne laser.

Interactions of prostaglandin E1, bradykinin and histamine and the increase of plasma fibrinogen in rats.

Considering that tissue injury caused by laparotomy significantly increases the liver synthesis of plasma fibrinogen, and that PGE1, bradykinin and histamine are released into the injured tissues, the effect of above mentioned inflammatory agents and of the adrenal medulla on plasma fibrinogen levels in rats was studied. The subcutaneous administration of PGE1, bradykinin or histamine does not modify plasma fibrinogen levels acting independently comparing with non-injected animals or injected with the drug vehicle. Bradykinin + histamine did not modify plasma fibrinogen levels either. However the administration of prostaglandin E1 + bradykinin + histamine reproduced the increase of fibrinogen characteristics of laparotomy. This increase was partially but significantly inhibited in rats that had undergone bilateral removal of the adrenal medulla or administration of PGE1 + bradykinin + histamine + bupivacaine (a local anesthetic), but it was not modified when the adrenal medullectomy was unilateral. It is concluded that plasma fibrinogen increase is obtained only when PGE1 acts in presence of bradykinin or histamine and the adrenal medulla should be partially responsible for said increase.

Rôle of histamine on plasma fibrinogen levels in rats with surgical injury (laparotomy).

The probable rôle of endogenous histamine in the increase of plasma fibrinogen in rats submitted to tissue injury (laparotomy) was studied. In laparotomized rats with 10 mg kg-1 day-1 of diphenhydramine (a H1-histamine receptor blocker) plasma fibrinogen decreased significantly as compared to the group of rats laparotomized only (P less than 0.02), reaching values similar to those observed in rats laparotomized with removal of the adrenal medulla or laparotomized with severing of splanchnic nerves. There is a significant difference between these latter groups and the normal noninjured group (P less than 0.01). Plasma fibrinogen did not modify (as compared with the uninjured group) in rats injected only with histamine (1 mg kg-1 day-1) or with diphenhydramine. Taking into account the results obtained and the mechanism of action of diphenhydramine, it would seen that endogenous histamine takes part in the increase of plasma fibrinogen in laparotomized rats, perhaps indirectly through stimulation of the adrenal medulla secretion.

Effects of indomethacin on plasma fibrinogen levels in rats with tissue injury.

The present investigation was designed to study the effect of indomethacin (5 mg kg-1 day-1) on plasma fibrinogen levels in laparotomized rats. Whereas tissue injury significantly increased plasma fibrinogen when compared to normal uninjured rats, indomethacin completely blocked that effect. Conversely, indomethacin did not prevent fibrinogen increase in laparotomized rats injected with epinephrine, with spinal cord transection + epinephrine or with adrenal medullectomy + epinephrine. Indomethacin or epinephrine administration to normal rats did not modify plasma fibrinogen. Taking into account that epinephrine is a key hormone in plasma fibrinogen response in laparotomized rats, and according to our results, prostaglandins might act by two possible pathways: 1) by decreasing of the pain threshold of the sensory nerve endings and stimulating sympathetic adreno-medullar system; 2) by entering into the blood stream and enhancing epinephrine action on plasma fibrinogen. It would appear that indomethacin inhibits both pathways.

Effects of the administration of progesterone and adrenal medullectomy on the plasma fibrinogen levels in rats with surgical injury (laparotomy).

The probable rôle played by the adrenal medulla in the decrease of plasma fibrinogen due to the administration of progesterone (0.5 mg kg-1 day-1 during 72 h) in rats submitted to surgical injury (laparotomy) was studied. The results obtained lead to assume that the decrease of plasma fibrinogen observed in laparotomized rats injected with progesterone is indirectly produced through inhibition of the adrenal medulla. The action of progesterone on the plasma fibrinogen would be a pharmacological effect of the drug, since in doses of 0.10 mg kg-1 day-1 the decrease of the fibrinogen is not observed in laparotomized rats. The administration of progesterone in non injured rats does not modify the plasma fibrinogen as compared to the group of non injected rats.

Effects of diethylstilbestrol, 17 beta estradiol, and progesterone on plasma fibrinogen levels in rats submitted to tissue injury (laparotomy).

Participation of estrogens (17 beta estradiol, diethylstilbestrol) and progesterone in the increase of plasma fibrinogen levels in female rats submitted to tissue injury (laparotomy) was studied. Ovariectomy avoided the increase of fibrinogen observed in laparotomized rats, while the administration of 17 beta estradiol or diethylstilbestrol to laparotomized-ovariectomized rats increased fibrinogen to levels similar to those observed in the group of laparotomized rats without other treatment. On the other hand, progesterone inhibited the increase of fibrinogen which is typical of laparotomy in both groups: one of laparotomized rats and the other of laparotomized rats injected with estrogens. Neither estrogens nor progesterone modify plasma fibrinogen levels in uninjured rats. It is concluded that estrogens might participate in the fibrinogen increase observed after tissue injury in female rats, and on the contrary, the administration of progesterone would render that increase null.