The impact of preventive health behaviour and social factors on visits to the doctor

Background

The aim of this study is to examine the joint impact of preventive health behavior (PHB) and social and demographic factors on the utilization of primary and secondary medical care under a universal health care system, as measured by visits to the doctor, who were categorized as either a General Practitioner (GP) or Specialist Doctor (SD).

Methods

An ordered probit model was utilized to analyze data obtained from the 2009 Israeli National Health Survey. The problem of endogeneity between PHB factors and visits to GP was approached using the two-stage residuals inclusion and instrumental variables method.

Results

We found a positive effect of PHB on visits to the doctor while the addition of the PHB factors to the independent variables resulted in important changes in explaining visits to GP (in values of the estimates, in their sign, and in their statistical significance), and only in slight changes for visits to SD. A 1% increase in PHB factors results in increasing the probability to visit General Practitioner in the last year in 0.6%. The following variables were identified as significant in explaining frequency of visits to the doctor: PHB, socio-economic status (pro-poor for visits to GP, pro-rich for visits to SD), location (for visits to SD), gender, age (age 60 or greater being a negative factor for visits to GP and a positive factor for visits to SD), chronic diseases, and marital status (being married was a negative factor for visits to GP and a positive factor for visits to SD).

Conclusions

There is a need for allowing for endogeneity in examining the impact of PHB, social and demographic factors on visits to GP in a population under universal health insurance.For disadvantaged populations with low SES and those living in peripheral districts, the value of IndPrev is lower than for populations with high SES and living in the center of the country. Examining the impact of these factors, significant differences in the importance and sometimes even in the sign of their influence on visits to different categories of doctors - GP and SD, are found.

     

Hypoglycemia as a predictor of mortality in hospitalized elderly patients

BACKGROUND: Hypoglycemia during hospitalization occurs in patients with and without diabetes. The aims of this study were to determine the incidence, associated risk factors, and short- and long-term outcome of hypoglycemia among hospitalized elderly patients. METHODS: This is a case-control study conducted at geriatric and medicine departments. All patients 70 years or older with documented hypoglycemia hospitalized within 1 year (n = 281) were compared with a nonhypoglycemic group of 281 elderly, randomly selected patients from the same hospitalized population. RESULTS: Among 5404 patients 70 years or older, 281 (5.2%) had documented hypoglycemia. Compared with the nonhypoglycemic group, we found the following characteristics to be true in the hypoglycemic group: there were more women than men (58% vs 44%, P =.001); sepsis was 10 times more common (P<.001); malignancy was 2.8 times more common (P =.04); the mean serum albumin level was lower (2.8 g/dL vs 3.4 g/dL, P<.001); and the mean serum creatinine and alkaline phosphatase levels were higher (P<.001 for both). Diabetes was known in 42% of the hypoglycemic group and in 31% of the nonhypoglycemic group (P =.03); 70 patients in the hypoglycemic group were taking sulfonylureas or insulin. Multivariate logistic analysis showed that sepsis, albumin level, malignancy, sulfonyurea and insulin treatment, alkaline phosphatase level, female sex, and creatinine level were all independent predictors of developing hypoglycemia. In-hospital mortality and 3-month mortality were about twice as high in the hypoglycemic group (P<.001). Multivariate analysis of mortality found that sepsis, low albumin level, and malignancy were independent predictors, while hypoglycmia was not. CONCLUSIONS: Hypoglycemia was common in elderly hospitalized patients and predicted increased in-hospital 3- and 6-month cumulative mortality. However, in a multivariate analysis, hypoglycemia was not an independent predictor for mortality, implying that it is only a marker.     

CD169+ macrophages in lymph node and spleen critically depend on dual RANK and LTbetaR signaling

CD169⁺ macrophages reside in lymph node (LN) and spleen and play an important role in the immune defense against pathogens. As resident macrophages, they are responsive to environmental cues to shape their tissue-specific identity. We have previously shown that LN CD169⁺ macrophages require RANKL for formation of their niche and their differentiation. Here, we demonstrate that they are also dependent on direct lymphotoxin beta (LTβ) receptor (R) signaling. In the absence or the reduced expression of either RANK or LTβR, their differentiation is perturbed, generating myeloid cells expressing SIGN-R1 in LNs. Conditions of combined haploinsufficiencies of RANK and LTβR revealed that both receptors contribute equally to LN CD169⁺ macrophage differentiation. In the spleen, the Cd169-directed ablation of either receptor results in a selective loss of marginal metallophilic macrophages (MMMs). Using a RANKL reporter mouse, we identify splenic marginal zone stromal cells as a source of RANKL and demonstrate that it participates in MMM differentiation. The loss of MMMs had no effect on the splenic B cell compartments but compromised viral capture and the expansion of virus-specific CD8⁺ T cells. Taken together, the data provide evidence that CD169⁺ macrophage differentiation in LN and spleen requires dual signals from LTβR and RANK with implications for the immune response.

