Efficacy and tolerability of the American Heartworm Society therapeutic protocol in dogs affected by heartworm disease without caval syndrome.

OBJECTIVES: The American Heartworm Society medical protocol represents the current standard of therapy for canine heartworm disease without caval syndrome. However, data on the tolerability of this protocol are limited. This study aimed to describe efficacy and prevalence of possible treatment-related side effects in dogs with heartworm disease treated using the American Heartworm Society protocol. MATERIALS AND METHODS: For this retrospective multi-centre cohort study, dogs diagnosed with classes 1 to 3 heartworm disease that completed the American Heartworm Society medical protocol were searched in four medical databases. Demographic, clinical, diagnostic, therapeutic and outcome data, including the number and type of possible treatment-related side effects, were retrieved. RESULTS: Thirty-five dogs were included. The median age and bodyweight were 6 years (1 to 13 years) and 17.3 kg (4.9 to 50 kg), respectively. Heartworm disease was classified as classes 1, 2 and 3 in 20 of 35, 11 of 35 and four of 35 dogs, respectively. In addition to the therapeutic recommendations of the American Heartworm Society, eight of 35 dogs underwent sedation to favour melarsomine administration, and 30 of 35 received ice at the injection site. After adulticide therapy, all dogs were hospitalised with cage rest [median time 12 hours (6 to 48 hours)]. All dogs survived the treatment. All dogs with long-term follow-up (32/35) became negative. Furthermore, treatment-related side effects were rare, mild and rapidly recovered without the need for supporting therapies; these included depression/lethargy (4/35 dogs), cough (2/35 dogs) and lameness, pain and gastrointestinal signs (1/35 dog each). CLINICAL SIGNIFICANCE: The American Heartworm Society medical protocol is efficient and safe in dogs with classes 1 to 3 heartworm disease.

Seasonal variations of plasma gonadotropin, prolactin, and testosterone levels in primary and secondary hypogonadism: evidence for an independent testicular role.

BACKGROUND: Seasonal hormonal rhythmicity of the hypothalamic-pituitary-gonadal axis may influence reproductive and sexual activity in mammals. AIM: To investigate whether pituitary-gonadal axis secretion seasonality occurs in men with primary and secondary hypogonadism and whether a hierarchical machinery regulates these variations. SUBJECTS AND METHODS: Six adult males with Klinefelter's syndrome (KS), eight with idiopathic normosmic hypogonadotropic hypogonadism (HH) and ten sex- and age-matched healthy controls were studied longitudinally for one year. Every three months, three plasma samples for assay of testosterone, LH, FSH, and prolactin were drawn and the mean value was used for statistical analysis. RESULTS: Healthy males showed a significant seasonality in LH (zenith in spring) and testosterone (zenith in autumn) but not in FSH and prolactin concentrations. Patients with KS and those with HH showed a seasonal rhythmicity only of testosterone values, even if with small amplitude, with the zenith in spring and summer respectively. CONCLUSION: The lack of dependence of testosterone on gonadotropin variations in normal men and the persistence of seasonal testosterone but not gonadotropin variations both in primary and secondary hypogonadism seem to indicate a possible independent testicular regulation of this seasonality. The shift of testosterone peak in hypogonadal men with respect to controls suggests that LH variations could play a synchronizing, rather than pace-making, role in seasonal testosterone variations. Since hormonal seasonality may also influence gonadal activity in humans, replacement therapy in hypogonadism should be aimed also at restoring a normal seasonal rhythmicity of pituitary-gonadal hormone concentrations.

Involvement of hypothalamus autoimmunity in patients with autoimmune hypopituitarism: role of antibodies to hypothalamic cells.

