Pubertal Gynecomastia Article Review

Length: 8 pages Sources: 1 Subject: Children Type: Article Review Paper: #47617157 Related Topics: Endocrine System, Spss, Puerto Rico, Human Growth Hormone
Excerpt from Article Review :

¶ … health effects of phthalates. To better explain, these are a group of industrial chemicals with numerous profitable uses comprising personal-care merchandises and plastic supplies. The authors explain within the abstract the most frequently used chemical is di-(2-ethylhexyl)-phthalate (DEHP). DEHP is known to possess estrogenic or antiandrogenic effects or both. Another chemical the authors discusses is MEHP. "Mono-(2-ethylhexyl)-phthalate (MEHP) is the main metabolite of DEHP. In this study, we aimed to determine the plasma DEHP and MEHP levels in pubertal gynecomastia cases" (Durmaz et al., 2010, p. e122). The study group used within the article consists of 40 new cases of diagnosed pubertal gynecomastia.

The cases involving pubertal gynecomastia were admitted to Hacettepe University Ihsan Do-ramaci Children's Hospital. Age-matched children were used in the control group that did not have pubertal gynecomastia or any other hormone related disorder.They measured both MEHAP and DEHP plasma levels utilizing high-performance liquid chromatography. They also measured serum hormone a physician's assessment. The results provided valuable insight into plasma DEHP and MEHP levels.

Those with pubertal gynecomastia had consistently higher plasma MEHP and DEHP levels. This means there is statistically noteworthy connection between plasma DEHP and MEHP in relation to pubertal gynecomastia. Although the authors state no connections can be made between plasma hormone levels and DEHP and MEHP levels, evidence explains pubertal gynecomastia may be affected by DEHP and MEHP.

b. The conclusion within the abstract offers a brief synopsis of the information and results. "DEHP, which has antiandrogenic or estrogenic effects, may be an etiologic factor in pubertal gynecomastia. These results may pioneer larger-scale studies on the etiologic role of DEHP in pubertal gynecomastia" (Durmaz et al., 2010, p. e122).

2. Introduction

a. Pubertal gynecomastia involves the benign growth of male breast tissue along with increased proliferation of ductile elements. Unfortunately due to the growing chemicals in food and other products, pubertal gynecomastia is a frequently seen problem happening within 65% of teenage males. Since male breast tissue has androgen and estrogen receptors, any chemicals that contain estrogenic properties will contribute to estrogen related proliferation. Where androgens inhibit breast tissue proliferation, estrogens stimulate. Pubertal gynecomastia produces an imbalance of these two hormones and leads to excess estrogen within the breast tissues leading to breast tissue proliferation. "…2 factors, which may be attributable to excessive estrogen activity, deficient androgen activity, increase aromatase enzyme activity, or a combination of these effects on breast tissue" (Durmaz et al., 2010, p. e123).

DEHP is reported to be an androgen antagonist which means it depletes androgens within the body, and in the case of pubertal gynecomastia, in the breast tissue. Since the disorder requires depletion of androgens for estrogens to proliferate breast tissue, DEHP may be a direct cause of pubertal gynecomastia. In the introduction, they discuss a possible estrogenic effect from DEHP although studies have attempted to tackle this possible correlation. The authors discuss the study and its purpose to identify the effects of MEHP and DEHP on hormone levels within patients along with effects of these chemicals on patients with pubertal gynecomastia.

b. The quote explains the lack of evidence in relation to DEHP/MEHP as it pertains to rising hormonal imbalances in male youths. "As far as we know there is no report in which the authors investigated the relationship between DEHP/MEHP levels and pubertal gynecomastia, which develops as a result of an imbalance between androgenic and estrogenic activity" (Durmaz et al., 2010, p. e123).

3. Materials and Methods

a. This section covers the materials utilized along with the different methods to measure and record during the study. Of the forty patients studied, only 19 had pubertal gynecomastia and the other 21 were healthy showing no signs of endocrine disorder. All subjects were male and aged between 11 and 15 years of age. The blood sampling was taken from the left arm cubital vein using a stainless steel needle.

Several hormone screening kits were used for the testing. "Commercial kits for luteinizing hormone (LH), follicle-stimulating hormone (FSH), estradiol, prolactin, thyrotropin, free triiodothyronine (FT3), and free thyroxine (FT4) were purchased from Abbott Architect (Abbott Park, IL), and the kits for the sex hormone-binding globulin (SHBG) were purchased from Zentech" (Durmaz et al., 2010, p. e124). These kits not only included estradiol, but also other...