CD169⁺ macrophages are strategically localized at the lymphatic sinuses of lymph nodes (LNs) and the marginal zone of the spleen, where they capture lymph- and blood-borne antigens, respectively (1). These macrophages reside close to B cells and mesenchymal stromal cells. B cells are a constitutive source of lymphotoxin (LT) α and LTβ that bind to the LTβ receptor (R) as LTα₁β₂ heterotrimer (2). Lack of B cells and unconditional or B cell–specific ablation of LTα or LTβ lead to loss of CD169⁺ macrophages in LNs and the spleen (3–6). Conversely, B cell–specific overexpression of LTαβ results in an increase of their numbers (7). Furthermore, administration of the decoy fusion protein LTβR-Fc or LTβR inactivation negatively affects their presence in both organs (3, 8, 9). However, although the myeloid cell lineage has been shown to express LTβR (10–12), it remains unclear whether the dependency on LTβR signaling is direct or implies an intermediate cell partner such as the adjacent stromal cells (9, 13, 14).We have recently shown that receptor activator of NF-κB ligand (RANKL) from marginal zone reticular cells (MRCs) regulates the differentiation of CD169⁺ macrophages in the LN (15). Like LTα and LTβ, RANKL is a member of the TNF superfamily and binds to the signaling receptor RANK (16). Stromal RANKL activates the lymphatic endothelial cells to form a cellular niche for macrophages and directly stimulates their differentiation into the CD169⁺ macrophages of the subcapsular sinus (subcapsular sinus macrophages, SSMs). However, a role of stromal RANKL for the splenic CD169⁺ macrophages has not been addressed. LTαβ and RANKL share many similarities in their biological functions. They are both indispensable for the organogenesis of secondary lymphoid organs (17, 18), are involved in the organogenesis of the thymus (19), and contribute to the formation of the intestinal microfold cells (20). However, RANKL stands out for its role in osteoclastogenesis (16), while LTαβ regulates the production of homeostatic chemokines and the differentiation of follicular dendritic cells (2).In the context of partially overlapping functions, we scrutinized the implication of the RANK–RANKL and LTβR–LTαβ axes in the differentiation of LN and splenic CD169⁺ macrophages. Using Cd169-directed conditional deficiency of RANK or LTβR, we report that direct RANK and LTβR signals are required for their differentiation in the LN and the spleen. In the absence of the receptors, LN CD169⁺ macrophages were replaced by myeloid cells phenotypically similar to the SIGN-R1⁺ medullary sinus macrophages. Deficiency of one copy of either Rank or Ltbr alleles sufficed for a prominent decrease in macrophage numbers, but the heterozygous deletion of both genes had a compound effect. Altered macrophage differentiation had a negative impact on lymph-borne antigen transport to B cells. In the spleen, Cd169-directed RANK or LTβR deficiency elicited a selective loss of the CD169⁺ MMMs. By the use of a RANKL reporter mouse together with RT-qPCR of sorted splenic stromal subsets, we identified CCL19⁺ splenic MRCs as a source of RANKL and demonstrated in Ccl19-cre RANKL-deficient mice that stromal RANKL participates in MMM differentiation. Their specific loss had no effect on the marginal zone B cell compartment but compromised viral capture and the formation of the virus-specific CD8⁺ T cell response. Taken together, the data provide evidence that CD169⁺ macrophage differentiation is dependent on the dual signals emanating from LTβR and RANK, with implications for the immune response to lymph- and blood-borne pathogens.     

