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PubMed1990

Prostaglandin E2-induced hyperplasia of the rat antral epithelium is followed by a secondary inhibition of the mitotic activity.

The aim of the study was to examine the mitotic activity in the antral and duodenal epithelium of Sprague-Dawley rats given trophic doses of E2 prostaglandins during a prolonged period of time. Natural prostaglandin E2 (dose range: 0.2-5.0 mg.k-1) and 15 (R) 15 methyl prostaglandin E2 (dose range: 0.03-2.0 mg.kg-1) were administered for 11 days, and mitoses were arrested with vincristine for 4 h before estimation of the cumulative mitotic index. A dose-related hyperplasia of the antral glands was observed after treatment with prostaglandin E2 and the synthetic analogue (p less than 0.05). The proliferative zone was enlarged in rats treated with high doses of the analogue but natural prostaglandin E2 did not affect the limits of the proliferative zone. A dose-related reduction of the mitotic index was observed in animals treated with prostaglandin E2 despite the presence of hyperplastic changes. All doses of the analogue induced antral hyperplasia without affecting the mitotic index except in rats given the highest dose who had a significantly lower mitotic index than controls (p less than 0.05). Hyperplasia of both crypts and villi was observed in the duodenum of rats given high doses of E2 prostaglandins (p less than 0.05) whereas the mitotic index and the growth fraction were not affected by treatments. It is concluded that hyperplasia by prostaglandins is developed in absence of changes of the mitotic activity. The observed reduction of the mitotic index is interpreted as a secondary phenomenon, possibly mediated by a regulatory mechanism of cell proliferation which is triggered to reduce further epithelial growth. It is suggested that prostaglandin E2 might influence such regulatory mechanisms.

Administration, Oral↗
PubMed1984

Gingival hyperplasia caused by nifedipine--a preliminary report.

We observed marked gingival hyperplasia, similar clinically and histologically to the hyperplasia caused by 5:5 sodium diphenylhydantoin (Dilantin) during the last 18 months in five patients treated by nifedipine. Histologically, marked epithelial hyperplasia-acanthosis, with moderate inflammatory reaction in the lamina propria, was observed in all the biopsy specimens. Evidence points to a strong relationship between the gingival hyperplasia and the administration of nifedipine.

Aged↗
PubMed1990

Butylated hydroxyanisole (BHA) does not cause forestomach hyperplasia by inhibiting the release of gastric mucus.

High doses of BHA cause hyperplasia and subsequent neoplasia in the rodent forestomach and can inhibit gastric prostaglandin (PG) synthesis in vitro. This paper examines the hypothesis that BHA induced forestomach hyperplasia occurs in response to a reduction of gastric mucus, with consequent irritation of the forestomach. This could result from inhibition of the formation of the PG's which mediate the synthesis and release of protective mucus. Groups of 10 rats received 0 or 2% BHA in the diet for 1 or 3 weeks and a positive control group was fed a diet containing indomethacin (3.5 mg/kg), a potent inhibitor of PG synthesis. After 1 week BHA caused focal erosion and ulceration of the forestomach consistent with an irritant effect, but 2 weeks later the epithelium was healed, thickened and markedly hyperplastic. Histochemical staining for mucus showed that the development of forestomach hyperplasia was associated with increased amounts of gastric and duodenal mucus and increased numbers of serotonergic-cells in the gastric and duodenal epithelium. In contrast, indomethacin caused a marked reduction in both gastric and Brunner's gland mucus. Neither BHA nor indomethacin exerted an effect on one specific type of mucus (viz: neutral, acidic or mixed) in the stomach. These results do not support the hypothesis that forestomach hyperplasia arises from an inhibition of either the synthesis or release of gastric mucus. It is possible that the increased numbers of serotonergic-cells are related to the initial ulcerative, or subsequent hyperplastic response.

Administration, Oral↗
PubMed1993

Ultrasonic tissue characterization of experimental venous intimal hyperplasia.

