Yale Journal Of Biology And Medicine Volume 32, April 1960
Sarcoidosis, psoriasis and gout: syndrome or coincidence?
Herbert Kaplan, Gerald Klatskin
Department of Internal Medicine, Yale, University School of Medicine
Last year we observed three patients with a combination of sarcoidosis, psoriasis and gout. Each of the patients had the classic clinical features of all three diseases, and in each of them the diagnosis of sarcoidosis and psoriasis was confirmed histologically. It is interesting to note that the skin lesion described by Jonathan Hutchinson in 1877 (1), which is considered the first report of sarcoidosis, developed in an elderly man with gout. In a later message, Hutchinson made the following remark: " I am inclined to believe that the skin disease in this patient is essentially due to gout.” In 1898, he described another patient with a combination of two diseases (2). To our knowledge, the relationship between sarcoidosis and gout has not been previously discussed in the literature, and the combination of sarcoidosis, psoriasis and gout has not been reported.
At first glance, the occurrence of three apparently unrelated but relatively common diseases in one individual suggests a coincidence. However, observation of three patients with this triad over a one-year period prompted us to investigate the possibility of a connection between these three diseases. To do this, we reviewed the medical records of patients diagnosed with sarcoidosis, gout, or psoriasis to find evidence of any combination of these three diseases. In addition, serum uric acid levels were determined in groups of patients with sarcoidosis and psoriasis.
The results of our study, together with some reports in the literature, suggest that the coexistence of sarcoidosis, psoriasis and gout may be associated with some as yet unknown relationships between these diseases.
In April 1958, LB, a 41-year-old white salesman, was admitted to Grace-New Haven Community Hospital with recurrent pain in his ankles and toes.
In 1950, he suddenly developed severe pain in the metatarsophalangeal joint of his right big toe. Swelling and severe pain then developed. The level of uric acid in the blood was high. A diagnosis of gout was made. Joint pain decreased with colchicine treatment, but increased 6 months after the end of therapy. During subsequent courses of colchicine, the pain recurred a month after the end of treatment. Treatment with benemide for one and two months had no effect on the frequency or severity of relapses. The serum uric acid level in 1958 was 8.5 mg%.
At the age of 20 years, the patient developed psoriasis. First, lesions developed on the scalp and legs. The psoriasis gradually progressed and lesions developed on the arms, abdomen, sacrum and groin. Numerous attempts at local therapy were ineffective. Although the patient had no respiratory symptoms, in 1954 a routine radiograph showed abnormalities that were interpreted as silicosis.
There was no family history of skin disease or arthritis. Physical examination revealed large, erythematous, well-defined lesions on the scalp, abdomen, sacrum, groin, and extensor surfaces of all four extremities. Blood pressure 140/100. The lacrimal and parotid glands were not enlarged. Ophthalmological examination showed no pathology. There was no peripheral lymphadenopathy. There were no signs of cardiac disease. The liver and spleen were not enlarged. Mild erythema and tenderness were noted on the right ankle. There were no lesions of other bones or joints.
Urinalysis, hematocrit, leukocyte count are normal. Serum protein 7.83 gm%, albumin 3.41 gm%, globulin 4.42 gm%. Serum calcium 10.2 mg%, inorganic phosphorus 3.6 mg%. The concentration of uric acid in two consecutive measurements was 11.4 and 10.8 mg%, respectively. Total bilirubin 1.18 mg%, direct bilirubin 0.41 mg%; bromosulfthalein retention after 45 minutes 17.8%; cephalin-cholesterol 2+ flocculation test at 24 and 48 hours; thymol test 4+; alkaline phosphatase 14.2 Shinowara-Jones-Reinhart units (modified Bodansky method); oxaloacetin glutamic transaminase 32 U. Excretion of phenolsulfophthalein was normal. The ECG showed no pathology.
A chest radiograph showed linear and nodular infiltrates in both lungs, most significant in the upper lobes, without evidence of hilar lymphadenopathy. X-rays of the bones of the arms and legs were normal. No dilation of the esophageal veins was observed. Pulmonary function testing showed low residual volume, hyperventilation, and an increased alveolar-arterial gradient of 18.8 mmHg. The reaction to intradermal injection of tuberculin was negative. Psoriasis responded to local treatment with tar ointment and ultraviolet irradiation. The patient was prescribed Benemide and was discharged from the hospital.
A month later, the patient was readmitted to the hospital for a liver biopsy to determine whether he actually had sarcoidosis. At this time there was no pain in the joints, and the skin lesions improved significantly. However, enlargement of the parotid gland was found. Leukocyte index 7.150/mm3, eosinophils 19%. Serum calcium 11.7 mg%, inorganic phosphorus 2.9 mg%. X-ray of the chest is unchanged. Liver biopsy showed numerous parenchymal granulomas consisting of compact clusters of epithelioid and giant cells consistent with sarcoidosis. Many granulomas were confluent and surrounded by collagen fibers that distorted the normal lobular architecture of the liver. In some areas, the parenchyma had a nodular pattern, suggesting early cirrhosis of granulomatous origin. Treatment with prednisone, 15 mg daily, was started, and benemide therapy was continued.
