Arterial stiffness in hyperthyroid patients is deteriorated due to thyroid hormones

ABSTRACT Objective The aim of this study is to evaluate and compare arterial stiffness, which is an independent risk indicator for cardiovascular diseases (CVDs), between patients with overt hyperthyroidism, subclinical hyperthyroidism, euthyroidism by antithyroid therapy and healthy volunteers with pulse wave analysis (PWA). Subjects and methods A total of 102 volunteers were included in the study (30 in the overt hyperthyroid group, 28 in the subclinical hyperthyroid group and 14 with euthyroidism by antithyroid therapy and 30 healthy). The arterial stiffness measurements of the participants in the study were performed with the Mobil-O-Graph PWA device (I.E.M. GmBH, Stolberg, Germany), which makes cuff based oscillometric measurement from the brachial artery. Results Systolic blood pressure, pulse rate, central systolic blood pressure, cardiac output, heart rate-corrected augmentation index (Aix@75) and pulse wave velocity (PWV) measurements were significantly higher in the hyperthyroid group than in the control group. The heart rate and PWV in the subclinical hyperthyroid group were significantly higher than the control group. In the euthyroid group, systolic blood pressure, central systolic blood pressure, cardiac output, cardiac index and PWV were found significantly higher than the control group. There was also a negative correlation between Aix@75 and thyroid-stimulating hormone (TSH), and a positive correlation between Aix@75 and free thyroid hormones. Conclusion In our study, we observed that the arterial stiffness was adversely affected by an overt or subclinical increase in thyroid hormones and this correlated with thyroid hormone levels. We recommend that PWV measurement, which is a simple method for detecting CVD risk, can be used in these patients.

An early stage in T4-induced hyperthyroidism is related to systemic oxidative stress but does not influence the pentose cycle in erythrocytes and systemic inflammatory status

ABSTRACT Objective Hyperthyroidism causes many injuries in its target organs and the consequences are reflected systemically. As systemic alterations in hyperthyroidism at earlier stages have received partial attention, this study aimed to investigate systemic redox and inflammatory status at an early stage of T4-induced hyperthyroidism. Materials and methods Male Wistar rats were assigned to control and hyperthyroid groups (n = 7/group). The hyperthyroid group received L-thyroxine (12 mg/L) in their drinking water for 14 days whereas control group received only the vehicle. Body weight was measured on the 1st and 14th day of the protocol. On the 14th day, animals were anaesthetized. Blood was then collected from the retro-orbital venous plexus and then the animals were euthanised. The blood was separated into plasma and erythrocytes. Plasma was used to measure ROS levels, sulfhydryl compounds, IL-10, TNF-α and LDH levels; erythrocytes were used for the analysis of thioredoxin reductase activity, glutaredoxin content, and pentose cycle enzymes (total G6PD, G6PD and 6PGD). Results Hyperthyroid animals presented body weight gain and final body weight reduction, which was associated with increased ROS levels and decreased sulfhydryl content in plasma. Thioredoxin reductase activity, glutaredoxin content, and pentose cycle enzymes levels in erythrocytes, as well as IL-10, TNF-α and LDH plasma levels were unaltered. Conclusion Taken together, our results suggest an impairment in corporal mass associated with systemic oxidative stress at this stage of hyperthyroidism. Meanwhile, the pentose cycle was not influenced and systemic inflammation and tissue damage seem to be absent at this stage of hyperthyroidism.

