Bertram J. Channick

The response of bone to metabolic acidosis in man.

Abstract A metabolic acidosis was produced in obese women by a fasting regimen with no caloric intake. The acidosis was then partially corrected by administering NaHCO 3 while continuing caloric starvation. During acidosis the net negative calcium balance was 156 mg. daily and during the alkali administration this calcium loss was reduced to 51 mg. daily. It was calculated that the anions lost from bone accompanying the calcium loss would combine with 4–8 mMoles H + daily and thus act as a buffer for the extracellular fluid during the acidosis.

Salivary Sodium-Potassium Ratio and Plasma Renin Activity in Hypertension

The cause of the suppression of plasma renin activity (PRA) in many patients with essential hypertension and normal aldosterone excretion is unknown. Since mineralocorticoid excess can lower PRA, we attempted to evaluate the activity of salt-retaining hormones in these patients by measuring the salivary Na/K ratio. The median Na/K ratio in 20 hypertensive patients with suppressed PRA and normal or low aldosterone excretion was 0.71. This was significantly lower than the median of 1.38 in 29 normal subjects and the median of 1.05 in 15 hypertensive patients with normal PRA.Excess dietary intake of salt is a possible cause of PRA suppression in these patients, but our findings indicate that high rather than low Na/K ratios would be expected if this were present. On the other hand, both the salivary electrolyte changes and the suppression of PRA are consistent with the hypothesis that mineralocorticoid excess is present in these patients, despite the failure to demonstrate elevated excretion of aldosterone.

Chronic Thyroiditis and Mitral Valve Prolapse

Mitral valve prolapse is more prevalent in patients with autoimmune diffuse toxic goiter, suggesting a possible etiologic association. The prevalence of mitral valve prolapse was determined in 75 patients with chronic lymphocytic thyroiditis, another autoimmune thyroid disorder, and in 50 healthy control subjects. Mitral valve prolapse was found in 31 of 75 (41%) patients with chronic lymphocytic thyroiditis and in 4 of 50 (8%) controls (odds ratio, 8.10; 95% confidence interval, 2.64 to 24.83; p less than 0.0005). The age-race adjusted odds ratio was 9.26 (95% confidence interval, 2.83 to 30.26; p less than 0.0005). No correlation between the prevalence of mitral valve prolapse and the presence of hypothyroidism, serum antithyroid antibodies, or the duration of chronic lymphocytic thyroiditis was found. The prevalence of mitral valve prolapse is substantially increased in patients with the autoimmune thyroid disorders.

The pressor response to angiotensin II in patients with low renin essential hypertension.

SUMMARY The etiology of low renin essential hypertension (LREH) has not been established with certainty, but mineralocorticoid excess has been implicated frequently in its pathogenesis. The finding of several investigators of a normal exchangeable sodium space and extracellular fluid volume, however, does not support this hypothesis. To evaluate the possible role of sodium and water retention in LREH, the pressor response to infused angiotensin II (A II) was determined and compared to that of normal subjects and that of subjects with normal renin essential hypertension (NREH). This approach was based on the known suprasensitivity of vascular receptors to A II in situations in which sodium and water compartments are expanded as they are, for example, in proven hypermineralocorticoid states such as primary aldosteronism. In this study, we found that subjects with LREH demonstrated no increased pressor response to graded doses of A II; this suggests that LREH is not primarily mediated by sodium and water retention.

Long-term follow-up of patients with Grave's disease treated by subtotal thyroidectomy

This long-term follow-up study of 83 patients with Graves disease who were treated by subtotal thyroidectomy reemphasizes the fact that postoperative hypothyroidism occurs primarily in the first postoperative year (27 percent of the study patients). In addition, there was no evidence of progressive increase in the incidence of hypothyroidism in subsequent years. Patients treated with radioactive iodine have a reported incidence of hypothyroidism of 70 percent 10 years postoperatively [4]. The 6 percent incidence of recurrent hyperthyroidism is much less than a reported incidence of 90 percent in patients treated with long-term antithyroid drugs [7]. Subtotal thyroidectomy continues to be an excellent method of treatment for patients with Graves disease and compared favorably with both radioactive iodine and long-term antithyroid drugs.

Dietary salt intake in hypertensive patients with normal and low plasma renin activity.