Ultrasonic tissue characterization (UTC) employing slope and Y-intercept parameters from the normalized power spectrum of backscattered echoes was employed in vivo to study compositional changes in the walls of pig jugular veins in which thrombi were experimentally induced. Light microscopy revealed these changes to be intimal hyperplasia with an early predominance of smooth muscle cells and a later mixture of smooth muscle cells and collagen deposits. UTC distinguished intimal hyperplasia from previously reported data from luminal thrombosis UTC. Furthermore, UTC was able to discriminate between early (predominantly smooth muscle cells) and older (smooth muscle cells plus collagen deposits) intimal hyperplasia. The study suggests that intimal hyperplasia in the experimental model used may be organized thrombus and that UTC may be able to follow both the development of wall changes as well as luminal changes occurring in venous thrombosis.

Animals↗
PubMed1996

Ultrasonic-pathologic comparison of postangioplasty myointimal hyperplasia and primary atheroma of the superficial femoral artery.

The purpose of this study was to characterize postangioplasty myointimal hyperplasia as compared to primary atheroma of superficial femoral arteries using color-coded duplex sonography (CCD), and to correlate sonographic findings with the histopathology of samples obtained from these lesions by catheter atherectomy (Redha-cut device). Preinterventionally, homogeneity, echogeneity, and the surface of plaques were described using CCD in nine cases with secondary stenoses after percutaneous transluminal angioplasty and in seven cases with primary atheroma. Myointimal hyperplasia of femoral restenoses showed a homogeneous (7 of 9 vs. 1 of 7) and hypoechogenic (7 of 9 vs. 0 of 7) wall thickening compared to primary atheromas (p < 0.05). Primary atherosclerotic plaques showed a rather heterogeneous, hypo- and hyperechogenic ultrasonic appearance with or without echo shadowing in six of seven cases. The surface of restenoses was more often regular than that of primary atherosclerotic lesions, but this finding did not reach statistical significance (6 of 9 vs. 2 of 7, p = 0.14). Thrombotic material appeared homogeneous and hypoechogenic in three of five cases and could not be discriminated from intimal hyperplasia. In summary, postangioplasty intimal hyperplasia is characterised by a hypoechogenic, homogeneous, rather regularly confined vessel wall thickening and can be differentiated from primary atheroma at CCD.

Aged↗
PubMed1996

Overexpression of her-2/neu in human prostate cancer and benign hyperplasia.

Overexpression of the neu oncoprotein has been described in several tumor models including breast and prostate cancer. Overexpression of neu has been reported to have prognostic significance in certain tumors but controversy continues regarding the role and frequency of neu overexpression in prostatic cancer. The objectives of the study were twofold. First, to characterize neu expression in prostate cancer in comparison to benign prostatic hyperplasia. Second, to determine whether neu expression correlates with Gleason grade in prostate cancer. Thirty-nine prostate cancers obtained from radical prostatectomy specimens and 10 benign prostatic hyperplasia specimens were included in the study. Specimens were formalin fixed and paraffin-embodied. neu expression was studied by immunohistochemical staining using a monoclonal neu specific AB-3 antibody. All 39 specimens (100%) of prostate cancer showed positive immunostaining of variable degree while 2 (20%) benign prostatic hyperplasia specimens showed positive staining. Thus, neu oncogene is overexpressed in localized prostate cancer compared to benign prostatic hyperplasia. The degree of neu immunostaining did not correlate with Gleason grade and there appeared to be a tendency towards an inverse relationship. The prognostic significance of the varying overexpression is unknown.

Biomarkers, Tumor↗
PubMed1996

Endometrial thickness assessed by transvaginal ultrasound insufficiently predicts occurrence of hyperplasia during unopposed oestrogen use.