Dynamic changes of central thyroid functions in the management of Cushing's syndrome

ABSTRACT Objective The aim of this study was to determine the frequency of central thyroid dysfunctions in Cushing's syndrome (CS). We also aimed to evaluate the frequency of hyperthyroidism due to the syndrome of the inappropriate secretion of TSH (SITSH), which was recently defined in patients with insufficient hydrocortisone replacement after surgery. Materials and methods We evaluated thyroid functions (TSH and free thyroxine [fT4]) at the time of diagnosis, during the hypothalamo-pituitary-adrenal axis recovery, and after surgery in 35 patients with CS. The patients were separated into two groups: ACTH-dependent CS (group 1, n = 20) and ACTH-independent CS (group 2, n = 15). Patients' clinical and laboratory findings were evaluated in five visits in the outpatient clinic of the endocrinology department. Results The frequency of baseline suppressed TSH levels and central hypothyroidism were determined to be 37% (n = 13) and 26% (n = 9), respectively. A negative correlation was found between baseline cortisol and TSH levels (r = -0.45, p = 0.006). All patients with central hypothyroidism and suppressed TSH levels showed recovery at the first visit without levothyroxine treatment. SITSH was not detected in any of the patients during the postoperative period. No correlation was found between prednisolone replacement after surgery and TSH or fT4 levels on each visit. Conclusion Suppressed TSH levels and central hypothyroidism may be detected in CS, independent of etiology. SITSH was not detected in the early postoperative period due to our adequate prednisolone replacement doses.

Does low serum TSH within the normal range have negative impact on physical exercise capacity and quality of life of healthy elderly people?

Objective Investigate the differences in cardiopulmonary (CP) capacity and Quality of Life (QOL) between healthy elderly (≥ 65 years) with different TSH levels (< 1.0 and ≥ 1.0 μIU/mL) both within the normal range. Also, evaluate the effects of TSH elevation on CP test and QOL, by administering methimazole to subjects with initial lower-normal TSH, in order to elevate it to superior-normal limit. Materials and methods Initially, a cross-sectional study was performed to compare CP capacity at peak exercise and QOL (using WHOQOL-OLD questionnaire) between healthy seniors (age ≥ 65 years) with TSH < 1.0 μIU/mL vs. TSH ≥1.0 μIU/mL. In the second phase, participants with TSH < 1.0 μIU/mL were included in a non-controlled-prospective-interventional study to investigate the effect of TSH elevation, using methimazole, on QOL and CP capacity at peak exercise. Results From 89 elderly evaluated, 75 had TSH ≥ 1 μIU/mL and 14 TSH < 1 μIU/mL. The two groups had similar basal clinical characteristics. No difference in WHOQOL-OLD scores was observed between groups and they did not differ in terms of CP function at peak exercise. QOL and CP variables were not correlated with TSH levels. Twelve of 14 participants with TSH < 1.0 μIU/mL entered in the prospective study. After one year, no significant differences in clinical caracteristics, QOL, and CP variables were detected in paired analysis before and after methimazole intervention. Conclusions We found no differences in CP capacity and QOL between health elderly with different TSH levels within normal range and no impact after one year of methimazole treatment. More prospective-controlled-randomized studies are necessary to confirm or not the possible harm effect in normal low TSH.

Synergic actions of polyphenols and cyanogens of peanut seed coat (Arachis hypogaea) on cytological, biochemical and functional changes in thyroid.

In animals, long-term feeding with peanut (Arachis hypogaea) seed coats causes hypertrophy and hyperplasia of the thyroid gland. However, to date there have been no detailed studies. Here, we explored the thyroidal effects of dietary peanut seed coats (PSC) in rats. The PSC has high levels of pro-goitrogenic substances including phenolic and other cyanogenic constituents. The PSC was mixed with a standard diet and fed to rats for 30 and 60 days, respectively. Animals fed with the PSC-supplemented diet showed a significant increase in urinary excretion of thiocyanate and iodine, thyroid enlargement, and hypertrophy and/or hyperplasia of thyroid follicles. In addition, there was inhibition of thyroid peroxidase (TPO) activity, 5’-deiodinase-I (DIO1) activity, and (Na+-K+)-ATPase activity in the experimental groups of rats as compared to controls. Furthermore, the PSC fed animals exhibited decreased serum circulating total T4 and T3 levels, severe in the group treated for longer duration. These data indicate that PSC could be a novel disruptor of thyroid function, due to synergistic actions of phenolic as well as cyanogenic constituents.