In January 1959, 8 months after starting steroid therapy, the patient was readmitted to the hospital due to worsening psoriasis. After starting treatment with prednisone and benemide, there was no recurrence of gout. However, an enlarged epitrochlear node was found on the right. Liver function improved, bromosulfthalein retention decreased to 6.9%. The cephalin-cholesterol flocculation test became negative, and alkaline phosphatase decreased to 10.0 U. A chest x-ray showed no changes, but pulmonary function improved slightly. Psoriasis responded to treatment with tar ointment and ultraviolet irradiation. Because of the apparent improvement in liver and lung function, the prednisone dosage was slowly reduced.
At last examination in May 1959, the patient was taking 7.5 mg of prednisone daily. There were no signs of sarcoidosis or gout, but there was a recent relapse of psoriasis. Serum uric acid was 4.7%, liver function remained unchanged compared to the results of 6 months ago. A skin biopsy showed characteristic features of psoriasis. A repeat liver biopsy showed the same changes noted 11 months earlier, except that many of the granulomas had undergone hyalinization.
This patient had extensive psoriasis for 10 years, after which he developed classic gout. Four years later, a chest x-ray showed the presence of asymptomatic pulmonary sarcoidosis. The possibility that the actual onset of sarcoidosis preceded the onset of psoriasis or gout cannot be excluded, since the “age” of the pulmonary lesions at the time of their discovery could not be assessed. Likewise, the possibility that hyperuricemia existed before the development of either of the other two diseases cannot be excluded. Therefore, no final conclusions can be drawn regarding the exact sequence of development of these diseases.
In February 1959, CD, a 51-year-old white university professor, was hospitalized due to severe shortness of breath. In July 1950, he was seen at the Ophthalmology Service of the Grace-New Haven Community Hospital for eye pain and blurred vision. One month prior, he developed erythema nodosum. Ophthalmological examination showed bilateral iridocyclitis. No lymphadenopathy, skin lesions, or salivary gland enlargement were noted. Systolic murmurs were heard in the heart. The liver was palpable two fingers below the costal margin, but there was no splenomegaly. Hemogram and urinalysis were normal. A chest radiograph showed bilateral emphysema and bilateral hilar lymphadenopathy. The preliminary diagnosis was sarcoidosis. A 10-day course of cortisone treatment was administered, which resulted in rapid improvement of ophthalmic symptoms. After 2 months, the patient developed bilateral secondary glaucoma, requiring iridectomy.
A year later, in June 1951, a relapse of uveitis, nonproductive cough, generalized myalgia and arthralgia developed. Apart from signs of bilateral uveitis and moderate hepatomegaly, there were no abnormalities. Leukocytes 4,200/mm3. Bilirubin, bromosulfthalein retention, cephalin-cholesterol flocculation test, and alkaline phosphatase were normal. Serum protein 6.53 gm%, albumin 3.38 gm%. Serum calcium and inorganic phosphorus concentrations were 10.5 and 3.9 mg%, respectively.
Skin tests with tuberculin, coccidioidin, histoplasmin and agglutination test for Brucella were negative. Gastric aspirate inoculated into a guinea pig did not lead to the development of tuberculosis. A chest radiograph showed bilateral hilar lymphadenopathy without pulmonary infiltrates. A liver biopsy revealed numerous noncaseating granulomas composed of epithelioid cells and giant cells. Staining of the biopsy material did not show the presence of acid-fast organisms. These findings were consistent with the clinical diagnosis of sarcoidosis. Treatment with intravenous ACTH for 8 days resulted in remission of ophthalmic symptoms that did not recur for 8 years.
In 1955, 5 years after the onset of sarcoidosis, dyspnea on exertion suddenly developed. X-ray showed bilateral pulmonary infiltrates. Over the next 3 years, the lung lesions increased in size, but the severity of the respiratory symptoms did not increase until 1958, when the shortness of breath became very severe.
In June 1956, the patient awoke during the night with severe pain in the metatarsophalangeal joint of his right big toe. The finger became red and hot and grew to twice its normal size. The erythema from the toe gradually spread to the entire dorsum of the leg. Treatment with colchicine resulted in rapid improvement. Unfortunately, blood uric acid levels were not measured at this time. A follow-up radiograph of the toe showed no abnormality. Two years later, in July 1958, pain in the big toe of the right foot developed again and again colchicine led to rapid improvement. Between 1957 and 1959, the patient had several episodes of pain and swelling of the knee joints, without redness or fever, each lasting approximately two weeks. Colchicine was not used for treatment because these episodes were not considered to be manifestations of gout. However, small doses of sodium salicylate relieved the pain.