In the present study, unopposed oestrogens were given to 184 non-hysterectomized women, for a duration varying from four weeks to 24 months, while the endometrial responses were monitored by transvaginal sonography (TVS) and backed up by endometrial sampling (conducted when the endometrial thickness reached 8 mm (double layer) or more, vaginal bleeding occurred during oestrogen administration, or after one year of unopposed oestrogen use). In cases where the endometrial thickness reached 8 mm or more, progestogens were administered for 12 days. In 64% of the women, administration of progestogen could be postponed until at least the fourth month of treatment under the pre-defined decision criteria. Eleven percent of the patients used oestrogens continuously during the two year study period, without any need of additional progestogen. In total, 338 endometrial biopsies were performed; 16 cases of hyperplasia were detected. In three cases, the corresponding endometrial thickness was below 8 mm (in one case, 5 mm). Endometrial thickness could not consistently predict occurrence of hyperplasia. In eight cases, hyperplasia occurred within 4 months of treatment, and in four cases, within only 2 months (of which only one case could possibly be attributed to previous hormone use and none to endogenous oestrogen production). The rapid occurrence of hyperplasia should be taken into account in studies of quarterly progestogen administration with hormone replacement therapy. It is concluded that postponement of progestogen administration with hormone replacement therapy under guidance of TVS only (without biopsies) would not be adequately safe to be recommended for clinical practice.

Adult↗
PubMed2005

Simvastatin does not inhibit intimal hyperplasia and restenosis but promotes plaque regression in normocholesterolemic patients undergoing coronary stenting: a randomized study with intravascular ultrasound.

BACKGROUND: Restenosis after coronary stenting is mainly caused by intimal hyperplasia. Both experimental and clinical studies suggest that statins may be able to inhibit intimal hyperplasia and, therefore, in-stent restenosis (ISR), by mechanisms beyond lipid lowering. METHODS: In a 12-month study, we randomized 71 normocholesterolemic patients to 20 mg simvastatin or no treatment, 2 weeks before elective coronary stenting. Patients were evaluated by quantitative coronary angiography and intravascular ultrasound, immediately after the index procedure and at the 12-month catheterization. RESULTS: Binary ISR was present in 15% and in 18% of simvastatin-treated patients and controls, respectively (P = NS). Intimal hyperplasia did not differ significantly between the 2 groups (3.6 +/- 1.8 vs 3.8 +/- 2.3 mm3/mm, 34% +/- 15% vs 35% +/- 23% for simvastatin vs controls, P = NS). However, persistent plaque decreased with simvastatin but increased in controls (-4.0 +/- 4.0 vs +1.6 +/- 3.8 mm3/mm, -14% +/- 10% vs +6% +/- 12%, P < .05). The same behavior was shown by intermediate plaques at nonstented sites (-2.5 +/- 3.0 vs +1.0 +/- 3.0 mm3/mm, -10% +/- 8% vs +9% +/- 9%, P < .05). Major adverse events at 12 months were present in 11% and 24% of simvastatin-treated patients and controls, respectively (P = .20). CONCLUSIONS: In normocholesterolemic patients undergoing coronary stenting, simvastatin does not prevent intimal hyperplasia or ISR, but it promotes atherosclerotic regression both at stented and at nonstented sites.

Coronary Angiography↗
PubMed2005

Lipid peroxidation triggers both c-Jun N-terminal kinase (JNK) and extracellular-regulated kinase (ERK) activation and neointimal hyperplasia induced by cessation of blood flow in the mouse carotid artery.

