M Katz

Middlesex University, UK, Londinium, England, United Kingdom

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Publications (18)53.31 Total impact

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    ABSTRACT: Androgenic stimulation of sebaceous glands is an important factor in the development of acne. We examined 36 females (aged 14-34 years), selected because none had received oral contraceptives, anti-androgen therapy, or systemic antibiotics during the previous year, or isotretinoin therapy, prior to their participation in the study. Subjects were divided into groups on the basis of acne severity, as follows: physiological, mild and moderate. Only two patients had polycystic ovaries on ultrasound examination. Seven patients had irregular menses; none had evidence of hirsutism. We found that the severity of acne, based on the acne grade, was highly correlated with the inflammatory lesion count, and less correlated with the sebum excretion rate. Either acne grade or inflammatory lesion count could be related to some of the five androgenic hormone determinants; free testosterone (TESTOS), δ4 androstenedione (DELTA 4), sex hormone binding globulin (SHBG), dehydroepiandrostenedione sulphate (DHEAS) and dihydrotestosterone (DHT). Multiple linear regression analysis determined the best model for predicting ACNE score as involving DELTA 4 and DHEAS (positive effects), and SHBG (negative effect), P < 0.005, R2= 0.36). In none of the patients were the levels of DHEAS or SHBG outside the normal range. The flndings in the two patients with polycystic ovaries did not differ signiflcantly from those in the remainder of the patients.
    No preview · Article · Jul 2006 · British Journal of Dermatology
  • R Chatterjee · M Katz
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    ABSTRACT: The objective of this study was to determine whether iron toxicity in blood transfusion dependent beta-thalassemic patients with pubertal failure was associated with gonadotrophin (GTH) insufficiency as assessed by spontaneous and dynamic tests. Gonadotrophin-releasing-hormone (GnRH)-GTH secretory dynamics were studied by serial ultradian GTH profiles and a 100 microg i.v. GnRH bolus test (GBT) in 28 male beta-thalassemia major patients with failed puberty (FP group). Five healthy, non thalassemic prepubertal males were studied for comparative purposes. According to the pulse profile, patients in the FP group were subdivided into apulsatile (no FSH and LH pulses, n = 16; AFP group) and pulsatile (defective pulse profile, n = 12; PFP group) subsets. The FP group had lower basal FSH (p < 0.01), LH (p < 0.01) and GnRH stimulated FSH (p < 0.001) and LH levels (p < 0.001) than the controls. However, basal and GnRH-stimulated FSH (p < 0.01 for basal and p < 0.001 for peak) and LH (p < 0.01 for both basal and peak) levels were lower in the AFP than the PFP group. Serum ferritin levels in GnRH-non-responders were higher than those in the responders (9,052.63 +/- 579.14 mg/l vs 5,933.33 +/- 1,819.65 mg/l; p < 0.05). Similarly, symptomatic organ damage was higher in the AFP than the PFP patients (81% vs 42%; p < 0.001). In conclusion, this study suggests that iron overloaded thalassemic patients with failed puberty had abnormal GnRH-GTH secretory dynamics. The severity of the defect was heterogeneous, ranging from very severe (apulsatile) to less severe (pulsatile) subsets. Comparison between spontaneous and dynamic test levels showed that there was concordance between the degree of pulse defect and magnitude of LH response to GBT. However, ultradian GTH profile was a more reliable method for identifying the degree of GTH insufficiency than GBT. Our data also showed that iron toxicity was the major cause of GnRH-GTH deficiency in thalassemic patients. Such information may be useful for better understanding of the pathophysiology of hypogonadotrophic hypogonadism (HH), thereby promoting therapeutic options for induction of puberty and spermatogenesis.
