IN RECENT years abuse of barbiturates has become a problem of increasing concern to physicians, various lay groups, law enforcement officers and legislators. The production of barbiturates has steadily increased and now appears to exceed greatly the amount needed for therapeutic purposes.1In 1948 the total production of barbiturates in the United States was 672,000 pounds (336,000 Kg.), an amount roughly equivalent to 3,057,730,000 capsules or tablets of 0.1 Gm. each, or approximately 24 doses for each person in the United States. Acute intoxication with barbiturates accounts for about 25 per cent of all patients with acute poisoning admitted to general hospitals2; and more deaths are caused by barbiturates, either accidentally ingested or taken with suicidal intent, than by any other poison.3Various articles in the lay press4have attributed automobile accidents and various crimes to barbiturate intoxication and have also stated that illegal trafficking in

CHRONIC BARBITURATE INTOXICATION: An Experimental Study

https://www.gastrojournal.org/article/0016-5085(87)90331-3/pdf

Cocaine-induced hepatotoxicity in humans

[Submicroscopic studies on the pathology of myocardial cells in phosphorus poisoning, hypertrophy, atrophy and potassium deficiency].

Disorders of potassium metabolism.

Pseudohyperkalemia, a rise in serum potassium concentration with concurrently normal plasma potassium concentration, is an in vitro phenomenon that was first described 50 years ago. It was originally attributed to the release of potassium from platelets during platelet aggregation and degranulation, and a significant correlation between pseudohyperkalemia and platelet count was established. During the last decade, new data were added to this phenomenon. In particular, pseudohyperkalemia was defined when serum potassium concentration exceeded that of plasma by more than 0.4 mmol/L provided that samples are collected under strict techniques, remain at room temperature and are tested within 1 hour from blood specimen collection. Moreover, it is positively correlated to (1) thrombocytosis due to the release of potassium from platelet granules during coagulation, (2) erythrocytosis due to the dilution of the released potassium in smaller volumes of serum, and (3) the presence of activated platelets, which have the capability of aggregation at a higher speed and release more potassium during degranulation. However, pseudohyperkalemia may be "masked" when in a state of hypokalemia because potassium moves back into the intracellular space in vitro, and the phenomenon is ameliorated or even not detected.

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Pseudohyperkalemia in Serum: A New Insight into an Old Phenomenon

Elevated serum potassium levels unassociated with manifestations of hyperkalemia have been observed in patients with thrombocythemia associated with the myeloproliferative disorder.1-3Studies indicate that potassium released from platelets during the process of blood coagulation is responsible, since serum prepared from platelet-free plasma has a normal potassium concentration. "Spurious hyperkalemia" has been suggested as a term for this syndrome.3We wish to reemphasize these findings with additional observations. Results and Comment Table 1 lists the clinical and laboratory data in a group of patients with elevations of leukocytes, erythrocytes, and platelets alone or in various combinations. Significant elevations of serum potassium levels above the normal level of 5 mEq. per liter were noted in Patients 1, 4, 5, 6, 7, 8, 9, and 14. In each of these patients there was a significant elevation of the platelet count. In the absence of thrombocythemia, elevations of the leukocyte or erythrocyte

Hyperkalemia Associated with the Myeloproliferative Disorder

THE RECENT observation of 2 fatal cases of acute phosphorus poisoning prompted an investigation of the incidence of phosphorus as a toxic agent and a review of the literature on the subject. Although at first glance its importance may seem slight, a further study of this condition brings to the foreground its serious nature and menace to the public health. INCIDENCE In the ten year period between 1934 and 1943, 14 patients with proved acute phosphorus poisoning were admitted to the Boston City Hospital, 7 of whom died, a mortality rate of 50 per cent. During this same period there were 1,443 admissions due to acute poisoning from other ingestants not including alcohol, with 90 deaths, a mortality rate of 6.2 per cent. Table 1 shows the incidence and mortality of the commonest toxic ingestants listed in order of their frequency. It will be noted that, although accounting for

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Acute phosphorus poisoning

Chromophobe adenomas of the pituitary are usually endocrinologically inactive and produce signs and symptoms only as a result of expansion. There are, however, some well-documented examples of this lesion associated with Cushing's syndrome. 1-7 The importance of recognizing this association has been emphasized by recent reports of progressive enlargement of chromophobe adenomas following adrenalectomy for Cushing's syndrome. 8-10 The evidence suggests the possibility that the pituitary tumor was present prior to surgery and that removal of the adrenals resulted in its expansion. The following case represents a 40-month follow-up of a patient with Cushing's syndrome associated with a radiologically demonstrable pituitary tumor. The patient was successfully treated by surgical removal of the tumor and irradiation of the sella turcica. The tumor was identified histologically as a chromophobe adenoma. Report of Case A 39-year-old white man was admitted to the Veterans Administration Hospital, Philadelphia, on Oct. 12, 1957. During the 10

Cushing's Syndrome Associated with Chromophobe Adenoma of Pituitary

Sarcoid involvement of the spleen with resultant splenomegaly is a fairly common manifestation of this disease.1-8Despite its frequency, splenic sarcoidosis rarely gives rise to objective and subjective manifestations. When present, they may take the form of either anatomical or functional complications. The former include rupture and abdominal discomfort due to increased splenic size.9-12The functional complication of sarcoidosis of the spleen is hypersplenism. Neutropenia, thrombocytopenia, and hemolytic anemia have been reported to occur alone or in various combinations with sarcoidosis.5,8,10,13-40Two cases of hypersplenism treated by splenectomy and with a three-year postoperative follow-up are presented in this paper. The difficulty in obtaining a preoperative diagnosis is well illustrated by these patients. Report of Cases A 41-year-old white man has been previously reported as an unusual instance of portal hypertension and bleeding esophageal varices secondary to sarcoidosis of the liver.19He was first admitted to the Veterans Administration Hospital in

Ralph M. Myerson

Papers

Hyperkalemia Associated with the Myeloproliferative Disorder

Acute phosphorus poisoning

Cushing's Syndrome Associated with Chromophobe Adenoma of Pituitary

The Role of Splenectomy in Sarcoidosis