We investigated whether lipid peroxidation might influence activation of the mitogen activated protein kinase (MAPK) extracellular regulated kinase (ERK1/2) and c-Jun N-terminal kinase (JNK) in neointimal hyperplasia induced by flow interruption of carotid artery in mice. C57/BL6 mice were subjected to a complete ligation of the left common carotid artery or to a sham ligation. Animals were randomized to receive either IRFI-042, a Vitamin E-like inhibitor of lipid peroxidation (20 mg/kg/i.p., immediately after artery occlusion) or its vehicle (1 ml/kg of a NaCl-DMSO solution). The extent of lipid peroxidation (investigated by the means of conjugated dienes levels) and JNK and ERK activation were evaluated by Western blot analysis after blood flow interruption. ICAM-1 expression in injured arteries was investigated 4 days after artery ligation by the means of reverse transcriptase polymerase chain reaction (RT-PCR) and quantification of the ICAM-1 protein levels. Morphometric analysis of the structural alteration caused by the disruption of the arterial blood flow was performed 4 weeks after surgery. Flow interruption in the carotid artery resulted at 10 min, following occlusion in a marked increase in conjugated dienes tissue levels (5.8+/-0.44 DeltaABS/mg protein), caused at 30 min after occlusion peak increase in both ERK1/2 (45+/-8 integrated intensity) and JNK (38+/-6 integrated intensity) activities, enhanced ICAM-1 expression (1.5+/-0.45 relative amount of ICAM-1 mRNA) and ICAM-1 protein levels (55+/-12 pg/mg protein) and produced a marked neointimal hyperplasia (mean intimal area=101+/-14 microm2). Injured arteries harvested from IRFI-042-treated mice had reduced conjugated dienes tissue levels (2.9+/-0.5 DeltaABS/mg protein), attenuated ERK1/2 (19+/-6 integrated intensity) and JNK (2.9+/-0.5 integrated intensity) activities, blunted ICAM-1 expression (0.38+/-0.1 relative amount of ICAM-1 mRNA) and protein levels (26+/-8 pg/mg protein) and decreased neointimal hyperplasia (mean intimal area=4.5+/-1.5 microm2). Our data indicate that ERK1/2 and JNK kinases play a crucial role in neointimal hyperplasia induced by flow cessation in the mouse carotid artery. Furthermore, the present data suggest that lipid peroxidation triggers ERK and JNK activation.

Animals↗
PubMed2005

Efficacy of peroxisome proliferative activated receptor (PPAR)-alpha ligands, fenofibrate, on intimal hyperplasia and constrictive remodeling after coronary angioplasty in porcine models.

Constrictive remodeling and intimal hyperplasia play a prominent role in restenosis after angioplasty. It has been reported that the severity of constrictive remodeling and intimal hyperplasia correlate with adventitial angiogenesis and inflammation. Experimental evidence indicates that inflammation participates in angiogenesis, and therefore inhibition of inflammation may impair neovascularization. We tested whether fenofibrate, peroxisome proliferative activated receptors (PPAR)-alpha specific ligand, inhibits the early inflammation, adventitial angiogenesis, constrictive remodeling and intimal hyperplasia after angioplasty using porcine coronary arteries. Fenofibrate was tested in vivo, in 30 coronary arteries of 10 pigs (1g/day, orally) and was compared to placebo. Quantitative intravascular ultrasound and histopathologic assessment showed that fenofibrate increased lumen (6.28 mm(2) versus 5.15 mm(2)), vessel area (7.34 mm(2) versus 6.69 mm(2)) and inhibited constrictive remodeling. Inflammatory cell infiltration was evaluated with scanning electron microscopy 3 days after angioplasty and was significantly decreased in the treated vessels compared to control. Adventitial angiogenesis 3 days after angioplasty was significantly reduced in the injured vessels derived from the fenofibrate treated group compared to placebo. In conclusion, pharmacological activation of PPAR-alpha inhibited constrictive remodeling and neointimal hyperplasia after angioplasty through inhibition of inflammation and adventitial neovascularization.

Angioplasty, Balloon, Coronary↗
PubMed2006

Alpha-lipoic acid inhibits fractalkine expression and prevents neointimal hyperplasia after balloon injury in rat carotid artery.

