Hyperprolactinemia and headaches

We investigated the frequency of headaches in women with menstrual abnormalities and hyperprolactinemia. Twenty-seven of 46 (58%) women with hyperprolactinemia indicated that headache episodes occur once or more per week; patients with sellar abnormalities (macroadenoma) or previous cranial or pituitary operation were excluded from this group of hyperprolactinemic patients. The headache episodes occurred significantly more frequently than in the control group (N = 56), where 27% indicated one or more headaches per week (p less than 0.01). In the vast majority of the women with hyperprolactinemia, headaches had preceded the finding of elevated prolactin levels for years and had not developed after the patients had become concerned about the pituitary gland. The clinical impression was that the headaches of these patients typically lack features of prodromal signs and unilaterality and resemble, in general, tension headaches; they may last for hours and often require medication. We could not demonstrate a relationship between prolactin levels and frequency or severity of these headache episodes. The etiology of these headaches is unclear. The therapeutic effect of bromocriptine deserves further investigation. In conclusion, we present data to suggest that headaches are commonly an associated finding in hyperprolactinemic women who have no evidence of significant pituitary enlargement.     

Hyperprolactinemia associated with acute intermittent porphyria

Galactorrhea as the result of hyperprolactinemia has been described in very rare cases associated to acute outbreaks of intermittent acute porphyria (IAP). In our country, any of such cases have been published or analytically documented. We present the case of a patient admitted in our hospital for the study of abdominal pain and galactorrhea, with latter diagnosis of IAP, supported by the assessment of the activity of the enzyme showing a deficit in the red blood cells.     

Hyperprolactinemia in males with systemic lupus erythematosus

Alanine dehydrogenase [EC 1. 4. 1. 1] was purified to homogeneity from a crude extract of Enterobacter aerogenes ICR 0220. The enzyme had a molecular mass of about 245 kDa and consisted of six identical subunits. The enzyme showed maximal activity at about pH 10.9 for the deamination of L-alanine and at about pH 8.7 for the amination of pyruvate. The enzyme required NAD+ as a coenzyme. Analogs of NAD+, deamino-NAD+ and nicotinamide guanine dinucleotide served as coenzymes. Initial-velocity and product inhibition studies suggested that the deamination of L-alanine proceeded through a sequential ordered binary-ternary mechanism. NAD+ bound first to the enzyme, followed by L-alanine, and the products were released in the order of ammonia, pyruvate, and NADH. The Km were 0.47 mM for L-alanine, 0.16 mM for NAD+, 0.22 mM for pyruvate, 0.067 mM for NADH, and 66.7 mM for ammonia. The Km for L-alanine was the smallest in the alanine dehydrogenases studied so far. The enzyme gene was cloned into Escherichia coli JM109 cells and the nucleotides were sequenced. The deduced amino acid sequence was very similar to that of the alanine dehydrogenase from Bacillus subtilis. However, the Enterobacter enzyme has no cysteine residue. In this respect, the Enterobacter enzyme is different from other alanine dehydrogenases.     

Hyperprolactinemia: an inductor of neoplastic changes in endometrium? A report of two cases

Mast cell stabilizers are commonly used in the treatment of asthma and allergic disorders. Although the role of mucosal mast cells in the pathogenesis of inflammatory bowel disease remains uncertain, mast cell stabilizers have been shown in animal models to attenuate the severity of experimental colitis. The authors' experience with ketotifen in three patients--one each with Crohn's disease, ulcerative colitis and collagenous colitis--who had demonstrated allergy to, or intolerance of, 5-aminosalicylic acid is reported.