    No preview · Article · Mar 2001 · Journal of pediatric endocrinology & metabolism: JPEM
  • R Chatterjee · M Katz
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    ABSTRACT: To determine the severity and reversibility of the lesion in the hypothalamic-pituitary (H-P) axis of male transfusion-dependent thalassaemic patients with failed puberty (FP). The hypothalamic-pituitary axes of 20 male thalassaemic patients (study group) were compared with two male subjects with idiopathic hypogonadotrophic hypogonadism (IHH) and five prepubertal healthy siblings (control group). GnRH-gonadotrophin insufficiency was characterized by nocturnal 12 h ultradian gonadotrophin profiles followed by a 100 microg GnRH bolus test (GBT) 4-6 times at 6 monthly intervals. Thalassaemic and IHH patients were then subjected to pulsatile subcutaneous GnRH infusions every 120 minutes for 3 months. Ultradian gonadotrophin profiles and GBT were repeated after 6 weeks of GnRH infusion and again at 3 months following infusion. FSH and LH were measured by radio-immunoassay. Ferritin was assayed by an immunoradiometric method. Patients with IHH who were apulsatile prior to infusion, developed normal gonadotrophin pulses with marked increment in their gonadotrophin responses to the GBT after 3 months of GnRH infusion. In contrast, the thalassaemic patients with apulsatile failed puberty (AFP) remained apulsatile (nonresponders) and had no increment in their gonadotrophin responses to the GBT after GnRH infusion. All patients with pulsatile failed puberty (PFP) had abnormal gonadotrophin pulses prior to GnRH infusion. Their pulse defects were either totally or partially corrected (responders) following infusion. The serum ferritin levels (9500 +/- 500 microg/l vs. 5966.67 +/- 1139 microg/l; P < 0.01) and percentage of organ dysfunction (87% vs. 17%; P < 0.01) were higher in the nonresponders than the responders. This study shows that thalassaemic patients with severe organ damage and iron overload are likely to be apulsatile with irreversible damage to their hypothalamo-pituitary axis, while those with less severe iron overload are likely to have potentially reversible hypogonadotrophic hypogonadism (HH). Our results also suggest that gonadotrophin pulse parameters, rather than the gonadotrophin response to a GnRH bolus following prolonged pulsatile GnRH infusion, may be more useful in discriminating reversible from irreversible hypogonadotrophic hypogonadism.
    No preview · Article · Jul 2000 · Clinical Endocrinology

  • No preview · Article · Jul 1998 · Annals of the New York Academy of Sciences
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    ABSTRACT: Androgenic stimulation of sebaceous glands is an important factor in the development of acne. We examined 36 females (aged 14-34 years), selected because none had received oral contraceptives, anti-androgen therapy, or systemic antibiotics during the previous year, or isotretinoin therapy, prior to their participation in the study. Subjects were divided into groups on the basis of acne severity, as follows: physiological, mild and moderate. Only two patients had polycystic ovaries on ultrasound examination. Seven patients had irregular menses; none had evidence of hirsutism. We found that the severity of acne, based on the acne grade, was highly correlated with the inflammatory lesion count, and less correlated with the sebum excretion rate. Either acne grade or inflammatory lesion count could be related to some of the five androgenic hormone determinants; free testosterone (TESTOS), delta 4 androstenedione (DELTA 4), sex hormone binding globulin (SHBG), dehydroepiandrostenedione sulphate (DHEAS) and dihydrotestosterone (DHT). Multiple linear regression analysis determined the best model for predicting ACNE scores as involving DELTA 4 and DHEAS (positive effects), and SHBG (negative effect), P < 0.005, R2 = 0.36). In none of the patients were the levels of DHEAS or SHBG outside the normal range. The findings in the two patients with polycystic ovaries did not differ significantly from those in the remainder of the patients.