Vascular inflammation induced by the proinflammatory cytokine/NF-kappaB pathway is one of the key mechanisms in the development of neointimal hyperplasia. Accumulating evidence suggests that a recently identified chemokine, fractalkine, is involved in arterial inflammation and atherogenesis. However, no study has examined the expression of neointimal fractalkine and the effects of pharmacological agents on this process. The purposes of this study were to measure neointimal fractalkine expression in the rat carotid artery following balloon injury and to determine if alpha-lipoic acid (ALA) inhibits fractalkine expression and neointimal hyperplasia. Balloon injury of the rat carotid artery induced fractalkine expression in the medial as well as neointimal regions. ALA inhibited this expression and consequently prevented neoinitmal hyperplasia in a balloon-injured rat carotid artery. Additionally, ALA inhibited TNF-alpha-stimulated fractalkine expression in cultured vascular smooth muscle cells (VSMCs), a process which is mediated through the NF-kappaB pathway. In addition to fractalkine, ALA successfully inhibited TNF-alpha-stimulated expression of vascular cell adhesion molecule-1 and monocyte chemotactic protein-1 in cultured VSMCs. These data suggest that the cytokine-fractalkine system is involved in the pathogenesis of restenosis. The present study supports the possibility that ALA, which inhibits the NF-kappaB/fractalkine pathway, may be used to prevent neointimal hyperplasia after angioplasty or stenting.

Angioplasty, Balloon↗
PubMedDate not supplied

Temporal and spatial characterization of cellular constituents during neointimal hyperplasia after vascular injury: Potential contribution of bone-marrow-derived progenitors to arterial remodeling.

BACKGROUND: Exuberant smooth muscle cells (SMCs) hyperplasia is the major cause of postangioplasty restenosis. We suggested that circulating smooth muscle progenitor cells might contribute to lesion formation after vascular injury. METHODS: We extensively investigated the cellular constituents during neointimal formation after mechanical vascular injury. RESULTS: A large wire was inserted into the mouse femoral artery, causing complete endothelial denudation and marked enlargement of the lumen with massive apoptosis of medial SMCs. At 2 h, the injured artery remained dilated with a thin media containing very few cells. A scanning electron microscopy showed fibrin and platelet deposition at the luminal side. One week after the injury, CD45-positive hematopoietic cells accumulated at the luminal side. Those CD45-positive cells gradually disappeared, whereas neointimal hyperplasia was formed with alpha-smooth muscle actin (SMA) positive cells. Bone marrow cells and peripheral mononuclear cells differentiated into alpha-SMA-positive cells in the presence of PDGF and basic FGF. Moreover, in bone marrow chimeric mice, bone-marrow-derived cells substantially contributed to neointimal hyperplasia after wire injury. CONCLUSION: These results suggest that early accumulation of hematopoietic cells may play a role in the pathogenesis of SMC hyperplasia under certain circumstances.

Actins↗
PubMed2005

Monoclonal B-cell hyperplasia and leukocyte imbalance precede development of B-cell malignancies in uracil-DNA glycosylase deficient mice.

Ung-deficient mice have reduced class switch recombination, skewed somatic hypermutation, lymphatic hyperplasia and a 22-fold increased risk of developing B-cell lymphomas. We find that lymphomas are of follicular (FL) and diffuse large B-cell type (DLBCL). All FLs and 75% of the DLBCLs were monoclonal while 25% were biclonal. Monoclonality was also observed in hyperplasia, and could represent an early stage of lymphoma development. Lymphoid hyperplasia occurs very early in otherwise healthy Ung-deficient mice, observed as a significant increase of splenic B-cells. Furthermore, loss of Ung also causes a significant reduction of T-helper cells, and 50% of the young Ung(-/-) mice investigated have no detectable NK/NKT-cell population in their spleen. The immunological imbalance is confirmed in experiments with spleen cells where the production of the cytokines interferon gamma, interleukin 6 and interleukin 2 is clearly different in wild type and in Ung-deficient mice. This suggests that Ung-proteins, directly or indirectly, have important functions in the immune system, not only in the process of antibody maturation, but also for production and functions of immunologically important cell types. The immunological imbalances shown here in the Ung-deficient mice may be central in the development of lymphomas in a background of generalised lymphoid hyperplasia.