effect of omega-3 on renal functions and structure in experimental hyperthyroidism: possible role of angiotensin-converting enzyme 1

Hyperthyroidism is associate with reduced serum creatinine and urea, renal hypertrophy and eventually chronic renal disease. The aim of the present study was to investigate the potential therapeutic value of omega-3 on renal functions and structural changes induced by hyperthyroidism and the effect of omega-3 on angiotensin-converting enzyme 1 [ACE1] as a possible mechanism. Thirty rats were randomly divided into three groups. Control group received the vehicle. Hyperthyroid group was treated with L-thyroxine 0.1 mg/kg/day for 6 weeks and hyperthyroid-omega-3 treated group received L-thyroxine 0.1 mg/kg/day alone for 2 weeks followed by concurrent treatment with L-thyroxine 0.1 mg/kg/day and 3 g/kg/day omega-3 orally for 4 weeks. Serum creatinine, blood urea nitrogen [BUN], serum total antioxidant capacity [TAC], renal ACE1 and kidney weight to body weight [KW/BW] ratio were determined. Histopathological studies using H and E, Masson trichrome were done. Administration of L-thyroxine induced a significant decrease in serum creatinine, BUN and TAC and a significant increase in renal ACE1 and KW/BW ratio. Moreover, renal cortex thickness was increased, glomerular capillaries were congested with an increase in mesangial matrix. Proximal convoluted tubules [PCTs] were degenerated with no structural changes were observed in distal convoluted tubules [DCTs], afferent and efferent arterioles. Omega-3 administration is nearly normalized serum creatinine, BUN, TAC and renal ACE1 levels and ameliorates L-thyroxine-induced renal hypertrophy, glomerular congestion and PCTs degenerative changes. In conclusion, omega-3 administration has protective effects against hyperthyroidism-induced functional and structural changes. These reno-protective effects are possibly mediated by reducing ACE1 activity and its antioxidant activity

Fetuin-A levels in hyperthyroidism

OBJECTIVE: Fetuin-A is a protein secreted from the liver that inhibits arterial calcification deposition and can contribute to insulin resistance. Hyperthyroidism is also associated with insulin resistance. It is not known whether hyperthyroidism has an effect on fetuin-A levels. METHODS: We measured fetuin-A levels and homeostasis model of assessment-insulin resistance before hyperthyroidism treatment was initiated and after euthyroidism was achieved. A total of 42 patients diagnosed with hyperthyroidism were enrolled in this study. Fetuin-A, insulin, high-sensitivity C-reactive protein, fasting blood glucose, free T3 (fT3), free T4 (fT4), and thyrotropin were measured before and after euthyroidism was established. RESULTS: Basal fasting blood glucose, high-sensitivity C-reactive protein, insulin, c-peptide, homeostasis model of assessment-insulin resistance, fT3, fT4 and fetuin-A levels were significantly decreased after euthyroidism was achieved (Table 1). Basal fasting blood glucose (r:0.407, p:0.008), high-sensitivity C-reactive protein (r:0.523, p<0.0001), insulin (r:0.479, p:0.001), homeostasis model of assessment-insulin resistance (r:0.541, p<0.0001), fT3 (r:0.492, p:0.001) and fT4 (r:0.473, p:0.002) were positively correlated with basal fetuin-A levels. Basal thyrotropin levels were significantly negatively correlated (r:-0.553, p<0.0001) with basal fetuin-A levels. CONCLUSION: Our findings suggest that hyperthyroidism influences fetuin-A levels.

