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Hypothyroidism can present a wide range of psychiatric manifestations, including personality disturbance, neurotic traits and psychotic features. Psychiatric treatment techniques without recognition and correction of the endocrine root of the mental disturbance will result in a failure of treatment. However, severe hypothyroidism can exist with a poverty of classical signs and symptoms such that both internist and psychiatrist may easily overlook endocrine dysfunction as a possible etiology of the mental disorder. A case of long-standing paranoid illness whose etiology was severe myxedema with such a poverty of signs and symptoms is presented. Failure to recognize the endocrinopathy may not only produce recovery difficulties but also psychiatric and endocrine repercussions if psychotropic medications are given in such masked cases. These problems are considered with particular reference to lithium, and screening criteria to avoid this problem are discussed.

The increasing tendency of doctors to base diagnosis on the results of laboratory investigations entails a corresponding decrease in the exercise of clinical judgment. This state of affairs can have harmful consequences for patients suffering from biochemically atypical forms of disorder, who may acquire functional psychiatric labels when they are in fact suffering from organic physical disorders. The author's personal experience of this invidious predicament is described. Although hypothyroidism was correctly diagnosed on clinical grounds within a few months of presentation, laboratory results were inconclusive and three years and three specialist consultations were to elapse before replacement therapy was obtained, and then only through unofficial channels. The handling of this case illustrates some unfortunate trends in contemporary medical practice with important implications for the health of patients.

The cutaneous mucinoses are a group of connective tissue disorders characterized by the deposition of mucin, either focally or diffusely, in the interstices of the dermis. The diseases may be a primary (metabolic) or secondary (catabolic) process. Systemic abnormalities are seen with most of these disorders. This review discusses the primary mucinoses in which the predominant dermal mucin is hyaluronic acid. Current therapy and proposed mechanisms for the mucinoses are considered.

The recognition of hypothyroidism may not always be easy in the emergency department setting. Laboratory evaluations of thyroid function are not usually performed on a 24-hour basis, and therefore the emergency physician, although suspecting the presence of hypothyroidism, may be unable to confirm the diagnosis while the patient is in the Emergency Department. It is not always the responsibility of the emergency physician to diagnose hypothyroidism, but in some clinical settings it may be important to include thyroid function tests in laboratory evaluation of patients to ensure adequate patient care and followup. Careful attention to nonspecific complaints, myxedematous changes, and signs of dysfunction of any organ system, especially in older female patients, may lead to the ultimate correct diagnosis. Myxedema coma is potentially fatal and must be recognized and treated emergently, usually prior to laboratory confirmation. Ventilatory support and thyroid hormone replacement are the two most important therapeutic maneuvers in the treatment of myxedema coma.

Every patient with myxedema has hypothyroidism, but not every hypothyroid patient has myxedema. It often is possible to diagnose myxedema on clinical grounds alone. Characteristic symptoms are weakness, cold intolerance, mental and physical slowness, dry skin, typical facies, and hoarse voice. Results of the total serum thyroxine and free thyroxine index tests usually will confirm the diagnosis. L-thyroxine is the treatment of choice for myxedema, but it must be given to elderly patients with extreme caution. The transition from the hypothyroid to the euthyroid state brings about changes that put an added burden on the heart. The patient's clinical status and results of thyroid function tests determine the proper maintenance dose. Myxedema coma is rare but often fatal. It occurs most often in elderly women and may be mistaken for one of the chronic debilitating diseases common to this age group. Primary treatment is prompt administration of adequate doses of thyroid hormone--either l-throxine given intravenously of L-triiodothyronine given by nasogastric tube. It also is essential to identify and treat the condition precipitating the coma.

An unusual, nodulocystic form of scleromyxedema (lichen myxedematosus) developed in a 48-year-old man with a six-year history of psoriasis. The scleromyxedema responded to intermittent therapy with melphalan and prednisone. Dermabrasion smoothed and softened the skin and increased the mobility of the perioral skin. Two months after remission of the skin lesions, psoriasis recurred.

A 61-year-old woman who presented with gross ascites is described. She had many of the clinical features of hypothyroidism, including a pericardial effusion and a normocytic normochromic anaemia. The ascitic fluid was exudative in type. The diagnosis of primary hypothyroidism was confirmed by the finding of low serum thyroxine and tri-iodothyronine levels, low 131I uptake, and high serum thyroid-stimulating hormone levels. The patient responded well to carefully graded thyroxine therapy.