Animals↗
PubMed2006

Leptin levels in serum depending on Body Mass Index in patients with endometrial hyperplasia and cancer.

UNLABELLED: Leptin levels in serum depending on Body Mass Index (BMI) in patients with endometrial hyperplasia and cancer. OBJECTIVES: Concentrations of leptin, a hormone secreted by white adipose tissue, correlate strongly with body mass. Leptin interacts with several other hormones, modifies the activities of some enzymes and proinflammatory cytokines, participates in hematopoiesis, thermogenesis, and angiogenesis, and is involved in the control of carbohydrate and lipid metabolism. This study was undertaken to determine whether serum concentrations of leptin in obese patients with endometrial hyperplasia and cancer deviate from values in patients with normal endometrium. STUDY DESIGN: We enrolled 86 obese postmenopausal women, including 40 with endometrial cancer and hyperplasia and 46 with normal endometrium. Depending on BMI, three subgroups were formed: I<30; II = 30-40; III > 40. Leptin concentrations were measured with immunoenzymatic test kits from IBL. Statistical comparison was done with the chi square (chi(2)) test and Statistica software package. RESULTS: Mean serum concentration of leptin in endometrial cancer and hyperplasia was 16737.1 pg/ml as opposed to 9048.7 pg/ml in patients without endometrial pathology (p<0.0001). Significantly, higher concentrations of leptin were noted in every BMI subgroup of patients with endometrial pathology in comparison to controls (p<0.005). CONCLUSIONS: Leptin appears to participate in proliferative processes of the endometrium. Obesity is an important risk factor in endometrial cancer.

Biomarkers↗
PubMed2005

Neutrophil accumulation promotes intimal hyperplasia after photochemically induced arterial injury in mice.

The role of leukocytes in the pathogenesis of coronary arterial disease has become a focus for clinical research. The aim of this study was to determine whether neutrophil accumulation would participate in the development of intimal hyperplasia after endothelial injury in mice, and whether d-myo-inositol hexakisphosphate (phytic acid) which inhibits the binding of L- and P-selectin to sialyl Lewis(X) could inhibit the development of intimal hyperplasia. Endothelial injury was inflicted in one femoral artery via the photochemical reaction between systemically injected rose bengal and transillumination with green light (wavelength: 540 nm). Scanning electron microscopic observation at 3 days after the injury showed an increase in the number of leukocytes adhering to the injury site. Histological observation at 21 days showed that in the neutropenia group administered anti-neutrophil antibody and in the phytic acid-treated group the progression of intimal hyperplasia was significantly attenuated by comparison with the corresponding control groups. These results suggest that neutrophil accumulation contributes to the initiation and/or development of intimal hyperplasia and L- and/or P-selectin may participate in their mechanisms.

Animals↗
PubMed2006

PEG-hirudin/iloprost coating of small diameter ePTFE grafts effectively prevents pseudointima and intimal hyperplasia development.

OBJECTIVES: Small diameter PTFE grafts are prone to thrombosis and intimal hyperplasia development. Heparin graft coating has beneficial effects but also potential drawbacks. The purpose of this study was to evaluate the experimental efficacy of PEG-hirudin/iloprost coated small caliber PTFE grafts. METHODS: Thirty-six femoro-popliteal ePTFE grafts (expanded polytetrafluoroethylene, diameter 4 mm) were inserted into 18 pigs. Grafts were randomised individually for each leg and grouped for 3 groups. Group I consisted of native ePTFE grafts, group II were grafts coated with a polylactide polymer (PLA) without drugs and group III grafts were coated with PLA containing a polyethylene glycol (PEG)-hirudin/iloprost combination. The follow-up period was 6 weeks. Patency rates were calculated and development of pseudointima inside the grafts was noted. Thickness of intimal hyperplasia at the distal anastomoses was measured using light microscopy. RESULTS: Patency rates for group I were 6/9 (67%), for group II 9/10 (90%) and 12/12 (100%) for group III. In groups I and II there was a significant reduction of blood flow proximal to the graft at graft harvest, to 29+/-12 and 28+/-20 ml/min respectively (both p<0.01 versus preoperative value), whilst in group III blood flow, 99+/-21 ml/min, remained at the preoperative level. Subtotal stenosis due to development of pseudointima was noted in each of the native and PLA coated grafts but not in group III grafts. Intimal hyperplasia at the distal anastomosis was lowest in group III. CONCLUSIONS: The PEG-hirudin/iloprost coating of ePTFE prostheses effectively reduced pseudointima and intimal hyperplasia development and led to superior graft patency.