Typical psoriatic lesions developed in December 1958. Erythematous, silvery, oval lesions with a clear border developed first on the flexor surface of the right forearm, then on the elbows, calves, and scalp. There was no family history of skin disease or arthritis. A physical in February 1959 showed typical psoriatic lesions on the scalp, both elbows and both calves. Ophthalmological examination showed postoperative damage to both pupils, with no evidence of active uveitis or conjunctivitis. The parotid and lacrimal glands were not enlarged. There was no peripheral lymphadenopathy. Cardiac examination showed tachycardia and systolic murmurs. The heart was of normal size. The edge of the liver was palpable in the right hypochondrium, the spleen was not enlarged. The right knee was slightly swollen and no fluid was found in the joint. The toes were normal, no gouty deposits were noted.
The volume of packed red blood cells was normal. Leukocytes 3,400/mm3. Eosinophils 12%. Trace amounts of protein were found in the urine, but the rest of the analysis was normal. Excretion of phenolsulfophthalein was normal. Serum uric acid concentration 4.2 mg%. Serum calcium and inorganic phosphorus levels were 10.0 and 3.3 mg%, respectively. Serum protein 7.54 gm%, albumin 3.44 gm%, globulin 4.10 gm%. Direct bilirubin 0.25 mg%, total bilirubin 1.2 mg%; bromosulfthalein retention after 45 minutes 18%; cephalin-cholesterol flocculation test negative; alkaline phosphatase 1.8 Shinowara-Jones-Reinhart units; oxaloacetin glutamine transaminase 38 U; Serological lipids are normal. Pulmonary function studies showed a low residual volume and a high alveolar-arterial gradient. The tuberculin skin test was negative. A chest radiograph showed bilateral hilar lymphadenopathy and fibrosis in the upper lobes. Histological examination of the skin was compatible with the diagnosis of psoriasis.
Due to worsening pulmonary function, treatment with prednisone, 60 mg per day, was started. After one month of therapy, respiratory symptoms and lung function improved significantly.
This patient developed sarcoidosis first. It progressed slowly over 6 years, affecting the eyes, lungs, hilar lymph nodes and liver, after which gout developed. After 2 years, a sudden worsening of pulmonary symptoms developed, possibly related to rapid dissemination of the granulomatous process in the lung, and psoriatic lesions also suddenly developed. Interestingly, as in Case 1, there was no family history of gout. However, all clinical features and rapid response to colchicine were typical of this disease. A normal blood uric acid level observed during the asymptomatic period is not sufficient evidence to exclude the diagnosis of gout (8). Whether the episodes of knee swelling were associated with gout or were manifestations of the nonspecific arthritis sometimes seen in sarcoidosis remains unclear.
JM, a 59-year-old black woman, presented to Grace-New Haven Community Hospital in March 1959 complaining of calf pain. In November 1954, the patient was seen in a dermatology clinic for randomly distributed, itchy, lichenified lesions on the calves, thighs and arms. Three months later, new lesions developed on both elbows. Over the next year they spread throughout the body except the palms and soles. In addition to lichenification, the lesions were surrounded by silvery scales consistent with psoriasis. In February 1956, the patient was hospitalized for the first time for treatment of a skin disease.
The liver was palpated two fingers below the costal margin. Liver function tests (serologic bilirubin, cephalin-cholesterol flocculation test, and alkaline phosphatase) were normal except bromosulfthalein retention, 21% at 45 minutes. Serum protein, calcium, and inorganic phosphorus were normal.
A chest radiograph showed no abnormalities. The itching decreased after a week's course of prednisone, but returned again after stopping therapy. Skin lesions showed no change after several types of topical therapy. In March 1957, a skin biopsy was performed which showed histological features typical of psoriasis. Serum protein at this time was 7.36 gm%, albumin 2.27 gm%, globulin 5.09 gm%.
Over the next two years, the skin lesions did not change significantly, except for a slight temporary improvement after treatment with prednisone, ultraviolet light, and tar ointment. In September 1958, thrombophlebitis developed. In March 1959, thrombophlebitis worsened, requiring hospitalization.
Review of the medical history revealed that the patient had had kidney stones for many years, beginning in childhood, with recurrent episodes of renal colic and hematuria, as a result of which nephrectomy was performed. Nine years ago, at the age of 50, a panhysterectomy was performed. A year later, in 1951, the first episode of acute gout probably occurred, although this diagnosis was not anticipated at this time. Similar episodes occurred several times a year. They usually began with a sudden, aching pain in the metatarsophalangeal joint of the right big toe, which then became swollen, red, hot and painful. Usually the exacerbation lasted about a week. During this time, the patient was unable to wear shoes, use bedding, or walk without crutches. Sodium salicylate provided temporary relief. Colchicine was not used for treatment.
