[A case report of diabetic scleredema in a patient with non-insulin-dependent diabetes mellitus].

A 70-year-old Japanese man with non-insulin-dependent diabetes mellitus showed scleredema diabeticorum. The patient complained of edematous feelings on his hands, both arms and face. The time of onset of these symptoms was not known. He had typical clinical and histopathological findings of diabetic scleredema. His diabetic control was poor and HbA1c level was 8.2% under insulin treatment. The patient had many complications such as diabetic retinopathy, diabetic nephropathy with benign nephrosclerosis, hyperlipidemia accompanied with a low level of high density lipoprotein cholesterol, hypertension and coronary heart disease. There were no abnormal laboratory findings except the diabetic controls and mild abnormal renal functions; however erythrocyte sedimentation rate was high.

Lateral hypothalamic injection of GABA(A) antagonist induces gastric vagus-mediated hypocalcemia in the rat.

The involvement of lateral hypothalamic area (LHA) neurons in the regulation of blood calcium homeostasis was investigated in unanesthetized rats. The microinjection of the gamma-aminobutyric acid A receptor antagonist bicuculline methiodide (BM, 4-40 ng x 0.5 microl(-1) x 5 min(-1)) into the LHA decreased the blood concentration of ionized calcium. Total serum calcium also decreased after the BM injection. This hypocalcemic effect was eliminated by a bilateral vagotomy of the gastric branches. An intravenous injection of atropine methyl bromide (a muscarinic antagonist), nadolol (a beta-adrenergic blocker), or ranitidine (a histamine H2 blocker) suppressed the BM-induced hypocalcemia, whereas phenoxybenzamine (an alpha-adrenergic blocker) proved to be ineffective. Although the intra-LHA injection of BM increased the serum gastrin, which is known to have a hypocalcemic effect, neither secretin nor somatostatin (gastrin-release inhibitors) blocked the hypocalcemic response. These results suggest that the hypocalcemia observed after the excitation of LHA neurons was mediated by muscarinic, beta-adrenergic, and histamine H2 receptors through the gastric vagus.

Hypothalamus regulates calcium metabolism in rats.

Hypothalamic mechanisms of blood calcium homeostasis and their functional heterogeneity were investigated in rats. Electrical and chemical stimulation of the lateral hypothalamic area (LHA), the paraventricular nucleus (PVN) and the ventromedial nucleus of the hypothalamus (VMH) induced hypocalcemia. The hypocalcemic effect of PVN stimulation was suppressed by vagotomy of the thyroid/parathyroid branches, while that of LHA and VMH stimulation was eliminated by gastric vagotomy. Immobilization (IMB) stress elicited hypocalcemia through VMH-gastric vagal activation. Both IMB- and LHA stimulation-induced hypocalcemia was antagonized by muscarinic antagonist and histamine H2 blocker. The former was also blocked by alpha-blocker and gastrin release inhibitor, while the latter was antagonized by an beta-blocker. The results suggest that hypothalamic nuclei are involved in regulation of blood calcium homeostasis via the gastric or thyroid/parathyroid vagus. Muscarinic, histamine H2, adrenergic and gastrin receptors mediate the hypocalcemic effect of the hypothalamo-vagal activation depending on behavioral conditions and receptor subtypes.

The stomach is the etiologic organ for immobilization-induced hypocalcemia in rats.

Our previous study revealed that the gastric vagus nerve plays an etiologic role in immobilization (IMB) stress-induced hypocalcemia. The purpose of the present study is to identify exactly what parts of the stomach are involved in the development of IBM-induced hypocalcemia and to determine whether or not gastric acid secretion is involved. A total gastrectomy, but not a resection of the upper intestine, eliminated the hypocalcemic effect of IMB. In addition, either an antrectomy (removal of the source of gastrin) or a fundectomy (depriving the origin of gastric histamine and gastric acid) was sufficient for eliminating IMB-induced hypocalcemia, while a partial (50%) fundectomy failed to suppress it. An intraperitoneal injection of galanin (an inhibitor of gastrin release) or ranitidine (a blocker of histamine H2-receptor) also suppressed the calcium-lowering effect of IBM, whereas omeprazole (an inhibitor of the proton pump) had no effect. These findings suggest that the antrum and the fundus of the stomach play essential roles in IMB-induced hypocalcemia through the vagus-induced release of gastrin and histamine but not through the secretion of gastric acid per se.

[A case of pulmonary sarcoidosis which exacerbated bronchial asthma in remission].

A 34-year-old woman had history of bronchial asthma in childhood, was admitted complaining of coughs and wheezes. Chest X-ray examinations showed bilateral hilar lymphadenopathy. A diagnosis of bronchial asthma was made because of her past history, reversible airflow limitation and moderate bronchial hyperreactivity. In addition, findings of chest X-ray films and TBLB specimens were indicative of pulmonary sarcoidosis. When bilateral hilar lymphadenopathy disappeared, her wheezes and bronchial hyperreactivity also improved. In this case, it was suggested that pulmonary sarcoidosis was a factor which worsened bronchial hyperreactivity and bronchial asthma which had been in remission.

[A case of silo-fillers' disease].

A 52 year-old male farmer was admitted to our hospital because of cough, sputum and dyspnea on exertion. Chest X-ray showed pulmonary edema and arterial blood gas analysis showed hypoxemia. Silo-fillers' disease was diagnosed because he had allegedly inhaled yellowish gas in the silo. The day following steroid therapy, symptoms and pulmonary edema improved. Silo-fillers' disease is chemical pneumonitis due to exposure to the oxides of nitrogen which are produced in silos. Although reported cases of silo-fillers' disease in Japan are rare it should be kept in mind in areas involved with dairy farming.