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Rev Neurol. 2002 Oct 16-31;35(8):741-2.
[Hypothyroidism concealed by Parkinson's disease]

[Article in Spanish]

Garcia-Moreno JM, Chacon J.

Servicio de Neurologia, Hospital Universitario Virgen Macarena, Sevilla, Espana. sinurrakis.es

AIMS: Although it is commonly recognised that diseases of the thyroids can simulate extrapyramidal disorders, a review of the causes of Parkinsonism in the neurology literature shows that they are not usually mentioned or, if so, only very briefly. The development of hypothyroidism in a patient with Parkinson s disease can go undetected, since the course of both diseases can involve similar clinical features. Generally speaking there is always an insistence on the need to conduct a thyroidal hormone study in any patient with symptoms of Parkinson, but no emphasis is put on the need to continue to rule out dysthyroidism throughout the natural course of the disease, in spite of the fact that the concurrence of both pathological conditions can be high and that, in the same way hypothyroidism can simulate Parkinson s disease, the latter can also conceal hypothyroidism. CASE REPORT: We report the case of a female patient who had been suffering from Parkinson s disease for 17 years and started to present on off fluctuations that did not respond to therapy. Hypothyroidism was observed and the hormone replacement therapy used to resolve the problem allowed the Parkinsonian fluctuations to be controlled. CONCLUSIONS: We believe that it is very wise to suspect hypothyroidism in patients known to be suffering from Parkinson s disease, and especially so in cases where the clinical condition worsens and symptoms no longer respond properly to antiparkinsonian treatment. These observations stress the possible role played by thyroid hormones in dopaminergic metabolism and vice versa.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12402227&dopt=Abstract

Gan To Kagaku Ryoho. 2002 Oct;29(10):1773-8.
[Low-dose cisplatin and UFT for hormone refractory prostate cancer]

[Article in Japanese]

Hoshi S, Ohyama C, Namiki S, Hagisawa S, Satoh M, Saito S, Ono K, Shirasaka T, Arai Y.

Dept. of Urology, Tohoku University School of Medicine.

OBJECTIVES: Biochemical modulation (BM) was initially used to enhance the effect of 5-fluorouracil (5-FU) by modulating its pharmacological action with the addition of other drugs. BM with low-dose cisplatin and 5-FU or UFT has been examined in cases of advanced gastric or pancreas cancer and 30 to 40% response rates have been reported. In the present study, the effect of BM on hormone refractory prostate cancer (HRPC) patients was examined. METHODS: BM consisting of 5 mg/body of cisplatin 3 times per week and 300-450 mg of UFT/day was given to 30 HRPC patients (median and range of age: 66 and 52-72, respectively). The ECOG performance status was 0 to 1. Gleason score was 7 in 8 patients, 8 in 10 patients and 9 in 12 patients, respectively. The metastatic site was bone in 29 patients (extent of disease on bone scan [EOD] grade 1: 10, 2: 10, 3: 8, 4: 1), lymph node in 8 and liver in 1. RESULTS: Among the 29 patients assessable for bone metastasis, 5 (17%) obtained marked improvement on bone scan. One was EOD grade 4 (super bone scan) and 4 were EOD grade 1-3. Eight (28%) were stable and 16 (55%) progressed on bone scan. Among 8 patients with lymph node metastasis, 4 (50%) showed partial response and 4 (50%) progression. One patient with liver metastasis showed complete response. Fourteen (47%) out of 30 patients showed a PSA decline of 50% or greater. Their median response duration was 8 months (range; 2 to 44 months). Among the 25 patients assessable for bone pain, 7 (28%) improved, 12 (48%) remained stable and 6 (24%) progressed. A side effect of Grade II anemia was seen in one patient. CONCLUSION: BM is effective in almost half of hormone refractory prostate cancer patients.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12402428&dopt=Abstract

Gan To Kagaku Ryoho. 2002 Oct;29(10):1795-9.
[A case of effective bisphosphonate therapy for bone metastasis from breast cancer with multiorganic metastases]

[Article in Japanese]

Sueyoshi K, Ogura Y, Komori T, Takahashi M, Tian TX, Tatsumi T, Matsuki M, Saika Y, Uesugi Y, Utsunomiya K, Inomata Y, Narabayashi I.

Dept. of Radiology, Osaka Medical College.

