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1.
Parasitol Res ; 119(7): 2207-2215, 2020 Jul.
Artigo em Inglês | MEDLINE | ID: mdl-32447517

RESUMO

Cystic echinococcosis (CE) is a disease of livestock and humans caused by the larval stage of the Echinococcus granulosus sensu lato (s.l.) species complex and occurs especially in areas where sheep breeding is widespread. This survey evaluates, after more than a decade since the last epidemiological survey, the current situation and trend of CE in sheep of the highly endemic island of Sardinia (Italy). From 2012 to 2018, out of a total of 1416 sheep, 65.3% were found positive for CE. Cyst fertility has increased slightly from 10.3% in 2006 (Scala et al. 2006) to 11.7% in the present survey (χ2 = 1.07; P = 0.30018) with a peak of 14.0% in the province of Sassari. Overall, 6815 hydatids were found and classified as sterile (26.2%), fertile (14.4%), caseous (5.3%), or calcified (54.1%) based on their morphology. All isolates were identified as E. granulosus sensu stricto (former G1/G3, strains). Results shown as the implementation of new European Council Regulations and in particular of 21/2004 that established a system for the individual identification and tracking of sheep could be a step forward towards a better control of animal movement, preventing illegal slaughtering on the island as well as in other countries experiencing similar problems. Even if at first sight the general situation of Sardinia regarding CE seems a little better compared with the past, our findings indicate that in some Provinces the epidemiological situation is not improved since 2006.


Assuntos
Equinococose/epidemiologia , Equinococose/veterinária , Echinococcus granulosus/isolamento & purificação , Doenças dos Ovinos/epidemiologia , Ovinos/parasitologia , Animais , Cistos/parasitologia , Genótipo , Humanos , Ilhas/epidemiologia , Itália/epidemiologia , Larva , Gado , Inquéritos e Questionários
2.
Radiol Case Rep ; 15(5): 534-541, 2020 May.
Artigo em Inglês | MEDLINE | ID: mdl-32180856

RESUMO

We report a case of a fibromyalgia (FM) patient with an history of brain-cancer presenting signs and symptoms of gadolinium toxicity following repeated administrations of a macrocyclic contrast agent, Gadovist. In the present report, we provide evidence supporting the hypothesis of a causal relationship linking gadolinium deposition to a clinical manifestation of disease, namely fibromyalgia. We unravel a role for gadolinium in the still unknown etiology of fibromyalgia as a metal toxicity disorder. Contrast agents are routinely administered in a clinical context. It is thus possible that the patients are mistakenly believed to show complaint of their primary disease, whereas, in some instances, their symptoms are associated with gadolinium deposition.

3.
Med Hypotheses ; 129: 109240, 2019 Aug.
Artigo em Inglês | MEDLINE | ID: mdl-31371082

RESUMO

Fibromyalgia (FM) is a chronic, painful, heterogeneous, and common disorder carrying a substantial socio-economical burden. It lacks effective cures and its aetiology is still unknown. There exists evidence for central and peripheral neurological contribution to the symptoms but grasping the real source of abnormal nervous system sensitization remains an ongoing challenge. There exists an association between an injury/trauma and the onset of the symptoms, but a causal relationship has not been yet sufficiently supported by scientific evidence. I postulate a role for gadolinium-based contrast agents and retention of gadolinium in the body. This conjecture breaks the hypothesis of a direct role for a physical injury/trauma per se in favour of an indirect one by the subsequent diagnostic procedures. It creates a new link between retention of gadolinium in the body and painful conditions as FM and unexplained chronic widespread pain reported after a trauma, surgery, or medical illness. Experimental evidence demonstrates possible retention of gadolinium species in human body, still lacking conclusive answers on their pathological consequences. Notwithstanding, there exist some initial data that report unexplained chronic widespread pain and symptoms of FM in those patients: they are suggestive for pathological consequences associated with gadolinium retention. Besides clear compelling symptoms overlapping, biochemical findings are provided to sustain the hypothesis of a role for gadolinium in the disease process focusing on neurotransmitters, endogenous metal cations, cytokines, and muscle tissue. Experimental findings strongly support the hypothesis of impairment at the cellular, intracellular, and systemic levels in FM. And these data are highly compatible with collateral effects associated with the interference of the gadolinium ion and its pharmaceutical chelates into biochemical pathways in vivo. The hypothesis presented in this article, along with the support of scientific evidence, links FM and unexplained chronic widespread pain reported after a trauma, surgery, or medical illness to retention of gadolinium in the body. If the hypothesis is confirmed, it could improve diagnosis and prevention, while providing a ground for development of new treatments.


