Gynaecomastia associated with cimetidine.

Spence, Rebecca; Celestin, Louis-Cyril

doi:10.1136/gut.20.2.154

Cited by 67 publications

(28 citation statements)

References 12 publications

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“…However, they differ from one study reporting thymic carcinoids as the most frequent cause of MEN1 related deaths (i.e. 24% compared to 10% for malignant PETs), and from 12 series in which either thymic carcinoids did not cause death of any patients 15,54,57,78,88,226,254,289,367,394,463 or caused only a small percentage of MEN1 related deaths (5–6%) 150,378,379,465 which was much less than seen with malignant PETS. Almost all of these latter series not reporting thmic carcinoids in MEN1 patients were older series.…”

Section: Discussioncontrasting

confidence: 84%

Causes of Death and Prognostic Factors in Multiple Endocrine Neoplasia Type 1

et al. 2013

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Multiple endocrine neoplasia type 1 (MEN1) is classically characterized by the development of functional or nonfunctional hyperplasia or tumors in endocrine tissues (parathyroid, pancreas, pituitary, adrenal). Because effective treatments have been developed for the hormone excess state, which was a major cause of death in these patients in the past, coupled with the recognition that nonendocrine tumors increasingly develop late in the disease course, the natural history of the disease has changed. An understanding of the current causes of death is important to tailor treatment for these patients and to help identify prognostic factors; however, it is generally lacking.To add to our understanding, we conducted a detailed analysis of the causes of death and prognostic factors from a prospective long-term National Institutes of Health (NIH) study of 106 MEN1 patients with pancreatic endocrine tumors with Zollinger-Ellison syndrome (MEN1/ZES patients) and compared our results to those from the pooled literature data of 227 patients with MEN1 with pancreatic endocrine tumors (MEN1/PET patients) reported in case reports or small series, and to 1386 patients reported in large MEN1 literature series. In the NIH series over a mean follow-up of 24.5 years, 24 (23%) patients died (14 MEN1-related and 10 non-MEN1-related deaths). Comparing the causes of death with the results from the 227 patients in the pooled literature series, we found that no patients died of acute complications due to acid hypersecretion, and 8%–14% died of other hormone excess causes, which is similar to the results in 10 large MEN1 literature series published since 1995. In the 2 series (the NIH and pooled literature series), two-thirds of patients died from an MEN1-related cause and one-third from a non-MEN1-related cause, which agrees with the mean values reported in 10 large MEN1 series in the literature, although in the literature the causes of death varied widely. In the NIH and pooled literature series, the main causes of MEN1-related deaths were due to the malignant nature of the PETs, followed by the malignant nature of thymic carcinoid tumors. These results differ from the results of a number of the literature series, especially those reported before the 1990s. The causes of non-MEN1-related death for the 2 series, in decreasing frequency, were cardiovascular disease, other nonendocrine tumors > lung diseases, cerebrovascular diseases. The most frequent non-MEN1-related tumor deaths were colorectal, renal > lung > breast, oropharyngeal. Although both overall and disease-related survival are better than in the past (30-yr survival of NIH series: 82% overall, 88% disease-related), the mean age at death was 55 years, which is younger than expected for the general population.Detailed analysis of causes of death correlated with clinical, laboratory, and tumor characteristics of patients in the 2 series allowed identification of a number of prognostic factors. Poor prognostic factors included higher fasting gastrin levels, presence of othe...

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Section: Discussioncontrasting

confidence: 84%

Causes of Death and Prognostic Factors in Multiple Endocrine Neoplasia Type 1

et al. 2013

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“…This accords with earlier studies investigating cimetidine in this respect, although gynaecomastia has sometimes been observed (Hall, 1976;Delle Fave et al, 1977;Spence & Celestin, 1979). However intravenous cimetidine and ranitidine increase prolactin concentrations (Delitala et al, 1979;Knigge et al, 1981).…”

Section: Discussionsupporting

confidence: 79%

The effects of ranitidine on pituitary‐thyroid function.

Kr¹,

Harrop²,

Hopton³

et al. 1984

Brit J Clinical Pharma

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Although several studies have examined the effects of cimetidine on pituitary-thyroid function, few have investigated ranitidine in this respect. We found no changes in thyroid-stimulating-hormone (TSH) or prolactin responses to TSH-releasing-hormone (TRH) in 10 patients with peptic ulcer disease given oral ranitidine. Serum total and free thyroxine (Ti4 and FT4) concentrations declined slightly, whereas total and free triiodothyronine (Ti3 and FIT3) increased slightly following ranitidine. None of these changes achieved statistical significance. Both the ratio of TT4ITi3 and FT4/FI3, however, declined (P < 0.05) following ranitidine. Thus ranitidine may have a minor influence on peripheral deiodination of thyroxine but has little effect on hormone production from the thyroid gland. The diagnostic value of biochemical tests of thyroid function is not seriously compromised in patients receiving ranitidine.

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“…Although the development of gynaecomastia in the contralateral breast may have been related to the intake of cimetidine at that time (Spence & Celestin 1979), it is most unlikely that the same drug was responsible for the development of the haemangioma because of the long time interval between stopping the drug and the appearance of the lesion. On the other hand, the strong family history of neoplastic diseases, including those of the breast, raises the possibility that this patient's breasts may have been genetically more susceptible than usual to the development of pathological lesions.…”

Section: Discussionmentioning

confidence: 99%