In addition to episodes of gout, the patient had chronic migratory arthritis of the knees, elbows, wrists and interphalangeal joints for 4 years. This condition was characterized by dull pain, sometimes with swelling of the joints. For the past three years, the patient has also had episodes of pain in both eyes, accompanied by lacrimation and blurred vision in the right eye. These episodes occurred approximately twice a year and lasted approximately a week.
There was no family history of skin disease or arthritis. The patient did not abuse alcohol and had adequate nutrition. Blood pressure 180/90. The lacrimal glands were greatly enlarged. The cornea and fundus were normal. Slit lamp examination showed no evidence of current or previous uveitis. The parotid glands were not enlarged and there was no peripheral lymphadenopathy. There were no wheezes in the lungs. The liver was palpated three fingers below the costal margin. The edge of the liver was hard. The spleen was not palpable. My calves were painful and hot. Apart from bilateral Heberden's nodes, the joints were normal. There were no gouty deposits in the joints.
Urinalysis and phenolsulfophthalein excretion were normal. Leukocytes 3,800/mm3. Calcium and inorganic phosphorus in serum are 11.9 and 4.9 mg%, respectively. Serum protein 7.61 gm%, albumin 2.79 gm%, globulin 4.82 gm%. Direct bilirubin 0.70 mg%, total bilirubin 1.4 mg%; Bromosulfthalein retention after 45 minutes is 2.3%; cephalin-cholesterol flocculation test negative after 24 and 48 hours; alkaline phosphatase 7.5 Shinowara-Jones-Reinhart units; glutamine oxaloacetin transaminase 59 U. Rheumatoid factor negative. The agglutination test for Brucella is negative.
The tuberculin test was negative (5 TU) and positive at 10 TU. Cultures of the gastric aspirate showed no growth of mycobacteria. Pulmonary function tests showed no abnormalities. The chest radiograph was normal. X-rays of the knees showed mild bilateral osteoarthritis and early osteoporosis of the arms and legs. An abdominal radiograph showed calcification in the area of the remaining kidney.
A liver biopsy showed diffuse portal fibrosis. Some septa contained numerous lymphocytes and local accumulations of large monocytes with large cytoplasm and large nuclei. In the periportal area, a large granuloma was found, consisting of a compact mass of epithelioid and giant cells, with a small area of eosinophilic necrosis in the center. Staining did not show the presence of acid-fast organisms. The histological picture was compatible with granulomatous cirrhosis caused by sarcoidosis.
Our experience described in cases 1 and 2 and the association of psoriasis with joint symptoms suggested the possibility that this patient had gout and that the hepatomegaly was caused by sarcoidosis. Ultimately, although not previously considered, this diagnosis was later confirmed.
This patient's clinical history and hyperuricemia were compatible with gout. As in the other two cases, there was no family medical history. Gout rarely occurs in black women (5,6). It may be significant that gout appeared shortly after panhystrectomy, since the onset of gout in women typically occurs in postmenopausal women (7). It is possible that the two episodes of thrombophlebitis were also associated with gout, as such an association has been previously reported (8).
The diagnosis of sarcoidosis was based on the results of a liver biopsy and was supported by the presence of enlarged lacrimal glands, a history of uveitis, the patient's race, place of birth in a rural area of the Southeast, and the finding of hyperglobulinemia and hypercalcemia. It is possible that nephrolithiasis, which the patient developed during childhood, was also associated with sarcoidosis. Although granulomatous liver lesions leading to cirrhosis are unusual in sarcoidosis, one of the authors of this article (GK) previously reported a similar case (9) and observed several others.
This patient developed gout 3 years before psoriasis. Hepatomegaly, which was associated with sarcoidosis, was discovered only 2 years later. However, it is not known exactly when hepatomegaly developed, since abdominal examination has not previously been performed. The development of nephrolithiasis in childhood and the later discovery of mild hypercalcemia suggests that this patient may have had sarcoidosis since childhood. This assumption is compatible with a very long illness, since the degree of liver fibrosis, apparently of granulomatous origin, was significant.
To look for a possible connection between sarcoidosis, psoriasis and gout, we reviewed the medical records of patients previously hospitalized with each of these diseases. We reviewed 73 cases of histologically verified sarcoidosis and 100 randomly selected cases of psoriasis and gout. To look for signs of sarcoidosis in the latter two groups, special attention was paid to skin and eye involvement, size of lymph nodes, liver and spleen, chest X-ray findings, globulin, calcium and alkaline phosphatase levels and any episodes of ocular inflammation or salivary gland enlargement. In addition, 25 cases of sarcoidosis and 45 cases of psoriasis were retested for the presence of hyperuricemia using a modified Brown method for measuring serum uric acid concentrations (10). A concentration of more than 6.0 mg% in men and 5.0 mg% in women was considered pathological.