CONTEXT: Antipituitary antibodies (APA) but not antihypothalamus antibodies (AHA) are usually searched for in autoimmune hypopituitarism. OBJECTIVE: Our objective was to search for AHA and characterize their hypothalamic target in patients with autoimmune hypopituitarism to clarify, on the basis of the cells stained by these antibodies, the occurrence of autoimmune subclinical/clinical central diabetes insipidus (CDI) and/or possible joint hypothalamic contribution to their hypopituitarism. DESIGN: We conducted a cross-sectional cohort study. PATIENTS: Ninety-five APA-positive patients with autoimmune hypopituitarism, 60 without (group 1) and 35 with (group 2) lymphocytic hypophysitis, were studied in comparison with 20 patients with postsurgical hypopituitarism and 50 normal subjects. MAIN OUTCOME MEASURES: AHA by immunofluorescence and posterior pituitary function were evaluated; then AHA-positive sera were retested by double immunofluorescence to identify the hypothalamic cells targeted by AHA. RESULTS: AHA were detected at high titer in 12 patients in group 1 and in eight patients in group 2. They immunostained arginine vasopressin (AVP)-secreting cells in nine of 12 in group 1 and in four of eight in group 2. All AVP cell antibody-positive patients presented with subclinical/clinical CDI; in contrast, four patients with GH/ACTH deficiency but with APA staining only GH-secreting cells showed AHA targeting CRH- secreting cells. CONCLUSION: The occurrence of CDI in patients with lymphocytic hypophysitis seems due to an autoimmune hypothalamic involvement rather than an expansion of the pituitary inflammatory process. To search for AVP antibody in these patients may help to identify those of them prone to develop an autoimmune CDI. The detection of AHA targeting CRH-secreting cells in some patients with GH/ACTH deficiency but with APA targeting only GH-secreting cells indicates that an autoimmune aggression to hypothalamus is jointly responsible for their hypopituitarism.

Simultaneous evaluation of the circulating levels of both Th1 and Th2 chemokines in patients with autoimmune Addison's disease.

BACKGROUND: Chemokines play a key role in the recruitment of the immune cells into the autoimmune process. Thus, the simultaneous evaluation of circulating levels of Th1-related chemokines, such as CX chemokine ligand 10 (CXCL10) and macrophage inflammatory proteins 1α (CCL3/MIP-1α), and Th2-related chemokines, such as macrophage inflammatory proteins 1 ß (CCL4/MIP-1ß) could be useful in the approach to some autoimmune diseases, including autoimmune Addison's disease (AAD). AIM: To evaluate plasmatic levels of MIP-1α, MIP-1ß, CXCL10 and adrenocortical antibodies in patients with AAD under treatment with corticosteroids. PATIENTS AND METHODS: Twelve women and 5 men (group 1) were divided in 2 subgroups: 9 subjects with isolated AAD (group 1a) and 8 with AAD associated with chronic autoimmune thyroiditis (group 1b). MIP-1α, MIP- 1ß and CXCL10 were evaluated in the serum of all patients and in 20 healthy controls, using a system for microarray suspension. RESULTS: The levels of MIP-1α, MIP-1ß and CXCL10 resulted significantly increased vs controls (p<0.001). An inverse significant correlation between the serum levels of MIP- 1ß and the duration of the disease was observed. CONCLUSION: High levels of MIP-1α and MIP-1ß associated with increased levels of CXCL10 in AAD seem to indicate a role of these chemokines in the autoimmune pathology of adrenal gland through the recruitment in loco of Th1 and Th2 cells. The simultaneous measurement of Th1-related chemokines (CXCL10 and MIP-1α) and of Th2-related chemokine MIP-1ß in the serum of patients with AAD would sustain a novel preliminary hypothesis on the immune microenvironment of chronic autoimmune inflammation within adrenal glands.

Autoimmunity as a possible cause of growth hormone deficiency.