Anastomosis, Surgical↗
PubMed2006

Thymic hyperplasia in a child treated with growth hormone.

OBJECTIVE: To report a case of thymic hyperplasia diagnosed three months after initiation of recombinant human growth hormone (GH) for the treatment of GH deficiency. DESIGN: Retrospective chart review was conducted to evaluate the temporal relationship between treatment with GH and thymic enlargement in a 7-year-old girl who had a history of embryonal rhabdomyosarcoma of the nasopharynx diagnosed at the age of 3 years. RESULTS: The diagnosis of GH deficiency was made based on clinical and auxological criteria, an insufficient response to clonidine-arginine stimulation testing (peak GH level of 4.8 microg/L) and low insulin-like growth factor 1 (IGF-1) level (30 ng/mL, -2.7 SD). The patient was started on GH at a dose of 0.3mg/kg/week. At the initiation of treatment with GH, the baseline growth velocity was 0.8 cm/year (-6.0 SD) and height was 112.5 cm (-1.7 SD). After three months of treatment with GH, her height increased by 4.2 cm (from -1.7 to -1.2 SD), and the IGF-1 level from -2.7 SD to -1.1 SD. A chest CT performed at that time for recurrence surveillance showed 89% increase in thymic volume relative to previous scan before treatment with growth hormone. A thoracoscopic biopsy of the thymus was performed and revealed hyperplasia with normal thymic architecture without evidence of malignancy. CONCLUSIONS: The timing of the development of thymic hyperplasia, along with data from in vitro and in vivo animal studies showing that GH and IGF-1 can directly stimulate growth of the thymus, suggests that GH contributed to the development of thymic hyperplasia in this patient.

Child↗
PubMed2006

Medical treatment of vulvar squamous cell hyperplasia.

OBJECTIVE: To evaluate symptomatic response and recurrence rates of graduated topical fluorinated corticosteroid in patients with vulvar squamous cell hyperplasia. METHODS: Nine hundred seventy-six patients with biopsy-proven vulvar squamous cell hyperplasia from 1990 to 2003 were reviewed in this retrospective study. All patients were treated with graduated topical fluorinated corticosteroid. Data were obtained from hospital records. Symptomatic remission and recurrence rates were noted following six months local therapy. RESULTS: The mean age was 42.55+/-10.93 (15-85). The remission rate was 93.8% in six months. The remission rate was non-significantly higher in postmenopausal patients than that in their premenopausal counterpart (94.9% vs 93.0%, p=0.15). The disease recurred in 6.9% of patients. Of the patients that suffered recurrence 47.5% had persistent disease initially. The patients with following factors older ages (>40 years), postmenopausal period had significantly higher recurrence rates. Four patients with recurrent disease and six patients with persistent disease in the form of vulvar intraepithelial neoplasia I-II or atypical squamous hyperplasia, were treated with skinning vulvectomy. CONCLUSION: Corticosteroid in the treatment of vulvar squamous cell hyperplasia yielded excellent response rates. In the evaluation of patients without symptomatic relief, the first step should be a vulvar biopsy to exclude the presence of atypical components.

Adolescent↗