    No preview · Article · Sep 1995 · British Journal of Dermatology
  • V De Sanctis · M Katz · C Vullo · B Bagni · M Ughi · B Wonke
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    ABSTRACT: The clinical picture of thalassaemia major has changed progressively over the years. Our study is a retrospective analysis of data on growth in a group of patients who have completed puberty spontaneously and have attained their adult height. Our objective was to evaluate the effect of different transfusion regimes and desferrioxamine administration on the growth pattern in beta-thalassaemia major. We studied 64 patients (28 males and 36 females). The patients were divided into three groups (A, B and C) according to the different transfusion regimes and the schedules of chelating therapy. Group A consisted of 16 patients who were transfused regularly at low haemoglobin levels (on average 8.5 g/dl) from an early age and started subcutaneous chelation therapy during adolescence. Group B consisted of 19 patients who were transfused regularly at high haemoglobin levels (on average 10 g/dl) from an early age and started subcutaneous therapy during childhood. Group C consisted of 29 patients who were transfused regularly at high haemoglobin levels (on average 10.5 g/dl) from an early age and started subcutaneous chelation therapy very early, at a mean age of 2 years. Standard auxological measurements were made at 3-monthly intervals throughout childhood and puberty until adult height was achieved. For group C patients the data on linear growth are provided only until the age of 12 years. Our study indicates that group A male and female patients did not grow significantly better than those in group B. Group C male and female patients, surprisingly, grew no faster than those who started chelation therapy late in childhood (group A). The most striking feature in the majority of both group A and B patients was reduced spurt in height at puberty. In addition, in both groups, a reduced sitting height due to spinal growth abnormality was found. An inverse correlation between sitting height and serum ferritin levels was observed in group A patients (r = -0.55, P < 0.05), whereas there was a direct correlation in group B patients (r = 0.42, P < 0.05). These data suggest that an ideal therapeutic regime has yet to be found which avoids the toxic effect of iron overload and on the other hand avoids interference with growth, secondary to desferrioxamine. Therefore we recommend that the growth of thalassaemia patients be monitored routinely at every follow-up visit and documented on growth velocity charts in order to detect early changes in their growth pattern and to establish an appropriate protocol for investigation and treatment.
    No preview · Article · Jul 1994 · Clinical Endocrinology
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    ABSTRACT: Pituitary-gonadal (P-G) function was evaluated 0-3 months before and 3-4 months after bone marrow transplantation (BMT) in 15 post-menarcheal females aged 17-30 (21.6 +/- 0.34) years with haematological malignancies. All patients had evidence of gonadal insufficiency prior to BMT in that their basal and human menopausal gonadotrophin (HMG)-stimulated oestradiol (E2) levels were significantly lower than those of control subjects. The patients also had markedly higher basal FSH levels and exaggerated responses to 100 micrograms iv gonadotrophin release hormone bolus compared with those of control subjects. However, the conditioning regimens employed prior to BMT, i.e. cytotoxic chemotherapy (CT) and total body irradiation (TBI), acting either singly or in combination, caused further ovarian damage. As a result, their gonadotrophins rose further into the menopausal range. Their oestradiol secretion diminished and ovaries became almost unresponsive 3-4 months after BMT. Pelvic ultrasound undertaken in 5 patients before and after BMT demonstrated a reduction in ovarian size associated with follicular depletion. All patients developed menopausal symptoms and became amenorrhoeic during this period. Contrary to expectation, the hormonal changes occurring acutely were similar in patients undergoing radiation-based regimens and those conditioned with high-dose chemotherapy alone. Also, the severity of ovarian dysfunction appeared independent of age at transplantation, the nature of the conditioning-regimen or the type of transplant. Gonadotrophic, thyrotrophic, lactotrophic and adrenocorticotrophic secretions were unaffected. These data indicate that the ovary suffers an acute insult during short-term chemotherapy but the anterior pituitary gland retains its trophic hormone reserve and secretory capacity.
    No preview · Article · Jun 1994 · Bone Marrow Transplantation
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    ABSTRACT: Thirteen post-pubertal male patients aged 17-25 years were assessed for pituitary-gonadal function 0-3 months prior to and 2-3 months post-bone marrow transplantation for haematological malignancy. All patients had multiagent cytotoxic treatment prior to transplantation and 30% were found to have germ cell dysfunction with abnormal semen parameters before high-dose therapy indicating damage to the germinal epithelium. They also had evidence of reduced Leydig cell reserve even before transplantation. During transplantation all patients sustained sustained gonadal injury, the effect on their germ cells being more pronounced than on the Leydig cells. Fifty per cent had reduction in testicular volume and all had azoospermia 2-3 months post-transplantation. Our results indicate that short-term chemoradiotherapy causes profound damage to the germ cell compartment of the testis, with less severe damage to the Leydig cells, but no overt injury to the anterior pituitary gland. The changes appeared to be identical in patients conditioned with total body irradiation-based protocols and those who received only high-dose chemotherapy prior to bone marrow transplantation.