Alternative complement pathway and factor B activities in rats with altered blood levels of thyroid hormone

Evaluating the activity of the complement system under conditions of altered thyroid hormone levels might help elucidate the role of complement in triggering autoimmune processes. Here, we investigated alternative pathway (AP) activity in male Wistar rats (180 ± 10 g) after altering their thyroid hormone levels by treatment with triiodothyronine (T3), propylthiouracil (PTU) or thyroidectomy. T3 and thyroxine (T4) levels were determined by chemiluminescence assays. Hemolytic assays were performed to evaluate the lytic activity of the AP. Factor B activity was evaluated using factor B-deficient serum. An anti-human factor B antibody was used to measure factor B levels in serum by radial immunodiffusion. T3 measurements in thyroidectomized animals or animals treated with PTU demonstrated a significant reduction in hormone levels compared to control. The results showed a reduction in AP lytic activity in rats treated with increasing amounts of T3 (1, 10, or 50 µg). Factor B activity was also decreased in the sera of hyperthyroid rats treated with 1 to 50 µg T3. Additionally, treating rats with 25 µg T3 significantly increased factor B levels in their sera (P < 0.01). In contrast, increased factor B concentration and activity (32 percent) were observed in hypothyroid rats. We conclude that alterations in thyroid hormone levels affect the activity of the AP and factor B, which may in turn affect the roles of AP and factor B in antibody production.

Hipertiroidismo y síndrome de Down: caso clínico / Hyperthyroidism and Down syndrome: a present diagnosis

A female patient with Down Syndrome and without cardiac defects. During infancy, she had low weight increment secondary to repeated hospital admissions due to obstructive respiratory tract episodes. In addition, she attends regularly to the gastroenterology clinic due to intermittent diarrhea. At the age of 9.4 years-old, she presented liquid stools 5-6 times/day, associated to a decrease of 7 kg in 5 months and marked hyperactivity. She is admitted with tachycardia, arterial hypertension and high liver enzymes (SGOT = 63 U/1 and SGPT = 97U/1). The ECG showed sinus tachycardia. She is discharged without etiological diagnosis. In the mean time, annual thyroid function requested for endocrinology control showed TSH < 0,1 uUI/ml, T3 = 482 ng/dl and total T4 = 15,4 ug/dl, evidencing clear hyperthyroidism and beginning therapy with propylthiouracil 10 mg/kg/day and propanolol 1,3 mg/kg/day. After 3 weeks, the patient showed less hyperactivity, normal stools, normal sleep-awake cycle and recovered weight. By 6 weeks, thyroid hormones and transaminases were within normal ranges.

Objetivo: Describir una asociación poco frecuente de Síndrome de Down con Hipertiroidismo. Caso Clínico: Paciente de sexo femenino, portadora de síndrome de Down, sin antecedentes de cardiopatía congénita. Evolucionó con mal incremento ponderal en el período de lactante, hospitalizaciones repetidas por cuadros respiratorios obstructivos. En control en gastroenterología por episodios de diarrea intermitente, y en genética en forma regular. Cuadro actual se inicia a los 9,4 años, caracterizado por deposiciones líquidas 5-6 veces al día, asociado a baja de peso aproximada de 7 kg en 5 meses e hiperactividad. Se hospitalizó para estudio y se pesquisaron cifras tensionales elevadas y taquicardia. En perfil bioquímico aparece SGOT 63 U/1 y SGTP 97 U/1. Electrocardiograma informa taquicardia sinusal. Alta sin etiología clara, se solicita función tiroidea: TSH < 0,1 uUI/ml, T3 482 ng/dl, T4 total 15,4 ug/dl realizándose diagnóstico de hipertiroidismo. Inició terapia con propiltiouracilo 10 mg/kg/día y propanolol 1,3 mg/kg/día. A las 3 semanas de iniciado el tratamiento, la paciente presenta menor hiperactividad, deposiciones normales, regulación de la hiperactividad y ciclo sueño-vigilia, recuperando peso. A las 6 semanas, los niveles de T3, T4 y transaminasas eran normales. El hipertiroidismo se observa con mucha menor frecuencia que el hipotiroidismo en niños y adultos con síndrome de Down. En series numerosas de pacientes con trisomía 21, se describen en general un bajo porcentaje de casos de hipertiroidismo, dentro de los cuales se incluyen la enfermedad de Graves y la Hashitoxicosis.