Sarcoidosis. None of the 73 patients with sarcoidosis had psoriasis or features of classic gout. However, 6 of the 25 patients whose blood uric acid levels were measured definitely had hyperuricemia. Only one of these patients had azotemia. Another patient had hypercalcemia but renal function was normal. Consequently, 20% of patients in this group had an unexplained increase in serum uric acid levels, which is significantly higher than previously reported for individuals without gout (7,11).
Migrating pain, often accompanied by joint swelling, was observed in 9 of 73 patients. Two of them had hyperuricemia, but articular manifestations were not characteristic of gout. One of these patients tested positive for rheumatoid arthritis with sheep red blood cells, while in the remaining patients the joint symptoms were interpreted as manifestations of sarcoidosis.
Psoriasis. When reviewing 100 case reports of patients with psoriasis, we found no cases of coexistence of sarcoidosis and gout. However, there was some evidence of sarcoidosis in a few patients. 16 patients from this group had arthritis. Although its manifestations were not typical of gout, in one patient the arthritis was accompanied by hyperuricemia of 6.8 mg% and in another patient the arthritis initially developed in the big toe. Although other joints subsequently developed involvement, serum uric acid levels were normal. 10 of the remaining 14 patients with joint symptoms had classic rheumatoid arthritis. Although no patient was diagnosed with sarcoidosis, 11 patients had radiographic evidence of unexplained pulmonary fibrosis, significant hyperglobulinemia, hepatomegaly, and/or splenomegaly.
Of particular interest was a patient who had psoriasis, mild hyperuricemia, pulmonary fibrosis, recurrent corneal ulcers, and significant hyperglobulinemia (5.08 gm%). In two cases, patients had small granulomas in the liver on needle biopsy. Sarcoidosis was considered as a differential diagnosis, but in the pathologist's opinion, the granulomas were too small to make a specific diagnosis. Liver biopsies in 3 other patients with hepatomegaly showed no granulomas. In other cases of hepatomegaly, hyperglobulinemia, or pulmonary fibrosis, the possibility of sarcoidosis was not considered and therefore not investigated.
18 of 47 psoriasis patients whose blood uric acid levels were measured had hyperuricemia. Renal function was impaired in 2 patients, was not studied in 5 patients, and was normal in the rest. Thus, at least 20% of patients in this group had unexplained hyperuricemia.
Gout. None of the 100 cases of gout had skin lesions suggestive of sarcoidosis or psoriasis. However, 2 patients had pulmonary fibrosis and one had hypercalcemia of unknown cause. Because these two patients did not have any evidence of sarcoidosis, this diagnosis was not considered during hospitalization and, therefore, was not excluded by appropriate studies.
Although we found no reports in the literature of the coexistence of sarcoidosis, psoriasis, and gout, other combinations of these diseases have been reported, including sarcoidosis and psoriasis, sarcoidosis and gout, and psoriasis and gout.
Sarcoidosis and psoriasis. Classic sarcoid skin lesions are easily differentiated from psoriasis based on their appearance, distribution, and histologic features. However, in the monograph by Longcope and Freiman (12), which described a form of cutaneous sarcoidosis resembling psoriasis, the authors' own observation was described and another patient was described by Combes (18). Although none of these patients had sarcoid granulomas in the skin, the possibility of coexistence of sarcoidosis and psoriasis cannot be definitively excluded. A literature search for cases of similar skin lesions in which typical sarcoid granulomas were found was unsuccessful. However, we found one case of coexistence of sarcoidosis and psoriasis (14). Whether the small number of reports of the combination of sarcoidosis and psoriasis truly reflects the rarity of this combination, or whether authors writing on sarcoidosis do not consider it necessary to report the occurrence of two apparently unrelated conditions in their patients, remains unclear.
Conjunctivitis, corneal ulcers, and iritis, which are known to occur in psoriasis (17), are very similar to the ophthalmic complications of sarcoidosis. However, the lack of evidence of sarcoidosis in these patients and the fact that these lesions were not granulomatous in nature (17) make it highly unlikely that the ocular lesions of these two diseases share a common pathogenesis. Lorincz (18) believes that psoriasis may be a hereditarily determined skin reaction that can be caused by a variety of etiological factors. Therefore, if an association between psoriasis and sarcoidosis does exist, it is possible that psoriasis may serve as a nonspecific stimulus for the development of sarcoidosis. A similar situation is associated with the well-known association between sarcoidosis and erythema nodosum (19), which is not granulomatous in nature and is not specifically associated with sarcoidosis.