A 50-year-old woman with a past history of breast cancer was referred to our department of radiology for detailed examination after abnormal shadows on chest x-ray were detected following a routine medical examination. After lung biopsy via thoracotomy, segmental resection of the lung was performed and mediastinal lymph nodes were dissected. A histopathological diagnosis of breast cancer with lung metastasis and mediastinal lymph-node metastases was made. Later, the patient complained of pain in the left lower extremity. A diagnosis of a left tibial metastasis was made according to bone scintigraphy and MRI. Radiation therapy at 50 Gy was then initiated. Chemotherapy and hormone therapy combined with bisphosphonate therapy (Bisphonal, once in 2 weeks), was also begun. During the treatment, the patient had multiple organ metastases including multiple brain metastases, and metastases to submental lymph nodes and the left adrenal gland. However, her bone metastasis was limited to the left tibial bone and no other bone lesions were detected by bone scintigraphy and MRI. She did not experience adverse effects from the bisphosphonate therapy. We consider that the inhibition of extension and further metastases of the tibial bone metastasis noted in this patient reflected the efficacy of bisphosphonate therapy, and that bisphosphonate therapy might become an essential treatment in patients with bone metastasis of breast cancer.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12402432&dopt=Abstract

Endocr J. 2002 Aug;49(4):503-9.
Body fat distribution and cardiovascular disease risk factors in pre- and postmenopausal obese women with similar BMI.

Ozbey N, Sencer E, Molvalilar S, Orhan Y.

Department of Internal Medicine, Istanbul Faculty of Medicine, Capa, Turkey.

The aim of this study is to determine the body fat distribution and cardiovascular disease risk factors in pre- and postmenopausal obese women matched for weight, height and body mass index (BMI). Study group consisted of 405 premenopausal overweight/obese (BMI > 27 kg/m2, mean 37.83 +/- 6.91 kg/m2) and 405 postmenopausal overweight/obese (BMI > 27 kg/m2), BMI-matched (mean 37.77 +/- 6.84 kg/m2) women. None of the women were on hormone replacement therapy. Insulin resistance was evaluated by "homeostasis model assessment" (HOMA) formula. Intraabdominal fat volume was calculated according to the following formula: IAF (L) = [(0.370 x abdominal sagittal diameter) - 4.85]. Age, waist circumference, waist to hip ratio (WHR) and intraabdominal fat volume were significantly higher in postmenopausals compared with BMI-matched premenopausal women (p < 0.001). Systolic and diastolic blood pressure, glucose, uric acid, cholesterol and triglyceride were significantly higher (p < 0.001) and HDL-cholesterol was significantly lower (p < 0.05) in postmenopausals. No significant differences were observed with respect to insulin and HOMA. When age-matched pre- and postmenopausal women were compared, only total cholesterol was significantly higher in the postmenopausal group. However, older postmenopausal women (> 50 years) had significantly higher systolic blood pressure, waist circumference, WHR, glucose and uric acid concentrations compared with younger (< or = 50 years) postmenopausals. It is concluded that an increase in abdominal fat accumulation and unfavorable alterations in risk factors disturb postmenopausal obese women even if total body weight and BMI do not change during menopause transition. Ageing, particularly throughout the postmenopausal years, has important effects on the detrimental changes associated with menopause.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12402983&dopt=Abstract

Biochemistry. 2002 Nov 5;41(44):13217-23.
Residue 19 of the parathyroid hormone: structural consequences.

Piserchio A, Shimizu N, Gardella TJ, Mierke DF.

Department of Chemistry, Brown University, Providence, Rhode Island 02912, USA.

Residue 19 of the parathyroid hormone (PTH) has been shown to play an important role in both binding to and activation of the PTH receptor; specifically, Arg(19)-containing analogues have improved biological function over similar Glu(19) peptides [Shimizu et al. (2002) Biochemistry 41, 13224-13233]. Additionally the juxtamembrane portion of the receptor is involved in the different biological responses. Here, we determine the conformational preferences of PTH analogues to provide a structural basis for their biological actions. On the basis of circular dichroism results, the Arg(19) --> Glu(19) mutations within the context of both PTH(1-20) and PTH(1-34) analogues lead to increases in helix content, ranging from a 8-15% increase. High-resolution structures as determined by (1)H NMR and NOE-restrained molecular dynamics simulations clearly illustrate the difference between Arg(19) and Glu(19)-PTH(1-20), particularly with the extent and stability of the C-terminal helix. The Arg(19)-containing analogue has a well defined, stable alpha-helix from Ser(4)-Arg(19), while the Glu(19) analogue is less ordered at the C-terminus. On the basis of these observations, we propose that position 19 of PTH(1-20) must be alpha-helical for optimal interaction with the juxtamembrane portion of the receptor. This mode of binding extends the current view of PTH binding (indeed ligand binding for all class B GPCRs), which invokes a bihelical ligand with the C-terminus of the ligand interacting with the N-terminus of the receptor (responsible for binding) and the N-terminus of the ligand interacting with the seven-helical bundle (leading to receptor activation).

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12403623&dopt=Abstract

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