...

Protection of samples was a key measure and was done so using aluminum foil followed by centrifugation and freezer storage.

Including the purchase of screening kits was purchase of DEHP and MEHP. DEHP and MEHP were bought from laboratories. In order to determine serum hormone levels, they measured using the 2-step chemiluminescence microparticle immunoassay method. Statistical analysis was done through use of the SPSS 13.0 software.

b. Other instruments used in thi section are as follows: "Determination of DEHP and MEHP concentrations was conducted by HPLC equipped with an auto sampler (Hewlett Packard Agilent 1100 Series, Vienna, Austria) using a UV detector (230 nm)" (Durmaz et al., 2010, p. e124).

4. Results

a. From the 40 patients tested, only 19 presented with pubertal gynecomastia while the remaining 21 were control patients. With the exclusion of one patient from the study that was in the group with pubertal gynecomastia, most of the results proved a significant correlation between DHEP and increased estrogenic activity and decreased androgenic activity. "1 patient from the gynecomastia group and 1 patient from the control group were excluded from analysis because the values were at the end points and changed the normal distribution curve" (Durmaz et al., 2010, p. e125).

DEHP levels were evident in all plasma samples and MEHP levels were measureable in all patients with pubertal gynecomastia, including 19 of the 20 control patients. As noted in the abstract, plasma MEHP/DEHP levels were statistically expressively higher in the pubertal gynecomastia group when compared to the control group. Even after a second round of measurements, the results were the same pointing to a correlation between exposure to DEHP and MEHP and development of hormonal imbalance as the patients with hormonal imbalances and pubertal gynecomastia showed higher levels of the two chemicals.

The results although pertaining to a small group, do show signs of possible connection between exposure to chemicals and hormonal imbalance. These results were measured using software that follows the suggested algorithm for the management of gynecomastia. It also was done with a second round of testing to ensure true and accurate results. Since the location where blood was drawn was the same for all participants in the study, the results can be viewed as having higher accuracy than if the blood drawn came from different locations.

b. The results of the study revealed significant correlation between pubertal gynecomastia and the two chemicals, DEHP and MEHP. "There was a statistically significant correlation between DEHP and MEHP values in the pubertal gynecomastia group (r 0.44, P .005); however, the correlation was not significant in the control group (r 0.43, P .065)" (Durmaz et al., 2010, p. e125).

5. Discussion

a. The discussion section of the article focuses on DEHP, and how it has become the most frequently used plasticize. The authors also highlight DEHP as an extensive universal environmental contaminant. Several reports show long-term toxic effects along with long-term tissue accumulation in animals. Dosage plays a part in level of toxicity along with duration of exposure. Studies reveal exposure and possible effects are increased during developmental stages and pregnancy such as infancy and puberty. Investigational animal models exhibited its effects on growing stages. "Although DEHP has been shown to have toxic effects for many systems, the most important effects after long-term) exposure are on the reproductive system" (Durmaz et al., 2010, p. e127).

In another study, the authors explains the effects of DHEP increased almost threefold when dosage was increased every 1 g/mL leading to increased risk in development of pubertal gynecomastia. This study presents a direct link between DHEP and development of pubertal gynecomastia. Plasma MEHP levels were also studied in order to augment the consistency of the results. The results from the study showed a high correlation between DEHP and MEHP levels. This means higher MEHP levels increases the risk of gynecomastia. This is the first study in which the authors examined the connection between pubertal gynecomastia and DEHP levels, making it difficult to relate with any other study results.

Environmental contamination is a crucial aspect of studies that must be controlled. As outlined in the Materials and Methods section, the authors of the article attempted their best to control the level of environmental contamination in the study. This meant they did not use any plastic material when conducting the study. "Blood was taken to the laboratory in 30 minutes. Plasma samples were separated and stored at 80°C immediately. The analyses of the pubertal gynecomastia cases and control blood samples were made simultaneously so if any contamination occurred it would have affected both groups" (Durmaz et al., 2010, p. e127). The inter-day and diurnal repetition of the DEHP examination technique was found to…

Sources Used in Documents:

References

Durmaz, E., Ozmert, E.N., Giray, B., Derman, O., Hincal, F., & Yurdakok, K. (2010). Plasma Phthalate Levels in Pubertal Gynecomastia. Pediatrics. 2010, 125(1), e122-129.


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