Use of xidifon for prevention and treatment of nephropathies with metabolic disorders in children

Xydofon was applied to the treatment of 68 children suffering from different renal diseases associated with metabolic disorders. The latter ones involved oxaluria (28 children), uraturia (17 children), cystinuria (14 children), and phosphaturia (9 children). To appraise the action of xydofon, use was made of the indicators of membranolysis, cellular homeostasis of calcium, lipid peroxidation, and of the level of beta 2-microglobulin in urine. The results obtained indicate that xydofon can be used as an effective remedy for the treatment of children suffering from nephropathies associated with metabolic disorders.     

The Effects of Hormones of the Hypothalamo-Hypophyseal-Adrenal, Renin-Angiotensin, and Thyroid Hormone Systems on the Formation of Dyscirculatory Encephalopathy

Measurements were made of plasma levels of free (f) thyroxine (fT4), triiodothyronine (fT3), thyrotropic hormone (TSH), adrenocorticotrophic hormone (ACTH), aldosterone, and renin in patients with dyscirculatory encephalopathy (DE). Their influences on the development of chronic circulatory insufficiency were assessed. A total of 39 patients were studied (aged 45-73 years) with DE stages I and II, without acute or chronic (in the exacerbation phase) somatic illness. These observations showed that diffuse lesions of brain tissues of different severities were accompanied by the following changes in thyroid homeostasis: 1) significant combined increases in TSH without alteration to the "fT3-TSH" negative feedback regulatory mechanism in patients with stage I DE; 2) significant combined decreases in TSH levels with marked suppression of the conversion of thyroxine into triiodothyronine and an interaction with impairments in the "fT3-hypophysis" system in patients with stage II DE. In addition, there were changes (increases) in cortisol levels with simultaneous decreases in renin levels in patients with stage II DE as compared with patients with stage I DE. Correlation analysis demonstrated the absence of any relationship between the age of the patients, the state of hormonal homeostasis, and the extent of vascular stenosis. These results suggest a role for hormones of the hypothalamo-hypophyseal-adrenal, thyroid, and renin-angiotensin systems in the mechanism by which DE develops as well as the possibility of using tests for these hormones as additional criteria for assessing the severity of diffuse brain lesions.     

emm typing of M nontypeable invasive group A streptococcal isolates in Israel

We performed emm typing of M nontypeable invasive group A streptococcal (GAS) isolates collected in a prospective population-based study in Israel. One hundred twenty of 131 isolates (92%) had emm sequences compatible with GAS, consisting of 51 different emm types. Eleven isolates were found to be group G streptococcus. Of the 120 isolates, 55 (46%) belonged to 32 types for which there were no typing sera available in the Streptococcal Reference Laboratory in Israel. The other 65 (64%) isolates, consisting of 19 types, had sera available and therefore could have been serotyped. Forty-three isolates had T and emm types which were not correlated according to standard M-typing protocols and were therefore missed. The principal effect of emm typing was the addition of 32 types not previously identified in Israel and the discovery of new associations between emm and T types. emm typing did not significantly change the proportion of M types; the five most common types were 3, 28, 2, 62, and 41. Twenty different types comprised 80% of all isolates. No new emm sequences were discovered. emm typing emphasized the unusually low incidence of M1 strains causing severe disease in Israel. As serological typing of GAS becomes more problematic due to lack of sera and the appearance of new emm types, reference laboratories should replace M typing with emm sequence typing. Development of a GAS vaccine relies on the emm type distributions in different geographical locations. In our study, 7% of isolates (types 41 and 62) are not included in a 26-valent vaccine that is being studied.     

The lipid composition of high-density lipoproteins in patients with psoriasis

Ten lipid fractions were detected in patients with psoriasis by the method of unidimensional chromatography in a thin layer of silica gel with two solvent systems designed for separating a lipid extract of high-density lipoproteins (HDLP). Four phospholipids fractions were identified as follows: three main ones, i.e. phosphatidylcholine, lisophosphatidylcholine and sphyngomielin, and one minor fraction, i.e. phosphatidylethanolamine. The HDLP lipid comprises free cholesterol and its esters. Three glyceride fractions were detected: mono-, di- and triglicerides and free fatty acids. The ratio of the individual phospholipid fractions, on the one hand, and of free to ester-bound cholesterol was found in HDLP by computer-aided densitometry of chromatograms and coincided with the routinely obtained data. The described method designed to evaluate the HDLP lipid composition can be handy in investigations of HDLP in patients with psoriasis.