    No preview · Article · Jun 1994 · Bone Marrow Transplantation
  • R Chatterjee · M Katz · T F Cox · J B Porter
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    ABSTRACT: We aimed to prospectively evaluate during 10 years the GnRH-gonadotrophin secretory dynamics in a cohort of 15 menstruating girls with beta-thalassaemia major to determine whether they sustained progressive damage to this axis. Patients were characterized by 12-hour gonadotrophin profiles (by sampling blood at 15-minute intervals) and assessment of gonadotrophin responses to 100 micrograms GnRH bolus (by sampling blood at 20-minute intervals for 1 hour and at 2 hours) sequentially during the follicular and luteal phases of their menstrual cycles, 12-14 months and 5-6 years after the onset of secondary amenorrhoea. We studied 15 post-menarcheal thalassaemic girls and five age-matched control subjects who were the healthy siblings of the patients. FSH and LH assays were determined using commercial RIA systems and double antibody techniques. Pulse detection used the Pulsar technique of Merriam and Wachter. We demonstrated that during their amenorrhoeic period, all thalassaemic patients had gonadotrophin pulse abnormalities and low-normal GnRH-stimulated gonadotrophin levels indicating that they had GnRH-gonadotrophin secretory insufficiency. During the subsequent 10 years there was progressive deterioration of hypothalamic-pituitary function in all patients; 66% became apulsatile and all had marked reduction in their GnRH-stimulated gonadotrophin levels. Our investigation suggests that thalassaemic patients with secondary amenorrhoea had severe and progressive damage to their hypothalamic-pituitary axes despite intensive chelation therapy.
    No preview · Article · Oct 1993 · Clinical Endocrinology
  • R Chatterjee · M Katz · T.F. Cox · H Bantock
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    ABSTRACT: Growth hormone (GH) secretion was determined by evaluating ultradian GH profiles for 12 h and GH responses to insulin stimulated hypoglycaemia (ITT) in 28 stunted boys with beta-thalassaemia major aged 15.2-17.4 years, who presented with pubertal failure (FP). Healthy non thalassaemia prepubertal boys (n = 10) aged 7.5-8.8 years, were studied as controls. All patients had normal responses to ITT with peak GH levels > or = 15 mU/l. Basal GH concentrations (mean +/- sem) (1.65 +/- 0.03 mU/l vs 2.58 +/- 0.27 mU/l; P < 0.05) and the stimulated GH responses (peak GH = 15.4 +/- 0.20 mU/l vs 21.08 +/- 0.78 mU/l; P < 0.001) were significantly lower in the patients with failed puberty than in the controls, indicating that the FP patients had diminished GH reserve and secretory capacity. Moreover, all the GH peak parameters including the maximum spontaneous concentrations (MX-GH) and the area under the GH curve (AUC) were significantly lower in the thalassaemic patients than in the controls (MX-GH = 5.2 +/- 0.21 mU/l vs 20.42 +/- 0.14 mU/l; P < 0.001; AUCb = 421.22 +/- 4.31 mU/l vs 712.20 +/- 3.42 mU/l; P < 0.001). These observations suggest that the thalassaemic patients had endogenous neurosecretory GH deficiency (GHND). Priming with sex steroid did not cause any improvement in the spontaneous or stimulated GH secretory patterns in thalassaemic patients. It was noteworthy that in neither the patients nor the control subjects, was there a significant correlation between the maximum stimulated and the MX-GH concentrations.(ABSTRACT TRUNCATED AT 250 WORDS)
    No preview · Article · Sep 1993 · European Journal of Pediatrics
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    ABSTRACT: To assess the pharmacokinetics of oral, intramuscular, or transdermal hormone replacement in patients with beta thalassaemia major. Oral (testosterone undecanoate 40 mg) and intramuscular (testosterone propionate 15 mg, phenylpropionate 30 mg, isocaproate 30 mg and decanoate 50 mg) testosterone and transdermal (17 beta oestradiol 25 micrograms and 50 micrograms) oestradiol were evaluated in 21 male (16-29 years) and 11 female (19-26 years) patients with beta thalassaemia major and various forms of hypogonadism. In male patients given oral testosterone, peak testosterone concentrations were observed either two to four hours or seven hours after administration; intramuscular testosterone produced peak values seven days after injection. Transdermal 17 beta oestradiol given to female patients produced a biphasic pattern with an initial peak concentration occurring at 36 hours and a secondary rise at 84 hours. The results indicate that oral androgens should be given twice daily in cases of hypogonadism, and where growth is incomplete, lower than recommended doses. If intramuscular testosterone is used, smaller doses of 10-25 mg should be given every one to two weeks. Transdermal administration of 25-50 micrograms 17 beta oestradiol generally produces a plasma E2 value in the early to mid-follicular phase range (100-300 pmol/l). This is appropriate in adults but excessive for prepubertal girls. Diffuse iron infiltration of tissues does not seem to interfere with the absorption of androgens and oestrogens from the gut, muscle, or skin.