Parathyroid surgery without instant PTH or radioguided Sestamibi scan

BACKGROUND: Radioguided Sestamibi scan and instant PTH (iPTH) are being used in minimally invasive parathyroid surgery (MIP). Experienced surgeons cure over 90-95% of the patients with primary hyperparathyroidism. PURPOSE/METHOD: To study the surgical results in treating hyperparathyroidism in a for profit community hospital lacking both iPTH and radioguided Sestamibi scan, we reviewed the patients operated from November 1, 2005 to October 31, 2006. RESULTS: The study comprised 56 patients: 52 with primary hyper-parathyroidism, three with secondary hyperparathyroidism and one with tertiary hyperparathyroidism. The only localizing test utilized pre-operatively was the Sestamibi Scan. PTH was measured immediately before and after surgery but the results was received seven to ten days later. The affected glands were removed in all patients. Fifty of 52 (96%) of the patients with primary hyperparathyroidism, the three patients with secondary hyper-parathyroidism and the patient with tertiary hyperparathyroidism are normocalcemic with normal PTH levels. Two patients have persistent mild hypercalcemia. Associated conditions were three papillary carcinoma of the thyroid, three multinodular goiter, four had a single thyroid nodule, one had an adrenal tumor and three were reoperations. CONCLUSION: Parathyroid surgery can be done safely and effectively in community hospitals without the utilization of radioguided Sestamibi scan and iPTH measurement.

131I-induced changes in rat thyroid gland function

Therapeutic doses of 131I administered to thyrotoxic patients may cause thyroid failure. The present study used a rat model to determine thyroid function after the administration of different doses of 131I (64-277 µCi). Thirty male Fisher rats in the experimental group and 30 in the control group (untreated) were followed for 6 months. The animals were 4 months old at the beginning of the experiment and were sacrificed at an age of 9 months. Hormone concentration was determined before 131I administration (4-month-old animals) and three times following 131I administration, when the animals were 7, 8, and 9 months old. The thyroid glands were removed and weighed, their volume was determined and histopathological examination was performed at the end of the experiment. Significant differences in serum triiodothyronine and thyroid-stimulating hormone concentration, measured at the age of 7, 8, and 9 months, were found in the experimental group. During aging of the animals, the concentration of thyroxin fell from 64.8 ± 8.16 to 55.0 ± 6.1 nM in the control group and from 69.4 ± 6.9 to 25.4 ± 3.2 nM in the experimental group. Thyroid gland volume and weight were significantly lower in the experimental than in the control group. Thyroid glands from the experimental group showed hyaline thickness of the blood vessel wall, necrotic follicles, a strong inflammatory reaction, and peeling of necrotic cells in the follicles. In conclusion, significant differences in hormone levels and histopathological findings indicated prolonged hypothyroidism after 131I administration to rats, which was not 131I dose dependent.

Thyroid dysfunction modulates glucoregulatory mechanism in rat.

The role of the thyroid gland in glucose homeostasis remains incompletely understood. To get a better insight hypo-and hyperthyroid conditions were experimentally induced in rat and found severe defects in glucose homeostasis. While blood glucose level returned to normal level after 2.5 hr of oral glucose challenge in control rats the blood glucose level remained high even after 24 hr of glucose load in both hypo- and hyperthyroid rats. These experimentally manipulated rats displayed higher levels of liver glycogen (10.45-22.8-fold) and serum glutamic pyruvic transaminase (1.48-9.8-fold). Liver histology of hyperthyroid treated rats revealed hepatotoxicity. From the results it can be concluded that thyroid gland plays an important role in glucose homeostasis.

Myelodysplastic syndrome and pancytopenia responding to treatment of hyperthyroidism: peripheral blood and bone marrow analysis before and after antihormonal treatment.