Assuntos
Dor Crônica/etiologia , Fibromialgia/etiologia , Gadolínio/efeitos adversos , Imageamento por Ressonância Magnética/efeitos adversos , Meios de Contraste/efeitos adversos , Citocinas/metabolismo , Humanos , Ligantes , Modelos Teóricos , Neurotransmissores/metabolismo , Segurança do Paciente , Fenótipo , Fator de Necrose Tumoral alfa/metabolismo
4.
Front Med (Lausanne) ; 5: 94, 2018.
Artigo em Inglês | MEDLINE | ID: mdl-29761101

RESUMO

A 34-year-old woman suffered from significant chronic pain, depression, non-restorative sleep, chronic fatigue, severe morning stiffness, leg cramps, irritable bowel syndrome, hypersensitivity to cold, concentration difficulties, and forgetfulness. Blood tests were negative for rheumatic disorders. The patient was diagnosed with Fibromyalgia syndrome (FMS). Due to the lack of effectiveness of pharmacological therapies in FMS, she approached a novel metabolic proposal for the symptomatic remission. Its core idea is supporting serotonin synthesis by allowing a proper absorption of tryptophan assumed with food, while avoiding, or at least minimizing the presence of interfering non-absorbed molecules, such as fructose and sorbitol. Such a strategy resulted in a rapid improvement of symptoms after only few days on diet, up to the remission of most symptoms in 2 months. Depression, widespread chronic pain, chronic fatigue, non-restorative sleep, morning stiffness, and the majority of the comorbidities remitted. Energy and vitality were recovered by the patient as prior to the onset of the disease, reverting the occupational and social disabilities. The patient episodically challenged herself breaking the dietary protocol leading to its negative test and to the evaluation of its benefit. These breaks correlated with the recurrence of the symptoms, supporting the correctness of the biochemical hypothesis underlying the diet design toward remission of symptoms, but not as a final cure. We propose this as a low risk and accessible therapeutic protocol for the symptomatic remission in FMS with virtually no costs other than those related to vitamin and mineral salt supplements in case of deficiencies. A pilot study is required to further ground this metabolic approach, and to finally evaluate its inclusion in the guidelines for clinical management of FMS.

5.
Front Med (Lausanne) ; 4: 198, 2017.
Artigo em Inglês | MEDLINE | ID: mdl-29250522

RESUMO

Fibromyalgia syndrome (FMS) is a chronic, complex, and heterogeneous disorder of still poorly understood etiopathophysiology associated with important musculoskeletal widespread pain, fatigue, non-restorative sleep, and mood disturbances. It is estimated to afflict 2-3% of the worldwide population, with clean prevalence among women. The objective of this paper is to propose a novel treatment for symptomatic remission of FMS, grounded in biochemistry and consisting in the withdrawal from the diet of molecules that can indirectly trigger the symptoms. The hypothesis develops from the evidence that low serotonin levels are involved in FMS. Serotonin is synthesized starting from the essential amino acid tryptophan. The presence of non-absorbed molecules in the gut, primarily fructose, reduces tryptophan absorption. Low tryptophan absorption leads to low serotonin synthesis that triggers FMS symptoms. Moreover not-absorbed sugars could also produce a microbiota deterioration activating a positive feedback loop: the increasing microbiota deterioration reduces the functionality of absorption both of fructose and tryptophan in the gut, entering a vicious circle. The therapeutic idea is to sustain serotonin synthesis allowing the proper tryptophan absorption. The core of the cure treatment is the exclusion from the diet of some carbohydrates and the marked reduction of some others. The main target is the limitation of total dietary fructose as marked as possible. It could be an effective strategy to get the remission of symptoms acting on the impaired biochemical pathways. The straying from the treatment is expected to cause the reappear of the symptoms.

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