It is not known why many patients with essential hypertension have low plasma renin activity. Since excessive intake of sodium could cause this abnormality, we attempted to estimate the dietary salt intake in 30 hypertensive patients by means of dietary histories and measurement of urinary sodium excretion while the patients ate their customary diet Fifteen patients with low plasma renin activity did not differ significantly from fifteen patients with normal renin activity in daily urinary sodium excretion (161.9 versus 141.2 mEq per 1.73 square meters) or in estimated dietary sodium intake (168.1 versus 203.5 mEq per 1.73 square meters). This suggests that excess salt ingestion is not a common cause for renin suppression in these patients.

The Salivary Sodium/Potassium Ratio in Hypertension: Relation to Race and Plasma Renin Activity

We have studied the relationship between plasma renin activity (PRA) and the salivary Na:K ratio, an index of mineralocorticoid effect, in 223 patients with essential hypertension. In 24 white patients with low PRA the median Na:K ratio was 0.74, which was significantly lower than the ratio of 1.40 in 54 normal white subjects (P less than .005) and the ratio of 1.10 in 34 white hypertensive patients with normal PRA (P less than .005). The Na:K ratio in 71 black patients with low PRA was 1.06, which was not significantly lower than the ratio of 1.50 in 38 black normal subjects or the ratio of 1.56 in 94 black hypertensive patients with normal PRA. These findings indicate a difference in salivary Na:K ratios between white and black patients with low renin essential hypertension, and suggest that mineralocorticoid excess may be a more frequent cause of low renin essential hypertension in white than in black patients.

Serum immunoglobulins in hypertension.

SUMMARY We measured serum immunoglobulins in 52 persons whose blood pressure was higher than 140/90 mm Hg, and 52 normotensive controls matched for age, sex and race. All were selected from a population of actively employed persons undergoing a routine health evaluation. Contrary to previous reports, the hypertensive subjects did not have higher levels of IgG or IgA than the controls. Sixteen hypertensive subjects with mean blood pressure higher than 115 mm Hg did not have elevated IgG or IgA levels when analyzed separately. Serum IgM was significantly lower in the 52 hypertensive subjects (125 ± 67 mg/dl vs 171 ± 85 mg/dl, p < 0.01).Our subjects failed to show the increase in immunoglobulins reported by others. The most likely reason for this is the mildness of their blood pressure elevation, although the absence of immunoglobulin elevation in the small number with more marked hypertension does not support this explanation.

BOECK'S SARCOIDOSIS SIMULATING HYPERPARATHYROIDISM

Excerpt That Boecks sarcoidosis could be mistaken for hyperparathyroidism was pointed out by Albright and Reifenstein1several years ago. They noted that bone changes, high serum alkaline phosphata...

Oral Clonidine for Rapid Control of Accelerated Hypertension

Thirty emergency‐room patients, 15 men and 15 women, from 27 to 64 years old with diastolic blood pressures (DBP) >115 mm Hg, were admitted to an open‐label, oral loading trial of clonidine. At this time, their supine mean arterial pressures (MAP) averaged 150 ± 2 mm Hg. An initial clonidine dose of 0.1 to 0.2 mg was to be followed every hour by another 0.1 mg until the DBP had been lowered to a level allowing treatment to be continued on an ambulatory basis or until a total of 0.5 mg had been given. A satisfactory response—defined as a reduction of the supine DBP to 105 mm Hg or lower if the baseline was between 115 and 135 mm Hg, or reduction of a baseline DBP >135 mm Hg by at least 30 mm Hg—was achieved in all but one of the patients in an average of 118 minutes; the mean dose required was 0.26 mg. The mean reduction from the baseline MAP was 23.1 ± 0.9%. Drug‐related adverse experiences comprised drowsiness and dry mouth in 13 patients. Thereafter, 28 of the patients were chronically treated with clonidine for an average of 73 days. In 24 patients treated for at least 80 days, the daily clonidine dose averaged 0.375 mg. All the patients required concurrent diuretic therapy. A satisfactory response (as defined above) to this maintenance treatment was shown by 85% of the patients, and full blood‐pressure control (supine DBP <95 mm Hg) was attained in 78%. The mean decreases from the baseline systolic and diastolic readings (taken before the acute treatment phase) amounted to 28.6% ± 2.5% and 19.8% ± 1.3%, respectively. Side effects were essentially the same as during the oral loading phase.