Hematological disorders, especially single lineage abnormalities, have been described in hyperthyroidism. Pancytopenia has been reported, without myelodysplastic syndrome or megaloblastic anemia. We studied the peripheral blood smear and the bone marrow aspiration and biopsy of a 65-year-old lady, who presented with pancytopenia and thyrotoxicosis due to multinodular goiter. She denied ingesting any toxic medication. At diagnosis: WBC: 2500/ul, platelets count: 58,000/ul, hemoglobin level: 6.5 g/dl. The bone marrow was moderately hyper cellular with moderate myelofibrosis and arrested hematopoiesis. The TSH level was: 0.02 mIU/l (N: 0.25-4), the fT3: 18 pmol/l (N: 4-10), the routine serum immunologic tests were negative. After treatment with single agent neomercazole (carbimazole), complete recovery of the blood cell counts was obtained within one month. The bone marrow aspiration, performed three months after starting therapy, showed normal hematopoiesis. The thyroid function tests returned to normal and no autoimmune reaction was detected on routine serum testing. Persistent response was observed six months later under medical treatment. The patient has refused surgical treatment. Reversible myelodysplastic syndrome may also be part of the changes in blood picture of patients with hyperthyroidism, probably due to direct toxic mechanism.

Osmotic fragility of red blood cells of hypothyroid, hyperthyroid patients and control subjects

Many hypo and hyperthyroid patients are anemic. Changes in concentration of thyroid hormones can affect Na+- K+ ATPase number and activity and also phospholipid composition of the cell membranes leading to changes in the surface to volume ratio and strength of membrane. In this study, the osmotic fragility of the red blood cells from non-treated hypo and hyperthyroid patients diagnosed on the basis of clinical examinations and paraclinical data were compared to that of control subjects. Written consent was obtained from all subjects. After washing three times with normal saline, red blood cells were placed in varying sodium chloride [NaCl] concentrations [0-0.9 gr%], following which, fragility was assessed with routine colorimetry methods. To do this, after the incubation period, tubes were centrifuged and the optical densities of the tubes was measured. Hemolysis percent in tubes was calculated on the basis of 100% hemolysis in the tubes containing 0 gr% of NaCl. The results indicate that the osmotic fragility of the cells from hyperthyroid patients in 0. 45gr% NaCl [74.6% +/- 30.2] was significantly [p < 0.01] lower than control subjects [93.8% +/- 9.1]. Osmotic fragility of red blood cells in 0. 5 g percent concentration of sodium chloride in hyperthyroid patients [27.8% +/- 26.0] was significantly less [p < 0.001] compared to the controls [63.5% +/- 27.5]. It appears that this change cannot be explained by changes observed in red blood cell indices [micrococytosis hypochromia]. According to the results of this study one can conclude that anemia reported in hypo- or hyperthyroid patients is not due to high osmotic fragility of the red blood cells and other causes need to be investigated

[Hematology and osmotic fragility of red blood cells in hyperthyroid rats]

Hyperthyroidism is associated with anemia. Since thyroid hormones, by acting on Na+/K+-ATPase activity and numbers, and also on the lipid composition of the membrane can alter the fragility of red cells, in this study, use compared the osmotic fragility of red cells in hyperthyroid rats to that of controls. Forty eight male Wistar rats [body weight, 221 +/- 4g] were divided in 4 groups. Group I consumed L-thyroxine [12mg/L in drinking water] for 30 days, group II was the control for group I, group III consumed L-thyroxine for 60 days and group IV was the control group for the group III. At the end of the intervention period, hormonal and biochemical measurements were done in blood samples. To assess the osmotic fragility, red blood cells [RBC] were incubated at 37°C for 30 min in different concentrations of NaCl and the extent of hemolysis was measured by colorimetry of the supernatant. Hemolysis percent was expressed in terms of percent hemolusis in presence of distilled water [100% hemolysis]. In this study although hemoglobin, haematocrit, mean corpuscular hemoglobin and mean corpuscular volume in group III were significantly [P<0.05] higher compared to group IV, osmotic fragility did not show any significant difference. The results indicate that hyperthyroidism in rat can not anemia and osmotic fragility of RBCs in hyperthyroid animals do not differ from control groups

Juvenile hyperthyroidism: an experience.

