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Biomedical subjects

M Horwith

Publications and source records attributed to M Horwith.

At least 19 recordsLinked to original sources
PubMed1988

Ectopic insulin production by a primary ovarian carcinoid.

An insulin-containing ovarian carcinoid was found at the autopsy of a 63-year-old woman with a 12-year history of episodic hyperinsulinemic hypoglycemia. In terms of histology, the carcinoid displayed both insular and trabecular patterns and contained a small focus of mucinous cystadenoma. Beta secretory granules were demonstrated by electron microscopy, and immunoreactivity for insulin was demonstrated in tumor cell cytoplasm by immunohistochemistry. Additional autopsy findings included a solitary parathyroid adenoma and a microscopic focus of pituitary hyperplasia. This is the first recorded case of insulin production by a primary ovarian neoplasm. The patient's constellation of endocrine findings may represent a variant of the syndrome of type I multiple endocrine neoplasia.

Carcinoid Tumor↗
PubMed1988

Usefulness of preoperative inferior petrosal vein sampling in Cushing's disease.

Adrenocorticotropic hormone (ACTH) levels from the inferior petrosal sinuses and peripheral veins were measured in 10 patients with Cushing's disease. All patients had normal or indeterminate computed tomography scans. In 9 of the 10 patients the petrosal vein sampling showed a gradient between pituitary ACTH and peripheral ACTH verifying the supposition of pituitary dependent hypercortisolism. In seven cases preoperative ACTH levels lateralized tumor to one side of the gland. In six of these cases tumor was found at that location at surgery. In the seventh case, no tumor was identified at surgery and that half of the gland was resected. Nine patients were cured following transsphenoidal excision of tumor.

Adenoma↗
PubMed1979

An electron microscopic investigation of human familial bone dysplasia. Inhibition of osteocytic osteolysis and induction of osteocytic formation of elastic fibers following calcitonin treatment.

Familial bone dysplasia with hyperphosphatasemia is characterized by excessive bone resorption early in life with resulting severe skeletal deformity. The disease can be ameliorated by treatment with human calcitonin. We have the studied the ultrastructure of bone from diseased patients before treatment and at intervals during 1 year of treatment with calcitonin. Pretreatment osteoblasts, osteoclasts, and osteocytes exhibited mitochondria which contained vast amounts of dense microcrystal deposits. Osteocytes were also distinguished by minimal organellar development. Osteoclasts were rare. Calcitonin treatment included a progressive development of a more normal bone structure. Intramitochondrial crystal deposits were absent in mitochondria of osteocytes and osteoclasts but were still present in mitochondria of osteoblasts. Surprisingly, the developing bony matrix during calcitonin treatment exhibited large numbers of elastic fibers. These appeared to develop normally in alignment with the surface membrane of osteocytes. Calcitonin treatment caused a proliferation of osteocyte organellar development. It is concluded that familial bone dysplasia is primarily a disease of osteocytes and that osteocytic activity is influenced by calcitonin.

Bone Diseases, Developmental↗
PubMed1977

Calcitonin treatment in hereditary bone dysplasia with hyperphosphatasemia: a radiographic and histologic study of bone.

Two children with bone dysplasia with hyperphosphatasemia (juvenile Paget's disease) were treated with synthetic human calcitonin. The progress of bone disease was monitored radiographically and histologically. Pretreatment radiographs showed markedly abnormal bone, characterized by lack of discrete cortex and absence of normal modeling. During treatment a discrete cortex was formed composed of compact bone, and more normal modeling occurred. This coincided with a histologic change from woven bone before treatment to a more lamellar type during treatment.

Alkaline Phosphatase↗
PubMed1976

Distribution of sulfur in urine of patients with cystathioninuria before and during administration of pyridoxine.

During administration of 400 mg daily of vitamin B6 as pyridoxine hydrocholoride to two patients with homozygous cystathioninuria, cystathionine excretion fell in a characteristic manner. Inorganic sulfate excretion did not change significantly when considered by itself. Total sulfur excretion, determined as sulfate after oxidation, decreased slightly in both patients and this decrease was statistically significant in one. The ratio of sulfate to total sulfur excretion increased significantly in both patients during vitamin B6 administration. The difference between total sulfur and free plus bound or ethereal sulfate is largely accounted for by cystathionine and lesser amounts of N-acetyl-cystathionine. The results indicate that cystathionine sulfur is not excreted other than as sulfate during vitamin B6 administration and support the hypothesis that cystathionase activity is enhanced by pyridoxine, the resultant cysteine, alpha-ketobutyrate, and ammonia being added to large body pools.

Amino Acid Metabolism, Inborn Errors↗
PubMed1976

Hereditary bone dysplasia with hyperphosphatasaemia: response to synthetic human calcitonin.

Four cases of familial bone dysplasia with hyperphosphatasaemia were treated with synthetic human calcitonin. Prior to therapy, all four cases were characterized by marked bone deformity, pain, tenderness and elevated levels of serum alkaline phosphatase and urinary hydroxyproline. Treatment with calcitonin produced in each case a striking clinical, biochemical and radiographic remission. Pain and tenderness was greatly diminished and urinary hydroxyproline and serum alkaline phosphatase levels were significantly decreased. Radiographic regression of the bony abnormalities was apparent as early as 4 1/2 months after the start of treatment. Prior to therapy bones exhibit no real organization. After calcitonin treatment, the radiographic appearance of a normal cortex and medullary cavity was clearly evident for the first time.

Adolescent↗
PubMed1971

Bilateral anorchia: discordance in monozygotic twins.

The bilateral absence of testes is described in one of two otherwise healthy and well-developed 12-year-old identical twin boys. The twins' father has only one palpable testis. The occurrence of complete anorchia in only one of otherwise identical twins constitutes relevant new data for considering the etiology of this rare condition and in assaying the role of the testis in growth and development between birth and puberty.

Body Height↗
PubMed1971

Gonadal dysgenesis in individuals with apparently normal chromosomal complements: tabulation of cases and compilation of genetic data.

Although usually associated with an abnormal sex chromosomal complement, gonadal dysgenesis is occasionally detected in individuals having apparently normal male (46,XY) or female (46,XX) chromosomal complements. Six individuals with XY or XX gonadal dysgenesis, four proven, two probable, are described. A review of histologically verified cases of XX and XY gonadal dysgenesis reveals frequent familial aggregation of affected individuals, a situation rarely encountered in the more frequent X-monosomic gonadal dysgenesis. Multiple affected sibs and frequent X-monosomic gonadal dysgenesis. Multiple affected sibs and frequent parental consanguinity suggest that XX gonadal dysgenesis is an autosomal recessive condition, while certain families suggest that XY gonadal Dysgenesis is an X-linked recessive or male-limited autosomal dominant condition.

Adolescent↗
PubMed1963

Cystathioninuria.

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Amino Acids↗