General and specific cutaneous findings associated with hyperthyroidism are reviewed. Familiarity with these findings may aid the practitioner in the early diagnosis of thyroid diseases. Several normally idiopathic cutaneous diseases can occasionally be controlled if underlying thyroid disease is considered as a cause, and appropriate testing performed.

A 33-year-old male consulted us with symptoms of band-like infiltration, thickenning and subcutaneous induration occurring in the face, chest, back, shoulder and upper extremities. In the following time he developed arthralgia, fever and ocular symptoms. Laboratory tests revealed normal thyroid functions and a normal bone marrow picture, but there were immunological abnormalities such as reduced cellular immunity, decrease in C 3 (beta 1c/la) and positive antinuclear antibody. Histologically, there was an increase in fibroblasts and deposits of hyaluronic acid were revealed histochemically. A diagnosis of lichen myxedematosus was established. At present, all symptoms and signs including skin rash have disappeared following corticosteroid therapy and the patient is being followed up. So far as we have been able to trace, reports on lichen myxedematosus associated with immunological abnormalities as described here have not been found. The relationship between this pathology and immunological abnormalities are discussed.

This article describes the clinical recognition of, and pathophysiological mechanisms underlying the development of, thyroid storm and myxedema coma. Effective therapeutic management of these conditions depends on a clear understanding of the physiological adaptations occurring in hyperthyroidism and hypothyroidism, and of how precipitating events may produce these decompensated states.

Postural abnormalities in a 66-year-old woman with ataxic myxoedema were recorded by stabilography during treatment. After replacement therapy, 3 Hz power in the sagittal plane was greater than before treatment; this peak shifted to a higher frequency and finally its ratio became normal. This is the first report of recovery of a 3 Hz body oscillation in ataxic myxoedema.

With special reference to diagnostic and therapeutic problems, a case of myxoedema coma with secondary hyperaldosteronism and raised LDH-concentration is described. The significance of different states of consciousness due to this endocrine disorder is pointed out with respect to the differential diagnosis and particularly to the clinical symptoms. In addition, experience with an intravenously administrable triiodothyronine compound is described and the different dosages previously mentioned in the leterature are discussed. The long interval of 5 weeks from the beginning of the therapy until the remission of the omatous state was surprising.

Erythrocyte carbonic-anhydrase-I (C.A.I.) concentration was measured by radial immunodiffusion in 30 thyrotoxic patients and 15 myxoedemic patients, the results being compared with those found in a control group of 90 euthyroid individuals. In thyrotoxicosis the erythrocyte-C.A.I. concentration was found to be below 10-29 mg/g haemoglobin, whereas the normal range varied from 11-1 to 22-5 mg C.A.I./g Hb. Low values were found in 4 patients with triiodothyronine(T3)-toxicosis. In myxoedema, the mean erythrocyte-C.A.I. concentration, though elevated at 20-37 mg/g Hb, fell within the normal range. In pregnancy, the erythrocyte-C.A.I. concentration rose with time, the mean value at tern being 20-6 +/-S.D. 3-3 mg/g Hb. In a group of women taking oral contraceptives, a low erythrocyte-C.A.I. concentration was noted--an effect which was most obvious among those taking low-oestrogen contraceptives. It is suggested that erythrocyte-C.A.I. estimation provdes a rapid screening test for thyrotoxicosis.

The manifestations of myxedema often occur insidiously over several months or years. Except for gastrointestinal symptoms, the diagnosis of hypothyroidism may not clinically evident. Especially in the elderly, symptoms of hypothyroidism are frequently unrecognized or simply dismissed as signs of old age.

The diagnosis of myxedema ascites is often difficult and delayed, from our experience and the reports of other investigators. To address this situation, previous reports on the diagnosis of ascites were pooled in order to distinguish the features of myxedema ascites from other forms of ascites. These features were confined to variables that would be obtained routinely from patients with ascites requiring paracentesis. The data of 26 patients with myxedema ascites, and 61 patients with ascites from another cause were analyzed. Discriminant analysis was used to select the variables that best separated patients into myxedema and non-myxedema groups. The variables selected were if the ascites was straw-colored or with a protein content less than 2.5 g/dl, if the patient was over age 40, and if there was periorbital edema or hepatomegaly. These variables correctly classified 90.8% of patients. However, considering the roughly 1% prevalence of myxedema ascites among patients with ascites, the predictive value of these variables, in combination, is only 8.7%. With this low rate, these variables should probably not be used to screen for myxedema ascites.