OBJECTIVE: To analyze the clinical profile of juvenile hyperthyroidism at presentation, their treatment outcome; predictors of remission and relapse. METHODS: Retrospective analysis of medical records of 56 patients with juvenile hyperthyroidism seen over a period of 16 years. A cohort of 38 females and 18 males with mean (+/-SD) age of 14.9 +/- 3.4 years (range 3 to 18 years) was analyzed. RESULTS: Majority of patients was in the age group of 12-16 years. Common symptoms observed at presentation were weight loss (82.1%), excessive sweating (78.6%), heat intolerance (76.8%), increased appetite (73.2%) and diarrhea in 48.2%. In addition, accelerated linear growth was observed in 7.1% of patients. Goiter was present in 98.2% of children; 94.5% of which was diffuse and 4.8% was multinodular. The mean ((+/-SD) T3 was 4.8 +/- 3.4 ng/mL (N, 0.6-1.6), T4 was 218 +/- 98 ng/mL (N, 60-155) and TSH was 0.44 +/- 0.36 (N, 0.5-5.5 microIU/mL). TMA positivity seen in 36.9% of patients. All patients were treated with carbimazole; subsequently 4 patients required thyroidectomy and one required radioactive iodine ablation. Mean (+/-SD) duration of follow-up in our patients was 4.9 +/- 3 years, ranging between 1.6 to 16 years and mean (+/-SD) duration of treatment was 34.4 +/- 22.6 months (range 12 to 120 months). Mean (+/-SD) duration to achieve euthyroidism was 5.2 +/- 4.7 months, ranging between 1-33 months. On intention to treat analysis, remission with carbimazole was achieved in 47.6%, remaining patients failed to achieve remission with drug treatment. CONCLUSION: Graves disease is the commonest cause of juvenile hyperthyroidism. Carbimazole is safe, effective, cheap, and easily available form of therapy. It is occasionally associated with serious side effects but requires prolonged follow up.

Subclinical hyperthyroidism as a potential factor for dysfunctional uterine bleeding

To evaluate the functional status of thyroid gland in apparently euthyroid women with dysfunctional uterine bleeding. Forty apparently euthyroid women with menorrhagia and no pathologic lesion in the genital tract were compared to 20 women having normal menstrual cycle as control group. All women were subjected to hormonal assay: total and free T3, T4 and TSH, Serum PRL, P [progesterone], total and free testosterone. A statistically significant difference in the values of TSH, total T3, free T3 and total T4 in the menorrhagia group compared to the control group. Prolactin was decreased significantly in the menorrhagia group. Subclinical hyperthyroidism can be a potential risk factor for dysfunctional uterine bleeding. Other studies are needed to confirm our findings

Diffuse Alveolar Hemorrhage Associated with Antineutrophil Cytoplasmic Antibody levels in a Pregnant Woman Taking Propylthiouracil

Propylthiouracil (PTU) is known to be a potential cause of antineutrophil cytoplasmic antibody (ANCA) positive small vessel vasculitis, resulting in glomerulonephritis and diffuse alveolar hemorrhage (DAH). Herein, we describe a 25-year-old pregnant woman who developed a perinulcear ANCA (p-ANCA) and myeloperoxidase ANCA (MPO-ANCA) positive DAH during PTU therapy. The patient improved after corticosteroid therapy and discontinuation of the PTU. Methimazole was prescribed in spite of the risk of recurrence of DAH because of the pregnancy. The patient is currently free from pulmonary problems. Our case shows that the alternative agent, methimazole, can be used to treat hyperthyroidism in a pregnant patient with PTU associated DAH.