An alternative possibility is that psoriasis may cause sarcoidosis. It also cannot be ruled out that both of these diseases are associated with the same etiological factor.
Sarcoidosis and gout. Apart from the two cases reported by Hutchinson (1,2), only one similar case is known (20), which was reported in a review of 90 cases of sarcoidosis associated with arthritis. There are very few reports of hyperuricemia in sarcoidosis (21, 22, 23). However, with the exception of our study, blood uric acid concentrations have not been measured in a large cohort of patients with sarcoidosis. Indeed, even in cases of sarcoidosis and arthritis, uric acid concentrations were measured in only two cases (24,25). It is generally accepted that the transient and migratory nature of articular symptoms (4,25–29) and the presence of granulomatous lesions in the synovial membranes of patients with sarcoidosis are inconsistent with the diagnosis of gout. However, given the fact that arthritis may be limited to a single joint (4, 26–29) and that radiographic bone changes in sarcoidosis and gout may be indistinguishable (12), it is possible that if the possibility of gout were investigated more frequently, the incidence of co-occurrence of sarcoidosis and gout would be higher than is currently believed.
Patients with gout are known to experience a variety of ocular inflammatory lesions, including uveitis and chorioretinitis (31–33). Although similar to the ophthalmic manifestations of sarcoidosis, they are associated with urate deposits rather than a granulomatous reaction.
Since gout is a fairly common disease, the few cases of its coexistence with sarcoidosis cannot be considered as adequate evidence of a connection between these diseases. However, we found hyperuricemia in 20% of 73 patients with sarcoidosis. One possibility that needs to be considered is that hyperuricemia is a consequence of impaired renal function, which in patients with sarcoidosis is a consequence of hypercalcemia (34) or granulomatous renal disease (35). This possibility seems unlikely since all but one of the patients with hyperuricemia had normal renal function. Only one of these patients had hypercalcemia, probably with mild deterioration of tubular function.
An alternative possibility is that, similar to that noted in leukemia, hyperuricemia occurs due to increased purine metabolism associated with the proliferation of reticuloendothelial cells from which sarcoid granulomas arise.
Psoriasis and gout. Of all the possible combinations of sarcoidosis, psoriasis and gout, only the combination of psoriasis and gout is reported quite often. In a group of 520 patients with gout (36), psoriasis was found in 4.0% of patients, which is significantly higher than the population average (0.27–1.4%) (37, 38). Although these data suggest an association between psoriasis and gout, the specificity of this association is questionable since the incidence of psoriasis was similarly high in rheumatoid arthritis and osteoarthritis (39).
There are no data regarding the incidence of gout in psoriasis. However, hyperuricemia was found in 35% of a group of 307 patients with psoriasis by two groups of researchers (40, 41). Our own observations support these results, but another study (42) with a smaller number of patients reached the opposite conclusion.
Because these data suggest that the incidence of hyperuricemia in psoriasis may be as high as 35%, it is unlikely that it is due to a single cause, such as undetected renal failure or the use of medications that can increase blood uric acid levels (43–46). One possibility that deserves consideration is that, similar to that noted in leukemia, hyperuricemia occurs due to increased purine metabolism associated with the accelerated proliferation of epidermal cells that occurs in psoriasis (18). The fact that there is no correlation between blood uric acid concentrations and the severity of psoriatic lesions would seem to contradict this hypothesis. However, a similar discrepancy may be seen in leukemia, where the concentration of uric acid does not necessarily change in parallel with the number of leukocytes in the peripheral blood.
The above data suggest a possible relationship between sarcoidosis, psoriasis and gout, but do not resolve the question of whether their coexistence was coincidental or a consequence of the interaction of these diseases. Because of the significant differences in pathogenesis, morphological features, and timing of onset, it is unlikely that all three diseases were initiated or accelerated by a single stimulus. The alternative possibility that one of the diseases caused the others seems more reasonable in view of the relationships between these conditions discussed above. The fact that these three diseases occurred in a different sequence in each of the patients (psoriasis, gout and sarcoidosis in case 1; sarcoidosis, gout and psoriasis in case 2; gout, psoriasis and sarcoidosis in case 3) at first glance contradicts this hypothesis. However, as stated above, it was impossible to determine the exact time of onset of sarcoidosis or hyperuricemia, so the exact sequence of events was, strictly speaking, unknown. A careful search for signs of sarcoidosis, psoriasis and gout in patients with these diseases will determine whether there really is a connection between these diseases.
Any joint disease is a serious pathology that requires timely treatment. After all, such diseases cause pain to the patient, disrupt the motor activity of the affected joint and make the patient incapacitated for a long time.
One of the most severe joint pathologies is gout. This disease has a number of characteristic symptoms and requires timely treatment. An advanced form of gout usually leads to disability, so at the first symptoms of the disease you should immediately consult a doctor and get tested.