A possible autoimmune aggression to pituitary somatotrophs has been suggested by the occurrence of antipituitary antibodies (APA) directed against GH-secreting cells in some cases of GH deficiency (GHD) both in adults and in children and in some patients with autoimmune poliendocrine syndrome. We also detected APA in some patients with idiopathic short stature (ISS) and suggested that the presence of these antibodies could identify those of them prone to develop GHD. In fact, patients with ISS, resulted positive for APA at the first observation, during a longitudinal follow-up showed an impaired GH response to the stimuli in subsequent years suggestive of acquired GHD. Also in such patients we demonstrated that the target of APA were the somatotrophs and that an autoimmune attack to these cells may be the underlying cause of hormonal impairment in several children with GHD positive for APA. In this connection we suggested that in these patients an early iso-hormonal therapy with recombinant GH may be useful to interrupt or delay the progression towards a clinical GHD.

Physiological effects of dietary cadmium acclimation and waterborne cadmium challenge in rainbow trout: respiratory, ionoregulatory, and stress parameters.

A suite of respiratory, acid-base, ionoregulatory, hematological, and stress parameters were examined in adult rainbow trout (Oncorhynchus mykiss) after chronic exposure to a sublethal level of dietary Cd (500 mg/kg diet) for 45 days and during a subsequent challenge to waterborne Cd (10 microg/L) for 72 h. Blood sampling via an indwelling arterial catheter revealed that dietary Cd had no major effects on blood gases, acid-base balance, and plasma ions (Ca(2+), Mg(2+), K(+), Na(+), and Cl(-)) in trout. The most notable effects were an increase in hematocrit (49%) and hemoglobin (74%), and a decrease in the plasma total ammonia (43%) and glucose (49%) of the dietary Cd-exposed fish relative to the nonexposed controls. Dietary Cd resulted in a 26-fold increase of plasma Cd level over 45 days (approximately 24 ng/mL). The fish exposed to dietary Cd showed acclimation with increased protection against the effects of waterborne Cd on arterial blood P(aCO2) and pH, plasma ions, and stress indices. After waterborne Cd challenge, nonacclimated fish, but not Cd-acclimated fish, exhibited respiratory acidosis. Plasma Ca(2+) levels declined from the prechallenge level, but the effect was more pronounced in nonacclimated fish (44%) than in Cd-acclimated fish (14%) by 72 h. Plasma K(+) was elevated only in the nonacclimated fish. Similarly, waterborne Cd caused an elevation of all four traditional stress parameters (plasma total ammonia, cortisol, glucose, and lactate) only in the nonacclimated fish. Thus, chronic exposure to dietary Cd protects rainbow trout against physiological stress caused by waterborne Cd and both dietary and waterborne Cd should be considered in determining the extent of Cd toxicity to fish.

Acute waterborne nickel toxicity in the rainbow trout (Oncorhynchus mykiss) occurs by a respiratory rather than ionoregulatory mechanism.

The acute mechanism of toxicity of waterborne nickel (Ni) was investigated in the rainbow trout (Oncorhynchus mykiss) in moderately hard ( approximately 140 mg l(-1) as CaCO(3)) Lake Ontario water, where the 96-h LC(50) for juvenile trout (1.5-3.5 g) was 15.3 mg (12.7-19.0, 95% C.L.) dissolved Ni l(-1). No marked impact of Ni exposure on average unidirectional or net fluxes of Na(+), Cl(-), or Ca(2+) was observed in juvenile trout exposed for 48-60 h to 15.6 mg Ni l(-1) as NiSO(4). Furthermore, when adult rainbow trout (200-340 g) were fitted with indwelling dorsal aortic catheters and exposed for 117 h to 11.6 mg Ni l(-1) as NiSO(4), plasma ions (Na(+), Cl(-), Ca(2+), and Mg(2+)) were all well conserved. However, mean arterial oxygen tension dropped gradually to approximately 35% of control values. This drop in P(aO(2)) was accompanied by an acidosis primarily of respiratory origin. P(aCO(2)) rose to more than double control values with a concomitant drop in arterial pH of 0.15 units. Acute respiratory toxicity was further evidenced by a significant increase in hematocrit (Ht), and plasma lactate, and a significant decrease in spleen hemoglobin (Hb). Following 117 h of exposure to 11.6 mg Ni l(-1), the gill, intestine, plasma, kidney, stomach, and heart accumulated Ni significantly, with increases of 60, 34, 28, 11, 8, and 3-fold, respectively. Brain, white muscle, liver, and bile did not significantly accumulate Ni. Plasma Ni exhibited a remarkable linear increase with time to levels approximately 30-fold higher than controls. We conclude that in contrast to most other metals, Ni is primarily a respiratory, rather than an ionoregulatory, toxicant at exposure levels close to the 96-h LC(50). The implications of a waterborne metal as an acute respiratory toxicant (as opposed to ionoregulatory toxicants such as Cu, Ag, Cd, or Zn) with respect to toxicity modeling are discussed.