    Preview · Article · Aug 1993 · Journal of Clinical Pathology
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    Full-text · Article · Feb 1990 · Annals of the New York Academy of Sciences

  • No preview · Article · Feb 1989 · Progress in clinical and biological research

  • No preview · Article · Feb 1989 · Progress in clinical and biological research
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    ABSTRACT: In an attempt to induce or to augment pubertal development and to achieve spermatogenesis, 10 gonadotropin-deficient thalassemic patients 15 to 23 years of age (mean 18.9 years) were treated with exogenous gonadotropins for 1 to 4 years (mean 2.1 years). Seven patients produced sperm during human chorionic gonadotropin (hCG) treatment given for 6 to 14 months. However, full spermatogenesis was achieved only when human menopausal gonadotropin was added to hCG regimen. In one patient, despite cessation of gonadotropin treatment, sexual potency, libido, and spermatogenetic capacity were maintained during the past 2 1/2 years. Our study indicates that it is possible to induce or to restore spermatogenesis in the majority of thalassemic patients and that gonadotrope cells may not be irreversibly damaged by iron deposition.
    No preview · Article · Jan 1989 · Fertility and Sterility
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    ABSTRACT: Eight thalassemic patients, aged 24-35 years, who developed amenorrhea 2-15 years after menarche, were studied. Mean basal serum LH and FSH levels and the peak levels after gonadotropin-releasing hormone were significantly less than corresponding values in normal controls. All patients showed low basal serum levels of estradiol and six had a poor or absent response to human menopausal gonadotropin. One subject had intact pituitary-gonadal function and one patient had an impaired LH and FSH response to gonadotropin-releasing hormone in the presence of a significant increase of estradiol after human menopausal gonadotropin stimulation. The findings regarding pituitary hormones other than gonadotropins suggest that iron overload damages tropic cells unequally and inconsistently. We conclude that both pituitary and gonadal damage may be responsible for the secondary amenorrhea in thalassemic patients.
    No preview · Article · Nov 1988 · Obstetrics and Gynecology
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    V De Sanctis · C Vullo · M Katz · B Wonke · R Tanas · B Bagni
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    ABSTRACT: Endocrine studies were made on 23 female patients aged 13 to 29 years, with delayed puberty or primary amenorrhoea and beta thalassaemia major, and 12 healthy controls, of whom six were prepubertal and six were in Tanner's stage 3-4. Each patient and control received a single intravenous dose of 100 micrograms gonadotrophin releasing hormone (GnRH), and one week later, 10 U/kg body weight of human menopausal gonadotrophin (hMG) to stimulate ovarian function. The patients had decreased gonadotrophin reserves when compared with those of normal controls, only one of 23 patients had an intact luteinising hormone and follicle stimulating hormone response. Most of the thalassaemic patients with delayed puberty showed normal gonad response to human menopausal gonadotrophin (hMG), but three had very low responses, when compared with that of controls. The gonadal failure was even more severe in four of six patients with primary amenorrhoea. It is important to assess hypothalamic-pituitary-gonadal function in young women with beta thalassaemia major, so that those with glandular dysfunction may be started on replacement therapy.
    Full-text · Article · Mar 1988 · Journal of Clinical Pathology

  • No preview · Article · Feb 1987 · Birth defects original article series