It is important to know that gout is a disease during which, for some reason, uric acid salts accumulate in the joints and kidneys. This pathology is called the disease of kings, as it occurs with heavy consumption of alcohol and meat. And such products in the past were available only to the rich. The peasants ate mainly vegetables.
True gout occurs very rarely; approximately 4 people out of 1000 suffer from it; in other cases, problems with the joint are associated with another cause. Most often, the disease is detected in mature men, up to about 45 years of age, less often in women during menopause and after it.
At a young age from 25 to 30 years, the disease rarely develops, mainly in men who lead a wild lifestyle. It is worth noting that in recent years the incidence of gout at the age of 30 has increased significantly, and in ancient times only mature and elderly people suffered from the pathology.
A distinctive feature of gout is that the disease affects all joints of the body. First, small joints on the hands and feet are affected, then the disease spreads and affects all large ones, for example, the knees and hips.
What gout is is now clear, and the cause of the pathology is a metabolic disorder in which the level of uric acid increases and remains at this level for a long time. Uric acid salts (urate crystals) begin to settle on the joints and gradually destroy them, causing the patient severe pain.
Disturbances in the body can occur due to hormonal imbalance or hereditary predisposition, but the impetus for the disease is given by an incorrect lifestyle. So people prone to gout who lead a healthy lifestyle will most likely never get sick.
Excess weight, alcoholism, and uncontrolled use of diuretics contribute to the development of the disease. Often the trigger for the onset of attacks is an injury, the joint is damaged, and at the site of the injury, urate crystals begin to be deposited in larger quantities, this leads to the rapid destruction of cartilage tissue.
Eating meat in very large quantities, especially fatty meat, causes gout. Red meat provokes an increase in uric acid in the blood; normally, the level decreases over time, but this does not happen with constant overeating.
This does not mean that you need to completely give up eating meat products. Animal proteins and fats are needed by the human body to function normally. The most important thing is that there should be moderation in everything; you should not overuse your favorite foods.
Gout is a disease whose symptoms do not appear for a long time. For many years, the level of uric acid in the body may be elevated, and urate is deposited in the joints. The disease occurs suddenly. This condition is called a gout attack. Signs of an attack:
As a rule, an attack of gout occurs abruptly and also passes abruptly; it usually lasts from 3 to 10 days.
Only a doctor can identify signs of gout and prescribe treatment, and solely on the basis of tests that can reveal elevated levels of uric acid and the presence of urate crystals in the joints. It is impossible to make a diagnosis on your own, since gout can be similar to an exacerbation of arthritis, arthrosis and other inflammatory and degenerative joint disorders.
To confirm the diagnosis, the following studies and tests are prescribed:
It is important to note that elevated uric acid levels do not always indicate the presence of gout. Therefore, doctors are not always in a hurry to make such a rare diagnosis and prescribe appropriate treatment. Treatment is often prescribed for other joint pathologies, but gout progresses.
Therefore, every patient with joint pain should become familiar with the symptoms of gout, and if there is a suspicion that it is gout, and the attending physician does not agree, it is best to consult other doctors and be examined again. It is worth understanding that doctors are people too, and they can make mistakes, and a person’s health is primarily in his hands.
Gout is considered an incurable disease, since it is very difficult to identify it in the early stages, and if gout attacks occur, the joints are already destroyed. It is worth noting that even during the period between attacks, the deposition of salts and the destruction of cartilage continues, so it is not recommended to delay going to the doctor.
Treatment of gout usually begins with pain relief, since patients go to the doctor during an attack, without anything bothering them before. If there is severe pain in the joint, then the first thing you need to do is call an ambulance, which will send the patient to the hospital where he will be treated, otherwise he will have to suffer from severe pain for a week.
You can alleviate the condition in the following ways:
Obviously, the hospital will help you get rid of the pain faster and prescribe treatment so as not to provoke a new relapse. Self-medication will not bring quick relief, and the risk of relapse will increase several times, so if you have joint pain, you should immediately go to the hospital.
If during a gout attack, doctors first prescribe medications to relieve pain and swelling, then subsequent treatment consists of normalizing metabolism. The patient is prescribed a diet, medications to reduce uric acid levels, and agents to restore cartilage tissue.
Any medications must be prescribed and selected by a doctor; this is very important, since potent drugs are used in the treatment of gout. Uncontrolled use of such drugs can cause disruption of the liver, kidneys, heart and gastrointestinal tract and significantly shorten the patient’s life.
The following medications are prescribed to treat gout:
As a rule, drug treatment will not completely stop the process of joint destruction, but by constantly monitoring uric acid levels, damage to other joints and the occurrence of new attacks can be avoided. Therefore, it is necessary to undergo treatment for a long time, and the sooner therapy begins, the better the prognosis for the patient.