Stainless steel bands in endodontics: effects on cuspal flexure and fracture resistance.

AIMS: This study investigated the effect of stainless steel bands on cuspal flexure and fracture resistance of extracted maxillary premolars. METHODOLOGY: Twenty extracted maxillary premolars (10 matched pairs) with mesio-occluso-distal (MOD) cavities and endodontic access were subjected to occlusal loading tests (100 N) using a servo-hydraulic testing machine. Cuspal deflections were measured by an extensometer, with and without the band present. Ten teeth (one of each pair) then had the band removed, and all teeth were subjected to loading until fracture. RESULTS: Mean cuspal flexure of teeth with bands was one-half of flexure without bands (P < 0.001). Teeth with bands fractured at higher load than their matched pairs with the band removed (P < 0.001), with mean loads at fracture of 1282 N and 729 N, respectively. CONCLUSIONS: The study showed that stainless steel bands used in endodontics reduce the cuspal flexure of maxillary premolars and increase their fracture resistance.

The quality of clinical fit of stainless steel bands used in endodontics.

Stainless steel bands are commonly advocated to protect posterior teeth against fracture during endodontic treatment and before final restoration. A poorly fitting band, however, may lead to a compromised coronal seal and gingival irritation. This radiographic study assessed the quality of fit and marginal adaptation in the proximal area of stainless steel bands placed during routine endodontic treatment. Clinical radiographs of 120 maxillary and mandibular premolars and molars were evaluated. All radiographs were taken during routine clinical endodontic treatment and randomly selected from cases completed by ten operators. Approximately one-half of cases did not meet the criteria of adequate marginal seal (mesial: 65/120; distal: 49/120). Only 11 teeth were found to have adequate fit of the band on both mesial and distal aspects of the tooth. The most common reason for inadequacy of fit was lack of band adaptation to the tooth contour in the cervical region. Stainless steel bands have a high possibility of poor marginal fit and should be used with the awareness that they may produce other clinical problems.

[Is there a correlation between cosmophysical factors and emergence of manic-depressive psychosis?]. / Sushchestvuet li korreliatsiia mezhdu kosmofizicheskim faktorami i vozniknoveniem maniakal'no-depressivnogo psikhoza?

Do the changes of the phases of bipolar, manic-depressive, behavior correlate with cosmic periodic processes? In a preliminary study, it was found that cosmic patterns such as planetary locations in relation to the lunar month could be correlated with the susceptibility to bipolar manic-depressive syndrome, in some cases. This paper describes the algorithms used to determine this correlation. The result suggest that it could be possible to anticipate cyclic patterns in some types of manic depressive disorders so that treatment could be more sensitive to the needs of the individual patient.

[Coma caused by meningoencephalitis as the initial manifestation of infectious mononucleosis. Description of a case]. / Coma da meningoencafalite come quadro di esordio della mononucleosi infettiva. Descrizione di un caso.

The clinical, anatomopathological and electroencephalographic aspects of C.N.S. impairment during I.M. are examined. The comparative frequency of such involvement, which generally presents in benign form, is confirmed together with the possible onset of forms that are extremely serious in terms of their course and prognosis. A case of I.M. which began with meningo-encephalitis-induced coma is reported. Stress is laid on the need to allow for mononucleosis infection when in the presence of viral encephalitis of unknown aetiology.