During the period of remission, the patient must lead an active lifestyle, eat right, engage in physical therapy and take medications as prescribed by the doctor. The main mistake of patients is their refusal of treatment as soon as the attacks pass, because of this fatal complications arise.
You cannot self-medicate for gout; this will certainly lead to complications. But in complex treatment, folk remedies can be very effective; the main thing is to take proven recipes and apply them according to all the rules and after consulting a doctor.
It is important to note that before using any product you need to make sure that there is no intolerance to its components. Lotions and ointments can be used only if there is no violation of the integrity of the skin at the site of exposure. It is also not recommended to mix folk remedies with pharmaceutical ointments; this can lead to an allergic reaction or chemical burn.
The following folk remedies are effective for gout:
Gout treatment cannot be effective if a person does not follow a diet. Nutrition should be correct, low-fat, balanced, tasty and healthy. It is necessary to eat often and in small portions, which is especially important for patients with large weight due to overeating. Eating small portions will help reduce the volume of the stomach, as a result of which a person will eat less and lose weight.
The following foods are prohibited for gout:
You are allowed to eat vegetables and fruits, cereals and dairy products, berries, and walnuts. The amount of meat and fish should be greatly limited; you can consume 150 grams 3 times a week during the period of remission. You need to cook yourself from natural and fresh products; it is better to avoid frying food in oil and fat, and steam, boil and bake food in foil.
If you have gout, it is important to drink a normal amount of water. Alkaline water is very useful, as it allows you to quickly remove purines from the body. Essentuki No. 4 and No. 17, Narzan and Borjomi are recommended for consumption. It is very important to buy water from trusted stores, and you should not buy suspiciously cheap water; counterfeit water will be of no use.
Gout can be cured completely only if it is detected at the initial stage, when the joints have not yet begun to actively deteriorate. But this happens extremely rarely, since nothing bothers the patient, and the increased acid level is not a 100% gout attack.
If the patient consulted a doctor at the first attack, began to receive responsible treatment and changed his lifestyle, then they speak of a favorable prognosis. In this case, attacks do not occur, the joints stop rapidly deteriorating, and the patient can live a normal life.
If a patient has been self-medicating for a long time and consults a doctor at an advanced stage, then returning to normal life is usually out of the question, since deposits over time affect not only the joint, but also the kidneys and other internal organs, and cause serious complications:
All these diagnoses are very serious, they occur in 80% of cases, sometimes separately, sometimes together, several diagnoses at once. Any disease from the list shortens the years of a person’s life, and if left untreated, leads to rapid death. Complications can only be prevented by a person’s responsible attitude towards their health and compliance with all doctor’s recommendations.
In the modern world, when joint diseases have spread among young people, special attention needs to be paid to the quality prevention of gout and other pathologies. In general, prevention of joint diseases consists of a healthy lifestyle.
To avoid getting gout, you need to follow these recommendations:
Psoriasis (scaly lichen) is a chronic relapsing skin disease.
Disorders of the nervous and endocrine systems, metabolism (especially the metabolism of amino acids - the main building material for cells, fat and carbohydrate metabolism), hereditary factor.
Pink-red nodules with a tendency to merge into plaques, covered with silvery-white, easily exfoliating scales; localization mainly on the elbows, knees, lower back, and scalp.
Psoriasis is a disease that requires long-term treatment; passes with remissions of several months or years and continues until the end of life. Pharmacotherapy for psoriasis depends on the stage of the disease:
1. During the progressive period, the following is prescribed:
2. In the hospital period (during the main manifestations of the disease) the following is prescribed:
3. During the period of symptom reduction, the following are also used:
4. To prevent relapses of psoriasis, it is recommended:
A predominantly plant-based diet with limited animal fats and carbohydrates is recommended, including butter, eggs, sugar, potatoes, white bread, refined and processed foods, all seasonings, tea, coffee. When the condition improves, you can add milk, kefir, and cheese to your diet. It is very useful to drink whey (in unlimited quantities). Alcohol abuse causes an exacerbation of the disease.
When the skin gradually begins to look normal, the second stage of treatment begins. But the composition of the ointment changes. Now it should include 5-5.5 parts of fresh egg white, 2-2.5 parts of flower bee honey, 1.5-2 parts of baby cream, 1-1.3 parts of celandine powder, solid oil.
With the beginning of the third stage of treatment, you stop taking Aralia tincture, and after two weeks it’s time to take Eleutherococcus extract, which is also taken 3 times a day, half an hour before meals.
During treatment, it is recommended to exclude eggs, fatty meat and spicy foods from the menu. In May-June, collect thistles, rinse, dry and mince - moisten the sore spots with the squeezed juice. Thistle juice is a proven remedy.